BACKGROUND:The coagulation function of patients after joint replacement is enhanced during the perioperative time, the coagulation disorder can easily lead to the deep vein thrombosis, which wil seriously affect the rehabilitation and prognosis of patients. The embolus fal ing off from venous thrombosis can lead to acute pulmonary embolism, severe cases can be life-threatening. So the early diagnosis of postoperative deep vein thrombosis and acute pulmonary embolism is very important.
OBJECTIVE:To review the research progress of clinical diagnosis of thrombosis in the perioperative patients after orthopaedic joint replacement.
METHODS:A computer-based retrieve in PubMed database and CNKI database were conducted by the first author for the articles on the clinical diagnosis of thrombosis in the perioperative patients after orthopaedic joint replacement from January 2008 to May 2013 with the key words of“arthroplasty, deep venous thrombosis, pulmonary artery embolism, risk factor, diagnostic approach, anticoagulant, perioperative period, research progress”in English and Chinese. A total of 165 articles were screened out, and final y 50 articles were included according to the inclusion criteria.
RESULTS AND CONCLUSION:After joint replacement surgery, various risk factors were associated with the etiology and pathogenesis of deep venous thrombosis, such as vascular and tissue impairments, limb fixation, pain stress, and hemorrhagic fluid caused coagulation disorder, were the main reasons to thrombosis. Deep vein thrombosis and pulmonary embolism had variety of clinical manifestations, many diagnostic approaches were widely applied in clinic, but each one has its laminations. So the positive diagnosis intervention should be performed according to the common clinical manifestations, general y begin from the routine examinations of ultrasound and electrocardiogram, and the combination of various methods was preferred if necessary in order to increase the positive diagnosis rate to the maximum extent, and take drug intervention immediately after diagnosis to avoid the happening of adverse events. Several new types of oral anticoagulants appear in clinical trials, and the outcomes are very promising, but the widely clinical application needs further observation.

Animals ; Astragalus Plant ; Cardiomyopathies ; Myocardial Ischemia ; Myocardium ; Rats

rAdinbitor was cloned from Gloydius blomhoffi brevicaudus in the laboratory. Previous researches had proved that rAdinbitor could inhibit proliferation of C6 glioma cells as well as promote their apoptosis. The molecular mechanism of rAdinbitor’s effects on C6 cells need to be further studied. rAdinbitor was expressed in E. coli BL21/pET23b-adinbitor and purified with Ni Sepharose 6 Fast Flow. The purified protein was confirmed by Western blotting. C6 cells were induced with fibronectin (FN). The effects of rAdinbitor with different concentrations on the expression of FAK, MEK1/2 and Caspase-3 as well as on activity of FAK and ERK1/2 in FN-induced C6 cells were studied by immunoblotting and immunoprecipitation. Results showed that rAdinbitor with different concentrations could obviously reduce the expression of FAK and MEK1/2, increase the expression of Caspase-3, as well as decrease ERK1/2 phosphorylation; besides 10 mg/L rAdinbitor, other concentrations’ rAdinbitor could inhibit FAK phosphorylation obviously. All those effects were dose-dependent. Results indicate that the effects of rAdinbitor on decreasing expression and activity of FAK and inhibiting Ras-MAPK signaling pathway play an important role in suppressing the proliferation of C6. Furthermore, the increase in Caspase-3 expression implies that the increase in apoptosis of C6 cells might be due to the suppression of rAdinbitor on the activity of ILK and PI-3K/Akt pathway.

Objective To explore the relationship between substance P(SP),somatostatin(SS) expression and change of morphology structure in jejunum of arsenism rats.Methods Acoording to sex and body mass,forty five clean grade SD rats were divided into control(0.0 mg.kg-1.d-1),low-dose arsenic(0.4 mg.kg-1.d-1) and high-dose arsenic(10.0 mg.kg-1.d-1) groups,n =15.The rats in low-and high-dose groups were treated with As2O3(2,50 mg/L) through drinking water for 4 months,respectively.Morphology changes of jejunum were observed by histological technique-HE staining and SABC immunohistochemistry.SP and SS positive cells in the jejunum were observed and counted,and its average gray value was analyzed with image analysis software (Biomias).Results Some jejunal villi were irregular in arsenism rats; with some brush border loss and irregular; goblet cells increased; infiltration of inflammatory cells in the lamina propria; and vacuoles in some intestinal gland cells.The differences of SP and SS positive cells between groups were statistically significant (F =608.54,227.59,all P ＜0.05).Compared with the control group (0.94 + 0.21,1.14 + 0.14),SP and SS positive cells in low-and highdose arsenic groups(1.85 + 0.25,1.83 + 0.24 and 4.24 + 0.33,3.31 ± 0.41) were significantly higher(all P ＜0.05),and high-dose arsenic group was significantly higher than the low-dose arsenic group(all P ＜ 0.05).The differences of average gray values of SP and SS positive cells between groups were statistically significant(F =68.43,26.57,all P ＜ 0.05).Compared with the control group(133.76 ± 3.61,137.57 ± 5.49),SP and SS positive cells in low-and high-dose arsenic groups(125.13 + 2.35,131.28 ± 5.66 and 118.30 ± 4.58,124.03 ± 3.94) were significantly lower(all P ＜ 0.05),and high-dose arsenic group was significantly lower than the low-dose arsenic group (all P ＜ 0.05).Conclusions Up-regulation of SP,SS may be related to jejunal mucosal injury and morphology structure in arsenic poisoning rats.

Objective To study the molecular mechanism of renal injury of chronic arsenic poisoning rats induced by the expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells.Methods Sixty healthy SD rats were divided into three groups,high-,low-dose group,and control group,n =20 in each group.The rats in high and low dose groups were treated with As203 through drinking water,10.0 and 0.4 mg/kg,respectively.The control rats were given distilled water.Four months later,serum and urinary arsenic level was determined,and kidney specimens were taken.The expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells was detected by histological technique-HE staining and SABC immunohistochemistry.In addition,cell number counting and image analyses were used in the study.Results The number of caspase-8 positive cells of renal proximal tubule in control group,low-and high-dose group was 3.33±1.32,31.14±8.02 and 46.50±7.20 cell number/visual fields,respectively,which was increased with dose increasing(all P ＜0.05);the average gray value was 151.34±6.40,133.58±4.63 and 128.34±16.28,respectively,decreased with dose increasing(all P ＜0.05).The number of P53 positive cells was 3.17±1.59,26.29±4.23 and 47.00±6.22 cell number/visual fields,respectively,increased with dose increasing (all P ＜ 0.05) ; the average gray value was 142.54±8.06,121.48±5.68 and 101.89±6.35,respectively,decreased with dose increasing (all P ＜ 0.05).Conclusion The increase of caspase-8 and P53 positive cells is one of the molecular mechanisms of renal injury induced by arsenic poisoning.

Background Neurotransmitter secretion disorder induced by chronic manganese poisoning has always been one of the important causes of body injury, but the mechanism of neurotransmitter secretion disorder caused by manganese is not clear at present. Objective To investigate the effects of presynaptic membrane intracellular protein 13-1 (Munc13-1) and synapse fusion protein binding protein 18-1 (Munc18-1) on dopamine secretion dysfunction induced by manganese chloride (MnCl₂) in human neuroblastoma (SH-SY5Y) cells. Methods A SH-SY5Y cell model induced by MnCl₂ was established. Cell viability was measured by MTT assay. Four experimental groups were set up: control group and low-, medium-, and high-dose manganese groups (0, 100, 200, and 400 μmol·L⁻¹ MnCl₂). They were treated with corresponding doses of MnCl₂ for 24 h. The secretion of dopamine was measured by enzyme-linked immunosorbent assay. The mRNA expression of Syntaxin-1 was detected by real-time quantitaive PCR. Total cell proteins were extracted, and the protein expression levels of Munc13-1, Munc18-1, and Syntaxin-1 were detected by Western blotting. The correlations of MnCl₂ exposure and dopamine secretion with the protein expressions of Munc13-1 and Munc18-1 were also analyzed by Pearson correlation. Results Compared with the control group, the cell viability rate decreased gradually with the increase of manganese exposure concentration, and the difference between the medium- and the high-dose manganese groups was statistically significant (P<0.05). The concentration of dopamine in cell culture medium of all manganese exposure groups decreased with the increase of manganese concentration, and compared with the control group and the low-dose manganese group, the medium- and the high-dose manganese groups were statistically significant (P<0.05). The expression of Syntaxin-1 at mRNA or protein level did not change significantly among groups (P>0.05). Compared with the control group, the protein expression of Munc13-1 decreased and that of Munc18-1 increased with the increase of manganese concentration (P<0.05). Compared with the low-dose manganese group, the changes of Munc13-1 protein in the high-dose manganese group and Munc18-1 protein in the medium- and high-dose manganese groups had statistical significance (P<0.05). Compared with the medium-dose manganese group, the protein changes of Munc18-1 in the high-dose manganese group were statistically significant (P<0.05). The correlation analysis showed that MnCl₂ dose was negatively correlated with Munc13-1 protein expression (r=−0.898, P<0.05), and positively correlated with Munc18-1 protein expression (r=0.678, P<0.05). Dopamine secretion was positively correlated with Munc13-1 protein expression (r=0.932, P<0.05), and negatively correlated with Munc18-1 protein expression (r=−0.817, P<0.05). Conclusion The inhibition of dopamine secretion in SH-SY5Y cells induced by manganese exposure is related to up-regulation of Munc18-1 and down-regulation of Munc13-1 expression levels, which may be one of the reasons for nerve injury caused by manganese.

OBJECTIVETo explore the neuroprotective effect and mechanism of picroside II on extracellular regulated protein kinases1/2 (ERK1/2) signal transduction pathway in cerebral ischemia injuryrats. METHODS The middle cerebral artery occlusion (MCAO) model was established by inserting a monofilament into middle cerebral artery. Totally 96 successfully modeled Wistar rats were divided into the modelgroup, the treatment (picroside II) group, the Lipopolysachcaride (LPS) group, and the U0126 group according to random digit table. Each group was further divided into 3 subgroups, i.e. 6, 12, and 24 h sub-groups. Picroside II (20 mg/kg) was peritoneally injected to rats in the treatment group 2 h after ischemia.LPS (20 mg/kg) and Picroside II (20 mg/kg) were peritoneally injected to rats in the LPS group 2 h after ischemia. U0126-EtOH (20 mg/kg)and Picroside II (20 mg/kg) were peritoneally injected to rats in the U0126group 2 h after ischemia. Equal volume of normal saline was peritoneally injected to rats in the control groupand the model group. The neurobehavioral function was evaluated by modified neurological severity score(mNSS) test. The structure of neurons was observed using hematoxylin-eosinstaining (HE) staining. Theapoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression of phosphorylated extracellular signal-regulated protein kinase1,2 (pERK1,2) in cortex was detected using immunohistochemistry (IHC) and Western blot.

RESULTSAfter cerebral ischemia injury neurological impairment score increased, the damage of neuron in the cortical area was aggravated, apoptotic cells increased in the model group as time went by. The expression of pERK1/2 increased more significantly in the model group than in the control group (P <0.05). The damage of neuron in the cortical area was milder, while apoptotic cells decreased, the expression of pERK1f2 obviously decreased more in the treatment group and the U0126 group (P < 0.05). The early damage of neuron in the cortical area was more severe, apoptotic cells and the expression of pERK12 were comparatively higher in early stage of the LPS group, but the expression of pERK1/2 was somewhat decreased in late stage.

CONCLUSIONSActivating ERK12 pathway could mediate apoptosis and inflammatory reactions of neurons after cerebral ischemia injury. Picroside II could protect the nerve system possibly through reducing activation of ERKI2 pathway, inhibiting apoptosis of neurons and inflammation reaction.

Animals ; Apoptosis ; Brain Ischemia ; drug therapy ; Cinnamates ; pharmacology ; Infarction, Middle Cerebral Artery ; drug therapy ; Iridoid Glucosides ; pharmacology ; MAP Kinase Signaling System ; drug effects ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar

Objective: To evaluate the clinical efficacy of sinew-regulating bone-setting manipulations plus exercise therapy in treating chronic non-specific low back pain (CNLBP). Methods: A total of 65 CNLBP patients were divided into two groups by the random number table method. Thirty-three cases in the treatment group were intervened by sinew-regulating bone-setting manipulations plus exercise therapy; 32 cases in the control group were intervened by medium-frequency electrotherapy plus exercise therapy. Before and after treatment, visual analog scale (VAS), dynamic and static muscle endurance of low back, median frequency (MF) of surface electromyography (sEMG) and Oswestry disability index (ODI) were used to evaluate the low back function. The therapeutic efficacy was estimated after treatment. Results: The two groups each had 2 dropouts during the study. The total effective rate was 90.3％ in the treatment group versus 66.7％ in the control group, and the between-group difference was statistically significant (P<0.05). After treatment, the VAS score, dynamic and static muscle endurance of low back, MF of sEMG and ODI score all changed significantly in both groups (all P<0.05); all the items in the treatment group were significantly different from those in the control group (all P<0.05). Conclusion: Sinew-regulating bone-setting manipulations plus exercise therapy can effectively release pain in CNLBP patients, increase muscle endurance of the low back and improve the quality of life, and its therapeutic efficacy is more significant than that of medium-frequency electrotherapy plus exercise therapy.

Objective To explore the correlation between adiponectin/leptin(A/L) ratio and metabolic syndrome diagnosis in elderly men. Methods A total of 256 elderly men (≥60 years) were enrolled and divided into metabolic syndrome group(n= 109) and non metabolic syndrome group (n= 147). Serum levels of adiponectin and leptin were measured by radioimmunoassay (RIA) and the A/L ratio was calculated. Metabolic syndrome diagnosis is based on the definition provided by China Diabetes Society (CDS) in 2004. Results (1) In metabolic syndrome group versus non metabolic syndrome group, the serum levels of leptin and adiponectin were (10. 3±7.0) vs (6.8±4.9)μg/L and(7.8±5.6)g/L vs (9.5±5.9)g/L, and A/L ratio was 0. 94±0. 78 vs 2.15±2.13 respectively. (2) A/L ratio was positively correlated with high density lipoprotein cholesterol (HDL-C) and negatively correlated with body mass index (BMI), triacylglycerol (TG) and serum uric acid(P< 0. 001). (3) The higher value of A/L ratio, the lower possibility of metabolic syndrome. When the A/L ratio was more than 5, the incidence of metabolic syndrome was decreased to O(X2 =34. 891 ,P< 0.001). (4) The more components of metabolic abnormality, the lower value of A/L ratio(F= 10. 876,P<0. 001). Conclusions The A/L ratio may be useful in evaluating the extent of metabolic disorder and diagnosing metabolic syndrome in elderly men.

Adrenal Glands ; Female ; Hematopoiesis, Extramedullary ; Humans ; Spherocytosis, Hereditary ; complications ; Young Adult