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

Background/aim: We calculated the homeostatic model assessment (HOMA) for estimating insulin sensitivity and beta-cell function in normal, healthy nondiabetics with infections (malaria, influenza, HIV, Helicobacter pylori, Chlamydia pneumoniae, and hepatitis C virus), type 2 diabetic black patients, and healthy controls from Kinshasa, DR Congo. Materials and methods: A case-control study was carried out between 2006 and 2007 for black Central African participants managed for HOMA.Results: In total, 219 patients and 110 healthy controls were matched for sex and age. The hyperbolic product for 85 infected patients occupied an intermediate position between the hyperbolic product for 110 controls and that of 134 type 2 diabetics. Inflammation/oxidative stress was present in all infected patients, as well as in the type 2 diabetics. Of the patients, 39.3% and 49.8% had insulin resistance and metabolic syndrome, respectively. Insulin resistance was more prevalent in nondiabetics with inflammation/oxidative stress (47.1%; P = 0.041) than in type 2 diabetics (34.3%). Type 2 diabetics had higher insulin sensitivity and lower beta-cell function but a similar HOMA-IR score. Conclusion: We recommend the assessment of insulin resistance in Central African patients with severe infections and type 2 diabetes.
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PMID:Hyperbolic relation between beta-cell function and insulin sensitivity for type 2 diabetes mellitus, malaria, influenza, Helicobacter pylori, Chlamydia pneumoniae, and hepatitis C virus infection-induced inflammation/oxidative stress and temporary insulin resistance in Central Africans 2930 46

Despite being in the midst of a global pandemic of infections caused by the pathogen Chlamydia trachomatis, a vaccine capable of inducing protective immunity remains elusive. Given the C. trachomatis mucosal port of entry, a formulation compatible with mucosal administration and capable of eliciting potent genital tract immunity is highly desirable. While subunit vaccines are considered safer and better tolerated, these are typically poorly immunogenic and require co-formulation with immune-potentiating adjuvants. However, of the adjuvants licensed for use in humans, very few drive robust cellular responses, a pre-requisite for protection against C. trachomatis infection. Recently, the cationic adjuvant formulations (CAF) have been shown to induce robust humoral and cellular immunity in pre-clinical models of chlamydia, malaria and tuberculosis (TB). Here, we demonstrate that CAF01 induces potent immune responses when combined with the major outer membrane protein (MOMP) of C. trachomatis following parenteral immunisation and also as part of a heterologous prime/boost regime. We show that a subcutaneous prime with CAF01-adjuvanted recombinant MOMP licenses antigen-specific immunity at distant mucosal sites which can be activated following oral antigen re-encounter in the absence of concomitant adjuvant stimulation. Finally, we shed light on the mechanism(s) through which CAF01 elicits robust antigen-specific immunity to co-formulated MOMP via type I interferon (IFN) signalling.
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PMID:Type I IFN signalling is required for cationic adjuvant formulation (CAF)01-induced cellular immunity and mucosal priming. 3172 5


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