Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta Androstenes steroid up-regulates immunity to increase resistance against lethal infection and lethal radiation, and mediates a rapid recovery of hematopoietic precursor cells after radiation injury. beta Androstenetriol increases the levels of the TH(1) cytokines, IL-2, IL-3, IFN gamma and counteracts hydrocortisone mediated immune suppression. In contrast, 17 alpha androstenediol inhibits proliferation and mediates apoptosis in tumor cells of murine and human origin. Its epimer 17beta androstenediol does not. The antiproliferative functions of 17 alpha androstenediol are not dependent on either the estrogen or androgen receptors. Our findings show that beta androstenes and analogs protect the host from lethal infection by DNA or RNA viruses such as, herpesvirus type 2, coxsackievirus B4, influenza, and arthropod borne viruses. These androstenes also protected the host from lethal bacterial infections by Enterococcus faecalis, Pseudomonas aeruginosa, and Klebsiella pneumonia and from parasites infections, i.e. Cryptosporidium parvum, and malaria. In vivo, the level of potency follows the order: dehydroepiandrosterone<<<androstenediol<androstenetriol with the latter being up to one hundred thousand times more potent in protecting the host from infections than the first. In vitro, their effects are also dramatically different from one another with only beta androstenetriol potentiating the cellular response by increasing lymphocyte activation and counteracting hydrocortisone immune-suppressive activity. Conceptually, the androstenes form a new and different subclass of steroid hormones with unique physiological properties. Following host injury, the balance between the epimers and isomers is a determining factor in the overall regulation of hematopoiesis, TH(l)/TH(2) balance, and host resistance to infections and tumor growth.
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PMID:Immune up-regulation and tumor apoptosis by androstene steroids. 1239 92

Infection may cause stillbirth by several mechanisms, including direct infection, placental damage, and severe maternal illness. Various organisms have been associated with stillbirth, including many bacteria, viruses, and protozoa. In developed countries, between 10% and 25% of stillbirths may be caused by an infection, whereas in developing countries, which have much higher stillbirth rates, the contribution of infection is much greater. In developed countries, ascending bacterial infection, both before and after membrane rupture, with organisms such as Escherichia coli, group B streptococci, and Ureaplasma urealyticum is usually the most common infectious cause of stillbirth. However, in areas where syphilis is prevalent, up to half of all stillbirths may be caused by this infection alone. Malaria may be an important cause of stillbirth in women infected for the first time in pregnancy. The two most important viral causes of stillbirth are parvovirus and Coxsackie virus, although a number of other viral infections appear to be causal. Toxoplasma gondii, Listeria monocytogenes, and the organisms that cause leptospirosis, Q fever, and Lyme disease have all been implicated as etiologic for stillbirth. In certain developing countries, the stillbirth rate is high and the infection-related component so great that achieving a substantial reduction in stillbirth should be possible by reducing maternal infections. However, because infection-related stillbirth is uncommon in developed countries, and because those that do occur are caused by a wide variety of organisms, reducing this etiologic component of stillbirth much further will be difficult.
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PMID:Infection and stillbirth. 1928 57