Objective To study the pulmonary function changes in patients cured from severe acute respiratory syndrome(SARS) Methods Pulmonary function tests were performed in 11 SARS patients one month after their discharge from hospital Results The subjects (3 males and 9 females) were aged from 21 to 62 years (31 0?10 0) The days after their discharge from hospital were 22 to 43 days (32 2?4 7) Pulmonary function showed:vital capacity(VC) (95 6?19 0)% predicted,forced vital capacity(FVC) (97 2?9 9)% predicted,forced expiratory volume in one second(FEV 1)(97 5?9 8)% predicted,FEV 1/FVC (85 9?5 6)%,total lung capacity(TLC) (102 4?10 4)% predicted,residual volume(RV)/TLC (32 6?5 0)%,RV (116 8?25 0)% predicted,and diffusing capacity of CO(DLCO) (73 6?10 9)% predicted Conclusion The patients cured from SARS demonstrated relatively normal ventilatory function but mild impaired diffusing capacity

Objective: To determine the role of cross-talk between calcineurin-dependent signal transduction pathway and protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and protein kinase A (PKA) in airway remodeling in asthma. Methods: Male guinea pigs were sensitized with intraperitoneal injections of ovabumin (OVA), then treated with cyclosporin A (CsA,5 mg/kg), an inhibitor of calcineurin, then inhaled OVA for 2 weeks 14 days later. Activities of calcineurin, PKC, MAPK, and PKA were was analyzed by phosphorylation and dephosphorylation. In primary cultures of rat airway smooth muscle cells (ASMC), activities of calcineurin, PKC, MAPK, and cross-talk induced by urotensin Ⅱ (UⅡ), a recently identified strong mitogen, were measured. Results: (1) The activities of calcineurin, MAPK and PKC increased by 19% (P0.05). (4) CsA 10 -6 mol/L inhibited UⅡ-stimulated PKC activity by 14% (P0.05). Conclusion:The signal transduction pathways between calcineurin and other protein kinases such as PKC, MAPK and PKA have cross-talk in airway remodeling in asthma.

Objective To analyze the situation of health-risk behaviors of the students in specialty medical science college of Yunnan and its relationship with negative life events, and provide scientific evidence for lowering the occurrence rate of health-risk behaviors. Methods The stratified randomised cluster-sampling method was used to select 576 students of specialty medical science college, and the occurrence rate of health-risk behaviors and life events conditions were estimated by Youth Health-Risk Behavior Questionnaire and Adolescents Self-Rating Life Events Checklist. Descriptive statistic analysis, Chi-square test and Logistic regression analysis was used to analyze the data. Results Among the students of specialty medical science college in Yunnan, the rate of smoking was 3.1%,the rate of drinking was 4.9%,the rate of food refusal was 39.6%, the rate of fighting was 13.5%,the rate of obsessed with the internet was 26.4%, and the rate of substance abuse was 3.1%. There were significant differences between the students of different genders (P<0.05) or specialities (P<0.05) . Logistic regression analysis showed total score of negative life events had positive influence on drinking (OR=1.017,P<0.05), food refusal (OR=1.018,P<0.05), fighting (OR=1.021,P<0.05), obsessed with the internet (OR=1.025, P<0.05), substance abuse (OR=1.025, P<0.05) . The factor of interpersonal relationship had positive influence on drinking (OR=1.162,P<0.05), food refusal (OR=1.102,P<0.05), substance abuse (OR=1.260, P<0.05) . The factor of punished had positive influence on fighting (OR=1.144, P<0.05), and had negative influence on drinking (OR=0.891, P<0.05) . The factor of study pressure had positive influence on fighting (OR=1.143, P<0.05), and the factor of loss had negative influence on fighting (OR=1.144, P<0.05) . Conclusion Negative life events are influencing factors for health-risk behaviors of the students in specialty medical science college of Yunnan, and there is difference on the way that the factor of life events influencing health-risk behaviors.

AIM: To study the effect of homocysteine (HCY) on proliferation of airway smooth muscle cells and fibroblasts and the effect of HCY on collagen prodution of airway fibroblasts. METHODS: [3H]-TdR incorpora- tion was measured in cultured airway smooth muscle cells. The [3H]-TdR and [3H]-proline incorporation were mea- sured in cultured airway fibroblasts. RESULTS: HCY induced proliferation of airway smooth muscle cells and fibroblasts in a concentration - dependent manner. HCY also induced collagen production of airway fibroblasts in a concentration - dependent manner. The inhibitors of protein kinase C, H7 and polymyxin B, inhibited HCY - induced proliferation of airway smooth muscle cells. CONCLUSIONS: HCY induced proliferation of airway smooth muscle cells and fibroblasts, HCY also induced collagen production of airway fibroblasts. The HCY - induced proliferation of airway smooth muscle cells may be related to the pathway of PKC signal transduction.

Objective To investigate the correlation between lesion pattern and etiological mechanism in acute isolated pontine infarction.Methods The clinical data in patients with acute isolated pontine infarction were collected retrospectively. Diffusion weighted imaging (DWI) was used to identify the lesion patterns. The correlation between the lesion pattern and etiological subtype was analyzed. Results A total of 146 patients with acute isolated pontine infarction were enrolled in the study, including 136 unilateral infarctions and 8 bilateral infarctions. The DWI lesion pattern analysis showed that there were 98 patients with paranasal infarction, 11 with anterolateral infarction, 18 with tegmentum infarction, and 19 with multiple infarction. Among all the etiological subtypes, basilar artery branch disease (BABD) accounted for the greatest proportion (n = 72, 49.3%), followed by large arterial occlusive disease ( n = 32, 21.9%), small arterial occlusive disease ( n = 25, 17.1%), and other causes/unknown causes ( n = 12, 8.2%). Cardioembolism was minimal (n =5, 3.4%). The distribution patterns of DWI lesions in acute isolated pontine infarction were significantly correlated with the etiological subtypes (C = 0.516, P < 0.001). Among them, 60 patients with paramedian infarction ( χ2 =16.915, P <0.001), 1 with anterolateral infarction ( χ2 =7.701, P = 0.006), 1 with tegmentum infarction ( χ2 =17.401, P <0.001) were closely associated with BABD; 9 patients with paramedian infarction ( χ2 =12.534, P <0.001), 6 with anterolateral infarction ( χ2 =24.365, P <0.001), and 10 with tegmentum infarction ( χ2 =18.312, P < 0.001) were significantly associated with small arterial occlusive disease. Conclusions There are significant correlation between the lesion pattern and etiological mechanism in acute isolated pontine infarction. The cause of acute isolated pontine infarction can be predicted in early stage by DWI revealed infarction distribution characteristics.

Objective To investigate the predictive factors of progressive motor deficits (PMD) after isolated pontine infarction. Methods Consecutive patients with isolated pontine infarction admitted to hospital within 48 hours after onset were enroled. They were divided into either a PMD group (increase ≥1 within 7 days) or a non-PMD group according to the clinical course and the changes of motor scores of the National Institutes of Health Stroke Scale (NIHSS). The pontine infarction patterns were classified as basal surface infarction and deep infarction, the sides were divided into left and right, the infarct levels were divided into upper, middle, and lower according to diffusion-weighted imaging. The demographics, baseline clinical data, and imaging features were compared between the two groups. Multivariable logistic regression models were used to analyze the predictive factors of PMD after isolated pontine infarction. Results A total of 101 patients with isolated pontine infarction admitted to hospital within 48 h of onset were enroled, including 16 in the PMD group and 85 in the non-PMD group. The proportions of pontine infarction involving the basal surface (87. 5% vs. 47. 1% , χ2 = 8. 851, P = 0. 003), the infarcts on the middle levels (56. 2% vs. 24. 7% , χ2 = 4. 851, P = 0. 028), and basilar artery stenosis or occlusion (62. 5% vs. 27. 1% ,χ2 = 7. 689, P = 0. 006) of the PMD group were significantly higher than those of the non-PMD group, while the proportions of the infarcts on the left sides (18. 8% vs. 56. 5% , χ2 = 7. 664, P = 0. 006) and the infarcts on the upper levels (37. 5% vs. 72. 9% , χ2 = 7. 689, P = 0. 006) of the PMD group was significantly lower than those of the non-PMD group. Multivariate logistic regression analysis identified that pontine infarction involving the basal surface (odds ratio 5. 650, 95% confidence interval 1. 011 - 31. 580, P = 0. 049) and basilar artery stenosis or occlusion (odds ratio 4. 075, 95% confidence interval 1. 127 - 14. 741, P = 0. 032) were the independent risk factors for PMD after isolated pontine infarction. Conclusions Infarction involving the basal surface and basilar artery stenosis or occlusion may be the predictors for PMD after isolated pontine infarction.

OBJECTIVETo investigate the role of calcineurin (CaN) in the lung fibroblast proliferation and collagen synthesis induced by basic fibroblast growth factor (bFGF).

METHODSWe used Western blot and immunohistochemical methods for investigating the content and distribution of calcineurin in the lung tissue. Calcineurin activity in different tissues was measured using (32)P-labelled substrate. In the primary culture of lung fibroblasts, (3)H-thymidine ((3)H-TdR) and (3)H-proline incorporation methods were used to study the effect of cyclosporin A (CsA), an inhibitor of calcineurin, on the lung fibroblast DNA and collagen synthesis stimulated by bFGF.

RESULTSWe found that calcineurin was expressed in lung tissue and has phosphatase activity (7.1 +/- 2.0 pmol Pi/mg pr/min). CsA (10(-8) - 10(-6) mol/L) inhibited lung fibroblast (3)H-TdR incorporation induced by bFGF in a dose-dependent manner, with the inhibitory rates by 20%, 46% and 66% (P < 0.01). CsA (10(-7) - 10(-6) mol/L) inhibited (3)H-proline incorporation in lung fibroblasts stimulated by bFGF, with the inhibitory rates by 21% and 37% (P < 0.01). In a culture medium, CsA (10(-8) - 10(-6) mol/L) inhibited (3)H-proline secretion induced by bFGF in a dose-dependent manner, with the inhibitory rates by 19%, 29% (P < 0.05) and 56% (P < 0.01). CsA (10(-7) mol/L) could inhibit calcineurin activity by 44% in lung fibroblasts (P < 0.01).

CONCLUSIONSCalcineurin is expressed in lung tissue and has phosphatase activity. It is involved in the bFGF stimulated lung fibroblast DNA and collagen synthesis.

Animals ; Calcineurin ; analysis ; physiology ; Cell Division ; Cell Survival ; drug effects ; Collagen ; biosynthesis ; Fibroblast Growth Factor 2 ; pharmacology ; Fibroblasts ; drug effects ; physiology ; Lung ; cytology ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley

Objective To investigate the correlations of P2Y1 and ITGB3 single nucleotide polymorphisms (SNP) with aspirin resistance (AR) in patients with large atherosclerotic stroke (LAA) in a Chinese Han population.Methods Patients with first-ever LAA from Anhui stroke registration system were enrolled.Thrombus elasticity diagram was used to detect the platelet function.TaqMan technology was used to detect the P2Y1 and ITGB3 genotypes.Results A total of 206 patients with LAA were enrolled.Thirty-one patients (15.0％) had AR and 175 (85.0％) were aspirin sensitive (AS).The frequency of P2Y1 rs701265 G allele in the AR group was significantly higher than that in the AS group (43.5％ vs.26.9％;x2 =7.074,P=0.008).The frequency of P2Y1 rs701265 AA genotype in the AR group was significantly lower than that in the AS group (32.3％ vs.53.7％;x2 =4.850,P=0.028).There were no significant significances in the frequencies of P2Y1 rs1065776 and ITGB3 rs5918 alleles and genotypes between the AR group and the AS group.Multivariate logistic regression analysis showed that P2Y1 rs701265 G allele was an independent risk factor for AR in patients with LAA (odds ratio 2.186,95％ confidence interval 1.190-4.016;P=0.012).Conclusion The P2Y1 rs701265 polymorphism is associated with AR in Chinese Han patients with LAA,while the P2Y1 rs1065776 and ITGB3 rs5918 polymorphisms are not.

OBJECTIVETo analyze diagnostic approach to severe acute respiratory syndrome (SARS) according to the diagnostic criteria issued by the Ministry of Health of China (MHC).

METHODSThe clinical data and the diagnostic results of 108 cases of SARS were retrospectively reviewed according to the MHC criteria.

RESULTSThere were 55 men and 53 women, with a median age of 34.5 years (range, 12 - 78 years). The interval between their first visit and clinical diagnosis was 3 days (range, 0 - 14 days). The diagnosis was made at the first visit in 7 (6.5%, 7/108) cases with a history of exposure to SARS patients and infiltrates on chest radiograph. Eighty-nine (82.4%) and 12 (11.1%) patients were categorized as probable cases and suspected cases respectively at their first visit and a clinical diagnosis of SARS was made subsequently. The interval between first visit and reaching the final diagnosis was 1 - 3 days in 72 (66.7%) cases and 4 days in 29 (26.9%) cases. The final diagnosis was made in 0 - 14 days (median, 2 days) for those (n = 59, 54.6%) with a history of close contact with SARS patients and 2 - 8 days (median, 3 days) for those (n = 49, 45.4%) living in Beijing but without such a history (P = 0.03). The chest radiograph was interpreted as unremarkable in 26 (24.1%) cases at their first visit, and the diagnosis was made in 4 days (range 2 - 8 days), which was significantly longer compared with other cases (P < 0.001). In patients without a history of close contact with SARS patients, all the five criteria were met after combination antibiotic therapy had failed.

CONCLUSIONSA chest radiograph without infiltrates at the early stage of SARS is an important factor responsible for delayed diagnosis. In patients without a history of close contact with SARS cases, antibiotic effect was a major factor influencing doctors' diagnosis.

Adolescent ; Adult ; Aged ; Child ; Female ; Humans ; Male ; Middle Aged ; Radiography, Thoracic ; Retrospective Studies ; Severe Acute Respiratory Syndrome ; diagnosis

Objective: To retrospectively analyze the potential correlation between cardiac magnetic resonance (CMR) imaging and clinical features and idiopathic arrhythmia in patients with straight back syndrome (SBS). Methods: Patients receiving CMR imaging examination from April 2015 to March 2016 at our department (n=1 432) were screened, 76 patients met the diagnosis criteria of flat chest (anteroposterior diameter/transthoracic diameter (APD/TTD) ratio<0.37 at the T8 vertebra). After excluding 33 patients with structural heart disease, 43 SBS patients were divided into two groups: SBS without obvious morphological change in the heart (group A, n=19) and SBS with morphological change of the heart (group B, n=24). CMR images were analyzed, focusing the heart morphological changes induced by SBS. The clinical data were collected to comprehensively analyze the medical history, electrocardiogram and electrophysiological examination in order to observe the relationship between SBS induced heart morphological change and the arrhythmia type and origin. Results: There were 21 male patients in this cohort, mean age was (28.5±11.5) years (13-58 years). APD/TTD ratio was similar between the two groups (0.30±0.03 vs. 0.29±0.04, P>0.05). LVEF tended to be lower in group B than in group A ((47.48±12.77)%vs. (59.31±9.04)%, P>0.05) . In group B, there were 15 patients with left ventricular enlargement, 2 with left ventricular wall thickening, 5 with uncoordinated ventricular wall motion, 5 with tricuspid regurgitation, 3 with mitral regurgitation, 2 with myocardial fibrosis, 5 with increased trabecular and 16 with decreased left ventricular function. Direct compression sign of right ventricle (disappeared precordial fat tissue space, secondary right atria enlargement and tricuspid regurgitation) and left atria (with or without secondary left ventricular enlargement and mitral regurgitation) were evidenced in patients of group B. CMR revealed that the arrhythmia origin corresponded the compression site of the heart in 8 cases (42.1%) in group A and 13 cases (54.2%) in group B, not corresponded to the compression site in 6 patients (31.6%) in group A and in 7 patients (29.2%) in group B, not attributable in 5 patients (26.3%) in group A and 4 patients (16.7%) in group B. The percent of arrhythmia origin corresponded the compression site of the heart tended to be higher in group B as compared to group A (P>0.05). Conclusion SBS can induce changes of cardiac morphology and cardiac function. SBS induced cardiac compression is linked with the development of arrhythmias and might be one of the reasons of arrhythmias in these patients.