Green tea,white tea,and Pelargonium purpureum increase the antioxidant capacity of plasma and some organs in mice

ObjectiveWe tested in mice the hypothesis that ingestion of infusions of green tea, white tea, or the aromatic plant Pelargonium purpureum increases total antioxidant capacity (TAC) of plasma and organs.MethodsTwenty-five mice were randomly assigned to five groups, each of which received by gavage 0.1 mL of infusion from green tea, white tea, or P. purpureum (8 g/100 mL of water) or catechin (0.01 g/100 mL) or water for 5 consecutive days. On the fifth day the animals were euthanized. Blood was taken by heart puncture and the heart, lungs, liver, spleen, kidney, and brain were removed. TAC was measured in plasma and in all organ homogenates with the ferric reducing antioxidant power assay and in selected organ homogenates by the total radical-trapping antioxidant parameter assay.ResultsGreen tea and P. purpureum increased TAC in the plasma and lungs, whereas green tea, white tea, and catechin increased TAC in heart homogenates. No effect was observed on the liver, brain, spleen, and kidney homogenates in comparison with the water control with the ferric reducing antioxidant power assay or the total radical-trapping antioxidant parameter assay.ConclusionThese results suggest that green tea, white tea, and P. purpureum exhibit antioxidant effects in vivo that may be observed not only in plasma but also in some organs.     

Female-specific issues in multiple sclerosis

Complex neuroendocrine mechanisms regulating the immune response can be recognized in all autoimmune diseases. Such mechanisms develop through endocrine loops and feedback processes along the hypothalamus-pituitary-gonads axis and the hypothalamus-pituitary- adrenal gland axis. Females are not only more susceptible to autoimmune diseases, but are also more exposed to relevant variations of hormonal levels that physiologically go along with women's life. This paper reviews female-specific issues in multiple sclerosis and how treatments must be considered accordingly. In particular, aspects related to puberty, menses, fertility, pregnancy, lactation and menopause are considered in addition to epidemiological and clinical issues.     

Sporadic vascular dementia as clinical presentation of a new missense mutation within exon 7 of NOTCH3 gene

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic disease characterized by ischemic stroke with early onset, migraine, seizures, and vascular dementia. CADASIL is associated with mutations within NOCT3 gene, mainly clustered in exons 3 and 4. We report a case of CADASIL presenting progressive subcortical dementia in the sixth decade. Neither family history, nor acute ischemic events were present. MRI findings were typical for CADASIL. NOTCH3 analysis disclosed a new missense mutation within exon 7, leading to the substitution of cysteine 366 with a tryptophan (Cys366Trp). Our finding suggests CADASIL diagnosis must be considered in patients with vascular dementia also in absence of stroke-like events and of family history.     

Strain-specific susceptibility for neurodegeneration in a rat model of autoimmune optic neuritis

Heterogeneity in clinical disease course and histopathology complicates the treatment of multiple sclerosis. We detected important differences in neurodegeneration in various subtypes of myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis. Dark Agouti (DA) rats showed a significantly higher survival of retinal ganglion cells in comparison to Brown Norway rats. After surgical transection of the optic nerve neuronal loss was similar in both rat strains. We identified an increased expression of interleukin 1beta and glial cell line-derived neurotrophic factor in DA rats as the possible mechanism of the observed endogenous neuroprotection in MOG-induced optic neuritis.     

Histological evaluation of biocompatibility of lyophilized bovine pericardium implanted subcutaneously in rats

Abstract:  This article aims at investigating in vivo evaluation of lyophilization procedure on the biocompatibility of bovine pericardium treated with glutaraldehyde (GA). The bovine pericardium was fixed with 0.5% glutaraldehyde during 10 days and preserved in 4% formaldehyde (FA). Two groups of samples were prepared from treated membranes: Group 1, nonlyophilized samples and Group 2, lyophilized samples. Male Sprague-Dawley rats (4 weeks after birth) were anesthetized (pentobarbital sodium 25 mg/kg of body weight) and in each one were implanted subcutaneously in the dorsal region a sample from Group 1 and another from Group 2. These samples were explanted after 30 days for histological analysis. No intercurrences took place after the surgery. No differences ( P  > 0.05) in the calcification, granulomatous reaction, mononuclear infiltration, and granulation tissue development was observed between both groups. The implanted lyophilized samples presented a trend for a reduced inflammatory reaction. Lyophilization of the bovine pericardium does not seem to increase the above listed tissue reaction.     

Calcium-sensing receptor attenuates AVP-induced aquaporin-2 expression via a calmodulin-dependent mechanism

Recent evidence suggests that arginine vasopressin (AVP)-dependent aquaporin-2 expression is modulated by the extracellular calcium-sensing receptor (CaSR) in principal cells of the collecting duct, but the signaling pathways mediating this effect are unknown. Using a mouse cortical collecting duct cell line (mpkCCD(cl4)), we found that increasing the concentration of apical extracellular calcium or treating with the CaSR agonists neomycin or Gd(3+) attenuated AVP-dependent accumulation of aquaporin-2 mRNA and protein; CaSR gene-silencing prevented this effect. Calcium reduced the AVP-induced accumulation of cAMP, but this did not occur by increased degradation of cAMP by phosphodiesterases or by direct inhibition of adenylate cyclase. Notably, the effect of extracellular calcium on AVP-dependent aquaporin-2 expression was prevented by inhibition of calmodulin. In summary, our results show that high concentrations of extracellular calcium attenuate AVP-induced aquaporin-2 expression by activating the CaSR and reducing coupling efficiency between V(2) receptor and adenylate cyclase via a calmodulin-dependent mechanism in cultured cortical collecting duct cells.     

Late restenosis following sirolimus-eluting stent implantation

Despite encouraging results from randomized trials, concerns exist about long-term results of sirolimus-eluting stent implantation. We sought to determine whether in-stent restenosis occurring >1 year ("late") after sirolimus-eluting stent implantation is a real clinical entity. We analyzed data on all sirolimus-eluting stents implanted in our institution before March 2003. During the study period 928 lesions in 433 patients were treated. Angiographic follow-up was performed in 306 patients (70.6%) with 679 lesions (73.2%). Angiography after 1 year was performed only in symptomatic patients. We considered restenosis "early" if it occurred during the first year and late if after 1 year. Late restenosis required demonstration of a widely patent stent at 6 to 9 months, with repeat angiography after 1 year demonstrating restenosis. Restenosis occurred in 160 lesions overall (23.5%). Of the 31 (4.6%) that were documented after 1 year, 13 were excluded from analysis due to absence of 6- to 9-month angiography; the remaining 18 (2.6%, 1.7 to 4.2) fulfilled our criteria for late restenosis (median time of documentation 607 days, interquartile range 511 to 923). In conclusion, late restenosis is an infrequent but real entity; its existence implies we should not discount the possibility of restenosis as the cause of symptoms that develop >1 year after sirolimus-eluting stent implantation.