Gelling and reducing agents are potential carbon and energy sources in culturing of anaerobic microorganisms.

Unlabelled: The majority of microorganisms in the environment have yet to be isolated in pure cultures, and the reasons behind this phenomenon remain elusive. In this study, we investigated the possibility of the commonly used gelling agent including agar and gellan gum as a source of carbon and energy in anaerobic roll-tube cultivation from one mangrove sediment sample and two high-temperature oilfield samples. Based on growth tests and genomic evidence, anaerobic gellan degraders were retrieved from genera of , , and lineages from the rarely cultivated phylum Atribacterota.

Coenzyme Q10 protects astrocytes from ROS-induced damage through inhibition of mitochondria-mediated cell death pathway.

Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes.

[Experimental studies on pharmacokinetics of three components in Buyanghuanwu injection on base of total quantum statistical moment].

Objective: To verify established the total quantum statistic moments model with astragaloside IV, paeoniflorin, tetramethylpyrazine in Buyanghuanwu injection, in order to establish a pharmacokinetic experimental method with multi-component traditional Chinese medicine (TCM) compound system.

Method: The RP-HPLC was adopted, with the chromatographic column of C18, 4.6 mm x 250 mm, 5 microm.

Association of selenoprotein p with Alzheimer's pathology in human cortex.

Selenium is known for its antioxidant properties, making selenoproteins candidate molecules for mitigation of neurological disorders in which oxidative stress has been implicated. The selenium transport protein, selenoprotein P, is essential for neuronal survival and function. We sought to determine whether selenoprotein P expression is associated with Alzheimer's disease pathology.

Cytotoxic withanolides from Physalis angulata L.

Four new withanolides, physagulins L-O (1-4), were isolated from the MeOH extract of the aerial parts of Physalis angulata L. (Solanaceae), together with seven known withanolides, compounds 5-11. Their structures were determined by spectroscopic techniques, including 1H-, 13C-NMR (DEPT), and 2D-NMR (HMBC, HMQC, 1H,1H-COSY, NOESY) experiments, as well as by HR-MS.

Mutation in Mpzl3, a novel [corrected] gene encoding a predicted [corrected] adhesion protein, in the rough coat (rc) mice with severe skin and hair abnormalities.

The rough coat (rc), an autosomal-recessive mutation, arose spontaneously in C57BL/6J mice. Homozygous rc mice develop severe skin and hair abnormalities, including cyclic and progressive hair loss and sebaceous gland hypertrophy. The rc locus was previously mapped to Chromosome 9.

Induction of heat shock proteins by hyperglycemic cerebral ischemia.

Hyperglycemia worsens the neuronal death induced by cerebral ischemia. A previous study demonstrated that diabetic hyperglycemia suppressed the expression of heat shock protein 70 (HSP70) in the liver. The objective of this study is to determine whether hyperglycemia exacerbates ischemic brain damage by suppressing the expression of heat shock proteins (HSPs) in the brain.

Activation of cell death pathway after a brief period of global ischemia in diabetic and non-diabetic animals.

Mitochondria play a critical role in the pathogenesis of cerebral ischemia. Acute hyperglycemia has been shown to activate the mitochondria-initiated cell death pathway after an intermediate period of ischemia. The objective of the present study was to determine if diabetic hyperglycemia induced by streptozotocin activates the cell death pathway after a brief period of global ischemia.

Up-regulation and altered distribution of lysyl oxidase in the central nervous system of mutant SOD1 transgenic mouse model of amyotrophic lateral sclerosis.

Mutations of the copper-zinc superoxide dismutase (SOD1) gene can result in the development of amyotrophic lateral sclerosis (ALS). The exact cellular mechanisms causing ALS are not known, but oxidative stress is thought to play a prominent role. Lysyl oxidase (LOX) is one of the genes that are known to be up-regulated in ALS patients.

Diabetes activates cell death pathway after transient focal cerebral ischemia.

It is well known that diabetes aggravates brain damage in experimental and clinical stroke subjects. Diabetes accelerates maturation of neuronal damage, increases infarct volume, and induces postischemic seizures. The mechanism by which diabetes increases ischemic brain damage is still elusive.