Animals ; Fibrosis ; Genetic Testing ; Interleukin-1 ; genetics ; Kidney ; pathology ; Kidney Diseases ; complications ; diagnosis ; genetics ; Male ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Transforming Growth Factor beta ; genetics ; Ureteral Obstruction ; complications ; Vascular Cell Adhesion Molecule-1 ; genetics ; Vascular Endothelial Growth Factor A ; genetics

OBJECTIVETo evaluate the clinical effects of hyperbaric oxygention (HBO) in treating hypermyotonia caused by spinal cord injury (SCI).

METHODSFrom March 2009 to April 2011, 80 patients with hypermyotonia caused by SCI were divided into treatment group and control group, with 40 cases in each group. There were 49 males and 31 females with an average age of (34.12 +/- 6.61) years (ranged, 17 to 60) in the study. Course of disease was from 14 to 30 d with an average of (20.16 +/- 5.08) d. The patients of the treatment group were treated with HBO, rehabilitation exercise and baclofen medication. With pressure of HBO was 2ATA, the treatment project including mask oxygen-inspiration for 20 minutes and resting 5 min, repeating 3 circulations as once, once every day and 10 times as a course of treatment, a total of 6 courses. In the control group, the patients were only treated with rehabilitation exercise and baclofen medication. Course of treatment was same with treatment group. The muscular tensions of patients were evaluated according to method of Modified Ashworth scale (MAS) at 3 courses and 6 courses after treatment.

RESULTSAfter 3 courses of treatment,5 cases were effective in treatment group and 4 cases were effective in control group. There was no significant difference between two groups. After 6 courses of treatment, 24 cases were effective and 5 cases were obvious effective in treatment group; 14 cases were effective and 2 cases were obvious effective in control group. Clinical effect of treatment group was better than that of control group after 6 courses of treatment.

CONCLUSIONHBO was effective to controlling hypermyotonia caused by SCI, it can be used widely as a routine adjuvant therapy in clinic, but adequate course of treatment is necessary.

Adolescent ; Adult ; Cohort Studies ; Female ; Humans ; Hyperbaric Oxygenation ; Male ; Middle Aged ; Muscle Hypertonia ; etiology ; therapy ; Spinal Cord Injuries ; complications

Objective To study the mechanism and protection of ulinastatin on organ functions in patients with severe disease.Methods Sixty patients in the intensive care unit(ICU)from October 2005 to July 2007 were randomly divided into a control group and an ulinastatin treatment group(each 30 cases).The patients in the control group received the conventional therapy,and the cases in the other treatment group accepted ulinastatin and conventional therapy.According to the disease situations,ulinastatin was administered 200-400 kU once,2-4 times a day,sequentially for 5-7 days.On the day of admission and 3, 5,and 7 days after admission in ICU respectively,blood samples were obtained for measuring alanine aminotransferase(ALT),aspartate aminotransferase(AST),creatinine(Cr),blood urea nitrogen(BUN), activated partial thromboplastin time(APTT),fibrinogen(FIB)and oxygenation index(PaO_2/FiO_2); whether breathing machine or hematodialysis was used and the end results were recorded.Results The rate of usage of breathing machine(23.3%),the incidences of hepatosis(3.3%)and renal dysfunction(10.0%) and fatality(3.3%)in ulinastatin treatment group were obviously lower than those of the control group (63.3%,23.3%,46.7%,10.0%,P0.05).Only one patient received bematodialysis in control group.Conclusion Ulinastatin can protect liver,renal and lung functions markedly and lower the incidence of multiple organ dysfunction syndrome and mortality in patients with severe disease.

Objective To investigate the toxic effect of hemin on primary cultured neurons,astrocytes,and brain capillary endothelial cells (BCECs),and the damage effect of hemin with different concentrations on the above cells. Methods (1) Primary cultured neurons,astrocytes and BCECs from the cortex of rats were exposed to different doses of hemin for 2 h,and continue culture of these cells for 24 to 96 h after withdrawing hemin was performed; the cellular morphology was examined under phase-contrast microscope; cellular survival rate was measured with Alama blue staining; and the releasing rate of lactate dehydrogenasing (LDH) was detected with regular biochemical method. (2) Primary cultured cells were exposed to different doses of hemin for 2 h,and continue culture of the cells for 4 h was performed after washing out the hemin; and then,concentrated formic acid was employed to dissociate the cells, and heme content in dissociated cells was measured with spectrophotometer. (3) Primary cultured cells was exposed to different doses ofhemin for 30,60 and 120 min,respectively,and continue culture of the cells for 4 h was performed after washing out hemin; and then,intracellular Fe3+was examined with Prussian blue staining. Results (1) Cultured neurons were injured by a low dose ofhemin (5 mmol/L) with a decreased survival rate by 40.2％ and an increased LDH releasing rate by 22.2％; and the pathological changes of cellular morphology were severe after 24 h of exposure to hemin.Following the increased doses ofhemin and time of post-exposure,the cellular death and LDH releasing were increased,and the morphological changes of cells were much severe. (2) The low and medium doses of hemin (5 mmol/L and 25 mmol/L) did not induce cellular death, LDH releasing and morphological changes in astrocytes; and a high dose ofhemin (50 mmol/L) could induce a death rate of astrocytes decreasing by 52.4％, a LDH releasing rate increasing by 31％ and obvious morphological changes of astrocytes; however, the injured astrocytes could regenerate fluent cellular monolayer 96 h after exposing to high dose of hemin treatment.(3) Hemin with either low or high dose did not induce any changes in cellular survival,LDH releasing and cellular morphology of BCECs.(4) The heme content in cultured neurons was significantly higher than that in astrocytes and BCECs after hemin treatment for 2 h.(5) The blue Fe3+ stained granules appeared in neurons as early as 30 min after neurons being exposed to hemin, and Fe3+ stained positive cells in neurons were significantly higher than those in astrocytes and BCECs at any dose ofhemin and any time point ofhemin treatment. Conclusion Hemin is highly toxic to neurons, but it can only injure astrocytes at a high dose and it can not induce direct damage in BCECs; free hemin could rapidly enter and accumulate in neurons,but less accumulate in astrocytes and not accumulate in BCECs.

Objective:To assess trend of clinical features,diagnosis,treatments and outcomes for in-hospital patients of acute ST-segment elevation myocardial infarction (STEMI) in Hebei province from 2001 to 2011.Methods:Our research was based on the information of China PEACE retrospective acute myocardial infarction (AMI) study.We conducted an analysis from 8 hospitals in Hebei province including 1 third class hospital and 7 second class hospitals for STEMI patients who were diagnosed,treated and discharged in those hospitals in 2001,2006 and 2011.The clinical features,process of diagnosis and treatment and outcomes were summarized.Results:A total of 832 medical records were enrolled.During 2001 to 2011,the mean age for in-hospital STEMI patients was increased as 63.5 years in 2001,65.0 years in 2006 and 66.0 years in 2011,P=0.0097;female ratio was similar as 30.1％ in 2001,30.7％ in 2006 and 30.3％ in 2011,P=0.9846;the ratio for cardiovascular risk factors were elevated as 69.9％ in 2001,87.1％ in 2006 and 87.0％ in 2011,P＜0.0010.In patients without documented contraindications,reperfusion rate was similar,P=0.8990 and primary percutaneous coronary intervention (PCI) conduction rate was similar.The following drug therapies were increased:aspirin (P＜0.0001),clopidogrel (P＜0.0001),β-blockers (P=0.0172),statins (P＜0.0001) and ACEI/ARB (P=0.0008).In 2001,2006 and 2011,the 7-day in-hospital mortality,the ratio of death and gave-up treatment were similar,P=0.5854 and P=0.3516 respectively.Conclusion:During 2001 to 2011,the onset age and the prevalence of cardiovascular risk factors were increased in STEMI patients in Hebei province;drug therapy for secondary prevention of coronary artery disease was elevated by years while the reperfusion rate was similar and 7-day mortality was similar.

OBJECTIVETo investigate the role of c-Jun N-terminal kinase (JNK)-c-Jun/activator protein-1 (AP-1) signal pathway in expression of monocyte chemoattractant protein-1 (MCP-1) in experimental rat glomerulonephritis.

METHODSNephrotoxic sera nephritis (NTN) was induced by injection of anti-GBM antibody into the tail veins of rats. Electrophoretic mobility shift assay (EMSA) and non-radioactive kinase assay were used to detect the activity of AP-1 and JNK in kidneys and angiotensin II-stimulated human mesangial cells. Ribonuclear protection assay was used to detect MCP-1 expression in cultured human mesangial cells.

RESULTSSignificant up-regulation of JNK and AP-1 was observed in NTN rats (3.82 +/- 0.58) folds and (5.36 +/- 0.61) folds, as compared with the controls. Supershift assay demonstrated that c-Jun and c-Fos were the predominant subunits involved. Activation of JNK and AP-1 significantly correlated with MCP-1 expression in NTN rats. Angiotensin II enhanced the expression of MCP-1 and activation of JNK and AP-1 in cultured human mesangial cells in a dose-dependent manner, with maximal stimulation seen at 100 nmol/L (20.99 +/- 4.71) folds, (6.91 +/- 1.65) folds and (7.82 +/- 1.32) folds respectively. Significant down-regulation of AP-1 activation and MCP-1 expression were observed in angiotensin II-induced human mesangial cells pretreated with JNK specific inhibitor SP600125.

CONCLUSIONSAngiotensin II and MCP-1 may play an important role in glomerulosclerosis via the JNK-c-Jun/AP-1 signal pathway.

Angiotensin II ; pharmacology ; Animals ; Cells, Cultured ; Chemokine CCL2 ; metabolism ; Glomerular Mesangium ; cytology ; metabolism ; Glomerulonephritis ; metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Male ; Proto-Oncogene Proteins c-fos ; metabolism ; Proto-Oncogene Proteins c-jun ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; drug effects ; Transcription Factor AP-1 ; metabolism

OBJECTIVETo investigate the role of NF-kappaB/IkappaB signal pathway in mediating the expression of monocyte chemoattractant protein-1 (MCP-1) in experimental rat glomerulonephritis.

METHODSNephrotoxic serum nephritis (NTN) was induced by injection of anti-GBM antibody into the tail veins of rats. Electrophoretic mobility shift assay (EMSA) and Western Blot were used to detect the activation of NF-kappaB, nuclear translocation of p65 subunit and degradation of IkappaBalpha and IkappaBbeta in rat renal tissue. MCP-1 expression in glomeruli and renal tubules was also assessed by immunohistochemistry and ribonuclease protection assay. This was further correlated with the activation of NF-kappaB.

RESULTSThere was an obvious expression of MCP-1 in glomeruli and renal tubules. Significant up-regulation of NF-kappaB activation, nuclear translocation of p65 subunit, and degradation of IkappaBalpha and IkappaBbeta were also observed in NTN rat renal tissue, as compared to the control group. A positive correlation was noted between NF-kappaB activation and MCP-1 expression.

CONCLUSIONSNF-kappaB/IkappaB signal pathway may play an important pathogenetic role in glomerulonephritis, with mediating the expression of MCP-1.

Animals ; Blotting, Western ; Chemokine CCL2 ; genetics ; metabolism ; Glomerulonephritis ; chemically induced ; genetics ; metabolism ; I-kappa B Proteins ; metabolism ; Kidney Glomerulus ; metabolism ; pathology ; Kidney Tubules ; metabolism ; pathology ; Male ; NF-kappa B ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction

This study was aimed to explore the effect of arsenic trioxide (ATO) on proliferation and apoptosis of mantle cell lymphoma (MCL) cell lines and the underlying mechanisms of the apoptosis. MCL cell lines (jeko-1, mino, JVM-2) were treated with different concentrations of ATO, then growth profile of these cells were detected by MTT. Apoptosis of ATO-treated jeko-1 cells were detected by flow cytometry with Annexin V-FITC/PI double staining. The loss of mitochondrial membrane potential of ATO-treated jeko-1 cells were detected by FCM with DiOC₆(3) staining. The expressions of cyclin D1 and apoptosis related proteins MCL-1, BCL-2, PUMA, NOXA, cCaspase-3 (cleaved caspase-3), cCaspase-9 (cleaved caspase-9), cPARP (cleaved PARP) were detected by Western blot. The results indicated that ATO inhibited cell growth, induced apoptosis of MCL cells and disrupted mitochondrial membrane potential. ATO could decrease expressions of MCL-1, PUMA and cyclin D1, increase expressions of cPARP, cCaspase-3, cCaspase-9 and the expressions of BLC-2 and NOXA were not changed. It is concluded that ATO can induce cell growth arrest and apoptosis of MCL cells. The mitochondrial pathway plays a very important role in cell apoptosis.
Apoptosis ; drug effects ; Apoptosis Regulatory Proteins ; metabolism ; Arsenicals ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphoma, Mantle-Cell ; metabolism ; Membrane Potential, Mitochondrial ; Mitochondria ; drug effects ; Oxides ; pharmacology

Adult ; Humans ; Male ; Myelodysplastic Syndromes ; complications ; pathology ; Pulmonary Alveolar Proteinosis ; etiology ; pathology

OBJECTIVETo study the clinical and pathological features of Alport syndrome in children.

METHODSThe clinical and histopathological data of 10 hospitalized children with Alport syndrome from February 2007 to February 2009 were retrospectively reviewed.

RESULTSThere were 7 males and 3 females, with the age ranging from 2 years to 6 years and 7 months (mean 3 years and 2 months). Five of 10 cases had positive family history. X-linked dominant inheritance Alport syndrome was diagnosed in 8 cases, and autosomal recessive inheritance Alport syndrome in 2 cases. Recurrent gross hematuria was found in 5 cases, hematuria and proteinuria in 3 cases, massive proteinuria in 1 case, and nephritic syndrome in 1 case. Under the light microscope, 8 cases presented with mesangial proliferation glomerulonephritis, and 2 cases with focal segmental glomerulosclerosis. Immunofluorescence assay showed that all cases had IgM deposition in glomerulus. Only 1 case showed typical glomerular basement membrane (GBM) pathological changes. All cases showed abnormal alpha-chain distribution in renal collagen IV.

CONCLUSIONSThe children with Alport syndrome have diverse clinical manifestations. Characteristic histopathological presentations could not be found under a light microscope, mesangial proliferation glomerulonephritis is the dominant pathological change, and IgM deposition in glomerulus is common. The GBM pathological change in children is not common. Immunofluorescence assay of alpha-chain in collagen IV is needed for the diagnosis of Alport syndrome.

Child ; Child, Preschool ; Collagen Type IV ; genetics ; Female ; Humans ; Kidney ; pathology ; Male ; Nephritis, Hereditary ; diagnosis ; genetics ; pathology