Determination of Ge in Au alloys using sodium hypophosphite and potassium iodate potentiometric titration method

This paper presents a new method of determining Ge in AuGe alloys by potassium iodate(KIO3)potentiometric titration when Ge(Ⅱ)and Au(0)are simultaneously reduced from Ge(Ⅳ)and Au(Ⅲ)by sodium hypophosphite rather than by distillation separation.The influences of such conditions as the reduction acidity,the dosage of sodium hypophosphite and the reduction time on the determination of Ge were studied.Ge in AuGe alloys such as AuGe_(12),AuGeNi_(12-2),AuAgGe_(18.8-12.5),and AuAgGeNi_(43.8-6-0.2)was measured with the relative standard deviation(RSD)of 0.10%-0.31%and the recoveries of added standard Ge in sample of 99.40%-100.40%under the conditions of 0.40-0.80 mol·L^(-1)HCl,3.3 mol·L^(-1)H^(3)PO^(4),15 g sodium hypophosphite,and reduction time of40 min.The new method presented is of high accuracy in results,good stability and sensibility in end-point,and easy operation and strong selectivity of determination.

Prediction of Short-Term Mortality after Valve Surgery： A Single Center＇s Perspective

To the Editor： Valve stenosis and regurgitation can lead to a series of symptoms, including chest distress and dyspnea. Valve replacement is an effective surgical procedure that improves patients＇ quality of life and life span and has played an increasingly important role in treating mitral valve diseases. Previous studies have reported different risk factors and independent predictors of increased mortality in patients with mitral valve replacement （MVR） and/or aortic valve replacement （AVR）. This study retrospectively reviewed data on patients undergoing valve surgery to determine the risk factors and predictors of short-term mortality in this patient population.

Microglia and astroglia:the role of neuroinflammation in lead toxicity and neuronal injury in the brain

Lead(Pb^(2+)),a ubiquitous environmental toxicant,may widely affect the function of many organs or systems of human beings,especially the brain.Although lead is believed to transport into the brain through the blood-brain barrier(BBB)and cause direct neuronal injury,growing data have shown that lead exposure could induce brain dysfunction by triggering microglial and astroglial activation,pro-inflammatory cytokine production and inflammatory response,generation of reactive oxygen species and oxidative stress,and finally result in BBB dysfunction and neuronal damage.This review summarizes recent studies regarding microglial and astroglial reaction,neuroinflammation,and neuronal death in the brain following lead insult,suggesting that reactive glial cells may represent a potential target for manipulation of lead-induced neuroinflammatory injury of the brain.

Astrocyte,reactive astrocytes and self-regulative apoptosis in the neuroinflammation

Astrocyte,one of the most abundant glial cell types,actively functions in stabilizing neural circuits and synaptic transmission in the central nervous system(CNS).Astrocytes not only provide metabolic and trophic supports to various CNS neurons and but also actively work in assisting synaptic transmission and plasticity.A line of growing evidences have documented that astrocytes present as an essential coordinatorin neural circuit function.[1]Firstly,calcium signaling or calcium wave calcium(Ca^(2+))between neighboring astrocytes contribute to establishment of a huge astrocytic glial network by gap-junctions,which has updated the understanding of astrocyte function in CNS,and led to an idea that astrocytes are powerful regulators of neuronal spiking.