BACKGROUNDRecent studies have indicated that chronic stress may give rise to brain damage, which is related to the genesis of depression. The purpose of this study is to investigate the effects of extract of Ginkgo biloba (EGb) and venlafaxine on depression.

METHODSRats were treated with chronic and comprehensive stress to create a depression model. Immunohistochemistry was used to detect the expression of brain-derived neurotrophic factor (BDNF) in the hippocampal CA3 neurons of rats treated with different drugs. Behavioral changes of these rats were also examined.

RESULTSThe expression of BDNF in the hippocampal CA3 neurons of the depression model decreased with a reduction in exploring behavior and a significant increase in fecal production. The expression of neuron nitric-oxide synthase (nNOS) protein also increased in the rats compared to normal controls. The rats treated with EGb and venlafaxine showed an increase in expression of BDNF and exploring behavior compared to untreated rats, but a decrease in nNOS and fecal production.

CONCLUSIONSRats sustain damage to the brain after being subjected to chronic and comprehensive stress. Our research has indicated that combined EGb with venlafaxine enhances the protection of neurons and decreases damage to the brain, while relieving the side effects of synthetic antidepressants.

Animals ; Antidepressive Agents, Second-Generation ; administration & dosage ; Brain Injuries ; complications ; metabolism ; Brain-Derived Neurotrophic Factor ; biosynthesis ; Cyclohexanols ; administration & dosage ; Depression ; drug therapy ; etiology ; Drugs, Chinese Herbal ; administration & dosage ; Ginkgo biloba ; chemistry ; Hippocampus ; metabolism ; Male ; Phytotherapy ; Rats ; Rats, Wistar ; Venlafaxine Hydrochloride

Nucleoside phosphorylases (NPases) were found to be induced in Enterobacter aerogenes DGO-04, and cytidine and cytidine 5'-monophosphate (CMP) were the best inducers. Five mmol/L to fifteen mmol/L cytidine or CMP could distinctly increase the activities of purine nucleoside phosphorylase (PNPase), uridine phosphorylase (UPase) and thymidine phosphorylase (TPase) when they were added into medium from 0 to 8 h. In the process of enzymatic synthesis of adenine arabinoside from adenine and uracil arabinoside with wet cells of Enterobacter aerogenes DGO-04 induced by cytidine or CMP, the reaction time could be shortened from 36 to 6 h. After enzymatic reaction the activity of NPase in the cells induced remained higher than that in the cells uninduced.
Cytidine ; pharmacology ; Cytidine Monophosphate ; pharmacology ; Enterobacter aerogenes ; enzymology ; Enzyme Induction ; Pentosyltransferases ; biosynthesis ; Vidarabine ; biosynthesis

OBJECTIVETo identify mutations of keratin 9 (KRT9) gene in a big Chinese family with epidermolytic palmoplantar keratoderma(EPPK) combined with knuckle-pad-like lesions and nail lesions.

METHODSGenomic DNA from peripheral blood of all available members in this family and 50 unrelated healthy individuals was used for amplification of the whole coding sequence and the intron-exon boundaries of KRT9 gene by PCR; The mutation was detected by direct sequence analysis and identified by restriction endonuclease Dde I.

RESULTSA mutation of AAT>AGT at codon 160 (N160S) was found in all patients but not in unaffected family members and 50 controls.

CONCLUSIONThe mutation of AAT>AGT at codon 160 (N160S) is the disease-causing mutation in this Chinese pedigree with EPPK.

Asian Continental Ancestry Group ; Codon ; DNA ; genetics ; DNA Mutational Analysis ; Exons ; genetics ; Female ; Genetic Predisposition to Disease ; Humans ; Keratins ; genetics ; Keratoderma, Palmoplantar ; genetics ; Male ; Pedigree ; Point Mutation ; Polymerase Chain Reaction

OBJECTIVETo report a Chinese Charcot-Marie-Tooth disease type 2 (CMT2) family.

METHODSAll the members in the family were studied clinically,and 6 patients were studied electrophysiologically. Sural nerve biopsy was performed in the proband. PMP22 gene duplications were detected by highly polymorphic short tandem repeat. Point mutation analysis of PMP22, MPZ and NEFL gene was screened by PCR-SSCP combined with DNA direct sequencing. A genome-wide screening was carried out to the family.

RESULTExcept 2 who had weakness and atrophy in both proximal and distal muscles of the lower limbs, all patients presented muscle wasting and a predominating weakness of distal parts of the lower limbs, and mild to moderate sensory impairments. In 6 patients who were subjected to elctrophysiological examinations, median-nerve conduction velocity (NCV) of the median nerve was normal. Electromyograms (EMGs) revealed signs of denervation with large motor unit potentials, fibrillation potentials and positive sharp waves. Sural nerve biopsy of the proband confirmed the presence of axonal neuropathy with an important loss of large myelinating fibers and a large number of clusters with mostly thinly myelinated axons. PMP22, MPZ and NEFL gene mutations were not found. The results of genome-wide screening revealed a linkage of CMT2 to a locus at chromosome 12q24.

CONCLUSIONThe results are consistent with the diagnosis of CMT2. This family represents a rare genetic type of CMT2 which can be designated as CMT2L.

Adolescent ; Adult ; Asian Continental Ancestry Group ; Charcot-Marie-Tooth Disease ; genetics ; pathology ; Chromosomes, Human, Pair 12 ; genetics ; Electromyography ; Female ; Humans ; Male ; Pedigree