2.Non-surgical treatment for fracture-disloction of ankle.
China Journal of Orthopaedics and Traumatology 2012;25(1):62-65
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
3.Effect of butylphthalide on the expression of S100 and glial fibrillary acidic protein in a rat model of Alzheimer disease.
De-Ren HOU ; Shun WAN ; Jun ZHOU ; Kun CHEN ; Yi TIAN
Journal of Southern Medical University 2009;29(6):1147-1149
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
4.Butylphthalide improves learning and memory abilities of rats with Alzheimer's disease possibly by inhibiting P38 mitogen-activated protein kinase and enhancing extra-cellular signal regulated kinase expressions.
De-ren HOU ; Yi TIAN ; Jun ZHOU ; Kun CHEN ; Shun WAN
Journal of Southern Medical University 2009;29(8):1592-1595
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
5.Butylphthalide improves learning and memory abilities of rats with Alzheimer's disease possibly by enhancing protein disulfide isomerase and inhibiting P53 expressions.
De-ren HOU ; Li XUE ; Jiao-chun TANG ; Jun ZHOU ; Juan-juan SUN
Journal of Southern Medical University 2010;30(9):2104-2107
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
6.Survivin and COX-2 expressions in giant cell tumor of bone and their relation to the prognosis.
Si-min LUO ; Ren-de LIU ; Wen-rui LI ; Jing-hui HOU
Journal of Southern Medical University 2009;29(1):156-159
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
7.Research progress of depression and the application of esketamine.
Fang-Bo LIN ; De-Ren HOU ; Qiu-Ping TANG
Journal of Southern Medical University 2016;37(4):567-inside back cover
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
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pharmacology
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Depression
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drug therapy
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Humans
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Ketamine
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pharmacology
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Receptors, N-Methyl-D-Aspartate
8.Effect of willed movement therapy on the expression of neurotrophin 3 and growth-associated protein 43 in rats with cerebral ischemia reperfusion.
De-ren HOU ; Shawuti SHADIKE ; Jin-feng DENG ; Jian-feng LIU ; Zhong-yang HU ; Jun ZHOU ; Li ZHOU ; Yuan-xin LIU
Journal of Southern Medical University 2011;31(8):1401-1404
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
9.Verification of a sporadic Alzheimer disease model in SORL1 gene knockout mice.
Fang-Bo LIN ; Xin LIU ; Jing-Wen XIE ; Jing LUO ; Xia-Lu FENG ; De-Ren HOU
Journal of Southern Medical University 2018;38(3):289-295
OBJECTIVETo compare the behavioral and pathological features of SORL1 gene knockout mice with those of normal mice and APP/PSE1 mice to verify the feasibility of using SORL1 knockout mice as a model of sporadic Alzheimer disease.
METHODSSORL1 gene of fertilized mouse eggs were edited using Crispr/Case9 technique. SORL1 mice were screened and identified by detecting the DNA sequence, and Western blotting was used to detect the expression of SORL1. SORL1 mice, control mice and APP/PSE1 mice all underwent Morris water maze test to assess their learning and memory abilities with positioning navigation and space exploration experiments. The expression of APP and Aβ in the brain of the mice was detected using immunohistochemistry and Western blotting, respectively.
RESULTSDNA sequencing showed CAAT deletion in SORL1 gene in two chromosomes of SORL1 mice, and the control mice had intact SORL1 gene without the deletion; Western blotting did not detect the expression of the SORL1 in the brain of SORL1 mice. Morris water maze test showed that in positioning navigation experiment, the average avoidance latency was similar between SORL1 mice and APP/PSE1 mice (P>0.05) but increased significantly in both mice as compared with the control group (P<0.05); similar results were obtained in the space exploration experiment. Immunohistochemistry and Western blotting revealed significantly increased APP and Aβ expression in the brain tissue of both SORL1 mice and APP/PSE1 mice compared with the control mice without significant differences between the two transgenic mice.
CONCLUSIONSORL1 mice exhibit similar behavioral and pathological changes with APP/PSE1 mice and can be used as a model of sporadic Alzheimer's disease.
10.Effect of willed movement therapy on GFAP and SYP expression in rats with cerebral ischemia-reperfusion.
De-ren HOU ; Shadike SHAWUTI ; Jian-feng LIU ; Hai-xia ZHU ; Jin-feng DENG ; Zhong-yang HU ; Jun ZHOU ; Yuan-xin LIU
Journal of Southern Medical University 2011;31(9):1543-1546
OBJECTIVETo determine the effect of willed movement on the expression of glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) in adult rats with cerebral ischemia-reperfusion, and explore the mechanism of willed movement in promoting nerve repair and regeneration.
METHODSAdult rat models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion (MCAO) for 2 h followed by a 24-h reperfusion. The models were then divided randomly into 3 groups, namely the model group, environmental modification (EM) group, and willed movement (WM) group. In each group, neurological deficits were evaluated at 3, 7 and 15 days after reperfusion. Immunohistochemistry and immunofluorescence assay were employed to examine the expression of GFAP and SYP in the brain tissue near the ischemic foci.
RESULTSThe rats in WM group showed lessened neurological deficits at 15 days and lowered expression of GFAP and SYP at 7 and 15 days after reperfusion compared with the model and EM groups (P<0.05). No significant difference was found in the expression of GFAP or SYP between the model group and EM group at any time points.
CONCLUSIONWilled movement can promote the functional recovery of neurological deficits following cerebral ischemia-reperfusion probably in relation to enhanced GFAP and SYP expressions in the ischemic brain tissues.
Animals ; Brain Ischemia ; metabolism ; therapy ; Disease Models, Animal ; Exercise Therapy ; methods ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; therapy ; Synaptophysin ; metabolism