Drowning ; Humans ; Male ; Middle Aged ; Organothiophosphorus Compounds ; poisoning

OBJECTIVETo summarize the clinical effects of the manipulative reduction and splint fixation for the treatment of fracture-dislocation of ankle.

METHODSFrom April 1990 to June 2010, 53 patients with fracture dislocation of ankle were treated with non-operative treatment including manipulative reduction, splint fixation, oral herbal soup and early functional exercises. There were 32 males and 21 females with an average age of 42.5 years (ranged, 25 to 60). There were 30 cases in left and 23 cases in right. Ankle joint function was evaluated according to standard of Mazur.

RESULTSFollow up time was from 6 to 60 months with an average of 33 months; all the fractures healed with an average of 4 months (ranged, 3 to 5). The mean of Mazur scoring was 90.11+/- 8.40, 36 cases got excellent results, 11 good, 3 fair and 3 poor.

CONCLUSIONWith non-operative treatment such as manipulative reduction and splint external fixation for fracture-dislocation of ankle can obtain satisfactory effects, which has advantage of simple operation, less trauma.

Adult ; Ankle Injuries ; therapy ; Female ; Follow-Up Studies ; Fractures, Bone ; therapy ; Humans ; Joint Dislocations ; therapy ; Male ; Manipulation, Orthopedic ; Medicine, Chinese Traditional ; Middle Aged ; Splints

OBJECTIVETo determine the expression of S100-beta protein and glial fibrillary acidic protein (GFAP) in hippocampal astrocytes of rats with Alzheimer disease (AD) model rats, and observe the effect of butylphthalide on their expression.

METHODSSixty male adult rats were randomized equally into model group, butylphthalide group, and control group, and in the former two groups, AD models were established by injecting beta-amyloid protein 1-40 into the hippocampus. Sixty days later, the rats were sacrificed and the bilateral hippocampuses were taken for immunohistochemistry.

RESULTSThe number of cells positive for S100 and GFAP in the hippocampus in butylphthalide group were significantly higher than that in the control group (P/0.01), but lower than that in the model group (P/0.05).

CONCLUSIONThe expression of S100 protein and glial fibrillary acidic protein increased significantly in the hippocampal astrocytes of rats with AD, and butylphthalide can inhibit the increase of their expression.

Alzheimer Disease ; chemically induced ; metabolism ; Amyloid beta-Peptides ; Animals ; Benzofurans ; pharmacology ; Disease Models, Animal ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; Male ; Nerve Growth Factors ; metabolism ; Neuroprotective Agents ; pharmacology ; Peptide Fragments ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; S100 Calcium Binding Protein beta Subunit ; S100 Proteins ; metabolism

OBJECTIVETo determine the effect of butylphthalide on the expressions of p38 mitogen-activated protein kinase and extra-cellular signal regulated kinases (ERKs) in the brain tissue of rats with Alzheimer's disease (AD).

METHODSSixty male adult rats were randomly divided to AD model group, butylphthalide group, and control group (n=20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats. Sixty days later, the learning and memory abilities of the rats were evaluated using Y-maze test, and the expressions of p38 and ERKs in the brain tissue of the rats were measured by immunohistochemistry. RESULTS Compared with the control group, the rats in AD model group exhibited significantly reduced learning and memory abilities, increased expressions of P38 in the hippocampus and lowered expression of ERK in the cortex (P<0.01). In comparison with the model group, the rats in the butylphthalide group showed significantly decreased P38-positive cells in the hippocampus and increased expression of ERK in the cortex (P<0.01).

CONCLUSIONSButylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P38 expression and enhancement of ERK expression in the brain tissues.

Alzheimer Disease ; enzymology ; metabolism ; physiopathology ; Animals ; Benzofurans ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Gene Expression Regulation, Enzymologic ; drug effects ; Hippocampus ; drug effects ; metabolism ; Male ; Memory ; drug effects ; Neuroprotective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.
Antidepressive Agents ; pharmacology ; Depression ; drug therapy ; Humans ; Ketamine ; pharmacology ; Receptors, N-Methyl-D-Aspartate

OBJECTIVETo determine the effect of butylphthalide on the expressions of protein disulfide isomerase (PDI) and P53 in the brain tissue of rats with Alzheimer's disease (AD).

METHODSSixty male adult rats were randomly divided into AD model group, butylphthalide group and control group (n = 20). AD models were established by injecting beta-amyloid protein 1-42 into the hippocampus of rats. Sixty days later, the learning and memory abilities of the rats were evaluated using Y-maze test, and the expressions of PDI and P53 in the brain tissue of the rats were measured by immunohistochemistry.

RESULTSCompared with the control group, the rats in AD model group exhibited significantly reduced learning and memory abilities, lowered expressions of PDI in the hippocampus and increased expression of P53 in the cortex (P > 0.01). In comparison with the model group, the rats in the butylphthalide group showed significantly increased PDI-positive cells in the hippocampus and decreased expression of P53 in the cortex (P < 0.01).

CONCLUSIONButylphthalide improves the learning and memory abilities of rats with experimental AD, the mechanism of which may involve inhibition of P53 expression and enhancement of PDI expression in the brain tissues.

Alzheimer Disease ; physiopathology ; Animals ; Apoptosis ; drug effects ; Benzofurans ; pharmacology ; Brain ; enzymology ; metabolism ; Disease Models, Animal ; Learning ; drug effects ; Male ; Memory ; drug effects ; Protein Disulfide-Isomerases ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tumor Suppressor Protein p53 ; metabolism

OBJECTIVETo investigate the expression of survivin and COX-2 in giant cell tumor of bone (GCT) and explore the prognostic factors for GCT.

METHODSThe expressions of survivin and COX-2 in 39 GCT tissues of three Jaffe grades and 4 normal bone tissues were detected by immunohistochemical staining, and the data were analyzed in relation to the clinicopathological features of the patients.

RESULTSThe expressions of survivin and COX-2 were significantly higher in the GCT tissues than in normal bone tissues (P<0.01). A positive correlation was found between survivin and COX-2 expressions and the pathological grade (P<0.01), but their expressions were not correlated to the patients' gender, age or surgical approaches (P>0.05). An obviously lowered recurrence rate was observed in patients with resection of the bone segment compromised by the tumor and subsequent bone grafting. Survivin and COX-2 were not independent risk factors of the prognosis of GCT.

CONCLUSIONSurvivin and COX-2 expressions may participate in the pathogenesis and development of GCT, but is not indicative of the prognosis.

Adolescent ; Adult ; Bone Neoplasms ; metabolism ; pathology ; Cyclooxygenase 2 ; genetics ; metabolism ; Female ; Giant Cell Tumor of Bone ; metabolism ; pathology ; Humans ; Inhibitor of Apoptosis Proteins ; Male ; Microtubule-Associated Proteins ; genetics ; metabolism ; Middle Aged ; Prognosis ; Young Adult

OBJECTIVETo observe the effect of willed movement therapy on the expression of neurotrophin 3 (NT-3) and growth associated protein 43 (GAP-43) in rats with cerebral ischemia-reperfusion (IR) and investigate the neuroprotective mechanism of willed movement therapy in nerve regeneration and repair.

METHODSCerebral IR model was established by middle cerebral artery occlusion (MCAO) in SD rats. The rats were randomly divided into MCAO group, environment modification group (EM group) and willed movement therapy group (WM group). The rats were evaluated for neurological deficits and decapitated on days 3, 7 and 15 after the reperfusion to examine the expressions of NT-3 and GAP-43 in the ischemic brain tissues by immunohistochemistry.

RESULTSCompared with MCAO and EM groups, the rats in WM group showed significantly lowered grade of neurological deficits (P<0.05) at 15 days and significantly increased the expressions of NT-3 and GAP-43 (P<0.05) at 7 and 15 days after the reperfusion. No significant difference was found in the expression of NT-3 and GAP-43 between MCAO and EM groups (P>0.05). The expression of NT-3 was positively correlated to that of GAP-43 in the ischemic tissues.

CONCLUSIONSWilled movement therapy increases the expression of NT-3 and GAP-43 in the ischemic brain area in rats with cerebral ischemia-reperfusion, which is probably related to nerve regeneration and repair.

Animals ; Brain Ischemia ; metabolism ; therapy ; Exercise Therapy ; methods ; GAP-43 Protein ; metabolism ; Infarction, Middle Cerebral Artery ; metabolism ; therapy ; Male ; Movement ; physiology ; Nerve Regeneration ; Neuronal Plasticity ; physiology ; Neurotrophin 3 ; metabolism ; Physical Exertion ; physiology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; therapy

OBJECTIVETo investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function.

METHODSThis case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group. The serum levels ofadiponectin in the participants were detected using enzyme-linked immunosorbent assay.

RESULTSSerum adiponectin level was significantly lower in the AD group than in the control group (P<0.05). Of the 3 subgroups of the AD patients, the moderate and severe AD groups showed significantly lower serum adiponectin level sthan the control group (P<0.05), but the difference in adiponectin levels was not significant between the mild AD group and the control group (P>0.05); serum adiponectin levels also differed significantly among the 3 subgroups of AD patients (P<0.05). Serum adiponectin level was positively correlated with the MMSE score in the AD patients (r=0.683, P<0.001).

CONCLUSIONSerum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

Adiponectin ; blood ; Alzheimer Disease ; blood ; Case-Control Studies ; Cognition ; Cognitive Dysfunction ; blood ; Enzyme-Linked Immunosorbent Assay ; Humans

The cDNA of human FGF-21 was subcloned into the pSUMO expression vector and the fusion protein was induced to express in Escherichia coli Rosetta (DE3). The recombinant hFGF-21 was expressed in soluble form in the pSUMO expression system. The recombinant fusion protein was purified by Ni-NTA column. The purified recombinant protein was dialyzed against PBS for re-nature. To obtain pure and active recombinant protein, the fusion protein was subjected to cleavage with SUMO protease I. To examine glucose regulation activity of hFGF-21, 3T3-L1 pre-adipocytes were differentiated into adipocytes, glucose up-take activity of hFGF-21 was examined by glucose oxidase and peroxidase (GOD-POD) assay. Compared with no stimulation control, the recombinant hFGF-21 treatment led to a significant increase in glucose consumption of adipocytes and a significant decrease in concentration of glucose in the medium (P < 0.05, P < 0.001).
3T3-L1 Cells ; Adipocytes ; metabolism ; Animals ; DNA, Complementary ; genetics ; Escherichia coli ; genetics ; metabolism ; Fibroblast Growth Factors ; genetics ; metabolism ; pharmacology ; Glucose ; metabolism ; Humans ; Mice ; Plasmids ; Recombinant Fusion Proteins ; genetics ; metabolism ; pharmacology ; Small Ubiquitin-Related Modifier Proteins ; genetics ; metabolism ; Solubility