what stages of the cell cycle do the nucleus and its content divide

. The typical cell has a cell cycle of roughly 24 hours. The whole process is divided into three major stages: mitosis orkaryokinesis (the division of the nucleus),cytokinesis (the division of the cytoplasm), andinterphase (the period during which DNA replication as well as the growth of the cell occur)

Chapter 8: The Cell Cycle

"Online Tutoring Archive Biology Chapter 8: The Cell Cycle Chapter 8: The Cell Cycle Learning Objectives:1. To become familiar with the balance between cell division and cell death2. To examine the phases of the cell cycle3. To become familiar with the overall regulation of the cell cycle4. To understand the significance of cell death5. To become familiar with mitosis and cancer Key Concepts:1. The development and continued existence of an animal (and perhaps other organisms) relfects a balance between cell division (mitosis) and cell death (apoptosis).2. A cell has choices: It may divide, specialize but not divide, repair damage, or die. The cell cycle describes the functional stages of a cell's existence.3. Biochemical checkpoints--a clock provided by shortening chromosome tips, and signals from outside and inside the cell regulate the cell cycle. Stem cells maintain the growth and specialization of a tissue.4. Cells that perish as a normal part of the life of an organism exhibit a characteristic choreography, almost a dance of death.5. Cancer is a derangement in cell cycle control. A cancer cell lacks a mitotic ""brake"" and has other characteristic features. Mutations, sometimes triggered by environmental factors, cause cancer. Chapter Concept 8.1: The Balance Between Cell Division and Cell Death The development and continued existence of an animal (and perhaps other organisms) relfects a balance between cell division (mitosis) and cell death (apoptosis). Textbook Reading Assignment: Pages 138 - 139Cells are the basis of life. They pass on their life history to their descendents through their genetic material. Each newly made cell contains a copy of the genetic information inherited from its parents as well as the necessary machinery needed to support the cell, such as organelles, membranes, small molecules, and macromolecules. Cell division accomplishes different tasks in single-celled and multicellular organisms. In single-celled organisms, cell division by mitosis creates new organisms that are clones of the original. In multicellular organisms, cell division by mitosis allows the organism to produce new cells for growth and replacement of dying cells. As indicated in the text, cell division and cell death are carefully balanced within multicellular organisms. Cell death ( apoptosis) is a normal part of development and, as discussed in the text, is used to carve distinctive structures such as toes and fingers. This chapter will introduce you to the mechanisms associated with both mitosis and apoptosis and conclude with a discussion of what happens when mitosis continues uncontrolled: cancer. Chapter Concept 8.2: The Cell Cycle A cell has choices: It may divide, specialize but not divide, repair damage, or die. The cell cycle describes the functional stages of a cell's existence. Textbook Reading Assignment: Pages 139 - 145Mitosis is just one stage in the life of the cell. The cell cycle includes everything that happens to a cell from its formation until it finishes its own division. For most of us, our bodies have reached some level of maturity, and many of our cells are no longer actively dividing. The idea of the basic cell cycle would best describe the life of a cell in a ten-year-old girl or boy who is still actively growing

Notice from the figure above (Figure 8.2) that cytokinesis occurs at the end of mitosis. Also notice from the same figure that interphase occupies most of the cell cycle. Since the ultimate fate of most cells is to eventually divide, interphase can be viewed as the period in which the cell is actively preparing to divide. Interphase is divided into three stages: G 1, S, and G 2. The cell begins as a new cell at the end of cytokinesis. It is in G 1, a growth phase. The cell that is going to divide (not all cells do) will pass through G 1 and enter the S stage. The S stage represents the period of time in which DNA synthesis occurs when the cell duplicates its DNA. G 2 is the final stage of the cell cycle in which the cell prepares to begin mitosis. The timing of the cell cycle is an important issue to consider. For example, how do cells know when to begin the cell cycle? How do they know when to stop? If cell division continued without stopping, single-celled organisms would soon outnumber their food supply. Multicellular organisms normally control cell growth. They tend to divide rapidly during periods of growth and slow down division once mature. How do cells do this? In order to prevent daughter cells from becoming smaller in each generation, most cells divide only after they have doubled their mass. Although the mechanisms behind how cells coordinate this are unclear, it has been demonstrated that a “go or no go” point exists at the end of G 1 of interphase, sometimes referred to as the G 0 phase. Once the cell reaches this “point of no return,” the cell must divide. Arrival at the start point depends upon nutrient availability, specialized proteins and signals from adjacent cells. At the beginning of mitosis the DNA wraps itself around specialized proteins to formchromosomes. Web Activity Use this link to see a model of specialized proteins and DNA which interact to form chromosomes. :http://www.cas.muohio.edu/~wilsonkg/bot203/W_and_C/basic_proteins/histone/histone.htm Chromosomes were first discovered during the 19 th century, yet no one knew their exact function at the time. Today, we know that chromosomes contain the genetic information ( chromatin —a tangled mass of DNA) responsible for the overall function of the cell. During the process of mitosis, each parent cell divides and provides a duplicate copy of its genetic information (DNA) to each of the new daughter cells formed. In other words, parental chromosomes are equally divided and distributed to each of the new cells during mitosis. Chromosomes can be of either the “one-legged” or “two-legged” variety. In a normal cell, chromosomes appear as long strands, like very thin spaghetti noodles. When a cell prepares to divide, however, the single strand duplicates itself, becoming a two-stranded chromosome. Each half of a two-stranded chromosome is termed a chromatid. Notice from the link below (and the image above - Figure 8.4) that the two chromatid halves are held together by a centromere. Here are two web links that will give you some idea about the basic structure of chromosomes. The first is at Colorado State University and the second is at Northwestern University:http://arbl.cvmbs.colostate.edu/hbooks/genetics/medgen/chromo/chromosomes.htmlhttp://www.cancergenetics.org/chrm-str.htm From looking at the two sister chromatids, you can see that they are identical to each other. The only reason for their formation is to allow them to separate during mitosis, with one going to one new cell, and the other going to the second new cell. In this way, each daughter cell receives the exact same genetic information. This section of the chapter focuses on the overall processes involved with the formation and eventual separation of chromatids during the process of mitosis. As indicated above, the goal of mitosis is to duplicate each of the chromosomes and separate the duplicated halves equally into the daughter cells. Such a situation provides the parent cell the ability to allocate identical copies of its DNA to each of the two daughter cells. Once the cell enters the M phase of the Cell Cycle, the chromosomes become visible and align themselves in the center of the cell. The individual chromatids then separate and move to the poles of the cell. In so doing, the genetic material found in the original chromosome is duplicated and shared with each of the new daughter cells. These events occur in four distinct steps or phases. The images below represent the four stages of mitosis (prophase, metaphase, anaphase and telophase). Keep in mind that mitosis is actually a continuous process, and the boundaries between these steps are somewhat vague. Nonetheless, we can still study what occurs during each of the four steps of mitosis. PLEASE REMEMBER: The overall goal of mitosis is to separate the duplicated halves of each chromosome (the sister chromatids) into the daughter cells. The first stage of mitosis is termedprophase. During prophase, the chromosomes appear, each consisting of two sister chromatids joined at the centromere. In order to split the sister chromatids of each chromosome efficiently, the physical position of the chromosomes must be manipulated during the process of cell division. In order to do so, themitotic spindle (also termed thespindle apparatus) forms during prophase. The mitotic spindle, demonstrated in Figure 8.5 below, consists of small fibers termed microtubules that are composed of protein. In animal cells, the microtubules attach at opposite ends of the cell to the centrioles (component of the centrosome / aster). The aster is an array of short microtubules associated with the centriole. Notice from the image below that the other end of each microtubule attaches to the kinetochore associated with the centromere of each chromosome. Altogether, the mitotic spindle can manipulate the physical location of each chromosome by lengthening or shortening microtubules. The second stage of mitosis is termed metaphase ( don't worry about the distinction made between metaphase and prometaphase made in the text). During metaphase, the microtubules of the spindle apparatus move each chromosome halfway between the two poles of the cell. The third stage of mitosis is anaphase. During anaphase, the sister chromatids separate into individual chromosomes and move toward opposite poles of the cell (refer to Figure 8.7 of text). The process of separating sister chromatids is termed karyokinesis. Anaphase is followed by the actual division of the cell into two new daughter cells. This final stage of mitosis is termed telophase. By the end of telophase, the mitotic spindle disappears, and the chromosomes uncoil to again form chromatin. The division of the cytoplasm, cytokinesis, usually follows mitosis. While mitosis is responsible for separating sister chromatids from one another, cytokinesis is responsible for separating the dividing cell into two new daughter cells. In animal cells, cytokinesis is performed with the use of acontractile ring. The contractile ring consists of protein wrapped around the dividing cell. As the proteins in the ring contract, they pinch the cell into two parts at the equator of the cell. Such a situation creates a deep groove termed thecleavage furrow. As cytokinesis continues, the cleavage furrow enlarges until two new cells are formed. Cytokinesis in plant cells differs from that in animal cells due to the presence of cell walls that prevent the pinching action observed in animal cells. As a result, cytokinesis in plant cells requires the construction of a new cell wall between the two daughter cells. The new wall begins as a flattened disk termed the cell plate, which eventually forms a true cell wall that separates the daughter cells from each other. Web Activity To see some photomicrographs of plant and animal cells in the various stages of actual mitosis and to do a self-test on recognition of these stages, use this link to a site at Cornell University: http://biog-101-104.bio.cornell.edu/Bio G101_104/tutorials/cell_division.html Use the following Web sites to review and study the information provided in this learning objective:www.biog-101-104.bio.cornell.edu/Bio G101_104/tutorials/cell_division.htmlwww.biology.arizona.edu/cell_bio/tutorials/cell_cycle/cells2.html Discussion Questions 1 and 2Why must the cell duplicate its DNA before it enters the M phase of the cell cycle? Diagram each stage of mitosis using three pairs of homologous chromosomes. What might happen if cells underwent mitosis without completing cytokinesis? Chapter Concept 8.3: Cell Cycle Control Biochemical checkpoints--a clock provided by shortening chromosome tips, and signals from outside and inside the cell regulate the cell cycle. Stem cells maintain the growth and specialization of a tissue. Textbook Reading Assignment: Pages 145 - 150As indicated in the text and in Figure 8.10 below, the cell cycle has several checkpoints that regulate the ""pace"" of the cell cycle. While we certainly are far from a complete understanding of how the cell cycle is regulated, we do know that telomeres (specialized chromosome tips) are important in overall regulation. Telomeres are composed of a repeated six base sequence that are lost during cell division. As indicated in the text, this means that chromosomes SHORTEN each time they divide. Interstingly enough, after 50 divisions of the cell the telomeres have been reduced in number to a point when they signal cell division to cease. Of course there are some exceptions, such as blood cells, bone marrow cells and cancerous cells as discussed in the text. The mechanism of telomere shortening is dependent upon the presence or absence oftelomerase, which functions to add DNA to the chromosome tips. Cells lacking telomerase activity divide about 50 times, those with high levels of the enzyme (sperm cells, cancer cells, etc.) can divide hundreds of times since their telomeres never shorten. While we have briefly covered what causes cells to stop division, we need to address the question as to what signals cells to divide. Biologists have discovered that cell division is stimulated and regulated by a variety of processes including:1) contact inhibition and hormonal control2) cyclin and kinase control3) control at the tissue level-- stem cells and cell populations. Contact inhibition--normal cells grow in culture until the formation of a monolayer. Once the cells touch each other and form a complete layer, cell division ceases. One of the problems with cancerous cells is their traditional lack of contact inhibition (refer to Figure 8.12 below). Various hormonal control factors regulate the cell cycle as well--familiarize yourself with these on pages 147 - 149 of the text. Both kinases and cyclins are involved in the regulation of the cell cycle. A kinase removes a phosphate from ATP and adds it to another protein. Kinases themselves, are activated by a protein called cyclin whose concentration varies throughout the cell cycle. Notice from Figure 8.13 below that the move from G 1 to S is initiated when S-kinase combines with S-cyclin. In addition, the move from G 2 to S is initiated when M-kinase binds with M-cyclin. According to the figure, cyclin concentrations increase at G 1 and G 2 only to decrease at S and M (mitosis). Stem cell regulation is an interesting phenomenon. Stem cells are capable of producing specialized cells throughout the body. When a stem cell divides to form two new daughter cells, one specializes (to form a skin cell for example) while the other remains a stem cell--ready to divide again. As a result, skin cells can be replaced without having to divide themselves. Note from the last section of this Learning Objective that some cells are post-mitotic, meaning they never divide. Brain cells and muscle cells are traditional examples of these. This explains why it takes so long (if ever) to overcome muscle and brain/spinal cord injuries. Chapter Concept 8.4: Cell Death Is a Part of Life Cells that perish as a normal part of the life of an organism exhibit a characteristic choreography, almost a dance of death. Textbook Reading Assignment: Pages 150 - 152The process of apoptosis (refer to Figure 8.15 below) is traditionally thought of as ""programmed cell death"". For example, cells located between the toes of a rooster are programmed to die during development yielding individual free toes. A lack of apoptosis during duck development results in webbed toes. As you can see, cell death should not be thought of as always being a ""negative"" process. The text does a wonderful job of discussing the mechanisms involved in the process of apoptosis on page 150. Make certain you are familiar with the following:death receptorthe function of caspasesblebs As indicated on pages 150-152, apoptosis is important in regulating neuronal activity (as in the case of NGF), fine tunes the immune system and helps in self-nonself regognition, and to detect and destroy cells that could grow uncontrollably (such as cancerous cells). At times abnormal apoptosis can affect the overall health of individuals. For example, too little apoptosis causes autoimmune disorders, cardiovascular disease, Alzheimer's disease and liver failure. Chapter Concept 8.5: Cancer--When the Cell Cycle Goes Awry Cancer is a derangement in cell cycle control. A cancer cell lacks a mitotic ""brake"" and has other characteristic features. Mutations, sometimes triggered by environmental factors, cause cancer. Textbook Reading Assignment: Pages 152 - 154Cancer is caused by a series of genetic mutations leading to the development of a tumor (an abnormal mass of cells). Cancer cells differ from normal cells in a number of ways:1. cancer cells lack differentiation and do not contribute to the overall functioning of the body.2. cancer cells repeatedly go through the cell cycle and, essentially, never die…they continue to grow uncontrollably.3. cancer cells have abnormal nuclei with mutated chromosomes. Ordinarily, cells with mutated DNA such as this undergo apoptosis and die…not cancer cells.4. cancer cells form tumors. Since cancer cells grow in an uncontrolled fashion, they continue to divide over and over again forming large masses of cells.5. cancer tumors can either be benign or malignant. Benign tumors are enclosed within a capsule and do not invade healthy tissue. Malignant tumors, on the other hand, spread throughout the body via metastasis and invade and destroy healthy tissue. Please review Table 8.3 of the text (page 153) to review the characteristics of cancer cells. In addition, make sure you understand the difference between oncogenes and tumor-suppressor genes on the regulation of the cell cycle (pages 153 - 154). Self Test1. ________ are threads of DNA and protein that carry the genetic information.a. Nuclear poresb. Histonesc. Chromosomesd. Microtubules2. Which of the following demonstrates an animal cell during anaphase (karyokinesis)?3. Which of the following is NOT a function of apoptosis?a. to elimate excess cells to carve out a functional structureb. to aid in ""self-nonself"" recognitionc. to destroy cells that could possibly grow uncontrollablyd. All of the above are functions of apoptosis.4. Interphase consists ofa. G 1b. G 2c. Sd. Interphase consists of all the above.5. What occurs during the S phase of interphase?a. growthb. mitosisc. DNA synthesisd. cytokinesis6. The goal of mitosis is to create identical daughter cells by separating ___________.a. sister chromatidsb. homologous chromosomesc. microtubulesd. cytoplasm7. The centromere attaches _____________ together.a. homologous chromosomesb. adjacent cellsc. adjacent nucleid. sister chromatids8. What is responsible for the movement of chromosomes during mitosis?a. cytoplasmb. the mitotic spindlec. the cell plated. homologous chromosomes9. During what stage of mitosis does the process of cytokinesis occur?a. prophaseb. metaphasec. anaphased. telophase10. In animal cells, a __________ forms during cytokinesis, while in plant cells a ________ forms.a. nucleus, cell wallb. cell plate, nucleusc. cleavage furrow, nucleusd. cleavage furrow, cell plate Answers to Self-Test Questions1. c2. c3. d4. d5. c6. a7. d8. b9. d10. d Answers/Insight into Discussion Questions1. If the DNA were not duplicated before cell division, the amount of DNA in the daughter cells would be cut in half each generation.2. This first part you can do by referring to Figure 8.7. Notice that the text goes through each stage of mitosis with two pairs of homologous chromosomes. All you need to do is add a third. The second part of this question is interesting. If the cell underwent mitosis without dividing the cytoplasm, you would end up with a single cell with multiple nuclei. "


does schizophrenia cause hallucinations

dit]In the case of psychotic patients the premier cause of auditory hallucinations is schizophrenia. In schizophrenia, patients show a consistent increase in activity of the thalamic and strietal subcortical nuclei, hypothalamus, and paralimbic regions; confirmed via PET scan and f MRI.

Auditory hallucination

"From Wikipedia, the free encyclopedianavigation search Paracusia Classification and external resources Specialty Psychiatry ICD - 10 R44.0ICD - 9-CM 780.1 [ edit on Wikidata]Neuropsychology Topics [show]Brain functions [show]People [show]Tests [show]Mind and brain portalv

t e A paracusia, or auditory hallucination, [1] is a form of hallucination that involves perceiving sounds without auditory stimulus.

A common form of auditory hallucination involves hearing one or more talking voices. This may be associated with psychotic disorders, and holds special significance in diagnosing these conditions. [2] However, individuals without any psychiatric disease whatsoever may hear voices. [3]There are three main categories into which the hearing of talking voices often fall: a person hearing a voice speak one's thoughts, a person hearing one or more voices arguing, or a person hearing a voice narrating his/her own actions. [4] These three categories do not account for all types of auditory hallucinations. Other types of auditory hallucination include exploding head syndrome and musical ear syndrome. In the latter, people will hear music playing in their mind, usually songs they are familiar with. This can be caused by: lesions on the brain stem (often resulting from a stroke ); also, sleep disorders such as narcolepsy, tumors, encephalitis, or abscesses. [5] This should be distinguished from the commonly experienced phenomenon of getting a song stuck in one's head. Reports have also mentioned that it is also possible to get musical hallucinations from listening to music for long periods of time. [6] Other reasons include hearing loss and epileptic activity. [7]In the past, the cause of auditory hallucinations has been attributed to cognitive suppression by way of executive function failure of the fronto-parietal sulcus. Newer research has found that they coincide with the left superior temporal gyrus, suggesting that they are better attributed to speech misrepresentations. [8] It is assumed through research that the neural pathways involved in normal speech perception and production, which are lateralized to the left temporal lobe, also underlie auditory hallucinations. [8] Auditory hallucinations correspond with spontaneous neural activity of the left temporal lobe, and the subsequent primary auditory cortex. The perception of auditory hallucinations correspond to the experience of actual external hearing, despite the absence of physical acoustic output . [9]Contents [ hide ]1 Famous examples2 Individual accounts3 History3.1 Ancient history3.1.1 Presentation3.1.2 Treatments3.2 Pre-modern3.2.1 Presentation3.2.2 Treatments4 Potential causes4.1 Schizophrenia4.2 Mood disorders and dementias4.3 Transient causes5 Diagnosis and treatments5.1 Pharmaceuticals5.2 Psychological therapies6 Non-conventional therapies7 Ongoing research7.1 Non-psychotic symptomology7.2 Methods7.3 Causes7.3.1 Internalization of the inner voice7.3.2 Disruption to internalization7.3.3 Re-expansion7.4 Treatments8 Affected Brain Regions9 See also10 References11 Further reading12 External links Famous examples [ edit]Robert Schumann, a famous music composer, spent the end of his life experiencing auditory hallucinations. Schumann’s diaries state that he suffered perpetually from imagining that he had the note A5 sounding in his ears. The musical hallucinations became increasingly complex. One night he claimed to have been visited by the ghost of Schubert and wrote down the music that he was hearing. Thereafter, he began making claims that he could hear an angelic choir singing to him. As his condition worsened, the angelic voices developed into demonic ones. [10]Brian Wilson, songwriter and co-founder of the Beach Boys, has schizoaffective disorder that presents itself in the form of disembodied voices. [11] They formed a major component of Bill Pohlad 's Love & Mercy (2014), a biographical film which depicts Wilson's hallucinations as a source of musical inspiration, [12] constructing songs that were partly designed to converse with them. [13] Wilson has said of the voices: ""Mostly [they're] derogatory. Some of it's cheerful. Most of it isn't."" [14] To combat them, his psychiatrist advised that he ""talk humorously to them"", which he says has helped ""a little bit"". [11]Individual accounts [ edit]The onset of delusional thinking is most often described as being gradual and insidious. Patients have described an interest in psychic phenomena progressing to increasingly unusual preoccupations and then to bizarre beliefs ""in which I believed wholeheartedly"". One author wrote of their hallucinations: ""they deceive, derange and force me into a world of crippling paranoia"". In many cases, the delusional beliefs could be seen as fairly rational explanations for abnormal experiences: ""I increasingly heard voices (which I'd always call ‘loud thoughts’)... I concluded that other people were putting these loud thoughts into my head"". [15] Some cases have been described as an ""auditory ransom note"". History [ edit]Ancient history [ edit]Presentation [ edit]The ancient world viewed hallucinations as it did most of the natural world - with awe and superstition. As such, it was viewed as either a gift or curse by God, or the gods (depending on the specific culture). During the reign of Tiberius (A. D. 14–37), a sailor named Thamus heard a voice that told him the God Pan was dead. The oracles of ancient Greece were known to experience auditory hallucinations while breathing in certain neurologically active vapors (such as the smoke from bay leaves), while the more pervasive delusions and symptomology were often viewed as possession by demonic forces as punishment for misdeeds. [10]Treatments [ edit]Treatment in the ancient world is ill documented, but there are some cases of therapeutics being used to attempt treatment, while the common treatment was sacrifice and prayer in an attempt to placate the gods. The Dark Ages saw the most horrific accounts where those with auditory hallucinations were subjected to trepanning or trial as a witch. [10] In other cases of extreme symptomatology individuals were seen as being reduced to animals by a curse, these individuals were either left on the streets or imprisoned in insane asylums. It was the latter response that eventually led to modern psychiatric hospitals. [16]Pre-modern [ edit]Presentation [ edit]Auditory hallucinations were rethought during the enlightenment. As a result, the predominant theory in the western world beginning in the late 18th century was that auditory hallucinations were the result of a disease in the brain (e.g. mania), and treated as such. [16]Treatments [ edit]There were no effective treatments for hallucinations at this time. Conventional thought was that clean food, water, and air would allow the body to heal itself ( Sanatorium ). Beginning in the 16th century Insane Asylums were first introduced in order to remove “the mad dogs” from the streets and left them chained to walls and living in their own filth. [16] These asylums acted as prisons until the late 18th century. This is when doctors began the attempt to treat patients. Often attending doctors would douse patients in cold water, starve them, or spin patients on a wheel. Soon, this gave way to brain specific treatments with the most famous examples including Lobotomies, shock therapy and branding the skull with hot iron. [16]Potential causes [ edit]In 2015 a small survey [17] reported voice hearing in persons with a wide variety of DSM-5 diagnoses, including: Bipolar disorder Borderline personality disorder Depression (mixed)Dissociative identity disorder Generalized anxiety disorder Major depression Obsessive compulsive disorder Post-traumatic stress disorder Psychosis (NOS)Schizoaffective disorder Schizophrenia However, numerous persons surveyed reported no diagnosis. In his popular 2012 book Hallucinations, neurologist Oliver Sacks describes voice hearing in patients with a wide variety of medical conditions, as well as his own personal experience of hearing voices. Schizophrenia [ e

[18] [19] Other research shows an enlargement of temporal white matter, frontal gray matter, and temporal gray matter volumes (those areas crucial to both inner and outer speech) when compared to control patients. [20] [21] This implies both functional and structural abnormalities in the brain, both of which may have a genetic component, can induce auditory hallucinations. [22]Auditory hallucinations attributed to an external source, rather than internal, are considered the defining factor for the diagnoses of schizophrenia. The voices hear are generally destructive and emotive, adding to the state of artificial reality and disorientation seen in psychotic patients. [8] The causal basis of hallucinations has been explored on the cellular receptor level. The glutamate hypothesis, proposed as possible cause for schizophrenia, may also have implications in auditory hallucinations, which are suspected to be triggered by altered gultamatergic transmission. [23]Studies using dichotic listening methods suggest that Schizophrenic patients have major deficits in the functioning of the left temporal lobe by showing that patients do not generally exhibit what is a functionally normal right ear advantage. [24] Inhibitory control of hallucinations in patients have been shown to involve failure of top-down regulation of resting-state networks and up-regulation of effort networks, further impeding normal cognitive functioning. [25]Mood disorders and dementias [ edit]Mood disorders have also been known to correlate with auditory hallucinations, but tend to be milder than their psychosis induced counterpart. Auditory hallucinations are a relatively common sequelae of Major Neurocognitive Disorders (formerly dementia) such as Alzheimer's disease. [26]Transient causes [ edit]Auditory hallucinations have been known to manifest as a result of intense stress, sleep deprivation, drug use, and errors in development of proper psychological processes. [ clarification needed] [27] Genetic correlation has been identified with auditory hallucinations, [28] but most work with non-psychotic causes of auditory hallucinations is still ongoing. [27] [29]High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon. [30]Diagnosis and treatments [ edit]Pharmaceuticals [ edit]The primary means of treating auditory hallucinations is antipsychotic medications which affect dopamine metabolism. If the primary diagnosis is a mood disorder (with psychotic features), adjunctive medications are often used (e.g., antidepressants or mood stabilizers). These medical approaches may allow the person to function normally but are not a cure as they do not eradicate the underlying thought disorder. [31]Psychological therapies [ edit]Cognitive-Behavioral Therapy has been shown to help decrease the frequency and distressfulness of auditory hallucinations, particularly when other psychotic symptoms were presenting. [32] Enhanced Supportive Therapy has been shown to reduce the frequency of auditory hallucinations, the violent resistance the patient displayed towards said hallucinations, and an overall decrease in the perceived malignancy of the hallucinations. [32] Other cognitive and behavioral therapies have been used with mixed success. [33] [34]Non-conventional therapies [ edit]Electroconvulsive therapy or ECT has been shown to reduce psychotic symptoms associated with schizophrenia [ citation needed], mania, and depression, and is often used in psychiatric hospitals. In recent years, repetitive transcranial magnetic stimulation (r TMS) has been studied as a biological method of treatment for auditory hallucinations. r TMS plays a role in altering neural activity over language cortical regions. Studies have shown that when r TMS is used as an adjunct to antipsychotic medication in treatment-resistant cases, the frequency and severity of auditory hallucinations can be reduced. [35]Another source of non-conventional techniques to cope with the voices are provided by the research and findings of the Hearing Voices Movement [36]Ongoing research [ edit]Non-psychotic symptomology [ edit]There is on-going research that supports the prevalence of auditory hallucinations, with a lack of other conventional psychotic symptoms (such as delusions, or paranoia), particularly in pre-pubertal children. [37] These studies indicate a remarkably high percentage of children (up to 14% of the population sampled [38]) experienced sounds or voices without any external cause, although ""sounds"" are not considered by psychiatrists to be examples of auditory hallucinations. Differentating actual auditory hallucinations from ""sounds"" or a normal internal dialogue is important since the latter phenomena are not indicative of mental illness. Methods [ edit]To explore the auditory hallucinations in schizophrenia, experimental neurocognitive use approaches such as dichotic listening, structural f MRI, and functional f MRI. Together, they allow insight into how the brain reacts to auditory stimulus, be it external or internal. Such methods allowed researchers to find a correlation between decreased gray matter of the left temporal lobe and difficulties in processing external sound stimulus in hallucinating patients. [8]Functional neuroimaging has shown increased blood and oxygen flow to speech related areas of the left temporal lobe, including Broca’s area and the thalamus. [8]Causes [ edit]The causes of auditory hallucinations are unclear. It is suspected that deficits in the left temporal lobe attribute that lead to spontaneous neural activity cause speech misrepresentations that account for auditory hallucinations. [8]Charles Fernyhough, of the University of Durham poses one theory among many but stands as a reasonable example of the literature. Given standing evidence towards involvement of the inner voice in auditory hallucinations, [39] he proposes two alternative hypotheses on the origins of auditory hallucinations in the non-psychotic. They both rely on an understanding of the internalization process of the inner voice. [27] [38] [40]Internalization of the inner voice [ edit]The internalization process of the inner voice is the process of creating an inner voice during early childhood, and can be separated into four distinct levels. [27] [38] [40]Level one (external dialogue) involves the capacity to maintain an external dialogue with another person, i.e. a toddler talking with their parent (s). Level two (private speech) involves the capacity to maintain a private external dialogue, as seen in children voicing the actions of play using dolls or other toys, or someone talking to themselves while repeating something they had written down. Level three (expanded inner speech) is the first internal level in speech. This involves the capacity to carry out internal monologues, as seen in reading to oneself, or going over a list silently. Level four (condensed inner speech) is the final level in the internalization process. It involves the capacity to think in terms of pure meaning without the need to put thoughts into words in order to grasp the meaning of the thought. Disruption to internalization [ edit]A disruption could occur during the normal process of internalizing one's inner voice, where the individual would not interpret their own voice as belonging to them; a problem that would be interpreted as level one to level four error. [27] [38] [40]Re-expansion [ edit]Alternatively, the disruption could occur during the process of re-externalizing one's inner voice, resulting in an apparent second voice that seems alien to the individual; a problem that would be interpreted as a level four to level one error. [27] [38] [40]Treatments [ edit]Psychopharmacological treatments include anti-psychotic medications. Psychology research shows that first step in treatment is for the patient to realize that the voices they hear are creation of their own mind. This realization is argued to allow patients to reclaim a measure of control over their lives. Some additional psychological interventions might allow for the process of controlling these phenomena of auditory hallucinations but more research is needed. [27]Affected Brain Regions [ edit]Left Temporal Lobe: processes semantics in speech and vision, includes primary auditory cortex [8]Broca's Area: speech and language comprehension [8]Superior Temporal Gyrus: contains primary auditory cortex [8]Primary Auditory Cortex: processes hearing and speech perception [8]Globus Pallidus: Regulation of voluntary movement [9]See also [ edit]Neuroscience portal Auditory imagery Earworm Hypnagogic hallucinations Intrusive thought Microwave auditory effect Speech synthesis Tinnitus References [ edit]^ ""Medical dictionary"".^ Yuhas, Daisy. ""Throughout History, Defining Schizophrenia Has Remained A challenge"". Scientific American Mind (March 2013). Retrieved 2 March 2013.^ Thompson, Andrea (September 15, 2006). ""Hearing Voices: Some People Like It"". Live Science.com. Archived from the original on 2 November 2006. Retrieved 2014-02-01.^ Semple, David. ""Oxford hand book of psychiatry"" Oxford press, 2005^ ""Rare Hallucinations Make Music In The Mind"". Science Daily.com. August 9, 2000. Archived from the original on 5 December 2006. Retrieved 2006-12-31.^ Young, Ken (July 27, 2005). ""IPod hallucinations face acid test"". Vnunet.com. Archived from the original on 2007-12-20. Retrieved 2008-04-10.^ Engmann, Birk; Reuter, Mike: Spontaneous perception of melodies – hallucination or epilepsy? Nervenheilkunde 2009 Apr 28: 217-221. ISSN 0722-1541^ a b c d e f g h i j Hugdahl K, Løberg E-M, Nygård M. Left Temporal Lobe Structural and Functional Abnormality Underlying Auditory Hallucinations in Schizophrenia. Frontiers in Neuroscience. 2009;3 (1):34-45. doi:10.3389/neuro.01.001.2009.^ a b Ikuta T, De Rosse P, Argyelan M, et al. Subcortical Modulation in Auditory Processing and Auditory Hallucinations. Behavioural brain research. 2015;295:78-81. doi:10.1016/j.bbr.2015.08.009.^ a b c Laqueur, Thomas (2007-09-03). ""Spirited Away"". pp. 36–42.^ a b ""Brian Wilson – A Powerful Interview"". Ability Magazine. Ability Magazine.^ Tapley, Kristopher (May 21, 2015). ""Bill Pohlad wants 'Love & Mercy' to take you inside the genius of Beach Boy Brian Wilson"". Hit Fix.^ Powers, Ann (July 7, 2015). ""Why Films About Musicians Leave So Much Music Off Screen"". NPR.^ Gilstrap, Peter (June 3, 2015). ""Inside Brian Wilson's room: The famed Beach Boy opens up about mental illness, medication, manipulation and the movie about his life"". Salon.^ Stanton, Biba (2000). ""First-person accounts of delusions"". Psychiatric Bulletin. 20 (9): 333–336. doi: 10.1192/pb.24.9.333.^ a b c d Boyer, Paul S: ""Insane Asylums."" The Oxford Companion to United States History. Oxford University Press. 2001. Encyclopedia.com. 22 Nov. 2009^http://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366%2815%2900006-1/fulltext^ Silbersweig, D. A.; Stern, E; Frith, C; Cahill, C; Holmes, A; Grootoonk, S; Seaward, J; Mc Kenna, P; Chua, SE; Schnorr, L.; Jones, T.; Frackowiak, R. S. J. (1995). ""A functional neuroanatomy of hallucinations in schizophrenia"". Nature. 378 (6553): 176–179. doi: 10.1038/378176a0. PMID 7477318.^ SHERGILL, SUKHWINDER S.; Nenadic, I; Volz, HP; Büchel, C; Sauer, H (2004). ""Neuroanatomy of 'Hearing Voices': A Frontotemporal Brain Structural Abnormality Associated with Auditory Hallucinations in Schizophrenia"". Cerebral Cortex. 14 (1): 91–96. doi: 10.1093/cercor/bhg107. PMID 14654460.^ Shin, Sang-Eun; Lee, J; Kang, M; Kim, C; Bae, J; Jung, G (2005). ""Segmented volumes of cerebrum and cerebellum in first episode schizophrenia with auditory hallucinations"". Psychiatry Research: Neuroimaging. 138: 33–42. doi: 10.1016/j.pscychresns.2004.11.005.^ SHERGILL, SUKHWINDER S.; Brammer, MJ; Fukuda, R; Williams, SC; Murray, RM; Mc Guire, PK (2003). ""Temporal course of auditory hallucinations"". British Journal of Psychiatry. 182 (6): 525–531. doi: 10.1192/bjp.182.6.525. PMID 12777344.^ Boksa, Patricia (2009). ""On the neurobiology of hallucinations"". J Psychiatry Neuroscience. 34 (4): 260–262.^ Bartha R, al-Semaan YM, Williamson PC, Drost DJ, Malla AK, Carr TJ, Densmore M, Canaran G, Neufeld RW Biol Psychiatry. 1999 Jun 1; 45 (11):1403-11.^ Green MF, Hugdahl K, Mitchell S Am J Psychiatry. 1994 Mar; 151 (3):357-62.^ Fox M., Raichle M. (2007). Spontaneous fluctuations in brain activity observed with functional magnetic resonance imaging. Nat. Neurosci. Rev. 8, 700–71110.1038/nrn2201 [Pub Med]^ WILSON, R.; GILLEY, D.; BENNETT, D; BECKETT, L.; EVANS, D. (2000). ""Hallucinations, delusions, and cognitive decline in Alzheimer's disease"". Journal of Neurology, Neurosurgery. 69 (2): 172–177. doi: 10.1136/jnnp.69.2.172. PMC 1737043. PMID 10896689.^ a b c d e f g Fernyhough, Charles; Jones, Simon R.: “Thinking Aloud About Mental Voices”^ Hugdahl, Kenneth (2008). ""Auditory hallucinations in schizophrenia: the role of cognitive, brain structural and genetic disturbances in the left temporal lobe"". Frontiers in Human Neuroscience. 1: 1–10. doi: 10.3389/neuro.09.006.2007.^ Stip, Emmanuel (2009). ""Psychotic Symptoms as a Continuum Between Normality and Pathology"". The Canadian Journal of Psychiatry. 54: 140–151.^ ""Too Much Coffee Can Make You Hear Things That Are Not There"". Retrieved 2 July 2016.^ Barker, P. (2009) Psychiatric and Mental Health Nursing- The craft of caring. 2nd Edition. England: Hodder Arnold.^ a b Penn, David L.; Meyer, PS; Evans, E; Wirth, RJ; Cai, K; Burchinal, M (2008). ""Professional A randomized controlled trial of group cognitive-behavioral therapy vs. enhanced supportive therapy for auditory hallucinations"". Schizophrenia Research. 109 (1–3): 52–59. doi: 10.1016/j.schres.2008.12.009. PMID 19176275.^ HAYASHI, NAOKI md, phd; IGARASHI, YOSHITO md; SUDA, KIYOKO md; NAKAGAWA, SEISHU md: Auditory hallucination coping techniques and their relationship to psychotic symptomatology Psychiatry and Clinical Neurosciences 61” 2007: 640–645^ Shergill, Sukhwinder S.; Murray, RM; Mc Guire, PK (1998). ""Auditory hallucinations: a review of psychological treatments"". Schizophrenia Research. 32 (3): 137–150. doi: 10.1016/S0920-9964 (98)00052-8. PMID 9720119.^ Waters F. Auditory hallucinations in psychiatric illness. Psychiatric Times. 2010;27 (3):54-58.^ see Intervoice^ Askenazy, Florence L.; Lestideau, Karine; Meynadier, Anne; Dor, Emmanuelle; Myquel, Martine; Lecrubier, Yves (2007). ""Auditory hallucinations in pre-pubertal children: A one-year follow-up, preliminary findings"". European Child & Adolescent Psychiatry. 16 (6): 411–415. doi: 10.1007/s00787-006-0577-9.^ a b c d e Jones, Simon R.; Fernyhough, C (2007). ""Neural correlates of inner speech and auditory verbal hallucinations: A critical review and theoretical integration"". Clinical Psychology Review. 27 (2): 140–154. doi: 10.1016/j.cpr.2006.10.001. PMID 17123676.^ ALLEN, PAUL; Aleman, Andre; Mc Guire, Philip K. (2007). ""Inner speech models of auditory verbal hallucinations: Evidence from behavioural and neuroimaging studies"". International Review of Psychiatry. 19 (4): 409–417. doi: 10.1080/09540260701486498.^ a b c d Fernyhough, Charles (2004). ""Alien voices and inner dialogue: towards a developmental account of auditory verbal hallucinations"". New Ideas in Psychology. 22: 49–68. doi: 10.1016/j.newideapsych.2004.09.001. Further reading [ edit]Johnson FH (1978). The anatomy of hallucinations. Chicago: Nelson-Hall Co. ISBN 0-88229-155-6. Bentall RP, Slade PD (1988). Sensory deception: a scientific analysis of hallucination. London: Croom Helm. ISBN 0-7099-3961-2. Larøi F, Aleman A (2008). Hallucinations: The Science of Idiosyncratic Perception. American Psychological Association (APA). ISBN 1-4338-0311-9. External links [ edit]INTERVOICE Online, website of the international hearing voices movement Hearing Voices Network""Anthropology and Hallucinations"", chapter from The Making of Religion""The voice inside: A practical guide to coping with hearing voices""Psychology Terms A salience dysregulation syndrome, from Jim van Os. The British Journal of Psychiatry, 2009. [ show]v t e Mood disorder ( F30–F39, 296) [ show]v t e Symptoms and signs: cognition, perception, emotional state and behaviour ( R40–R46, 780.0–780.5, 781.1)Categories: Hallucinations Effects of psychoactive drugs Psychosis Medical signs Symptoms and signs: Cognition, perception, emotional state and behaviour "


the difference between rugs and carpets is size.

ug?• A rug is smaller than a carpet. In other words, a rug is less than 2m (6.5 feet) in length.• People call a wall to wall covering as a carpet and prefer to call smaller pieces that are either kept in the center of a room or below a bed as rugs.• The size difference can be put in the following manner as well.

Difference Between Carpet and Rug

"Difference Between Carpet and Rug Posted on April 10, 2011 by koshal Last updated on: January 16, 2015Carpet vs Rug Difference between carpet and rug is not that hard to understand. One can say that carpets are used all over the world as flooring, and rug is just another word that is referred to this flooring. It is half true because a rug is also used as flooring. However, a carpet and a rug are not the same thing. As a result, you cannot say a rug is just another word to refer to carpet. So, we cannot use these words as synonyms as there are differences between a carpet and a rug that will be highlighted in this article. These differences are very easy to understand. What is a Rug? Rugs are not usually longer than 2m or in other words, 6.5 feet. People prefer to call smaller pieces that are either kept in the center of a room or below a bed as rugs. If it covers less than 40 square feet area of the room, it is a rug. When it comes to removing, rugs are just placed on the floor and can be moved here and there. This proves to be a plus point in favor of rugs, and this is why many prefer to keep rugs in rooms and other places in their homes rather than getting carpets installed that prove to be difficult in cases of shifting. Rugs are made of materials like cotton, wool, hemp, and jute, and also they come in different patterns and textures. Here also, smaller size of rugs helps as they can be made in more textures and patterns than carpets. When it comes to cleaning, rugs can be easily cleaned at home. What is a Carpet? A carpet is anything larger than 2m or in other words, 6.5 feet. People call a wall to wall covering as a carpet. Irrespective of the size of the room, if the flooring is such that it covers the entire room, it is a carpet. When it comes to the ease with which it can be removed, carpets tend to be difficult in removing from the floor or the wall. Carpets are made of materials like cotton, wool, hemp, and jute, and also they comein different patterns and textures. In general, carpets are thicker than rugs, and they give a luxurious feel when they are thicker. When it comes to cleaning, professionals may be required to get cleaning of carpets done. What is the difference between Carpet and R

Irrespective of the size of the room, if the flooring is such that it covers the entire room, it is a carpet, but if it covers less than 40 square feet area of the room, it is a rug. Though this is an arbitrary differentiation, it helps in deciding whether the piece of flooring is a carpet or a rug.• Another difference lies in the ease with which flooring can be removed. While carpets tend to be difficult in removing from the floor or the wall, rugs are just placed on the floor and can be moved here and there.• Rugs and carpets, though both are made of similar materials like cotton, wool, hemp, and jute, differ in terms of patterns and textures. Rugs can come in more patterns than carpets.• Cleaning of rugs is easier than carpets and professionals may be required to get cleaning of carpets done. On the other hand, rugs can be easily cleaned at home.• In general, carpets are thicker than rugs, and they give a luxurious feel when they are thicker.• When it comes to price, the manufacturer decides the price depending on the way the carpet or the rug was made. For example, a hand woven rug can be more expensive than a machine made rug. Same can be said about carpets. So deciding which is more expensive, rug or carpet, depends on the situation.• Floor to floor and wall to wall coverings are called carpets.• Rugs require little maintenance and can be easily moved while it is difficult to clean a carpet and also to move it from one place to another. Images Courtesy: Carpet by Dainis Matisons ( CC BY 2.0)Fakhrali rug via Wikicommons (Public Domain)Related posts: Difference Between Cooler and Air-Conditioner Difference Between Electric Fireplace and Gas Fireplace Difference Between Marble and Granite Difference Between Eurotop and Pillowtop Difference Between Super Glue and Epoxy Help us to improve our writing. Please Rate. (No Ratings Yet)Cite This Page ""Difference Between Carpet and Rug."" Difference Between. Com. April 10, 2011. < http://www.differencebetween.com/difference-between-carpet-and-vs-rug/ >Filed Under: Household Tagged With: carpet, carpet and rug, carpet definition, carpets, flooring, rug, rug definition, rugs "


which sexually transmitted disease has three stages, the first of which involves development of a chancre?

10The sexually transmitted disease known as syphilis has three major stages of infection and one inactive or latent stage. The first stage of a syphilis infection manifests itself typically as the formation of a small ulcer or chancre on the site of the in

Syphilis: What You Don't Know Can Hurt You By Brandon Marlow | Submitted On October 25, 20

fection. This chancre typically develops twenty-one days after infection, though it could appear as as soon as ten to twenty days, or later, some twenty-two to ninety days after being infected. Once the chancre is evident at any set time from ten to ninety days, the disease becomes highly infectious, and any contact with it will almost invariably result in an infection. One can become infected by coming into contact with ulcer or spirochetes-rich chancre. Even the use of condoms may not be able to prevent infection if the chancre is outside of the female's vagina, or is located in the male's scrotum. If the ulcer is located in the mouth, even a simple kiss is enough for one to become infected. This chancre will eventually disappear after three to six weeks, but may reappear at a later time as secondary syphilis if treatment was not received or given. Though an initial infection may heal on its own in most cases, especially in women, but 25% of these cases will progress to the secondary stage of syphilis. This generally develops after a couple of weeks or after a month, and can last as long six weeks. Because of the systemic nature of the secondary stage of syphilis, it affects more organs. Typical symptoms of this secondary stage include skin rashes on the palms of the hands and the soles of the feet. They are not typically itch, and sometimes they are even obscure. Other manifested symptoms of this secondary stage include hair loss, white patches on the skin, such as on the mouth, nose, or vagina, sore throat, as well as headache and fever. Lesions that look like genital warts may also appear on the genital area. These warts, as well as the rashes are highly contagious. Since the rashes usually appear on the palm of the hand, even something as slight as a handshake can transmit the infection to another person. After the second stage, syphilis will enter the latent, or symptom free stage. This stage lasts for twenty or more years, but even if an infected person has not gone through the latent stage, one may still progress to the third and final stage. This is the stage of the disease in which syphilis will cease to become infectious, but since it is systemic, a plethora of complications will arise. The methods for treating syphilis vary according to the stage or progress of the disease, and the clinical manifestations shown. A very effective way of curing syphilis involves the intramuscular injection of penicillin. This drug is able to cure not just the primary, but even the tertiary stage of the disease. In order for it to be effective however, constant and rigorous treatment is necessary. In cases of penicillin allergies, other alternative drugs, just like oral doxycycline or tetracycline may be used. Vibramycin, Oracea, Adoxa, Atridox, Achromycin, among others are some of the drugs used for syphilis treatment. Pregnant ladies who are infected with syphilis can pass on the disease to the fetus. Penicillin is one of the best known cures because it is the only antibiotic which can pass through the placental barrier, and thus rid the fetus of the infection. If left untreated, the child can be born blind, or it can die within the womb. Syphilis is not something to be easily ignored. If you think you are infected with syphilis, or if you are showing some signs and symptoms, it is important that you seek out medical help as soon as possible. Syphilis---a disease that needs rigorous attention, especially in cases of infection in women. Learn more about the symptoms and treatment of this dangerous disease. Don't wait call our toll-free number today to speak to one of our caring counselors.1 (888) MAX-LABS or 1 (888) 629-5227 or visit us at Local STD Testing Labs [http://localstdtestingclinics.com/]Article Source: http://Ezine Articles.com/expert/Brandon_Marlow/643042


what is ladder move

ry. Up is not the only way forward Climbing the ladder is the traditional model for career growth, taking a single pathway upward through the corporate hierarchy. However, it's not the only way to move forward.

"Your next career move: The ladder or the lattice? Share Share What's This? Image: Flickr, fdecomite By Jo Miller Dec 13, 2014When it comes to moving forward in your career, there are two paths you can take: The ladder or the lattice. For example, one mid-level manager took a calculated risk when she accepted a lower position with a much larger company. On her resume, it looked like a step down the career ladder — but after less than a year in the role, she had gained recognition as a high-potential emerging leader. She has since rotated through a number of assignments that have given her broad exposure to different areas of the company. Having long felt like a golden bullet that just needed to be aimed in the right direction, she now feels that this series of lateral moves has pointed her in the right long-term career trajecto

Cathy Benko, vice chairman with Deloitte, has done a lot to popularize the term ""career lattice"" to refer to a more flexible type of trajectory that offers multiple pathways for career growth, including upward, lateral and even downward moves. Her book, The Corporate Lattice, opens with the observation that,""The world of work is at an inflection point. The hierarchical corporate ladder is giving way to a multidimensional corporate lattice. """"The world of work is at an inflection point. The hierarchical corporate ladder is giving way to a multidimensional corporate lattice. ""There is more than one method for building a career, and moving up the ladder is not the only way to move your career forward. Which of these paradigms fits best for you at this phase in your career? You'll know you're ready for a ladder move when you're capably performing your current role, are happy with your current company and are ready to step up to more responsibility and leadership. But a lattice move might be worth considering if you want to network, gain skills, alter your long-term trajectory or if you're bored and ready for a new intellectual challenge. You might also want to consider a lattice move if: You love your work, but you don't love your boss. If your boss is putting a lid on your career development, don't stay too long. You'll do much better with a boss that's supportive. The same goes for working in a toxic team culture or for a company that doesn't value its employees. Your life outside work takes precedence. If you're in a phase where family, balance or other needs are simply more important than your career, a lattice move can help you maneuver into a role that better supports your current situation. Your job leads into a career dead-end. If you're on a path with limited opportunities to grow, consider a sideways move into an area with more potential for future advancement (and make your move sooner rather than later, or risk career paralysis). The same goes for when you're working for a business that is stagnating. Ultimately, your career will too, unless you jump ship. You aspire to become a business leader, not a subject-matter specialist. Moving laterally can broaden your exposure to different functional areas or business divisions, burnishing your resume for future business leadership positions. Either model -– ladder or lattice -– can lead you on a path to career growth, leadership and a successful and satisfying career. The choice really is yours. Mashable Job Board Listings The Mashable Job Board connects job seekers across the U. S. with unique career opportunities in the digital space. While we publish a wide range of job listings, we have selected a few job opportunities from the past several weeks to help get you started. Happy hunting!Web & Social Media Analyst at Imagination Publishing in Chicago, Illinois Creative Director at LEWIS Pulse in San Francisco, California Design Lead — Nike+ Design at Nike in Portland, Oregon Jo Miller Jo is Founding Editor of Be Leaderly, CEO of Women’s Leadership Coaching, Inc., and creator of the Women’s Leadership Coaching® system, a roadmap for women who want to break into leadership. She has traveled i... More Topics: Business, Job Search Series, Jobs, mashable careers Get our hottest stories delivered to your inbox. Sign up for Mashable Newsletters to get personalized updates on top stories and viral hits. "


what is the medication to treat dementia

There are national guidelines for people with dementia that can help your specialist decide which treatment to choose. One of the following is usually recommended: donepezil, galantamine and rivastigmine for people with mild or moderate Alzheimer's disease, providing that:

Medication and Treatment for Dementia

Brain / Nerves / Neurology Save Print Share Actions Medication and Treatment for Dementia Authored by Dr Mary Harding, 21 May 2015In this series: Memory Loss and Dementia Causes of Memory Loss and Dementia Lewy Body Dementia Medicines for dementia are used to help with symptoms that affect thinking and memory, as well as symptoms that affect mood and behaviour. But there are also many non-drug treatments that can help support a person with dementia. In this article What non-medicine treatment options are there? How do treatments for dementia work? When are medicines for dementia usually prescribed? Which dementia treatment is usually prescribed? How well do dementia treatments work? How should I take these medicines? What is the usual length of treatment? What about side-effects? Who cannot take medicines for dementia? Can I buy medicines for dementia? What non-medicine treatment options are there? Support and care is the most important part of treatment When someone is diagnosed with dementia, a full assessment may be suggested to look at their practical skills, their ability to look after themself, their safety in their home, etc. This usually involves assessment by a number of different healthcare professionals. An individual care plan may be drawn up that outlines the person's specific needs. The aim is to maintain the independence of someone with dementia as much as possible and for as long as possible. Most people with dementia are cared for in the community. Often, the main carer is a family member. It is important that carers get the full support and advice which is locally available. Support and advice may be needed from one or more of the following healthcare and allied professionals, depending on the severity of the dementia and the individual circumstances: District nurses can advise on day-to-day nursing care. Occupational therapists can advise on changes to the physical environment, which may help a person with dementia. For example, handrails and grab bars, labelling of objects, removing items that are not needed in the home. Physiotherapists can help. For example, with exercises to help maintain mobility. Community psychiatric nurses can advise on caring for people with mental illness. Sometimes a specialist assessment by a psychiatrist may be needed. Social Services can advise on local facilities such as daycare centres, benefits, help with care in the home, sitting services, respite care, etc. People who can advise on financial and legal matters, such as Lasting Power of Attorney. Voluntary organisations can be a good source of advice. If you care for a person with dementia, it is well worth getting information about the help that is available in your local area. In most areas of the UK there are organisations that provide support and advice for carers of people with dementia. Your local library or Citizens Advice Bureau will often have contact details. The level of care and support needed often changes over time. For example, some people with mild dementia can cope well in their own home which is very familiar to them. Some may live with a family member who does most of the caring. If things become worse, a place in a residential or nursing home may be best. The situation can be reviewed from time to time to make sure the appropriate levels of care and support are provided. Many carers struggle on beyond the point where they need more help. If you are a carer, you can ask a GP or district nurse to assess a person with dementia if you feel that you need a greater level of support. There are a number of local carer support groups on the internet, which may also be able to provide support and advice. For example, information about respite/short-break services for carers. Other possible treatments There are some other treatments and options that may be helpful for some people with dementia, particularly in certain situations. These include the following. Measures to help simplify the daily routine and enhance memory may help some people. For example, planning out and writing down a daily routine. This may include writing reminders to do certain things such as putting the rubbish out, locking the door at night-time, etc. Making sure that clothing, keys, glasses or other things that are used often are put in prominent places where they can be found easily may also be helpful. Labelling of commonly used objects may be another useful tool. An occupational therapist may be able to advise. Reality orientation is thought to help in some cases. This involves giving regular information to people with dementia about times, places, or people to keep them orientated. It may range from simple things, such as having a board in a prominent place, giving details of the day, date, season, etc, to staff in a residential home reorientating a person with dementia at each contact. Cognitive stimulation (stimulating the brain) may help to improve memory, language and problem-solving ability. For example, by recreational activities, problem-solving activities and talking to the person with dementia. In addition, recreational activities may enhance quality of life and well-being. Regular physical activity, if possible, such as walking, dancing, etc, may help to slow down the decline in mobility that is common in people with dementia. It may also help if depression is a problem. Reminiscence therapy may help in some cases. This involves encouraging people to talk about the past so that past experiences are brought into their current thoughts. It relies on long-term memory which is often quite good in people with mild-to-moderate dementia. Cognitive behavioural therapy is sometimes tried to help treat depression that is quite common in people with dementia. Behavioural therapy may also be used to treat any problems related to behaviour that someone with dementia may have. This type of therapy looks for possible reasons for certain behaviours. For example, someone who wanders a lot may in fact be doing this because they are feeling quite restless. In this situation, taking part in regular physical activity may help. Animal-assisted therapy may sometimes be suggested to help people with dementia who have challenging behaviour such as agitation or aggression. For example, allowing the person to spend time with and interact with a trained dog. Sensory stimulation - for example, using music, lights, sounds, smells, massage and aromatherapy to stimulate the brain. This may also be helpful for some people with dementia - for example, to improve their mood or feelings of restlessness. What medicines are used to treat dementia? Medicines for dementia are used firstly as a treatment to help with symptoms that affect thinking and memory (cognitive symptoms). Secondly, they are used as treatment to help with symptoms that affect mood and how someone behaves (non-cognitive symptoms). These medicines do not cure dementia and they may only work for some people. They also may only work for a short time (6-12 months). Medicines for dementia are always started by a doctor who specialises in treating dementia. There are four medicines available in the UK which can be prescribed for dementia. These are donepezil, rivastigmine, galantamine and memantine. They are available as tablets, liquids, tablets that dissolve in water, or patches. They come in various brand names. In addition, there are a number of other medicines that may be prescribed to people who have dementia. For example: An antidepressant may be advised if depression is suspected. Depression is common in people with dementia and may be overlooked. Aspirin and other medicines to treat the risk factors for stroke and heart disease may be appropriate for some people. This is especially the case for those with vascular dementia. Sleeping tablets are sometimes needed if difficulty sleeping is a persistent problem. A tranquilliser or an antipsychotic medicine is sometimes prescribed as a last resort for people with dementia who become easily agitated. Research continues looking for new medicines to help with dementia. How do treatments for dementia work? Medicines for dementia work by increasing the levels of certain chemicals in the brain. Acetylcholinesterase inhibitors These include donepezil, rivastigmine and galantamine. They work by increasing the level of acetylcholine. This is a chemical in the brain that is low in people with Alzheimer's disease. These medicines are not a cure for Alzheimer's disease. However, they may help to treat some of the symptoms affecting thinking and memory in about half of people with Alzheimer's disease. In the UK, the National Institute for Health and Care Excellence (NICE) recommends that donepezil, galantamine and rivastigmine can be considered as treatment options for people with mild or moderate Alzheimer's disease, providing that: The medicine is started by a specialist in the care of people with dementia. A person receiving treatment has regular reviews and assessments of their condition. (Reviews are usually carried out by a specialist team. Carers' views on the person's condition should also be asked before the medicine is started and should be considered during the reviews. )The medicine is only continued for as long as it is thought to be having a worthwhile effect on a person's symptoms. Common side-effects of these medicines may include feeling sick, muscle cramps, tiredness, headache and diarrhoea. Your doctor should be able to give you more details about possible side-effects. The medicine rivastigmine is also licensed to be used in people with mild-to-moderately severe dementia who also have Parkinson's disease. So, doctors may suggest this medicine for this group of people. Also, an acetylcholinesterase inhibitor medicine may sometimes be suggested for people with dementia with Lewy bodies (DLB) who have problems with challenging or disruptive behaviour (non-cognitive symptoms). Memantine Memantine is also licensed for the treatment of Alzheimer's disease in some people. It works by reducing the amount of a brain chemical called glutamate. It is thought that this may help to slow down the damage to brain cells affected by Alzheimer's disease. Like the medicines above, this is not a cure. Some research studies have shown that it seems to slow down the progression of the symptoms in some cases. NICE recommends that it can be considered as a treatment option for: People who have moderate Alzheimer's disease and who for some reason cannot take, or are intolerant to, the acetylcholinesterase inhibitor medicines. People who have severe Alzheimer's disease. When are medicines for dementia usually prescribed? Your GP will usually refer you to a doctor who specialises in treating dementia, to confirm that you have dementia. The specialist will then decide if you should have treatment. This decision to start treatment and which treatment to start depends on various things. These include what has caused your dementia, what your symptoms are and how severe your dementia is. Dementia is usually classed as being mild, moderate or severe. Which dementia treatment is usually prescribed? Your specialist will decide which treatment is right for you.

The medicine is started by a specialist in the care of people with dementia. A person receiving treatment has regular reviews and assessments of their condition. (Reviews are usually carried out by a specialist team. Carers' views on the person's condition should also be sought before the medicine is started and should be considered during the reviews. )Memantine can be considered as a treatment option for: People who have moderate Alzheimer's disease and who, for some reason, cannot take, or are intolerant to, the acetylcholinesterase inhibitor medicines. People who have severe Alzheimer's disease. These medicines are not usually used for people with other types of dementia. However, rivastigmine can be used for people with mild-to-moderately severe dementia who also have Parkinson's disease. So, doctors may suggest this medicine for this group of people. Also, an acetylcholinesterase inhibitor medicine may sometimes be suggested for people with DLB who have problems with challenging or disruptive behaviour (non-cognitive symptoms). How well do dementia treatments work? It is thought that about half the people treated with a cholinesterase inhibitor will see an improvement in symptoms that affect thinking and memory. Whether they help with other symptoms such as aggression and agitation has still not been confirmed. The improvement in symptoms is usually only seen for about 6-12 months. For memantine, some studies have shown that it can slow down the progression of symptoms in some cases. How should I take these medicines? It is usual to start with a low dose. This is then increased over a period of weeks to a target treatment dose. The dose is increased slowly because when you first start taking these medicines you may develop some unpleasant side-effects - for example, diarrhoea, feeling sick (nausea) and being sick (vomiting). Most people who develop side-effects find that after a period of time they go away. If you are tolerating a low dose well, your doctor will increase your dose, if needed. How often the dose is increased depends upon which medicine you are taking. For example, if you are taking galantamine, the dose is increased every four weeks. If you are taking rivastigmine tablets, the dose is increased every two weeks. See the leaflet that came with your medicine for more information. What is the usual length of treatment? Medicines for dementia are usually only continued for as long as they are thought to be having a worthwhile effect on symptoms. What about side-effects? Medicines for dementia cause side-effects in some people. However, if side-effects do occur, they are usually minor and often go away after a few months. The most common side-effects of anticholinesterase inhibitors include: Diarrhoea. Muscle cramps. Feeling tired (fatigue). Feeling sick (nausea). Being sick (vomiting). Not sleeping well (insomnia). Headache. Being incontinent of urine. Other less common side-effects include: Symptoms of the common cold. Loss of appetite. Mental health disorders. Fainting and seizures. Dizziness. A thumping heart (palpitations). Flushing or sweating. Rash. Itching. Memantine may cause: Dizziness. Headache. Feeling out of breath. Constipation. Drowsiness. High blood pressure. Other less common side-effects include: Vomiting. Blood clots (thrombosis). Heart problems. Confusion. Feeling tired. Seeing things or hearing things which are not real (hallucinations). Problems with walking. The above is not an exhaustive list but highlights the more common possible side-effects. For a full list of side-effects see the information leaflet that comes with the medicine. Who cannot take medicines for dementia? In general, most people are able to take these medicines. Caution may be needed in people with certain medical problems. For example, people with severe liver or kidney problems may not be able to take them, or they may need a lower dose. Care also needs to be taken in people who have had fits in the past. Can I buy medicines for dementia? No - you cannot buy medicines for dementia. They are only available on prescription. How to use the Yellow Card Scheme If you think you have had a side-effect to one of your medicines you can report this on the Yellow Card Scheme. You can do this online at www.mhra.gov.uk/yellowcard. The Yellow Card Scheme is used to make pharmacists, doctors and nurses aware of any new side-effects that medicines or any other healthcare products may have caused. If you wish to report a side-effect, you will need to provide basic information about: The side-effect. The name of the medicine which you think caused it. The person who had the side-effect. Your contact details as the reporter of the side-effect. It is helpful if you have your medication - and/or the leaflet that came with it - with you while you fill out the report. Next page: Lewy Body Dementia Previous page: Causes of Memory Loss and Dementia Did you find this information useful? Further reading and references Related Information Memory Loss and Dementia Alzheimer's Disease Pro Galantamine (Reminyl)Donepezil for dementia (Aricept)Weight Loss (Unintentional)View all How to make shopping easier for people with dementia6 minutes reading time How to reduce your risk of dementia5 minutes reading time How does diet affect dementia?5 minutes reading time I am so lost in this illness. No Dr. has said how bad he is. He is moody, bi-polar, verbally abusive and nasty at times. At other times is he decent, quiet, distant, has developed a extra over the... Sandy1953Join the discussion on the forums Health Tools Feeling unwell? Assess your symptoms online with our free symptom checker. Start symptom checker Article Information Last Checked 21 May 2015Next Review 20 May 2018Document ID 13892 (v2)Author Dr Mary Harding Peer reviewer Dr John Cox The information on this page is written and peer reviewed by qualified clinicians. Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Patient Platform Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.


name lennart

The name Lennart is a German baby name The German meaning of Lennart is: Lion-hearted

Lennart

Lennart1.8K shares Share Pin it! Tweet 968Lennart The name Lennart is a Male name. German meaning:

Language Analysis of Lennart The name Lennart has 2 syllables The name Lennart begins with the letter LBaby names that sound like Lennart: Lamorat Lenard Lennard Leonard Leonarda Leonardo Leonhard Leonrd Lnrd Baby names that are similar to Lennart: Benat Benner Bennet Bennett Bernard Denna Dennet Dennit Feenat Genna Numerology of Lennart The name Lennart has a numerology value of 7In numerological terms, this means the following Thought The product of mental activity; that which one thinks. A single act or product of thinking; idea or notion. The capacity or faculty of thinking, reasoning, imagining, etc. A consideration or reflection. Consciousness The thoughts and feelings, collectively, of an individual or of an aggregate of people. the moral consciousness of a nation. Awareness of something for what it is; internal knowledge. Concern, interest, or acute awareness. Spirit The principle of conscious life; the vital principle in humans, animating the body or mediating between body and soul. The soul regarded as separating from the body at death. Interactivetools Gender Predictor Baby Names Due Date Calculator Ovulation Calculator1.8K shares Share Pin it! Tweet 968Tell us what you think!


parasympathetic dominance definition

Sometimes people can have a Sympathetic and Parasympathetic Dominance which means your body has a difficult time maintaining balance between the two states; it swings like a pendulum between both extremes and indicates a need for nutritional support for both sides. Primary indicators of Sympathetic Dominance symptoms:

Sympathetic Dominance The Autonomic Nervous regulates the internal body processes that require no conscious awareness: for example, the rate of heart contractions, the rate of breathing, amount of stomach acid secreted, and the speed at which food passes through the digestive tract. We divide the Autonomic Nervous System into the Sympathetic and Parasympathetic sides and they can be easily thought of as our body’s gas pedal and brakes. The Sympathetic side relates to the speeding up of body processes, it responds to stresses both external and internal like infection, and at its extreme influence we are in what may be referred to as “fight or flight” mode which is our response to extremely stressful or emergency situations (like flooring the gas pedal). While the Sympathetic dominances is necessary, even life saving, at times, it prevents the proper operation of the Parasympathetic side which is equally important. Each of the two sides uses specific counterbalancing minerals and nutrients to fuel their controlling mechanisms. Think of Sympathetic dominance as an indicator for the need to supply the missing minerals and nutrients that support the opposite, Parasympathetic side – primarily alkaline ash minerals including Potassium. Too much acceleration means we need more brakes. Sympathetic Dominance can be indicated by the presence of symptoms that both show a keyed up, hyper functioning, over-alertness, and an under-functioning of the Parasympathetic side such as poor digestion, difficulty relaxing or getting a good night’s sleep, racing or erratic pulse, or difficulty with bathroom functions.

Acid foods upset Get chilled often“Lump” in throat Dry mouth-eyes-nose Pulse speeds after meal Keyed up – fail to calm Cut heals slowly Gag easily Unable to relax; startles easily Extremities cold, clammy Strong light irritates Urine amount reduced Heart pounds after retiring “Nervous stomach”Appetite reduced Cold sweats often Fever easily raised Neuralgia-like pains Staring, blinks little Sour stomach often Nutrition is essential to overall health! Feeding the body properly keeps our systems working well and working together. A deficiency within one system may cause an array of issues throughout the body. Like Us Office Hours Day Morning Afternoon Monday 7:30am-1:00pm 2:30pm-6:30pm Tuesday 7:30am-1:00pm 2:30pm-6:30pm Wednesday 7:30am-1:00pm 2:30pm-6:30pm Thursday 7:30am-1:00pm 2:30pm-6:30pm Friday 7:30am 1:00pm Our Location An Optimal Spine Equals Optimal Health Salina Family Chiropractic1605 West Garland Avenue Spokane, WA 99205 Phone: (509) 467-2888Map and Directions


how many miles in altitude is the united states satellite constellation

A GPS satellite is a satellite used by the NAVSTAR Global Positioning System (GPS). The first satellite in the system, Navstar 1, was launched February 22, 1978. [1] The GPS satellite constellation is operated by the 50th Space Wing of the United States Air Force. The GPS satellites circle the Earth at an altitude of about 20,000 km (12,427 miles) and complete two full orbits every day.

GPS satellite blocks

"From Wikipedia, the free encyclopedia (Redirected from GPS (satellite))navigation search See also: List of GPS satellites GPS satellite constellation (not to scale)Various earth orbits to scale; green dash-dot line is medium earth orbit, a typical GPS orbit.

[2]Contents [ hide ]1 Block I satellites2 Block II satellites2.1 Initial Block II series2.2 Block IIA series2.3 Block IIR series2.4 Block IIR-M series2.5 Block IIF series3 Block III satellites3.1 Block IIIA series3.2 Block IIIF series4 References Block I satellites [ edit]A Navstar GPS satellite undergoing pre-launch testing. Rockwell International was awarded a contract in 1974 to build the first eight Block I satellites. In 1978 the contract was extended to build an additional three Block I satellites. Beginning with Navstar 1 in 1978, ten ""Block I"" GPS satellites were successfully launched. One satellite, ""Navstar 7"", was lost due to an unsuccessful launch on 18 December 1981. [3]The Block I satellites were launched from Vandenberg Air Force Base using Atlas rockets that were converted intercontinental ballistic missiles. The satellites were built by Rockwell International at the same plant in Seal Beach, CA where the S-II second stages of the Saturn V rockets had been built. [4]The Block I series consisted of the concept validation satellites and reflected various stages of system development. Lessons learned from the 11 satellites in the series were incorporated into the fully operational Block II series. Dual solar arrays supplied over 400 watts of power, charging Ni Cd batteries for operations in Earth's shadow. S-band communications were used for control and telemetry, while a UHF channel provided cross-links between spacecraft. A hydrazine propulsion system was used for orbital correction. The payload included two L-bandnavigation signals at 1575.42 MHz (L1) and 1227.60 MHz (L2). The final Block I launch was conducted on 9 October 1985, but the last Block I satellite was not taken out of service until 18 November 1995, well past its 5-year design life. [5]Block II satellites [ edit]Initial Block II series [ edit]The Block II satellites were the first full scale operational GPS satellites, designed to provide 14 days of operation without any contact from the control segment. The prime contractor was Rockwell International, which built a SVN 12 qualification vehicle after an amendment to the Block I contract. In 1983 the company was awarded an additional contract to build 28 Block II/IIA satellites. Block II spacecraft were 3-axis stabilized, with ground pointing using reaction wheels. Two solar arrays supplied 710 watts of power, while S band communications were used for control and telemetry. A UHF channel was use for cross-links between spacecraft. A hydrazine propulsion system was used for orbital correction. The payload included two L band navigation signals at 1575.42 MHz (L1) and 1227.60 MHz (L2). Each spacecraft carried 2 rubidium and 2 cesium clocks, as well as nuclear detonation detection sensors, leading to a mass of 1,660 kilograms (3,660 lb). [6]The first of the nine satellites in the initial Block II series was launched February 14, 1989; the last was launched October 1, 1990. [7] The final satellite of the series to be taken out of service was decommissioned on March 15, 2007, well past its 7.5 year design life. Block IIA series [ edit]The Block IIA satellites were slightly improved versions of the Block II series, designed to provide 180 days of operation without contact from the control segment. However, the mass increased to 1,816 kilograms (4,000 lb) [8]Nineteen satellites in the Block IIA series were launched, the first on November 26, 1990 and the last on November 6, 1997. Only one satellite of the Block IIA ( SVN-34) is still in service, broadcasting the PRN 18 signal. [9]Two of the satellites in this series, numbers 35 and 36, are equipped with laser retro-reflectors, [10] allowing them to be tracked independently of their radio signals, providing unambiguous separation of clock and ephemeris errors. Block IIR series [ edit]Artist's impression of a GPS-IIR satellite in orbit. The Block IIR series are ""replenishment"" (replacement) satellites developed by Lockheed Martin. Each satellite weighs 4,480 pounds (2,030 kg) at launch and 2,370 pounds (1,080 kg) once on orbit. [11] The first attempted launch of a Block IIR satellite failed on January 17, 1997 when the Delta II rocket exploded 12 seconds into flight. The first successful launch was on July 23, 1997. Twelve satellites in the series were successfully launched. Block IIR-M series [ edit]Artist's impression of a GPS-IIRM satellite in orbit. The Block IIR-M satellites include a new military signal and a more robust civil signal, known as L2C. [12] There are eight satellites in the Block IIR-M series, which were built by Lockheed Martin. [13] The first Block IIR-M satellite was launched on September 26, 2005. The final launch of a IIR-M was on August 17, 2009. [14]Block IIF series [ edit]Main article: GPS Block IIFArtist's impression of a Navstar-2F satellite in orbit. The Block IIF series are ""follow-on"" satellites developed by Boeing. The satellite has a mass of 1,630 kilograms (3,600 lb) and a design life of 12 years. The first Block IIF space vehicle was launched in May 2010 on a Delta IV rocket. [15] The twelfth and final IIF launch was February 5, 2016. [16]Block III satellites [ edit]Block IIIA series [ edit]Main article: GPS Block IIIAArtist's impression of a GPS Block IIIA satellite in orbit. GPS Block IIIA is the first series of third-generation GPS satellites, incorporating new signals and broadcasting at higher power levels. In September 2016, the Air Force awarded Lockheed Martin a contract option for two more Block IIIA satellites, setting the total number of GPS IIIA satellites to ten. [17] As of December 2017, the first GPS IIIA launch is scheduled for May 2018 by Space X. [18]Block IIIF series [ edit]Main article: GPS Block IIIFThe Block IIIF series (or ""tranche"") is the second set of GPS Block III satellites, which will consist of up to 22 space vehicles. [19] Block IIIF launches are expected to begin no earlier than 2025 and continue through 2034. [20]References [ edit]^ ""Navstar 1"". NASA. 27 April 2016. Retrieved 25 July 2016.^ ""The Global Positioning System"". harvard.edu.^ ""BLOCK I SATELLITE INFORMATION"". USNO.^ ""Site: Boeing North American, Inc"". WTEC.^ ""GPS (Navstar)"". skyrocket.de.^ ""GPS-2 (Navstar-2)"". skyrocket.de.^ ""BLOCK II SATELLITE INFORMATION"". USNO.^ ""GPS-2A (Navstar-2A)"". skyrocket.de.^ ""GPS CONSTELLATION STATUS"". U. S. Coast Guard Navigation Center. Retrieved 25 January 2016.^ ""CDDIS Bulletin - June 1994, Volume 9 No. 5"". NASA Goddard Space Flight Center. Archived from the original on 2009-03-20.^ ""Global Positioning management System IIR"". Lockheed Martin Space Systems Company.^ ""GLOBAL POSITIONING SYSTEM"". USAF. Archived from the original on 2007-11-16.^ ""Latest GPS IIR-M Sat Goes ""Gold"" For Lockheed Martin"". Sat News. Archived from the original on 2008-01-23.^ ""ULA Delta II Completes 20 Year Era With Successful Air Force GPS IIR-21 Launch"" Archived 2009-10-01 at the Wayback Machine.^ ""Boeing Satellite Launch Schedule"". Boeing. January 15, 2008. [ permanent dead link]^ ""Air Force successfully launches GPS IIF-12 satellite"". GPS World. February 8, 2016.^ ""SMC exercises contract options to procure two additional GPS III satellites"". September 22, 2016.^ Gruss, Mike (April 27, 2016). ""Space X wins $82 million contract for 2018 Falcon 9 launch of GPS 3 satellite"". Space News. Space News. Retrieved December 2, 2017.^ Divis, Dee Ann (November 22, 2017). ""Next Tranche of GPS Satellites to be called GPS IIIFs"". Inside GNSS. Gibbons Media & Research LLC. Retrieved December 1, 2017.^ Gleckel, Gerry (November 15, 2017). ""GPS Status & Modernization Program"" (PDF). GPS.gov. U. S. Air Force. Retrieved December 1, 2017. [ hide]v t e NAVSTAR Global Positioning System satellites List of GPS satellites Block I1 2 3 4 5 6 7 † 8 9 10 11Block II1 2 3 4 5 6 7 8 9Block IIA1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19Block IIR1 † 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21Block IIRM1 2 3 4 5 6 7 8Block IIF1 2 3 4 5 6 7 8 9 10 11 12Block IIIA1 2 3 4 5 6 7 8 9 10Block IIIF1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22Italics indicate future missions. Signs † indicate launch failures. Categories: Global Positioning System Satellites of the United States GPS satellites "