IgG4-related diseases with autoimmune hemolytic anemia: A case report / 中南大学学报(医学版)

IgG4-related disease (IgG4-RD) is a rare autoimmune fibrosis disease characterized by elevated serum IgG4 and tissues as well as organs infiltrated with IgG4-positive cells, resulting in swelling and damage.It is currently treated as first-line treatment with glucocorticoids. Autoimmune hemolytic anemia (AIHA) is also a relatively rare disease that caused by autoreactive erythrocyte antibodies. Although both are autoimmune-related diseases, they rarely overlap. The relationship between them is not clear. A case of IgG4-RD combined with AIHA is reported. The patient has shortness of breath, cough, and sputum after physical activity. Physical examination showed appearance of anemia, yellow staining of skin and sclera, palpable neck and multiple swollen lymph nodes. Laboratory examination, bone marrow biopsy, and lymph node biopsy confirmed the diagnosis. Therefore, clinicians should develop ideas and raise awareness of such diseases.

The realisation of evidence-based medicine / 中国医师杂志

The new model of evidence-based medicine (EBM) that appeared in last century has experienced the global development of nearly 30 years, which praise and question all have.How to develop this medical model scientifically.? This article will talk about personal thinking about this from three aspects.Ⅰ.Looking back and relearning evidence-based medicine;Ⅱ.What is the current misunderstanding of evidence-based medicine? Ⅲ.Medical ethics to be reaffirmed in evidence-based medical practice.

Investigation and analysis for current situation and pathogenesis relevant to pulmonary hypertension / 中南大学学报(医学版)

Objective:To investigate the demographic characteristics and the causes for pulmonary hypertension (PH) in adult patients.Methods:A total of 2 508 adult patients diagnosed as PH,who came from the Second Xiangya Hospital of Central South University from January 2010 to December 2014,were retrospectively investigated.All subjects underwent the clinical diagnosis,or the echocardiographic diagnosis,or thetraditional hemodynamic criteria by right heart catheterization (RHC).The patient's data including hospital numbers,gender,ages,primary diseases,etc,are collected and analyzed.Results:In this study,the number of patients diagnosed as PH was increased year by year.The median age of 2 508 patients was 47 (18-93) years old,and there were 933 males (37.2％),the ratio of male to female was 1:1.69 (P＜0.05).Female was more common in Class Ⅰ PH (pulmonary arterial hypertension) and Class Ⅱ PH (pulmonary hypertension due to left heart disease)(＞70％),but there were more male patients (74.5％) in Class Ⅲ PH (pulmonary hypertension due to lung diseases and/or hypoxia).In our study,896 cases (35.73％) were the Class Ⅰ PH,1 163 cases was the Class Ⅱ PH (46.37％),411 cases was the Class Ⅲ PH (16.39％),and the Class Ⅳ PH (chronic thromboembolic pulmonary hypertension) and the Class Ⅴ PH (PH with unclear and/ or multifactorial mechanisms) were diagnosed in 32(1.27％) and 6 patients (0.24％),respectively.The diseases with largest number of patients for the top 7 primary PH were rheumatic heart disease (1 090,43.48％),congenital heart disease (692,27.60％),chronic obstructive pulmonary disease (358,14.28％),connective tissue related disease(156,6.22％),valvular heart disease (66,2.63％),idiopathic PH (46,1.83％) and pulmonary embolism (27,1.08％).Conclusion:Adult PH patients' peak incidence age is 41-50 years old.This disease is more common among women,and the Class Ⅰ/Ⅱ PH are common in women while the Class Ⅲ is more common in men.Rheumatic heart disease and congenital heart disease may be the most common cause for pulmonary hypertension in China,and chronic obstructive pulmonary disease is the most common cause for the Class Ⅲ PH,in which the patients are old.

Relationship between main pulmonary artery diameter and process of chronic pulmonary disease / 中南大学学报(医学版)

OBJECTIVE@#To explore the relationship between main pulmonary artery diameter and process of chronic pulmonary disease.
@*METHODS@#We retrospectively reviewed 9 cases without pulmonary diseases (control group) and 100 cases with chronic pulmonary diseases, which were divided into 3 groups: the simple chronic pulmonary disease (A group, 37 cases), the compensatory period of chronic cor pulmonale (B group, 20 cases) and the decompensatory period of chronic cor pulmonale (C group, 43 cases). Main pulmonary artery diameter (MPAD) was measured by chest CT. The differences of MPAD among these 4 groups were analyzed.
@*RESULTS@#There was a strong positive correlation between pulmonary artery diameter and process of chronic pulmonary disease. Mean MPAD in the group C was higher than that in the group B (P<0.05), and mean MPAD in the group B was higher than that in the group A (P<0.05). Mean MPAD in control group was the smallest one among all groups (P<0.05).
@*CONCLUSION@#Main pulmonary artery diameter could reflect the process of chronic pulmonary disease.

Measurement of Rho-kinase and CD4+CD25+ regulatory T cells in the peripheral blood in asthmatic patients / 中南大学学报(医学版)

OBJECTIVE@#To determine the levels of Rho-kinase and CD4+CD25+ regulatory T cells in patients with asthma, and the relationship between Rho-kinase and CD4+CD25+ regulatory T cells.@*METHODS@#We included 16 patients with moderate to severe asthma in the research group and 14 healthy people as the control group. The levels of Rho-kinase in the 2 groups were measured by ELISA. The level of CD4+CD25+ regulatory T cells in the 2 groups was measured by flow cytometry. The pulmonary function was measured by spirometer.@*RESULTS@#The level of Rho-kinase in the research group was higher than that in the healthy controls (P0.05). The level of CD4+CD25+ regulatory T cells in the peripheral blood of the 2 groups showed a positive correlation with FEV1% (r=0.380, P=0.038). There was no correlation between the level of Rho-kinase and the level of CD4+CD25+ regulatory T cells in the peripheral blood of the 2 groups (r=-0.438, P>0.05).@*CONCLUSION@#Rho-kinase and CD4+CD25+ regulatory T cells may play a key role in the pathogenesis of asthma.

Atorvastatin attenuates involvement of RhoA/Rho-kinase pathway and NF-κB activation in hypoxic pulmonary hypertensive rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hypoxic pulmonary hypertension (HPH) contributes to the pathogenesis of cardiopulmonary diseases. Several lines of evidence indicate that the Rho A/Rho-kinase pathway play an important role in the progress of pulmonary hypertension. Stains have been shown exert numerous biological effects that are independent of their cholesterol-lowering property. We hypothesized that the Rho A/Rho-kinase pathway is involved in the pathogenesis of HPH, and that atorvastatin would attenuate involvement of the Rho A/Rho-kinase pathway in a HPH rat model.</p><p><b>METHODS</b>Thirty-two Wistar rats were randomly divided into four groups: control group, hypoxic group, atovastatin group, and normal saline group. The control group was kept in a normoxia environment. The other groups were exposed to hypoxia for three weeks. Atovastatin was administered daily via a gastric gavage in the atovastatin group. We measured the mean pulmonary arterial pressure (mPAP), the ratio of the right ventricular weight to the sum of the weights of the left heart ventricle and septum (RV/(LV+S)), arteriole wall thickness/vascular external diameter (WT%), vascular area/total vascular area (WA%), expression of RhoA and phos-MYPT-1 protein in lung tissue, and NF-κB activation in pulmonary vascular smooth muscle cells.</p><p><b>RESULTS</b>Compared with the control group, mPAP, RV/(LV+S), WT%, WA%, NF-κB activation, expression of RhoA, and phos-MYPT-1 were increased in the hypoxic and normal saline groups (P < 0.05). Compared with the hypoxic group, mPAP, RV/(LV+S), WT%, WA%, NF-κB activation, expression of RhoA, and phos-MYPT-1 were decreased in the atovastatin group (P < 0.05). Correlations between phos-MPTY-1 and mPAP, WA%, WT%, and NF-κB activation were all positive.</p><p><b>CONCLUSIONS</b>The Rho A/Rho-kinase pathway plays an important role in the development of HPH. Atorvastatin reversed HPH by inhibiting the activity of Rho A/Rho-kinase and NF-κB.</p>

Measurement of Rho-kinase in peripheral blood monocytes in patients with pulmonary arterial hypertension related to chronic obstructive pulmonary diseases / 中南大学学报(医学版)

OBJECTIVE@#To determine effects of the RhoA/Rho kinase signaling pathway on patients with pulmonary arterial hypertension related to chronic obstructive pulmonary diseases by testing levels of Rho-associated coiled-coil containing protein kinase 1(ROCK1) in peripheral blood monocytes in healthy subjects, patients with chronic obstructive pulmonary diseases (COPD), and patients with pulmonary arterial hypertension related to COPD.@*METHODS@#Ten healthy subjects (Group A), 10 patients with COPD (Group B), and 10 patients with pulmonary arterial hypertension related to COPD (Group C) were enrolled, all of whom were hospitalized in the Third Hospital of Changsha between Dec. 2010 and Apr. 2011. Twenty milliliters of blood was collected from each subject. The peripheral blood mononuclear cells (PBMC) were separated by Percoll and, monocytes were incubated. Levels of ROCK1 in the three groups were measured by ELISA. The pulmonary function was measured by spirometric tests, and the pulmonary arterial systolic pressure (PASP) was detected by color Doppler echocardiogram.@*RESULTS@#1)The PASP in Group C was significantly higher than that of Groups A and B(P0.05).@*CONCLUSION@#Rho kinase plays a key role in the pathogenesis of pulmonary arterial hypertension. The ROCK1 may be a marker of the severity of pulmonary arterial hypertension related to COPD.

Atorvastatin attenuates hypoxic pulmonary hypertension in rats by inhibiting RhoA/Rho kinase pathway / 中南大学学报(医学版)

OBJECTIVE@#To investigate whether atorvastatin treatment can improve the symptoms of hypoxia-induced pulmonary hypertension in rats by inhibiting RhoA/Rho kinase pathway.@*METHODS@#A total of 32 Westar rats was divided into 4 groups: normoxic controls (Group A), hypoxic controls (Group B), hypoxia plus atorvastatin [10 mg/(kg.d)] group(Group C), and hypoxia plus the vehicle of atorvastatin (Group D). Rats for hypoxia treatment were maintained under the condition of 10% FiO2 6 h/d for 4 weeks. At the end of 4 weeks, rats were anesthetized and the mean pulmonary arterial pressure (mPAP) was measured by right heart catheterization. The ratios of arteriole wall thickness to vascular external diameter (WT%), and vascular area to total vascular area (WA%) were measured by a computerized image analyzer. RhoA and phos-MYPT-1 expression in the pulmonary artery were determined by Western blot.@*RESULTS@#Comparing with Group A, the mPAP [(29.6 ± 1.1)mmHg vs (16.8 ± 0.7)mmHg], RV/(LV+S) [(39.0 ± 0.7)%vs (29.4 ± 0.5)%], WT% [(35.6 ± 2.4)% vs (22.3 ± 1.2)%] and WA% [(56.5 ± 5.1)% vs (36.6 ± 2.3)%] in Group B were all significantly increased (P<0.05). Comparing with Group B, the mPAP [(25.3 ± 3.2)mmHg], RV/(LV+S) [(36.3 ± 2.1)%], WT%[(29.2 ± 3.2)%] and WA% [(48.1 ± 2.7)%] in Group C were significantly decreased. The vehicle of atorvastatin had no such effect. The expression of RhoA and phos-MYPT-1 in the pulmonary artery was increased in Group B, but it was decreased in Group C.@*CONCLUSION@#RhoA/Rho kinase pathway plays an important role in the development of hypoxic pulmonary hypertension. Atorvastatin can improve the symptoms of hypoxic pulmonary hypertension by inhibiting RhoA/Rho kinase activity.

Effect of atorvastatin on lipopolysaccharide-induced expression of C-reactive protein in human pulmonary epithelial cells / 中南大学学报(医学版)

OBJECTIVE@#To determine the effect of atorvastatin on lipopolysaccharide-induced expression of C-reactive protein in cultured A549 cells.@*METHODS@#A549 cells were incubated in DMEM medium containing lipopolysaccharide in the absence or presence of various concentrations of atorvastatin. After the incubation, the medium was collected and the level of C-reactive protein was measured by enzyme-linked immunosorbent assay. The cells were harvested and C-reactive protein mRNA was analyzed by reverse transcription polymerase chain reaction.@*RESULTS@#Incubation with lipopolysaccharide significantly induced a time and dose dependent increase in the mRNA expression and the production of C-reactive protein in A549 cells (P<0.05). Atorvastatin significantly decreased the lipopolysaccharide induced the mRNA expression and the production of C-reactive protein in a dose dependent manner in A549 cells (P<0.05).@*CONCLUSION@#Atorvastatin downregulates lipopolysaccharide-induced expression of C-reactive protein in cultured A549 cells, which may be its mechanism of anti-inflammation.

Effect of atorvastatin on inflammatory infiltration in the lung of rabbits with hypercholesterolemia / 中南大学学报(医学版)

Objective To determine the effect of atorvastatin on the hypercholesterolemia in-duced lesion in the lung. Methods Fifteen male New Zealand rabbits were randomly assigned into a control group (n=5) , a high-cholesterol forage group (n=5) , and an atrovastatin treatment group (n=5). The control group received normal forage, but the high-cholesterol group and atrovastatin treatment group received high-cholesterol forage. From the 9 th week, the atrovastatin treatment group was added atorvastatin, and the experiment stopped at the end of the 14th week. At the beginning of the experiment and at the 8 th, 14 th week, blood cholesterol and body weight were detected. At the 14th week, bronchial alveolar lavage (BAL) was performed in vitro after the rabbits were executed; pathological examinations were determined in the lung tissues by staining with hamatoxylin-eosin. Oil red 0 and the activities of NF-κB in the alveolar macrophages (AMs) were investigated by immuno-cytochemistry. Proliferative cell nuclear antigen in the lung tissues was adopted by immunohistochem-istry, and the concentrations of IL-6 in the serum, BALF and the culture supematants of AMs were measured by ELISA. Pulmonary tissue paraffin section was stained with hamatoxylin-eosin. Results Atorvastatin reduced inflammatory infiltration, AM NF-κB activation, and cell proliferation in the lung, but raised IL-6 level. Conclusion Hypercholesterolemia-induced pulmonary inflammation is attenuated by atorvastatin.

Atorvastatin Reduces the LPS-induced COX-2 Expression in Cultured Human Pulmonary Epithelial Cells / 中国医师杂志

Objective To assess the effect of atorvastatin on the Lipopolysaccharide (LPS)-induced cyclooxygenase-2 (COX-2) expression in cultured human pulmonary epithelial cells (A549). Methods A549 cells were incubated in the medium containing LPS and different concentrations of atorvastatin(0,10,15,20?M/ml, respectively) for 12h. Then the total cellular RNA and proteins from the cells treated with different experimental conditions were extracted for RT-PCR and western blot analysis,respectively. Results In cultured human pulmonary epithelial cells, atorvastatin reduced the expression of COX-2 mRNA and protein induced by LPS in a dose-dependent manner. Conclusion Atorvastatin may down-regulate LPS-induced COX-2 expression in cultured human pulmonary epithelial cells.

A measure of Chronic respiratory disease questionnaire for clinical trail / 中南大学学报(医学版)

Objective　The aim of this paper was to investigate the reliability and validity of the Chronic respiratory disease questionnaire (CRQ) in China. Method　Sixty-eight patients with chronic respiratory disease who were in hospital from January to November, 1999 were surveyed with CRQ. Eighteen patients were investigated repeatly with CRQ in one week to test the reliability; before and the 10th day after treatment, 50 patients were surveyed twice with CRQ and the peakflow of these patients were also detected. The same doctor explained questionnaires and tested peakflow. Results　The correlated analysis of reliability was positive (r=0.732, P<0.01). The correlatied analysis between the difference of twice-questionnaire scores and the difference of twice-peakflow value was also positive (r=0.565, P<0.01).Conclusion　CRQ can be used by the clinical doctors of China.

Changes of [Ca~(2+)]_i and the activity of ACE in alveolar macrophages of rabbits with high-fat diet / 中国病理生理杂志

AIM:To investigate the effects of high-fat diet on the level of intracellular free calcium ([Ca2+]i) and the activity of angiotensinⅠconverting enzyme (ACE) in alveolar macrophages (AMs) of rabbits. The association between asthma and high-fat diet was also observed. METHODS: Twelve male New Zealand rabbits were medially divided into normal diet group and 1.2% high-cholesterol diet group randomly. 8 weeks later, bronchial alveolar lavage was performed in vitro. [Ca2+]i was determined by Fluo-2/am.The activity of ACE was detected with ultraviolet method. RESULTS: The levels of [Ca2+]i in AMs greatly increased (P