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It may be that amino acid changes in hemagglutinin between antigenically variant strains are sometimes selected by memory helper T cells cheap phenergan 25 mg line. However order 25 mg phenergan visa, for amino acid replacements in hemagglutinin purchase 25mg phenergan with visa, it isdiculttoseparate the potential role of memory helper T cells from the obviously strong eects of anti- body memory. The level of memory helper T cells can be measured by the time re- quired for naive B cells to switch from initial IgM secretion to later IgG se- cretion. When assessed by this functional response, helper T cell mem- oryappears to be short-lived for inuenza (Liang et al. Other assays nd that memory helperTcells remain for several months after initial infection (Gupta et al. Preliminary data suggest that patterns of immunodominance in the primary response do notnecessarily carry through to the memory pool (Belz et al. In some cases, it seems that T cell clones increased to high abundance in the primary response suf- fer greater reductions as the cellular populations are regulated in the memory phase (Rickinson et al. The parasites race against immune eectors, which may eventually kill parasites faster than they are born. Each kind of parasite has its particular site of infec- tion, pattern of spread between tissues, and rate of increase. Immuno- logical memory therefore inuences the host-parasite race in a dierent way for each kind of parasite. I discuss memory-parasite in- teractions with regard to the type of immune cell involved, the kinetics of parasite spread, and the kinetics of immune eector response. There are four main classes of immune cells that canbeenhanced by primary infection to provide greater protection against later infections: plasma B cells, memory B cells, eector T cells, and memory T cells (Ahmed and Gray 1996). These eector B cells usually pro- duce mature immunoglobulins such as IgG in systemic sites and IgA on mucosal surfaces. IgG can sometimes prevent infection by binding to in- oculum before the parasites replicate in the host. IgA antibodies provide eective protection against pathogens that initially invade mucosal sites, such as inuenza through the nasal mucosa, rotaviruses and many bacterial pathogens via the intestinal mu- cosa, and gonorrhea via the urethral epithelium (Mims 1987; Ada 1999). However, IgA titers decline relatively rapidly after infection, lasting on the order of months rather than years, as is often the case for IgG. Memory B cells proliferate and dierentiate into plasma cells upon secondary infection. If the pathogen is not immediately cleared by ex- isting antibodies and the pathogens initial replication is relatively slow, then the memory B cells may have time todierentiate into plasma cells and clear the pathogen before widespread infection develops. Once widespread infection becomes established, memory B cells can help to produce a more specic, rapid,andintense antibody response. However, the relative roles of antibodies and T cells in clearing estab- lished infection vary depending on the attributes of the pathogen (Mims 1987; Janeway et al. Antibodies play a key role in clearing cytopathic viruses on mucosa or circulating in the blood. The dynamics of this race could be analyzed by mathematical models that compare the viruses birth and death rates in light of the killing action mediated by antibodies and eector T cells. For viruses that circulate in systemic infections, memory IgG anti- bodies may often protect against infection. By contrast, for mucosal infections such as those by rotaviruses and many bacterial pathogens, memory IgA antibodies often decline below protection level, but mem- ory B cells can play an important role in defense by dierentiating IgA- secreting plasma cells (Ahmed and Gray 1996). Thus clearance before signicant infection develops can occur by various scenarios. First, recent stimulation by antigen can boost eector T cell density to protective levels. Stimulation can occur by persistent antigen maintained in the host or by recurrent infection. Second, slowly spreading infections may allow dierentiation of eector T cells from memory T cells in time to control initial spread of the pathogen. Third, memory antibody may clear the pathogen before the initial infection becomes established. Lack of symptoms during secondaryinfectionmayresultfromrapid clearance of the parasite or from control of the infection that still al- lows some parasite replication and transmission. It is important to dis- tinguish between clearance and controlled infection when studying the population dynamics and evolution of the parasite. In summary, parasite attributes determine the type of host memory that impedes secondary infection. For example, the number of parasites in the inoculum frequently inuences whether an infection is cleared quickly or spreads widely. These various parasite attributes and the rate parameters that gov- ern parasite birth and death within hosts must be measured against the kinetics of immunological memory and the response to secondary infection. The quantitative outcome inuences the selective pressure imposed on various parasite epitopes by host memory. Such selective pressure, in turn, shapes the distribution of antigenic variation in para- site populations. The immunological prole of each host and the variation of proles between hosts inuence the selective pressures imposed on parasite antigens. For the prole of each host, consider as a simple measure of immunodominance the number of epitopes to which a host retains protective antibody. If a host retains protection against n epitopes, then avariantparasite strain must dier in at least n sites to avoid all mem- ory. If the mutationratepersiteis,thenthe probability is n that aprogenyoftheoriginal strain is an escape variant with all of the n necessary dierences. Several laboratory experiments of inuenza have studied the origin of escape variants when neutralizing antibody pressure is imposed against viral epitopes (Yewdell et al. For anti- bodies against only a single epitope, escape variants arise often because only a single mutation is needed. The mutation rate of inuenza is on the order of = 105 per nucleotide per generation. Thus, a moderate- size population of viruses likely has at least a few escape mutants. By con- trast, a more focused immunodominant response allows the rapid evo- lution of escape variants. To determine the selective pressures imposed on parasite popula- tions, the immunodominance of each hosts memory prole must be placed in the context of variationinmemoryproles between hosts. A parasite with genotype A/B at the two sites sweeps through the popula- tion, infecting all hosts. One-half ofthe host population maintains mem- ory against both antigens, one-quarter has immunodominant memory against A only, and one-quarter has immunodominant memory against B only. Now consider how this distribution of memory proles inuences the success of antigenic variants. Thism utant can attack the quar- ter of the host population with memory only against B. Asthepara- site spreads, a second mutation to A /B allows attack of the remaining hosts. This example shows that strongly immunodominant host proles lim- ited to one or a few sites allow parasite mutants with few changes to succeed.

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Symptom Estimated prevalence (%) Location Estimated prevalence (%) Dysmenorrhea 78 purchase phenergan toronto. In most of the cases order phenergan without a prescription, are overexpressed in macrophages of women with endome- hematoxylineosin staining allows the diagnosis; immuno- triosis when compared with controls (3) purchase cheap phenergan on line. The mechanisms by which endometriosis Auto-antibodies (Abs) causes infertility are still largely not well defined. These Anti-endometrial Abs include anatomical changes that lead to adhesions or Antiphospholipid Abs Auto-Abs against carbonic anhydrase tubal obstruction, potential negative effects of peritoneal Auto-Abs against transferrin and follicular fluid on egg maturation and sperm motility, Auto-Abs against a2-Heremans-Schmidt glycoprotein potential oocyte maturational abnormalities and hormonal Auto-Abs against oxidatively modified lipoproteins variations, and the effects of endometriosis on uterine Auto-Abs against laminin-1 Antithyroid Abs receptivity for implantation. Endometriosis 273 specific for endometriosis and are also associated with women with endometriosis, none of them has been proved other gynecological and non-gynecological disorders to be useful for predicting the presence of the disease. Anti-endometrial Abs have cohort studies and seven case-control studies including been widely demonstrated to be increased in women with women with infertility or chronic pelvic pain (6). The exact antigen remains unknown; sensitivity was only 28%; if the sensitivity was increased to therefore, no simple antigen-antibody assay is currently 50%, the specificity decreased to 72%. When the analysis available (8) and the measurement of these Abs is not used was limited to women with advanced endometriosis, the in clinical practice. For a cardiolipin, ethanolamine, and beta-2-glycoprotein 1 have specificity of 89%, the sensitivity was 47%; an increase of increased levels in women with endometriosis but up to now the sensitivity to 60% resulted in a decrease of the specifi- there is no evidence that these Abs can be used in a clinical city to 81%. Serum protein-containing glycotopes such as sialy- lated T antigen might induce Abs response in patients with There are a limited number of reports on the significance endometriosis. Aberrant immunological mechanisms includ- secreted from the endometrium and endometriotic ing the production of auto-Abs may be involved in the implants; its serum levels may be slightly increased in pathogenesis of endometriosis-related infertility. Infertile women with endometriosis however the measurement of patients with endometriosis have increased prevalence of this molecule does not allow to discriminate patients with auto-Abs against laminin-1, which is a multifunctional gly- endometriosis from controls. Thyroid autoimmunity has also been documented in triosis but up to now it has not been largely investigated. Angiogenin, which may promote the establish- marker will yield sufficient sensitivity and specificity to be ment of new blood supply for the lesions, has increased used in clinical practice. However, in recent years, proteo- serum levels in women with endometriosis during the folli- mic technology has been applied to the research of new cular phase of the menstrual cycle and has recently been markers of endometriosis with promising results (12). It is contro- Contraceptives (to be reassessed) versial whether histology should be obtained if peritoneal Oral contraceptives disease alone is present; visual inspection is usually adequate Contraceptive patch but histological confirmation of at least one lesion is ideal. In Contraceptive ring Progestogens cases of ovarian endometrioma and in deeply infiltrating dis- Derivative of progesterone ease, histology should be obtained to identify endometriosis Medroxyprogesterone acetate and to exclude rare instances of malignancy (13). It is possible Megestrol acetate to suspect the presence of endometriosis on the basis of symp- Dydrogesterone toms reported by the patients and findings at gynecological Derivative of 19-nortestosterone Norethindrone examination, but limited information can be obtained on the Norgestrel extent of lesions. Therefore, preoperative imaging is required Lynestrenol for determining the location and severity of disease. Recently, multislice- conceive although they may have an anti-ovulatory effect computed tomography combined with colon distension by when taken at mid-cycle. Several studies proved that water enteroclysis has been proved to have high accuracy in suppression of ovarian function for 6 months reduces determining the presence of bowel endometriotic nodules with endometriosis-associated pain (13). Minimal lesions are more difficult to of the potential effects on the ectopic lesions and on the diagnose during clinical consultation, and they are usually immune system (4, 17, 18). Therapy Both gonadotropin-releasing hormone analogs and dana- zol have been used in the treatment of endometriosis; Medical therapy aims primarily to eradicate painful however, they may cause several adverse effects. In the symptoms; there is no evidence that currently available last 20 years, our understanding of the pathogenesis of medical therapies can enhance fecundity and reduce the endometriosis at the molecular and cellular levels has extent of endometriosis. Differences in character- and they may improve our ability to eliminate endome- istics among 1,000 women with endometriosis based on triotic lesions when present or more likely to prevent extent of disease. Fertil Steril 2002; ciated with improvements not only in pain symptoms but 78(4): 7339. Laboratory testing for endome- women with endometriosis, and this technique decreases triosis. An Laparotomy should be reserved for patients with advanced association of IgG anti-laminin-1 autoantibodies with endo- stage disease in whom laparoscopy is judged to be not metriosis in infertile patients. Pregnancy loss and endometriosis: Pathogenic role of anti- There is no solid evidence that the development of endo- laminin-1 autoantibodies. Hum unclear whether lifestyle (regular exercise, cigarette smok- Reprod 2005; 20(10): 2698704. Future perspectives in the medical treatment of endome- macrophages in endometriosis: Correlation between the triosis. Some of these patterns are related with global autoimmune regulation whereas others may be related with inflammatory autoimmunity against ovarian antigens. This syndrome (amenorrhea, hot flushes, genital autoantibodies are detected in patients with Addisons dis- atrophy, infertility) was first described by Atria in 1950. In the first one, there is a bodies, which are also present in just 1520% of patients complete absence of ovarian follicles, and it is characteristic with Addisons disease but without amenorrhea. Autoantibodies against other endocrine systems: Auto- are the target of autoimmune attack. Antireceptor antibodies: Antireceptor antibodies are pellucida binding, and recognition of porcine oocytes targeted against membrane hormone receptor. These appears to be highly non-specific because it occurs in sera antibodies may act mimicking the physiologic hormo- from 60% of healthy fertile women and even occurs in nal action or blocking the hormone function depending 40% of male serum samples. Some investigators zona pellucida autoantibodies may be more in the order have described the presence of antibodies directed of 2. However, such antibodies have also been detected in patients with iatrogenic ovarian failure (4). In experimental animal models, immune conditions varies somewhat between different these antibodies have been able to inhibit the follicular development (15). These patients with normal represent secondary effects of a more global endocrine number of ovarian follicles present gonadotrophin resis- autoimmune dysfunction. Autoimmune Ovarian Failure 279 and it has been suggested that estrogen may modulate the interfering with zona pellucida antigens, thereby disrup- T-cell activation arguing that T-cell activation observed in ting ovulation and/or fertilization (4). Furthermore, hormonal repla- include those methods that target zona pellucida; thus, cement therapy may decrease the number of activated immunization with heterologous zona pellucida antigens T cells (16). The T-killer cells are also diminished in number results in autoimmune oophoritis characterized by follicle and function as monocytes are (16). An inflammatory oophoritis such as that observed following immunization with ovarian homogenate, however, does not occur (18). The inflammation and other; they also determined different type of T cells subsides after 14 weeks, and the ovaries become atrophic. They also included two control This type of experimental oophoritis in mice is similar to groups. The authors concluded that subclinical ovarian failure is not an Conclusion autoimmune alteration. Serum ovarian present a greater incidence of type I diabetes and myasthe- antibodies appear after 28 days and may passively transfer nia gravis than general population. A novel autoantigen in patients with premature ovarian fail- J Clin Endocrinol Metab 1991; 73: 3607. Silva, Eduardo Ferreira Borba, Marcello Cocuzza, Jozelio Freire de Carvalho and Elosa Bonfa Abstract Testicular autoimmune disease may be primary or secondary. The former is characterized by an isolated infertility and autoantibodies directed to sperm, basement membrane, or seminiferous tubules without evidence of a systemic autoimmune disease.

As the attacks are triggered after exposure to cold buy generic phenergan on line, part of the examination can also be made by way of a simple cold provocation test where the person in question keeps his/her fingers under cold running water or inserts the finger in ice water for 5 minutes in order to provoke a white-finger attack Photo documentation generic phenergan 25 mg line. When an attack occurs purchase 25mg phenergan with mastercard, a witness confirms the white fingers by way of a photo of the person reporting the white fingers. The photo needs to show the face and hands of the person in question Certification by a doctor. An examining doctor (for example a specialist of occupational medicine) certifies that, in the examination, he or she has seen white finger attacks in the person in question with a detailed symptom description as set out below Perhaps a vascular-physiological examination. The examination is performed in a special laboratory with registration of finger blood pressure before and after finger cooling. However, if a vascular-physiological examination shows a positive white finger result, the disease is regarded as having been documented. Description of symptoms Regardless of the documentation method used, there always has to be a clear symptom description which sets out in detail which fingers and how much of the fingers may react with colour changes and a dead feeling. Furthermore there needs to be a detailed description of the delimitation and of the course of the attacks (prevalence, frequency, and duration). Work-related vibration disorders are usually reviewed by specialists of occupational health, but the documentation of attacks can also take place in other ways, see above. When the attack is subsiding, the lividness is replaced by a blue/red discolouration accompanied by a tickling sensation. Objective signs The diagnosis of white fingers is basically made in a clinical examination. Findings in a clinical examination while the person in question is having a white finger attack will be sharply delimited white fingers, involving one or more fingers on one or both hands. In a large number of cases there will be a need for the person in question to have supplementary medical examinations made: A. Assessment of wrist pulses when lifting arms and turning head sideways at the same time C. Examples of pre-existing and competitive diseases/factors Like most other diseases, white fingers can develop or become aggravated as a consequence of other diseases or factors not connected with work. Therefore the National Board of Industrial Injuries will make a concrete assessment of whether the nature and extent of any disclosed competitive factors may give grounds for turning down the disease entirely or whether, if the claim is recognised, there are grounds for making a deduction in the compensation. Examples of possible competitive factors which may affect the onset or the course of the disease: Familiar disposition (white fingers can be hereditary) Information of Raynauds disease of the toes Previous arm fractures Other vascular diseases of the arms Connective tissue diseases (real arthritis/rheumatoid arthritis and other autoimmune diseases) Polycytemy (a condition with abnormal increase in the number of red blood cells) Symptoms or information of any arteriosclerotic diseases, i. We cannot demand invasive examinations, but this type of examination can also be made non-invasively with surface electrodes Furthermore it may be beneficial to take a blood sample in order to rule out that substantially competitive conditions such as alcoholism, diabetes, B12 vitamin deficiency or folic acid deficiency may be the primary cause of the disease Peripheral neuropathy means injury to the distal nerves (impact on nerve ends or degeneration of nerve roots) and may occur in hands as well as feet. Peripheral means that there is damage to the ends/roots of one or more nerves with diffuse neuropathic complaints as a consequence of an impact on several big main nerves (nervus medianus, nervus ulnaris and nervus radialis) of the forearm. The disease needs to involve at least one of the three said main nerves of the forearm with consistent symptoms. Usually the disease will affect several of the mentioned three nerves (polyperipheral 136 neuropathy), but the disease can also be limited to a single nerve (monoperipheral neuropathy). The sensory nerve impulses have the effect that you for instance feel touch, pain, temperature, and pressure. This means that peripheral neuropathy may become manifest as fine motor and sensory complaints, but not necessarily both at the same time. Peripheral neuropathy can also be an accompanying disease to white fingers (Raynauds disease) and will in that case accompany the white finger attacks as opposed to an independent peripheral neuropathy, where the symptoms typically will be of a more permanent nature. The peripheral neuropathy will then in principle be regarded as a consequence of white fingers, which may qualify for recognition on the basis of the list, and therefore will not be processed as an individual disease. Cases of neuropathy in other regions than hands and fingers are not covered by this item of the list of occupational diseases. If there is peripheral neuropathy of hands as well as feet, this will furthermore be indicative of the disease having other causes than hand-arm vibrations in the workplace. For carpal tunnel syndrome, as opposed to peripheral neuropathy radiating from the medianus nerve, there will be a well-delimited pressure neuropathy at the wrist. If impingement/impact on the nervus medianus (carpal tunnel syndrome), nervus ulnaris or nervus radialis has been established, with accompanying peripheral neuropathy, it is not possible to recognise the peripheral neuropathy as a separate disease under item C. We cannot demand invasive examinations, but this type of examination can nowadays also be made non-invasively with surface electrodes. Competitive diseases/factors: Like most other diseases, peripheral neuropathy can develop or become aggravated as a consequence of other diseases or factors not connected with work. Competitive diseases/factors Like most other diseases, degenerative arthritis of the elbow or wrist can develop or become aggravated as a consequence of other diseases or factors not connected with work. Examples of possible competitive factors which may affect the onset or the course of the disease: Previous fractures of the wrist or elbow Connective tissue diseases (real arthritis/rheumatoid arthritis and other autoimmune diseases) 1. Exposure requirements for white finger and peripheral neuropathy For the diseases white fingers (Raynauds syndrome/Raynauds disease) and peripheral neuropathy of hands/fingers there must in principle have been relevant stressful work for a consecutive period of time consistent with the stresses compared with time in table 1 under item 8. A condition for recognising white fingers and peripheral neuropathy of hands/fingers is that there must have been vibration through hands and arms from hand-held tools, hand-held machines or stationary machines, the exposure happening through some kind of object. The intensity is measured by vibration acceleration, the so-called frequency-weighted acceleration, which is indicated by a 2 2 measuring unit in metres per second2 (m/s ) or decibel (dB). More specific requirements to the vibration exposure will depend on the severity of the exposure as well as the extent of the use of heavily vibrating hand tools per day and over time with reference to the form. For the purposes of making an assessment, if it is not possible to get information on the concrete acceleration level of the tool, there is a form with an indicated average level, see form 2 in paragraph 8. It should be noted that old tools usually have a higher vibration level than new tools, which are often vibration dampened. It is furthermore a prerequisite for recognition that there should be a good time correlation between the disease and the work with vibrating tools. For white fingers and peripheral neuropathy the relevant time correlation is that the first symptoms of the disease are seen some time after commencement of the stressful work of hand and arm. Depending on the extent and severity of the load, some time usually means about one year and up to several years. However, the assessment must stress whether for instance there have been extraordinarily severe, daily stresses. In such cases, from a medical point of view, there will be a time correlation between the work and the development of the disease, even if the onset of the first symptoms is a short while after commencement of the wrist-loading work. However, the disease must not have been manifest as a chronic disease before commencement of the stressful work. The load needs to be assessed in relation to the persons size and physique, and furthermore there needs to be a good time correlation between the exposure and the onset of the disease. When processing the claim, the National Board of Industrial Injuries may obtain a medical certificate from a specialist of occupational medicine. The medical specialist will furthermore make an individual assessment of the importance of stress factors for the development of the disease in the examined person in question. Exposure requirements for recognition of degenerative arthritis (arthrosis) of wrist and elbow joint Degenerative arthritis (arthrosis) of wrist and elbow joint only qualifies for recognition under item C.

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