Methamphetamine: Effects on the brain, gut and immune system

Methamphetamine (METH) is a powerful central nervous system stimulant which elevates mood, alertness, energy levels and concentration in the short-term. However, chronic use and/or at higher doses METH use often results in psychosis, depression, delusions and violent behavior. METH was formerly used to treat conditions such as obesity and attention deficit hyperactivity disorder, but now is primarily used recreationally. Its addictive nature has led to METH abuse becoming a global problem. At a cellular level, METH exerts a myriad of effects on the central and peripheral nervous systems, immune system and the gastrointestinal system. Here we present how these effects might be linked and their potential contribution to the pathogenesis of neuropsychiatric disorders. In the long term, this pathway could be targeted therapeutically to protect people from the ill effects of METH use. This model of METH use may also provide insight into how gut, nervous and immune systems might break down in other conditions that may also benefit from therapeutic intervention

Hrvatska liturgijska pjesmarica: Pjevajte Gospodu pjesmu novu (III. popravljeno i dopunjeno izdanje)

Bananas have enormous health benefits as a food for both animals and humans. They have been used as a complimentary medicine to treat pathological conditions since ancient times. Recently, there has been increased interest in the scientific validity of the beneficial effects of bananas in alleviating and treating disease conditions including, ulcers, infections, diabetes, diarrhea, colitis and blood pressure. Herein, we write on the potential therapeutic and functional benefits of certain species of bananas when consumed green as well as considering the properties of extracts from the non-fruit parts of the plant. We conclude that green bananas appear to deliver an array of health and therapeutic benefit

Curcumin activates the p38MPAK-HSP25 pathway in vitro but fails to attenuate diabetic nephropathy in DBA2J mice despite urinary clearance documented by HPLC

<p>Abstract</p> <p>Background</p> <p>Curcumin has anti-inflammatory, anti-oxidant, and anti-proliferative properties, and depending upon the experimental circumstances, may be pro- or anti-apoptotic. Many of these biological actions could ameliorate diabetic nephropathy.</p> <p>Methods/Design</p> <p>Mouse podocytes, cultured in basal or high glucose conditions, underwent acute exposure to curcumin. Western blots for p38-MAPK, COX-2 and cleaved caspase-3; isoelectric focusing for HSP25 phosphorylation; and DNase I assays for F- to G- actin cleavage were performed for <it>in vitro </it>analyses. <it>In vivo </it>studies examined the effects of dietary curcumin on the development of diabetic nephropathy in streptozotocin (Stz)-induced diabetes in DBA2J mice. Urinary albumin to creatinine ratios were obtained, high performance liquid chromatography was performed for urinary curcuminoid measurements, and Western blots for p38-MAPK and total HSP25 were performed.</p> <p>Results</p> <p>Curcumin enhanced the phosphorylation of both p38MAPK and downstream HSP25; inhibited COX-2; induced a trend towards attenuation of F- to G-actin cleavage; and dramatically inhibited the activation of caspase-3 in <it>vitro</it>. In curcumin-treated DBA2J mice with Stz-diabetes, HPLC measurements confirmed the presence of urinary curcuminoid. Nevertheless, dietary provision of curcumin either before or after the induction of diabetes failed to attenuate albuminuria.</p> <p>Conclusions</p> <p>Apart from species, strain, early differences in glycemic control, and/or dosing effects, the failure to modulate albuminuria may have been due to a decrement in renal HSP25 or stimulation of the 12/15 lipoxygenase pathway in DBA2J mice fed curcumin. In addition, these studies suggest that timed urine collections may be useful for monitoring curcumin dosing and renal pharmacodynamic effects.</p

Effect of endothelium-derived relaxing factor on renin secretion from isolated mouse renal juxtaglomerular cells

This study aimed to examine the direct influence of native endothelium derived relaxing factor (EDRF) on renin secretion. To this end isolated mouse renal juxtaglomerular cells were cocultured with bovine aortic endothelial cells which produced and released significant amounts of EDRF as assayed by guanylate cyclase activities which were measured separately in endothelial and juxtaglomerular cells as well as in the cocultures of juxtaglomerular with endothelial cells. EDRF production was blunted in the absence of extracellular L-arginine and in the presence of N omega-nitro-L-arginine (L-NAG; 200 microM). Inhibition of endothelial EDRF production by removal of arginine or addition of L-NAG was associated with a significant decrease of renin secretion from the cocultures while the same regimen had no effect on renin secretion from JG cells alone. Exogenous generation of nitric oxide by the addition of sodium nitroprusside (100 microM) stimulated renin secretion in the cocultures both at normal and inhibited EDRF formation as well as from juxtaglomerular cells alone. These findings suggest that native EDRF released from vascular endothelial cells is a stimulatory signal for renin secretion from renal juxtaglomerular cells