Annals of medicine
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Many studies in several species, including humans, have identified a subset of primary afferent nerve fibres that are activated by potential or actual tissue-damaging stimuli. Discharge patterns of these nociceptive afferents faithfully reproduce some aspects of the applied stimuli (e.g. shape of the stimulus-response function) but not others (e.g. time-course of a sustained stimulus). ⋯ Therefore, the painfulness of a stimulus cannot be deduced from nociceptor discharges alone; central processing needs to be taken into account, particularly central summation. In addition to the immediate responses of nociceptive afferents to external stimulation, acute pain mechanisms also comprise the short-term plasticity of the nociceptive system as a consequence of prolonged noxious stimulation.
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Vulvodynia is a complex multifactorial and multidisciplinary clinical syndrome of unexplained vulvar pain, sexual dysfunction, and psychological disability. Because of the absence of abnormal physical findings among such patients, vulvodynia was long thought to be solely a psychosomatic syndrome. The incidence or prevalence of vulvodynia has not been well studied. ⋯ The most common subtypes are vulvar vestibulitis syndrome, cyclic vulvovaginitis and dysesthetic vulvodynia. Simple practice guidelines can be developed to facilitate the evaluation and management of such patients. Systematic epidemiological, etiological and therapeutic studies of vulvodynia are urgently needed.
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The adipsin-ASP pathway provides a mechanism by which the adipocyte is able to regulate its rate of de novo triglyceride synthesis and reesterification. The adipocyte can synthesize and secrete the three proteins necessary for the formation of the effector molecule, acylation stimulating protein (ASP). ASP increases membrane transport of glucose and the activity of diacylglycerol acyltransferase and by virtue of both of these effects markedly increases the rate of triglyceride synthesis. ⋯ Accordingly, the concept of microenvironmental metabolic regulation of triglyceride hydrolysis at the endothelial surface and triglyceride synthesis within the adipocyte will be presented. In addition, the pathogenetic sequence by which dysfunction of this pathway can lead to dyslipoproteinaemia will be reviewed. Emphasis, however, will be placed on the role this pathway may play in the pathogenesis of obesity and the adaptation to negative caloric balance in the obese.
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The pathogenesis of nutritional rickets is not well-understood. While the etiologies include deficiencies of vitamin D, calcium (Ca) or phosphate (PO4), and perhaps aluminium toxicity, the role these nutrients play in the development of tissue level anomalies characteristic of rachitic cartilage and bone has yet to be defined. Reported alterations in the biochemistry of rachitic bone and cartilaginous matrix which could adversely affect mineralization and endochondral ossification are of questionable significance since the tissues mineralize rapidly when exposed to Ca and PO4 salts in vivo and in vitro. ⋯ In healing rickets, the Ca and PO4 content of these tissue fluids increases in the same time-frame it takes to experimentally remineralize the matrices. However, it is not certain what determines the Ca and PO4 content of the ECF. Cytokines which may play a role in the cellular regulation of Ca and PO4 and maintain processes which contribute to normal patterns of endochondral ossification could provide a mechanism common to the pathogenesis of rickets from a variety of causes.
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Insulin-dependent diabetes mellitus (IDDM), or type I diabetes, is the end result mainly of a T-cell mediated autoimmune destruction of pancreatic islet beta cells. Genetical and environmental factors are both of importance in the pathogenesis. Genes in the HLA complex seem to be the most important genetical factors. ⋯ Thus, the recognition of certain islet beta cell derived peptides by self-reactive CD4+ T cells, may be an initial event in the pathogenesis. The DQ molecules involved in IDDM susceptibility or protection may exert their function either during thymic development of potential self-reactive CD4+ T cells, or by preferential presentation of certain beta-cell derived peptides to CD4+ T cells, or both. The finding that certain DQ molecules as such confer IDDM susceptibility may lead to new methods to prevent IDDM, for example by using blocking peptide analogues.