To study the relationship between the burden of Pneumocystis carinii (P. carinii) and the inflammatory reaction and biochemical markers in bronchoalveolar lavage fluids (BALF) in a rat model of P. carinii pneumonia (PCP).Clean grade 50 male Sprague-Dawley rats were immunosuppressed by a subcutaneous injection of 25 mg cortisone acetate twice a week for 8-12 weeks; the PCP model was successfully induced in 14 rats. The inflammatory reaction and biochemical markers of the activity of lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and type IV collagenase (matrix metalloproteinases, MMP-2, MMP-9) as well as the values of total protein (TP) and albumin (ALB) in BALF between the mild burden group of P. carinii (involved alveoli < 25% per 100 alveoli, Group A) and the moderate to severe burden group (involved alveoli > or = 25% per 100 alveoli, Group B) were measured. The other six clean grade SD rats served as normal control group (Group C).The total white cell count in BALF was higher in Group B [(6.8 +/- 1.7) x 10(6)/L] than in Group A [(3.8 +/- 1.2) x 10(6)/L] (P < 0.01); however, there were no differences in white cell differentiation. Assays of biochemical markers showed that ALB in BALF in Group B (0.893 +/- 0.469 g/L) was increased in comparison with Group A (0.262 +/- 0.169 g/L); it was only 0.026 +/- 0.021 g/L in Group C. The contents of TP and activities of LDH were higher in Group B (TP 1.756 +/- 0.706 g/L, LDH 2580 +/- 550 U/L) than in Group A (TP 0.784 +/- 0.553 g/L, LDH 1410 +/- 620 U/L); the values of TP and LDH were 0.063 +/- 0.020 g/L and 370 +/- 250 U/L respectively in Group C. The activity of Type IV collagenase, including MMP-2 and MMP-9, was higher in Group B than in Group A (P < 0.01) (MMP-2: 1102 +/- 169 grey value vs 459 +/- 274 grey value; MMP-9: 1218 +/- 257 grey value vs 449 +/- 225 grey value). There was no activity of Type IV collagenase in BALF of Group C. No statistically significant difference was observed in ALP between the groups B and A.These results indicate that there is a significant correlation between the burden of P. carinii in lung tissues and the inflammatory reaction as well as biochemical markers of the resultant activity of lung injury.
Objective. The measurement of the static compliance of the respiratory system (Cstat) during mechanical ventilation requires zero end-inspiratory flow. An inspiratory pause maneuver is needed if the zero end-inspiratory flow condition cannot be satisfied under normal ventilation.Approach. We propose a method to measure the quasi-static respiratory compliance (Cqstat) under pressure control ventilation mode without the inspiratory pause maneuver. First, a screening strategy was applied to filter out breaths affected strongly by spontaneous breathing efforts or artifacts. Then, we performed a virtual extrapolation of the flow-time waveform when the end-inspiratory flow was not zero, to allow for the calculation ofCqstatfor each kept cycle. Finally, the outputCqstatwas obtained as the average of the smallest 40Cqstatmeasurements. The proposed method was validated against the gold standardCstatmeasured from real clinical settings and compared with two reported algorithms. The gold standardCstatwas obtained by applying an end-inspiratory pause maneuver in the volume-control ventilation mode.Main results. Sixty-nine measurements from 36 patients were analyzed. The Bland-Altman analysis showed that the bias of agreement forCqstatversus the gold standard measurement was -0.267 ml/cmH2O (95% limits of agreement was -4.279 to 4.844 ml/cmH2O). The linear regression analysis indicated a strong correlation (R2 = 0.90) between theCqstatand gold standard.Significance. The results showed that theCqstatcan be accurately estimated from continuous ventilator waveforms, including spontaneous breathing without an inspiratory pause maneuver. This method promises to provide continuous measurements compliant with mechanical ventilation.
Total 732 subjects aged 30-60 years undergoing health check-up at Beijing Hospital Medical Examination Center in 2009, who had no history of non-alcoholic fatty liver disease (NAFLD) were recruited in the study.According to the quartile of hemoglobin (HGB) level, the subjects were divided into 4 groups: Q1: HGB≤131 g/L (n=192), Q2: HGB>131 g/L and ≤140 g/L (n=178), Q3: HGB>140 g/L and ≤152 g/L (n=184), Q4: HGB>152 g/L (n=178). All participants were followed up for 4 years, the prevalence rates of NAFLD in groups Q1, Q2, Q3 and Q4 were 8.3% (16/192), 17.4% (31/178), 23.4% (43/184) and 25.3% (45/178), respectively (P<0.05). Logistic regression showed that the rates of NAFLD in groups Q2, Q3 and Q4 were 2.32 (1.22-4.41), 3.36 (1.81-6.21) and 3.72(2.02-6.87) times higher as group Q1(P<0.05). Multiple logistic regression analysis showed that the hemoglobin level, TG and BMI were the independent risk factors of NAFLD.
Key words:
Fatty liver; Hemoglobins; Cohort studies
Gliomas are the most aggressive intracranial tumors accounting for the vast majority of brain tumors with very poor prognosis and overall survival (OS). Cancer-derived immunoglobulin G (cancer-IgG) has been found to be widely expressed in several malignancies such as breast cancer, colorectal cancer, and lung cancer. Cancer-IgG could promote tumorigenesis and progression. However, its role in glioma has not been revealed yet.We mined open databases including the Chinese Glioma Genome Atlas (CGGA), The Cancer Genome Atlas (TCGA), and the Gene Expression Omnibus (GEO) to study the role of IGHG1, which encodes cancer-IgG in glioma. Examination of the differential expression of IGHG1 was carried out in the GEO and TCGA databases. Furthermore, its expression in different molecular subtypes was analyzed. Stratified analysis was performed with clinical features. Subsequently, immune infiltration analysis was conducted using single-sample gene set enrichment analysis (ssGSEA). GSEA was performed to reveal the mechanisms of IGHG1. Lastly, immunohistochemistry was processed to validate our findings.In this study, we found that the expression of IGHG1 was higher in glioma and molecular subtypes with poor prognosis. The overall survival of patients with a high expression of IGHG1 was worse in the stratified analysis. Immune infiltration analysis indicated that the expression level of IGHG1 was positively correlated with the stromal score, ESTIMATE score, and immune score and negatively correlated with tumor purity. Results from the GSEA and DAVID demonstrated that IGHG1 may function in phagosome, antigen processing and presentation, extracellular matrix structural constituent, antigen binding, and collagen-containing extracellular matrix. Finally, immunohistochemistry assay validated our findings that patients with a high expression of cancer-IgG had poor OS and disease-free survival (DFS).Cancer-IgG is a promising biomarker of diagnosis and treatment for patients with glioma.
Introduction: Mouse models of chronic heart failure (HF) have been widely used in HF research. However, the current HF models most often use the C57BL/6 mouse strain and do not show the clinically relevant characteristics of pulmonary congestion. In this study, we developed a robust mouse model of HF in the BALB/c mouse strain, exhibiting pulmonary edema and pleural effusion, and we validated the model using the standard pharmacological therapies in patients with chronic HF and reduced ejection fraction (HFrEF) or acute decompensated HF. Methods: After induction of myocardial infarction (MI) by permanent ligation of the left coronary artery in BALB/c mice, the cardiac function, pulmonary congestion, disease biomarkers, and survival were evaluated using the angiotensin converting enzyme inhibitor enalapril or the loop diuretic furosemide. Enalapril was administered 4 weeks post-MI for 6 weeks or furosemide was given 10 weeks post-MI for 4 days, when pulmonary congestion was evident. Results: Compared to sham controls, MI mice developed systolic dysfunction, exhibited lung weight increase at 4 weeks, and progressively developed pleural effusion (60% of the animals) at 10 weeks. Compared to the vehicle, enalapril significantly reduced the lung weight and pleural effusion, preserved systolic function, and improved survival. Furthermore, furosemide completely abolished the pleural effusion. Enalapril or furosemide also reduced the plasma brain natriuretic peptide concentration. Discussion: The post-MI HF in BALB/c mice shows reproducible and robust pulmonary congestion and may be a clinically relevant model for novel drug testing for treatment in patients with HFrEF or acute decompensated HF.
Objective
To explore the effects of gradient pressure treatment on rehabilitation of limb function and lymphedema in post-operation patients with breast cancer.
Methods
A total of 567 patients with modified radical mastectomy for breast cancer were randomly divided into experimental group (284 cases, routine nursing for breast and functional rehabilitation exercises guided by professional nurses at early stage after operationan and gradient pressure treatment) and control group (283 cases, routine nursing for breast and functional rehabilitation exercises guided by professional nurses at early stage after operation). Shoulder mobility and incidence rate of lymphedema were all observed at 5 weeks and 12 weeks after operation.
Results
The shoulder mobility in experimental group [(26.17±4.77)° for adduction, (70.13±10.55)° for outreach, (142.54±6.09)° for forward bend and upward lift, (36.47±2.86)° for extension] was superior to that in the control group (F=261.27, 31.62, 46.03, 33.37; P<0.01). 5 weeks after operation, but affected limb function was almost same in two groups 12 weeks after operation. The incidence rate of lymphedema was 7.04% in the experimental group and 16.61% in the control group 12 weeks after operation with statistically significant difference (χ2=12.447, P<0.01).
Conclusions
Gradient pressure treatment applied for post-operation patients with breast cancer can improve limb function and decrease the incidence rate and degree of lymphedema, so as to improve patients′ life quality.
Key words:
Breast neoplasms; Lymphedema; Affected limb function; Gradient pressure treatment
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