Disorders of Hippocampus Facilitated by Hypertension in Purine Metabolism Deficiency is Repressed by Naringin, a Bi-flavonoid in a Rat Model via NOS/cAMP/PKA and DARPP-32, BDNF/TrkB Pathways.

Individuals who are hypertensive have a higher tendency of predisposition to other genetic diseases including purine metabolism deficiency. Therefore, the search for nontoxic and effective chemo protective agents to abrogate hypertension-mediated genetic disease is vital. This study therefore investigated the repressive effect of naringin (NAR) against disorder of hippocampus facilitated by hypertension in purine metabolism deficiency. Male albino rats randomly assigned into nine groups (n = 7) were treated for 35 days. Group I: control animals, Group II was treated with 100 mg/kg KBrO3, Group III was treated with 250 mg/kg caffeine, and Group IV was treated with 100 mg/kg KBrO3 + 250 mg/kg caffeine. Group V was administered with 100 mg/kg KBrO3 + 100 mg/kg haloperidol. Group VI was administered with 100 mg/kg KBrO3 + 50 mg/kg NAR. Group VII was administered with 250 mg/kg caffeine + 50 mg/kg NAR, and Group VIII was administered with 100 mg/kg KBrO3 + 250 mg/kg caffeine + 50 mg/kg NAR. Finally, group IX was treated with 50 mg/kg NAR. The sub-acute exposure to KBrO3 and CAF induced hypertension and mediated impairment in the hippocampus cells. This was apparent by the increase in PDE-51, arginase, and enzymes of ATP hydrolysis (ATPase and AMPase) with a simultaneous increase in cholinergic (AChE and BuChE) and adenosinergic (ADA) enzymes. The hypertensive-mediated hippocampal impairment was associated to alteration of NO and AC signaling coupled with lower expression of brain-derived neurotrophic factor and its receptor (BDNF-TrkB), down regulation of Bcl11b and DARPP-32 which are neurodevelopmental proteins, and hypoxanthine accumulation. However, these features of CAF-mediated hippocampal damage in KBrO3-induced hypertensive rats were repressed by post-treatment with NAR via production of neuro-inflammatory mediators, attenuation of biochemical alterations, stabilizing neurotransmitter enzymes, regulating NOS/cAMP/PKA and DARPP-32, BDNF/TrkB signaling, and restoring hippocampal tissues.

Kytococcus sedentarius and Micrococcus luteus: highly prevalent in indoor air and potentially deadly to the immunocompromised - should standards be set?

The multifarious types of infections contracted from indoor environments show that buildings can serve as a reservoir for infectious bacteria. This study is an investigation into the type and concentrations of bacteria in the indoor and outdoor environments of an electronic factory, an office and a winery in Malaysia. Trypticase soy agar (TSA) (with ambient air incubation) and TSA supplemented with haemin and NADH (with CO2 enhanced incubation) were used for the isolation of bacteria. The plates were incubated at 37ºC for 3 days. A random selection of bacterial isolates were Gram stained and identified using the BD BBL Crystal Identification Systems. Kytococcus sedentarius and Micrococcus luteus were the predominant bacterial species identified from indoor air. These bacteria were present at relatively high concentrations in indoor air, at times, above 800 colony forming units per cubic meter (CFU/m3) of air. This indicates that both K. sedentarius and M. luteus can survive a wide range of adverse conditions, including chemical contamination and ultraviolet exposure. M. luteus is a known cause of pneumonia in immunocompromised individuals and has also been implicated in skin infections. Recent reports suggest species of kytococci as emerging opportunistic pathogens of the immunocompromised, paediatrics and the elderly. We postulate that opportunistic bacteria, such as the kytococci and the micrococci, may also have a potential role in instigating subclinical, more subtle symptoms of disease in inmmunocompetent individuals.

Effects of low-iron status and deficiency of essential fatty acids on some biochemical constituents of rat brain.

The effects of iron and essential fatty acids (EFA) on the development of the brain were studied in young rats. Male weanling rats were maintained on diets deficient in EFA, low in iron (9 ppm) or deficient in both EFA and iron. The low-iron status aggravated signs of EFA deficiency indicating decreases in both growth and brain weight. While the protein content of the brain was considerably reduced, the alkaline phosphatase (ALP) activity increased in all dietary regimes. The lipids and fatty acid components of the brain were affected both qualitatively and quantitatively by the diets. Myelin lipids and docosahexaenoic acid (DHA, 22:6) were reduced by the iron deficient diets and the effect was found to be greater in the deficiency of both EFA and iron. It appears that dietary iron has a significant role to play in the biosynthesis of prostaglandins and in the proper configurational development and functioning of the brain.