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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chilling injury is the major limiting factor for successful cryopreservation of both human and animal oocytes. Maternal hyperthermia is the main reason for summer infertility in dairy cows. In this paper, we will present evidence for the involvement of membrane lipid composition and its thermotrophic behavior and the mechanism by which chilling injury and/or heat stress disrupt oocytes' developmental competence. Although oocyte and single zygote are similar in shape and size, the oocyte is known to be very sensitive to cryopreservation, whereas, the zygote is successfully cryopreserved. Recently, we have shown that the lipid-phase transition (LPT) in human MII oocytes occurs at about 20 degrees C, while the LPT temperature of zygotes is lower by 10 degrees C. Similarly, the LPT in oocytes collected from dairy cows was found to be elevated by 10 degrees C in the summer vs. the winter. This feature was associated with alterations in membrane lipid composition. In particular, during the winter, the oocyte membrane is composed mainly of mono- and polyunsaturated fatty acids while in the hot summer, it is composed of more saturated fatty acids. In another study, we showed that exposure of bovine oocytes to physiologically relevant heat shock increases the proportion of oocytes that undergo apoptosis, presumably via sphingomyelin hydrolysis and ceramide formation (i.e. the sphingomyelin apoptosis pathway). Using a mouse model, we have recently shown that hyperthermia of 1.5 degrees C affects the follicle enclosed oocyte as determined by lower developmental competence. Given the importance of the membrane's composition and integrity, it appears that alterations in the oocyte-membrane underlie the disruption of developmental competence in mammalian oocytes exposed to thermal stress (i.e. chilling injury or heat shock).
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PMID:Do chilling injury and heat stress share the same mechanism of injury in oocytes? 1824 81

The National Institutes of Health (NIH) has redefined prostatitis into four distinct entities. Category I is acute bacterial prostatitis. It is an acute prostatic infection with a uropathogen, often with systemic symptoms of fever, chills and hypotension. The treatment hinges on antimicrobials and drainage of the bladder because the inflamed prostate may block urinary flow. Category II prostatitis is called chronic bacterial prostatitis. It is characterized by recurrent episodes of documented urinary tract infections with the same uropathogen and causes pelvic pain, urinary symptoms and ejaculatory pain. It is diagnosed by means of localization cultures that are 90% accurate in localizing the source of recurrent infections within the lower urinary tract. Asymptomatic inflammatory prostatitis comprises NIH category IV. This entity is, by definition, asymptomatic and is often diagnosed incidentally during the evaluation of infertility or prostate cancer. The clinical significance of category IV prostatitis is unknown and it is often left untreated. Category III prostatitis is called chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). It is characterized by pelvic pain for more than 3 of the previous 6 months, urinary symptoms and painful ejaculation, without documented urinary tract infections from uropathogens. The syndrome can be devastating, affecting 10-15% of the male population, and results in nearly 2 million outpatient visits each year. The aetiology of CP/CPPS is poorly understood, but may be the result of an infectious or inflammatory initiator that results in neurological injury and eventually results in pelvic floor dysfunction in the form of increased pelvic muscle tone. The diagnosis relies on separating this entity from chronic bacterial prostatitis. If there is no history of documented urinary tract infections with a urinary tract pathogen, then cultures should be taken when patients are symptomatic. Prostatic localization cultures, called the Meares-Stamey 4 glass test, would identify the prostate as the source for a urinary tract infection in chronic bacterial prostatitis. If there is no infection, then the patient is likely to have CP/CPPS. For healthcare providers, the focus of therapy is symptomatic relief. The first therapeutic measure is often a 4- to 6-week course of a fluoroquinolone, which provides relief in 50% of men and is more efficacious if prescribed soon after symptoms begin. Second-line pharmacotherapy involves anti-inflammatory agents for pain symptoms and alpha-adrenergic receptor antagonists (alpha-blockers) for urinary symptoms. Potentially more effective is pelvic floor training/biofeedback, but randomized controlled trials are needed to confirm this. Third-line agents include 5alpha-reductase inhibitors, glycosaminoglycans, quercetin, cernilton (CN-009) and saw palmetto. For treatment refractory patients, surgical interventions can be offered. Transurethral microwave therapy to ablate prostatic tissue has shown some promise. The treatment algorithm provided in this review involves a 4- to 6-week course of antibacterials, which may be repeated if the initial course provides relief. Pain and urinary symptoms can be ameliorated with anti-inflammatories and alpha-blockers. If the relief is not significant, then patients should be referred for biofeedback. Minimally invasive surgical options should be reserved for treatment-refractory patients.
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PMID:Chronic prostatitis: management strategies. 1919 37

Case Presentation. Mrs. X, 35 years old, case of primary infertility, was diagnosed to have genital tuberculosis on the basis of PCR positive and hysterolaparoscopy findings and received category I ATT for 6 months. Following ATT completion, her USG revealed no evidence of tuboovarian mass or hydrosalpinx. Since her tubes were patent, she underwent 3 cycles of ovulation induction and 2 cycles of IUI. The women presented with acute PID, five days after IUI, and was conservatively managed. She again presented 24 days after IUI with persistent low grade fever and abdominal pain. Suspecting relapse of genital tuberculosis, she was started on category II ATT. She had acute episodes of high grade fever with chills 2 weeks after starting ATT and MRI revealed bilateral TO masses suggestive of pyosalpinx. Emergency laparotomy was done, pus was drained, and cyst wall was removed and HPE was suggestive of chronic inflammation with few granulation tissues. ATT was continued for one year and the woman improved. Conclusion. The possibility of flare-up of PID (pelvic inflammatory disease) in treated case of tuberculosis undergoing infertility management should be kept in mind and aggressive management should be done.
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PMID:A Rare Case of Flare-Up of PID in Infertility Treatment. 2660 Sep 59