OBJECTIVETo explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension (PAH) in patients of chronic obstructive pulmonary disease (COPD) associated with chronic cor pulmonale (CCP) during exacerbation.

METHODSSeventy patients of COPD and CCP with acute exacerbation were randomly and equally divided into control group and treatment group. The control group received standard treatment with antibiotics, antiasthmatic and expectorant medications, and oxygenation; and the ligustrazine treatment group received ligustrazine treatment (80 mg/d; i.v.; for 2 weeks) in addition to the standard treatment. Before and at the end of 2 week treatment, the clinic responses of the two regimens were evaluated, plasma levels of endothelin-1 (ET-1) and nitric oxide (NO) were determined; arterial oxygen partial pressure (PaO2, mean pulmonary arterial pressure (mPAP), outflow tract of right ventricle (RVOT), and internal diameter of right ventricle (RV) were measured.

RESULTSGood clinic benefits were achieved in both the standard and ligustrazine regimens, plasma level of ET-1, values of mPAP, RV and RVOT decreased significantly, plasma level of NO and PaO2 values decreased (all P < 0.01 vs pre-treatment to all parameters). Compared with the control group, ligustrazine greatly enhanced the clinic efficacy from 77.1% to 97.1% (P < 0.05), and also resulted in more significant changes of all these parameters (P < 0.01 vs control group for all parameters). For both groups, the levels of plasma ET-1 were positively correlated with values of mPAP, RVOT, and RV (r = 0.710, 0.853, and 0.766, respectively, all P = 0.000), and negatively correlated with plasma NO and PaO2 (r = - 0.823, and - 0.752, respectively, all P = 0.000).

CONCLUSIONLigustrazine is effective in treating pulmonary artery hypertension during acute exacerbation of COPD and CCP in patients from the plateau area. The observed changes in the plasma levels of NO and ET-1 in response to ligustrazine treatment suggest that ligustrazine may act through the selective effect on pulmonary blood vessels to enhance the synthesis and release of NO and suppress those of ET-1 from lung vascular endothelial cells, thus reducing pulmonary artery pressure and decreasing pulmonary arterial hypertension.

Altitude ; Blood Gas Analysis ; Chronic Disease ; Endothelin-1 ; blood ; Humans ; Hypertension, Pulmonary ; drug therapy ; Nitric Oxide ; blood ; Pulmonary Artery ; physiopathology ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; Pyrazines ; therapeutic use ; Respiration

Age Factors ; Child Nutritional Physiological Phenomena ; Child, Preschool ; Diet ; Eating ; Female ; Humans ; Male ; Sex Factors

BACKGROUND:The molecular mechanism of traumatic deep vein thrombosis is complex.Numerous studies focus on clinical observation and epidemiology,but its molecular mechanism has not been a new breakthrough.OBJECTIVE:By use of gene array technology,this study was aimed to study the expression changes of matrix metalloproteinases in rat models of traumatic deep vein thrombosis,and to explore the roles of matrix metalloproteinases in traumatic deep venous thrombosis.METHODS:A total of 150 SD rats,SPF grade,of 8-12 weeks old,body weight of 250-300 g,were divided at random into normal control group (n=10) and model group (n=140).Rat traumatic deep venous thrombosis models were set up by clamping the femoral vein and fixing the bilateral hind limbs,and the fixation of hip spica with plaster bandage was conducted in each group.Then rats were divided into 7 subgroups:post-traumatic 0.5 hours,post-traumatic 2.5 hours (initial period of thrombosis),post-traumatic 25 hours (thrombogenesis at thrombotic crest-time),post-traumatic 25 hours non-thrombogenesis at the thrombotic crest-time),post-traumatic 72 hours (thrombus resolution),post-traumatic 72 hours thrombus insolution) and post-traumatic 168 hours (nonthrombosis).At the corresponding phasess,the femoral vein tissues were incised,and total RNA of femoral vein was extracted using Trizol one-step method.Applying Genechip Rat Genome 430 2.0 genechips,the gene expressions in femoral vein were detected in different groups.The rate of traumatic deep venous thrombogenesis and non-thrombogenesis,the rate of thrombi solution and insolution were observed;the expressions of matrix metalloproteinases and tissue inhibitor of metalloproteinases at different time phases was detected by gene array data analysis.RESULTS AND CONCLUSION:Three model rats died and the remaining 147 rats were involved in the final analysis.At the post-traumatic 25 hours,the rate of thrombogenesis was 50.5% and nonthrombogenesis was 49.5%.To the post-traumatic 168 hours,the rate of thrombus solution was 56.7% and thrombus insolution was 43.3%.Both matrix metalloproteinases and tissue inhibitor of metalloproteinases exhibited differential expressions in the course of traumatic deep venous thrombosis.Under the thrombus insolution state,matrix metalloproteinases continued to show a high expression,tissue inhibitor of metalloproteinase expression was down-regulated in the thrombus formation,was significantly inhibited in the thrombus insoluUon process.In the process of traumatic deep vein thrombosis and insolution,matrix metalloproteinase was closely related to traumatic deep vein thrombosis,the matrix metalloproteinase/tissue inhibitor of metalloproteinases are likely to affect the biological state of thrombosis.

BACKGROUNDThe difference between renal oncocytomas (RO) and renal clear cell carcinomas (RCCs) presents the greatest diagnostic challenge. The aim of this study was to retrospectively determine if RO and RCCs could be differentiated on computed tomography (CT) images on the basis of their enhancement patterns with a new enhancement correcting method.

METHODSForty-six patients with a solitary renal mass who underwent total or partial nephrectomy were included in this study. Fourteen of those were RO and 32 were RCCs. All patients were examined with contrast-enhanced CT. The pattern and degree of enhancement were evaluated. We selected the area that demonstrated the greatest degree of enhancement of the renal lesion in the corticomedullary nephrographic and excretory phase images. Regions of interest (ROI) were also placed in adjacent normal renal cortex for normalization. We used the values of the normal renal cortex that were measured at the same time as divisors. The ratios of lesion-to-renal cortex enhancement were calculated for all three phases. The Student's t-test and Pearson's Chi-square test were used for statistical analyses.

RESULTSAll RCCs masses showed contrast that appeared to be better enhanced than RO on all contrast-enhanced phases of CT imaging, but there was no significant difference in absolute attenuation values between these two diseases (P > 0.05). The ratio of lesion-to-cortex attenuation in the corticomedullary phase showed significantly different values between RO and RCCs. The degree of contrast enhancement in RCCs was equal to or greater than that of the normal renal cortex, but it was less than that of the normal cortex in RO in the corticomedullary phase. The ratio of lesion-to-cortex attenuation in the corticomedullary phase was higher than the cut off value of 1.0 in most RCCs (84%, 27/32) and lower than 1.0 in most RO (93%, 13/14) (P < 0.05). In the nephrographic phase, the ratio of lesion-to-cortex attenuation was higher than that in the corticomedullary phase in most RO (71%, 10/14), showing a prolonged enhancement pattern; and was lower than that in most RCCs (97%, 31/32), showing an early washout pattern (P < 0.05). In the differentiation of RO from RCCs, the sensitivity was 93%, specificity 84%, positive predictive value 72%, negative predictive value 84%, and accuracy for RO was 87, if the ratio of lesion-to-cortex attenuation in a cortex phase was lower than the cutoff value of 1.0. The sensitivity was 71%, specificity was 97%, positive predictive value was 91%, negative predictive value was 91%, and accuracy for RO was 89%, if the ratio of lesion-to-cortex attenuation in nephrographic phase was higher than that in the corticomedullary phase.

CONCLUSIONSThe ratios of renal lesion-to-cortex attenuation ratios may be helpful in differentiating RO from RCCs.

Adenoma, Oxyphilic ; diagnosis ; diagnostic imaging ; Adult ; Aged ; Carcinoma, Renal Cell ; diagnosis ; diagnostic imaging ; Female ; Humans ; Kidney Neoplasms ; diagnosis ; diagnostic imaging ; Male ; Middle Aged ; Tomography, X-Ray Computed

Objective To evaluate the clinical significance of epithelial cellular adhesion molecule (Ep-CAM)expression in esophageal squamous cell carcinoma(SCC).Methods The Ep-CAM expression was immunohistochemically investigated in 70 normal esophageal mucosas,SCCs and 72 lymph nodes.Results Ep-CAM expression was observed in 94.3% of the tumors,but no expression in the normal mucosa.The Ep- CAM expression was not significantly different between different tumor scales and tumors invading depths,its expression level was relevant with the tumors differentiation and lymph node metastases(P

Objective To develop the clinical practice guidelines for the management of medication adherence to highly active antiretroviral therapy (HAART) in China. Methods The development methods included qualitative interview of 31 stakeholders, questionnaire survey of 423 PLHIV, adaptation of 30 clinical practice guidelines related to AIDS care, and overviews of reviews of 44 systematic reviews/Meta-analysis. Results 10 clinical practice guidelines and 10 systematic reviews/Meta-analysis were included. The clinical practice guidelines for the management of HAART were formed. Conclusions The formed clinical practice guidelines showed better applicability and higher general quality. It is recommended to use the guidelines in AIDS care.

To determine heat-shock protein (Hsp)90 expression is connected with cellular apoptotic response to heat stress and its mechanism, chicken (Gallus gallus) primary myocardial cells were treated with the Hsp90 promoter, aspirin, and its inhibitor, geldanamycin (GA), before heat stress. Cellular viability, heat-stressed apoptosis and reactive oxygen species level under different treatments were measured, and the expression of key proteins of the signaling pathway related to Hsp90 and their colocalization with Hsp90 were detected. The results showed that aspirin treatment increased the expression of protein kinase B (Akt), the signal transducer and activator of transcription (STAT)-3 and p-IKKα/β and the colocalization of Akt and STAT-3 with Hsp90 during heat stress, which was accompanied by improved viability and low apoptosis. GA significantly inhibited Akt expression and p-IKKα/β level, but not STAT-3 quantity, while the colocalization of Akt and STAT-3 with Hsp90 was weakened, followed by lower cell viability and higher apoptosis. Aspirin after GA treatment partially improved the stress response and apoptosis rate of tested cells caused by the recovery of Akt expression and colocalization, rather than the level of STAT-3 (including its co-localization with Hsp90) and p-IKKα/β. Therefore, Hsp90 expression has a positive effect on cellular capacity to resist heat-stressed injury and apoptosis. Moreover, inhibition of Hsp90 before stress partially attenuated its positive effects.
Apoptosis* ; Aspirin ; Cell Survival ; Chickens* ; Heat Stress Disorders ; Heat-Shock Proteins* ; Hot Temperature* ; HSP90 Heat-Shock Proteins ; In Vitro Techniques* ; Proto-Oncogene Proteins c-akt ; Reactive Oxygen Species ; Transducers

OBJECTIVETo study the pulmonary pathology in patients died of fatal human influenza A(H1N1) infection.

METHODSEight cases of fatal human influenza A (H1N1) infection, including 2 autopsy cases and 6 paramortem needle puncture biopsies, were enrolled into the study. Histologic examination, immunohistochemitry, flow cytometry and Western blotting were carried out.

RESULTSThe major pathologic changes included necrotizing bronchiolitis with surrounding inflammation, diffuse alveolar damage and pulmonary hemorrhage. Influenza viral antigen expression was detected in the lung tissue by Western blotting. Immunohistochemical study demonstrated the presence of nuclear protein and hemagglutinin virus antigens in parts of trachea, bronchial epithelium and glands, alveolar epithelium, macrophages and endothelium. Flow cytometry showed that the apoptotic rate of type II pneumocytes (32.15%, 78.15%) was significantly higher than that of the controls (1.93%, 3.77%).

CONCLUSIONNecrotizing bronchiolitis, diffuse alveolar damage and pulmonary hemorrhage followed by pulmonary fibrosis in late stage are the major pathologic changes in fatal human influenza A (H1N1) infection.

Adolescent ; Adult ; Aged ; Alveolar Epithelial Cells ; pathology ; Antigens, Viral ; metabolism ; Apoptosis ; Autopsy ; Biopsy, Needle ; Bronchiolitis, Viral ; pathology ; Child ; Child, Preschool ; Female ; Hemagglutinin Glycoproteins, Influenza Virus ; metabolism ; Humans ; Influenza A Virus, H1N1 Subtype ; immunology ; Influenza, Human ; metabolism ; mortality ; pathology ; virology ; Lung ; immunology ; metabolism ; pathology ; Male ; Middle Aged ; Nuclear Proteins ; metabolism ; Pulmonary Alveoli ; pathology ; Pulmonary Fibrosis ; pathology ; Young Adult

OBJECTIVETo study the expression changes of matrix metalloproteinases (MMPs) in traumatic deep vein thrombosis (TDVT) in a rat model with the aid of gene chip technology and to explore the roles of MMPs in TDVT.

METHODSTotally 150 Sprague Dawley rats were randomly divided into control group (n equal to 10) and model group (n equal to 140). Rat models of TDVT were established by clamping the femoral vein and fixing the bilateral hind limbs. Then fixation of the hip spica with plaster bandage was conducted. According to the observation phases and/or biological situations of the femoral vein thrombosis, the model rats were further divided into 7 groups. Vascular tissues were obtained from each group through noninvasive incision into the femoral vein at corresponding time points. We adopted the Trizol one-step method for total RNA extraction, Affymetrix RAT 230 2.0 array for detection of RNA expressions and fold change (FC) analysis for changes of differential expressions of MMPs in each group. The main outcome parameters measured included expressions of MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-10, MMP-11, MMP-12, MMP-13, MMP-14, MMP-16, MMP-23 and MMP-24. Gene array data of these MMPs were analyzed by the Affymetrix Microarray Analysis software (Version 5.0).

RESULTSFC analysis showed differential expressions of MMPs in each group during the course of TDVT. At the initial period of thrombosis, MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-10, MMP-11, and MMP-24 had significantly high expression, while MMP-12, MMP-13, MMP-14, MMP-16 and MMP-23 had relatively low expression. MMPs were all highly expressed at the peak time of thrombosis. In the process of thrombus resolution, MMP-2, MMP-10, MMP-16 and MMP-24 have relatively low expression, while MMP-12, MMP-13, MMP-14, MMP-16 and MMP-23 have significantly high expression.

CONCLUSIONMMPs may affect the process of TDVT through transcription regulation of the fibrinolysis-anti-fibrinolytic system during the course of thrombosis and thrombus resolution.

Animals ; Disease Models, Animal ; Matrix Metalloproteinases ; physiology ; Rats ; Rats, Sprague-Dawley ; Venous Thrombosis ; enzymology ; etiology ; Wounds and Injuries ; complications