Adrenomedullin ; metabolism ; Child ; Endothelin-1 ; metabolism ; Female ; Heart Defects, Congenital ; complications ; Humans ; Hypertension ; metabolism ; Hypertension, Pulmonary ; metabolism ; Male ; Nitric Oxide ; metabolism

Objective To evaluate the efficacy and safety of argatroban in the treatment of progressive cerebral infarction.Methods Three hundred hospitalized patients with progressive cerebral infarction from October 2006 to September 2011 were collected,among which 150 cases who agreed to the use of argatroban as experimental group,and 150 cases who didn' t agree to the use of argatroban for economic reasons as control group.Experimental group was treated with venous argatroban.It was 60 mg/d within the first 2 days and 24 h continuous intravenous drip.From the beginning of the 3rd day,the dosage was changed to 10 mg each time,twice a day for 5 days.Additionally,75 mg clopidogrel was given once a day for 12 days.Control group was only treated with 75 mg clopidogrel once a day for 14 days.The degree of neurological deficit was compared using the National Institutes of Health Stroke Scale (NIHSS) scoring and the rehabilitation condition was evaluated by Barthel index (BI) and modified Rankin Scale (mRS) scoring between 2 groups before treatment and 3 d,14 d,30 d and 90 d after treatment respectively,and further compared to patients with large artery stenosis and anterior or posterior circulation infarction.The indexes of coagulation function of 2 groups were monitored meanwhile.Results The degree of neurological deficit was significantly improved in the short term (before treatment:NIHSS 15.19 ± 2.70,after treatment of 3 d 10.75 ±2.09,t =2.l14,P =0.037 ;14 d 8.77 ± 1.50,t =2.092,P =0.039;30 d 6.89 ± 0.79,t =2.520,P =0.013 ;90 d 4.85 ± 0.38,t =2.723,P =0.008),and the activities of daily living were significant enhanced in the experimental group (after treatment of 30 d BI 70.89 ± 12.69,90 d 88.16 ± 11.96,90 d mRS 1.57 + 0.39) when compared with the control group (after treatment of 30 d BI 60.26 ± 11.85,t =2.292,P=0.023;90 d 69.90 ± 12.63,t =2.790,P =0.006;90 d mRS 2.14 ±0.52,t =2.124,P =0.035).For large artery stenosis or posterior circulation infarction,the efficacy of argatroban was better.The indexes of coagulation function were in the normal range both before and after medication.No serious adverse reaction occurred during treatment.Conclusion Argatroban which has a higher security probably improves the prognosis and reduces the disability of patients with progressive cerebral infarction.

OBJECTIVE: To study ApoB gene genetic polymorphism of Han nationality and Mongolian nationality in midwest area of Inner Mongolia. METHODS: Some unrelated individuals of Han nationality and Mongolian nationality in midwest area of Inner Mongolia were selected. Polymerase chain reaction-restriction fragment length polymorphism technology was used to check the presence of Xba I (X+) and EcoR I (E-) sites of rare alleles. The genotype frequency, allelic frequency and population genetics parameters were calculated. RESULTS: The frequencies of Xba I (X+) and EcoR I (E-) rare alleles were 2% and 4.6% in Han population. There was no Xba I (X+) or EcoR I (E-) rare alleles found in Mongolian nationality. CONCLUSION The allelic frequencies of ApoB gene Xba I and EcoR I sites are very different in different races. These sites may be used in identification of ethnicity.
Alleles ; Apolipoprotein B-100/genetics* ; Asian People/genetics* ; China ; Ethnicity ; Gene Frequency ; Genotype ; Humans ; Mongolia ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length

Animals ; Education, Medical ; trends ; Humans ; Medicine, Chinese Traditional ; methods ; trends

Objective To investigate the protective effects of simvastatin on cobalt choride ( CoCl2 ) -induced hypoxia and reoxygenation injury on alveolar type Ⅱ cells and the underlying mechanisms.Methods CoCl2 was used to establish the hypoxia and reoxygenation injury model on AT Ⅱ cells.Blank,control and variant doses simvastatin-treated groups ( 5,10,20,30,50,100 μ mol/L) were designed in the present study.The proliferation of AT Ⅱ cells was evaluated by Cell Counting Kit-8 ( CCK-8 ) assay.The percentage of apoptotic cells was assessed by flow cytometry AV/PI double-staining.The protein levels of surfactant protein-C (SP-C) and proliferating cell nuclear antigen (PCNA) in AT Ⅱ cells was determined by Western blot.Results As compared with the control group,pretreatment with low dose (5 - 20 μmol/L),but not high dose simvastatin (50 - 100 μmol/L) markedly reduced A549 cells apoptosis,and increased their proliferation and the protein levels of SPC and PCNAin vitro.The protective effect could be reversed in vitro by L-mevalonate,a simvastatin competitive inhibitor,which indicated that the inhibition of mevalorate pathway was involved in the simvastatin induced AT Ⅱ cells function restoration.Condusion Low doses simvastatin reversed CoCl2-induced hypoxia and reoxygenation injury of AT Ⅱ cells.The inhibition of mevalonate pathway contributed to simvastatin induced AT Ⅱ cells function restoration.

OBJECTIVETo observe the expression of urotensin II (UII) on the lung of patients with pulmonary hypertension (PH) with congenital heart disease and investigate the meaning of this phenomenon.

METHODThirty eight patients with CHD were divided into three groups according to pulmonary arterial systolic pressure (PASP) measured in cardiac catheterization and surgery: normal pulmonary pressure group (N group, PASP < 30 mm Hg, n = 10), mild PH group (M group, PASP ≥ 30 mm Hg, n = 15), severe or moderate PH group (S group, PASP ≥ 50 mm Hg, n = 13). The expression of UII protein and UII mRNA in pulmonary arterioles were measured separately by immunohistochemical (IHC) analysis and in situ hybridization (ISH) analysis.

RESULT(1) The results of UIIIHC staining: The UII protein expression of group M was higher than that of group N (20.22 ± 3.58 vs. 14.34 ± 2.18, P < 0.01), but less than group S (20.22 ± 3.58 vs. 28.92 ± 3.22, P < 0.05). (2) The results of UIIISH mRNA staining were similar to IHC staining, the A value of group M was higher than group N (12.51 ± 2.02 vs. 8.85 ± 1.41, P < 0.05), less than that of group S(12.51 ± 2.02 vs. 25.35 ± 4.33, P < 0.01). (3) Correlation study: there was a positive correlation between the A values of UIIIHC and pulmonary hypertension (r = 0.64, P < 0.01, n = 38), a positive correlation between the A values of UIIISH and pulmonary hypertension (r = 0.58, P < 0.01, n = 38).

CONCLUSIONThere was the expression of Urotensin II protein and mRNA in the lung of pulmonary hypertension patients with congenital heart disease, and these expression may involve the formation of pulmonary hypertension of congenital heart disease.

Adolescent ; Blood Pressure ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Heart Defects, Congenital ; complications ; metabolism ; physiopathology ; Humans ; Hypertension, Pulmonary ; etiology ; metabolism ; physiopathology ; Immunohistochemistry ; In Situ Hybridization ; Infant ; Lung ; metabolism ; physiopathology ; Male ; Pulmonary Artery ; metabolism ; physiopathology ; RNA, Messenger ; genetics ; metabolism ; Severity of Illness Index ; Urotensins ; genetics ; metabolism

OBJECTIVETo investigate the effects of cyclosporine A (CsA), a powerful inhibitor of mitochondrial permeability transition pore (MPTP), on pneumocyte apoptosis, the release of cytochrome C and the activity of caspase-3 after lung ischemia/reperfusion, and explore the mechanisms.

METHODSSingle lung in situ ischemia/reperfusion animal model was used. 30 SD rats were randomly divided into three groups (n = 10): sham (S) group, ischemia/reperfusion (I/R) group and cyclosporine A (CsA) group. Apoptosis of pneumocyte was assessed by TUNEL method, cytochrome C (CytC) in cytoplasm was detected by immunohistochemistry techniques, and the activity of caspase-3 was measured with spectrophotometer.

RESULTSThe content of CytC in cytoplasm, the activity of caspase-3, and the value of apoptosis index (AI) in ischemia/reperfusion group were evidently higher than that in S group (P < 0.01). CsA suppressed apoptosis as well as CytC release and caspase-3 activity (P < 0.01).

CONCLUSIONCsA can prevent the release of cytochrome C, block the apoptosis of pneumocyte accordingly maybe by closing the MPTP.

Alveolar Epithelial Cells ; cytology ; drug effects ; Animals ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cyclosporine ; pharmacology ; Cytochromes c ; metabolism ; Lung ; blood supply ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology

Objective To evaluate the clinical and radiographic characteristics and function of erosive hand osteoarthritis (EOA) patients. Methods Data were obtained from 19 patients with EOA, including their social conditions, clinical conditions, radiographic scores and hand function evaluation. The number of hand osteoarthritis (HOA) patients was 312. The control group consisted of non-EOA patients with hand osteoarthritis with a ratio of 4:1 to EOA patients. A non-parameter test analysis was performed. All data were analyzed by SPSS 23.0 statistical analysis, t test, χ2 test, Fisher exact probility and Spearman's correlations analysis were used for statistical analysis. Results Totally data of 19 patients were collected. Eighteen were female. Onset age was (56±8). Average duration was 56 (12~120) months. FIHOA scores of all the EOA patients were at least 5. All the erosions of 39 joints were characteristically central and erosive changes in 7 joints (18%) showed up as gull-wing. Among 39 erosive joints, including 12 (31%) E and 27 (69%) R, 34 (87%) distal interphalangeal joints were involved. Data analysis found out that EOA patients had longer disease duration (Z=2.610, P=0.009), more severe K-L level (44 ±11 vs 26 ±7, t=7.134, P<0.01), higher AUSCAN total score (28±6 vs 21±7, t=3.781, P<0.01) and higher AUSCAN function score (18±6 vs 12±6, t=4.042, P<0.01). The differences of ESR and CRP were not significant between EOA and non-EOA patients. Conclusion Erosions seen in EOA patients are centrally located gull-wing in the DIP joints. EOA patients have longer duration, more severe radiographic damage and worse joint function.

Objective To compare the value of conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound in the display capacity of periampullary carcinoma and its relationship with the surrounding tissue.Methods A total of 18 patients with the periampullary carcinoma were diagnosed pathologically or by endoscopic biopsy.Each patient had three imaging modalities by conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound.The display capacity and the relationship between the mass and surrounding tissue were compared with three modalities.Results The display rates of limpid visibilities of carcinoma on conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound were 16.7%(3/18),22.2%(4/18) and 94.4%(17/18),respectively;The display rates of duodenum protrusion on three modalities were 0(0/18),38.9% (7/18) and 72.2% (13/18),respectively,with significant differences among conventional ultrasound,hydrosonography and double-contrast enhanced ultrasound.The double-contrast enhanced ultrasound showed two cases of peripheral vascular invasion and one case of intrahepatic metastasis.Conclusion The double-contrast enhanced ultrasound can increase the display capacity of periampullary carcinoma as a new diagnostic modality for periampullary carcinoma.

Objective: To observe the effects of microwave on the activity of SOD and the contents of MDA in renal cortex and testis of mice. Methods: Microwave generator(2 450 MHz, 10 mW/cm2) was used to expose mice; NBT,DTNB and TBA were used to mearure the activity of SOD and the contents of MDA in renal cortex and testis of the mice after microwave exposure.Results: The content of MDA in renal cortex and testis of the mice increased progressively on days 1,6,12 and reached the highest level on day 24 after the microwave exposure (P<0.01). The activity of SOD in renal cortex and testis of the mice decreased progressively on days 1, 6, 12 and reached the lowest level on day 24 after the microwave exposure (P<0.01). Conclusions: Microwave exposure can produce reactive oxygen free radicals and lead to depress SOD activity.