Buyang Huanwutang Promoted Proliferation and Differentiation of Neural Stem Cells via Regulating Autophagy Following Oxygen-glucose Deprivation/Reoxygenation Injury / 中国实验方剂学杂志

Objective:To investigate the effect of Buyang Huanwutang （BHT） on proliferation and differentiation in neural stem cells （NSCs） after oxygen-glucose deprivation/reoxygenation （OGD/R） injury. Method:NSCs isolated from the hippocampus of SD rats were cultured and randomly divided into a normoxia group， a model group， a BHT group， a rapamycin （Rapa） group， and a combination group ［autophagy inhibitor 3-methyladenine （3-MA） combined with BHT］. The 20% blank serum was used in the normoxia group， and 20% BHT-medicated serum in the BHT group. The doses of Rapa and 3-MA were 1 μmol·L^-1 and 5 mmol·L^-1， respectively. The cells were subjected to OGD/R except those in the normoxia group. The cell morphology was observed under a light microscope. NSCs were confirmed by immunofluorescence detection of nestin expression. The viability and proliferation of NSCs were assessed by cell counting kit-8 （CCK-8） assay and 5-ethynyl-2-deoxyuridine （EdU） labeling， respectively. Furthermore， Ad-mCherry-GFP-LC3B fluorescence assay was performed to investigate autophagy. The effect of BHT on autophagy-related protein expression was detected by western blot assay. Brain derived neurotrophic factor （BDNF）， <italic>β</italic>-tubulin Ⅲ， and glial fibrillary acidic protein （GFAP） were evaluated by immunofluorescence assay. Result:OGD/R significantly reduced the cell viability of rat NSCs as compared with the normoxia group. Compared with the model group， the BHT group exhibited significantly improved viability of rat NSCs （<italic>P</italic><0.01）. BHT induced the production of autophagosomes in NSCs after OGD. The BHT group showed increased expression of microtuble-associated protein 1 light chain 3Ⅱ (LC3Ⅱ） and Beclin-1 （<italic>P</italic><0.05，<italic>P</italic><0.01） and slightly changed p62 compared with the normoxia group， and significantly up-regulated LC3Ⅱ and Beclin-1 （<italic>P</italic><0.05，<italic>P</italic><0.01） and down-regulated expression of p62 （<italic>P</italic><0.01） compared with the model group. The Rapa group had similar effect as the BHT group （<italic>P</italic><0.05，<italic>P</italic><0.01）， while the combination group inhibited the activity of autophagy （<italic>P</italic><0.01）. As indicated by the results of ad-mCherry-GFP-LC3B， compared with the normoxia group， the model group showed increased fluorescence intensity （<italic>P</italic><0.01）， and the BHT and Rapa groups could further increased the fluorescence intensity of autophagy （<italic>P</italic><0.01）， while the combination group inhibited autophagy activity （<italic>P</italic><0.01）. Immunofluorescence results revealed that compared with the normoxia group， the model group displayed significantly reduced positive cells of EdU， <italic>β</italic>-tubulin Ⅲ， GFAP， and BDNF （<italic>P</italic><0.01）， and the BHT and Rapa groups exerted similar protective and promoting effects （<italic>P</italic><0.05，<italic>P</italic><0.01）， while the combination group partially blocked the neuroprotection and differentiation ability of BHT （<italic>P</italic><0.05）. Conclusion:BHT pretreatment can effectively protect rat NSCs against OGD-induced injury and promoted proliferation and differentiation by up-regulating autophagy.

One-stage surgery in patients with both cardiac and non-cardiac diseases / 北京大学学报(医学版)

OBJECTIVE@#To investigate the possibility and feasibility of one-stage cardiac and non-cardiac surgery.@*METHODS@#From July 1999 to August 2018, one hundred and eleven patients suffering from cardiac and non-cardiac diseases were treated by one-stage cardiac and non-cardiac operation in Department of Cardiac Surgery and Thoracic Surgery, General Surgery, Urinary Surgery, and Gynecology, Peking University First Hospital. There were 83 males (74.8%) and 28 females (25.2%), aged 41 to 84 years [mean age: (64.64±8.97) years]. The components of the cardiac disease included coronary heart disease, valvular heart disease, cardiac tumors, chronic constrictive pericarditis and congenital heart disease. The components of the non-cardiac diseases included lung benign and malignant diseases, thymoma and thymic cyst, breast cancer, chest wall giant hemangioma, digestive tract benign and malignant diseases, urinary system carcinoma and gynecological diseases.@*RESULTS@#Two patients died after operations in hospital; thus, the hospital mortality rate was 1.8%. One patient died of multiple organ failure on the 153th days after emergency coronary artery bypass grafting (CABG) combined with radical resection of bladder cancer. The other of pericardium stripping with lung cancer operation died of the multiple organ failure on the tenth day after surgery. The remaining 109 patients recovered and were discharged. There were 13 cases of complications during the days in hospital. The total operative morbidity was 11.7%: postoperative hemorrhage in 2 cases (1.8%), pulmonary infection and hypoxemia in 3 cases (2.7%), hemorrhage of upper digestive tract in 1 case (0.9%), incisional infection in 3 cases (2.7%), subphrenic abscess in 1 case (0.9%), and postoperative acute renal failure and hemofiltration in 3 case (2.7%). Of the 109 patients discharged, 108 patients were followed up. All the patients survived for 6 months, and 21 patients died due to tumor recurrence or metastasis within 1 to 5 years of follow-up, but no cardiogenic death. During the follow-up period, 1 patient developed cardiac dysfunction, 1 patient underwent percutaneous coronary intervention (PCI), 1 patient had cerebral hemorrhage due to excessive postoperative anticoagulation, and 1 patient suffered from incisional hernia.@*CONCLUSION@#One-stage surgeries in patients suffering from both cardiac and non-cardiac benign or malignant diseases are safe and possible with satisfactory short-term and long-term survival.

Research Progress on Automatic Assessment of Bone Age / 法医学杂志

Bone age is an important indicator of human growth and development, which can objectively reflect the growth level and maturity of individuals. Traditional manual bone age assessment usually compares the X-ray of the left wrist with the reference standard to obtain the corresponding bone age. This method is time-consuming and its results vary with different observers. In recent years, with the continuous development of computer science, bone age assessment has began to change from traditional manual assessment to automatic assessment. Although there has already been numerous researches on automatic bone age assessment, most of them are still in the experimental stage. This paper reviews related research and progress on automatic bone age assessment at home and abroad in recent years, in order to provide reference and research ideas for relevant researchers.

Death pattern and cause analysis in mice after establishment of the liver alveolar hydatid model / 中国人兽共患病学报

We studied the death pattern and the main causes of death after artificial liver inoculation with alveolar hydatid model,and explored the risk factors and prevention of major complications resulting from death after modeling.The 50 healthy Kunming mice were inoculated with open-staring liver puncture and the physiological changes of the mice were observed dy-namically within 1 5 days after operation.The time and amount of death were recorded,and the causes of death and related fac-tors were analyzed emphatically.On the 1 5 day after surgery,1 9 died;1 died in the ninth day,and the remaining 1 8 died with-in 7 days of the operation.The postoperative death rate began to rise in the second day,and gradually decreased to 1 after the peak of the 4 th and 5 th days.The main causes of death of the mice after inoculation were closely related to the complications of surgical methods,anaesthesia,infection,antigenicity of vesicle,and liver injury.Effective prevention of these complications is the key to improve the survival rate.

Abnormal calcium re-uptake in myocardium sarcoplasmic reticulum in rabbits with heart failure and the influencing factors / 生理学报

The aim of the present study was to investigate the abnormal calcium re-uptake function of myocardium sarcoplasmic reticulum (SR) in rabbits with heart failure, as well as potential mechanisms. Heart failure model was established in rabbits through aortic insufficiency and constriction of abdominal aorta. The SR Ca(2+) re-uptake function was measured with a calcium imaging device. The activity of myocardium SR calcium adenodine triphosphatase 2a (SERCA2a) was measured by inorganic phosphate. The protein expressions of SERCA2a, CaMKII, PKA, PP1α, phospholamban (PLB), PLB-Ser(16) and PLB-Thr(17) were evaluated by Western blot. The activities of PKA and CaMKII were detected by γ-(32)P substrate incorporation. The results showed that, compared with the sham operation group, the heart failure group exhibited reduced Ca(2+) re-uptake amount (P < 0.01) and the expression and activity of SERCA2a (P < 0.05 or P < 0.01), decreased expression of PLB and its phosphorylation status in sites of Ser(16) and Thr(17) (P < 0.05), increased expressions and activities of PKA and CaMKII (P < 0.05 or P < 0.01), and increased expression of PP1α (P < 0.05). These results suggest that the abnormal Ca(2+) re-uptake function in heart failure is related with reduced expression and activities of SERCA2a, as well as reduced expression of PLB and its phosphorylation status. Both PLB-Ser(16) and -Thr(17) may be involved in the regulation of myocardium SR calcium pump activity in heart failure.

Expression of Cysteinyl leukotriene receptor 1 in bronchial epithelial cell regulated by tumor necrosis factor-α / 中华实用儿科临床杂志

Objective To explore whether TNF-α involves in the modulation of Cysteinyl leukotriene receptor 1 (CysLT1) expression in bronchial epithelial cells.Methods The bronchial epithelial cell lines 16HBE cells were stimulated with different concentration (0.00,0.05,0.50,5.00,20.00 μg/L) of TNF-α for 48 hours,and CysLT1 mRNA in 16HBE cells was measured by reverse transcription(RT)-PCR.CysLT1 expression was detected by immunohistochemistry.Results 16HBE cells did not express CysLT1,after the cells were treated with TNF-α,obvious expression of CysLT1 were detected by immunohistochemistry.The weak CysLT1 mRNA expression was observed by RT-PCR in 16HBE cells,and after the cells were treated with TNF-α for 48 hours,CysLT1 mRNA expression were upregulated.When the concentrations of TNF-α were 0.00,0.05,0.50,5.00,and 20.00 μg/L respectively,the relative intensities of CysLT1 mRNA/β-actin were 0.048,0.105,0.177,0.182,0.495,respectively.Conclusions TNF-α can upregulate CysLT1 mRNA expression in 16HBE ceils in a dose-dependent manner.When infected by virus,respiratory tract produces abundant TNF-α.The TNF-α can upregulate the expression of CysLT1 in epithelial cells,enhance inflammation reaction in respiratory tract.This may explain partially the mechanism of exacerbation of asthma induced by respiratory tract infection.

Effect of metoprolol on sarcoplasmic reticulum Ca2+ leak in a rabbit model of heart failure / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Studies have shown that β-blockers can improve cardiac performance in heart failure (HF) by reversing protein kinase A (PKA)-mediated sarcoplasmic reticulum (SR) Ca2+ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor (RyR2) hyper-phosphorylation is a critical regulator of SR Ca2+ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca2+ leak by other potential mechanisms.</p><p><b>METHODS</b>New Zealand white rabbits were randomly divided in three groups (n=7 in each group): normal group, metoprolol-untreated group and metoprolol-treated group. Cardiac function was determined by echocardiography and hemodynamic assays. The SR Ca2+ leak was measured by a calcium-imaging device, and the expression and activities of related proteins were evaluated by Western blotting and auto-phosphorylation.</p><p><b>RESULTS</b>In the metoprolol-untreated group, there was significantly increased ventricular cavity size, reduced systolic function, increased SR Ca2+ leak, reduced associated amount of FK506 binding protein 12.6 (FKBP12.6), increased expression and activity of PKA and Ca2+/calmodulin-dependent protein kinase II (CaMKII), and increased phosphorylated RyR2 phosphorylation sites (with unchanged RyR2-P2030). In the treated group, there was partly increased ventricular cavity size with preserved systolic function, but no prominent Ca2+ leak, with unchanged expression and activity of PKA, CaMKII and their RyR2 phosphorylation sites.</p><p><b>CONCLUSION</b>Chronic administration of metoprolol prevented the SR Ca2+ leak by restoring not only PKA-dependent but also CaMKII-dependent hyper-phosphorylation of RyR2, which may be one of the potential mechanisms by which β-blockers improve cardiac function and reduce the incidence of fatal arrhythmia in HF.</p>

Pulmonary pathology in fatal human influenza A (H1N1) infection / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the pulmonary pathology in patients died of fatal human influenza A(H1N1) infection.</p><p><b>METHODS</b>Eight 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.</p><p><b>RESULTS</b>The 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%).</p><p><b>CONCLUSION</b>Necrotizing 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.</p>

Effects and mechanism of protein tyrosine kinase inhibitor on blood-retinal barrier breakdown / 中华实验眼科杂志

Background Several cytokines,especially interleukin-1β (IL-β) involve in the breakdown of blood-retina barrier,and the signal of cytokine is transduced through protein tyrosine kinase (PTK) pathway.Objective This study was to investigate the effects of PTK inhibitor,Genistein,on IL-1β-induced blood-retinal barrier breakdown and possible mechanism.Methods The animal models of blood-retinal barrier breakdown were induced through intravitreal injection of IL-1β(10ng) in 24 clean healthy SD rats and assigned to IL-1β group and Genistein group.5μl IL-1β+1μl Genistein with 0.2,1,5μg were intravitreally injected in 12 model rats and 5μl IL-1β (2mg/L)+1μl DMSO was used at the same way in other 12 models.Evans Blue was injected in rats via jugular vein in 1 hour before sacrifice of animals and the arterial blood was collected for the detect of serum Evans Blue.The retinas of the rats were obtained in 4 and 48 hours after injection of vitreous cavity to assay the content of Evans Blue in retina.The changes of vessels and infiltration of inflammatory cells were observed with hematoxylin-eosin stain.RT-PCR was employed to determine the expression of IL-8 and MCP-1mRNA in neuroretina after intravitreal injection.Expression of MCP-1 protein was localized by immunohistochemistry.Results The ratio of retinal Evans Blue and plasma Evans Blue was significantly decreased after intravitreal injection of different doses of Genistein among Genistein groups and IL-8 group with a statistical difference (4 hours:F=7.510,P=0.010;48 hours:F=5.960,P=0.019).With the increase of time after injection of Evans Blue,the ratio of retinal Evans Blue and plasma Evans Blue was gradually reduced in comparison to IL-1β group (P＜0.05).After injection of IL-1β,the dilation of retinal vessel and adhesion of leukocyte to vessel wall were seen under the light microscope,but infiltration of less inflammatory cells was found in Genistein group.The expressions of IL-8 and MCP-1mRNA were obviously declined in retina of rats in Genistein groups compared with IL-8 group (P＜0.05).Immunochemistry indicated that the expression of MCP-1 protein in neuroretina tissue was weaker in Genistein group compared with IL-8 group.Conclusion PTK inhibitor,Genistein,can decrease IL-1β-induced permeability of vessel and maintain the integrity of blood-retinal barrier by downregulating the expression of chemokines and infiltration of leukostasis in retinal vessels.This study imply that PTK pathway plays an important role in IL-1β-induced blood-retinal barrier breakdown.

Pericyst may be a new pharmacological and therapeutic target for hydatid disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Most hydatid cysts with calcified walls are biologically and clinically silent and inactive. Transforming growth factor-beta 1 (TGF-β1) plays a critical role in the calcification process of cells. The aim of this study was to assess the effect of modulating TGF-β1 signaling on the calcification of hydatid cysts.</p><p><b>METHODS</b>Pericyst cells isolated from hepatic hydatid cysts were cultured with osteogenic media. These cells were assessed for alkaline phosphatase activity and mineralization capacity using Alizarin Red staining. Cells were also treated with recombinant human TGF-β1 and TGF-β inhibitor, and the expression profiles of osteoblast markers (RUNX2, osterix, and osteocalcin) were analyzed using Western blotting. The effects of inhibiting TGF-β1 signaling on calcification of pericyst walls were assessed using different doses of TGF-β inhibitor for 7 weeks in a preclinical disease model of liver cystic echinococcosis.</p><p><b>RESULTS</b>Cells within the pericyst displayed high levels of alkaline phosphatase activity and mineralized nodule formation, as induced by osteogenic media. These activities, as well as expression profiles of osteoblast markers (RUNX2, osterix, and osteocalcin) could be inhibited by addition of recombinant human TGF-β1 (rhTGF-β1) and enhanced by TGF-β inhibitor. In the animal model of cystic echinococcosis, inhibition of TGF-β1 signaling increased calcification of the pericyst wall, which was associated with decreased cyst load index and lower viability of protoscoleces.</p><p><b>CONCLUSIONS</b>Cells within the pericysts adopt an osteoblast-like phenotype and have osteogenic potential. Inhibition of TGF-β1 signaling increases hydatid cyst calcification. Pharmacological modulation of calcification in pericysts may be a new therapeutic target in the treatment of hydatid disease.</p>

Frequency, distribution of CD4+, CD8+ T cells and expression of CD38 in gastric mucosa of HIV infections / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To investigate the frequencies and distribution of CD4+ T cells and CD8+ T cells as well as the changes of immune activation in gastric mucosa of HIV-infected individuals.</p><p><b>METHODS</b>42 HIV-infected individuals were recruited into this investigation, and 36 patients had definite diagnosis of clinical stage. Biopsy of gastric mucosal tissues was performed by fiberoptic gastroscope including 10 normal people as a control group. Then, immunohistochemistry was used to detect expression of CD4, CD8 and CD38 in gastric mucosa, and the distinctions among three groups were analyzed with LEICA Qwin image analysis system.</p><p><b>RESULTS</b>(1) Compared with asymptomatic HIV carriers and control group, CD4 T cells remarkably decreased in the gastric mucosa of AIDS patients (P < 0.01). In gastric mucosa of asymptomatic HIV carriers, there were still some CD4+ T cells in lymphoid follicles and stroma where CD4+ T cells were unevenly distributed, the frequency of CD4+ T cells was not significantly different between asymptomatic HIV carriers and control group (P > 0.05); (2) Phenomenon of CD8+ T cells infiltrating mucosal epithelium and gland was general in HIV-infected individuals. CD8+ T cells took on local excessive hyperplasia in gastric mucosa of some individuals. As compared with control group, CD8+ T cells markedly increased in gastric mucosa of infected individuals (P < 0.01), but the distinction of asymptomatic HIV carriers and AIDS patients was not significant (P > 0.05); (3) CD38-expressing cells mainly distributed over gastric mucosal surface to superficial layer(1/3-2/3 layer) of HIV-infected individuals, and was more intensive than control group (P < or = 0.01), but there was not noticeable difference between asymptomatic HIV carriers and AIDS patients (P > 0.05).</p><p><b>CONCLUSION</b>The frequencies and distribution of gastric mucosal CD4+ T cells of HIV-infected individuals were closely correlated with progression of disease. Disfunction of mucosal immune system which was resulted from HIV infection and injury of CD4+ T cells could be an important cause of CD8+ T cells increasing and CD38-expressing enhancement.</p>

Comparison of cardiac function and expression and activity of myocardial calcium regulatory proteins in rabbit systolic and diastolic heart failure models / 生理学报

The aim of the present study is to investigate the differences in cardiac function, and the expression and activity of calcium regulatory proteins between rabbit systolic heart failure (SHF) and diastolic heart failure (DHF) models. New Zealand white rabbits were randomly divided into three groups: sham operation (SO) group, DHF group (receiving abdominal aortic constriction) and SHF group (receiving aortic valve destruction and abdominal aortic constriction). The cardiac function was detected by echocardiographic and hemodynamic assays. The mRNA expression levels of sarcoplasmic reticulum Ca(2+) ATPase 2a (SERCA2a) and phospholamban (PLB) were evaluated by RT-PCR. The protein expression levels of SERCA2a, PLB, phosphoserine 16-PLB (pSer-16-PLB) and protein kinase A (PKA) were evaluated by Western blot, and the phosphorylation status of PLB was determined by the ratio of pSer-16-PLB protein level to that of PLB. The activity of SERCA2a was measured through inorganic phosphate. The activity of PKA was measured by gamma-(32)P ATP-binding assays. Compared with SO group, there were significantly increased ventricular wall thickness, raised left ventricular end diastolic pressure (LVEDP), reduced diastolic function in DHF group (P<0.05 or P<0.01), and significantly increased ventricular cavity size and LVEDP, reduced systolic function in SHF group (P<0.05 or P<0.01). The expression levels of SERCA2a in DHF and SHF groups were lower than that in SO group (P<0.05), while the expression and activity of PKA in DHF and SHF groups were higher than that in SO group (P<0.05 or P<0.01), and there was no significant difference between DHF and SHF groups. The expression levels of PLB and pSer-16-PLB as well as the phosphorylation status of PLB and activity of SERCA2a in SHF group were lower than those in DHF and SO groups respectively. Posing a contrast, the phosphorylation status of PLB and activity of SERCA2a in DHF group were higher than that in SO group (P<0.05). These results indicate that the SHF and DHF models were successfully established, and there are some differences in the expression and activity of calcium regulatory proteins between two models.

Correlation between premature ejaculation and redundant prepuce / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the correlation between redundant prepuce and premature ejaculation.</p><p><b>METHODS</b>Fifty-two cases suffering from premature ejaculation and redundant prepuce were treated with circumcision. They were asked to fill the investigating questionnaire about the changes of ejaculatory latent period, patients' and their wives' satisfaction with sexual life before and after the treatment.</p><p><b>RESULTS</b>During 12 months after circumcision, 28 cases were cured and 11 cases were efficacious. The curative rate was 54.9% and effective rate was 76.5%. Twelve cases with no responding continued to be treated with routine methods, such as psychotherapy, daub narcotic to glans of penis and taking medicine to treat chronic prostatitis, which were used before circumcision but still no effects. During 18 months after circumcision, 4 cases were cured and 5 cases were efficacious.</p><p><b>CONCLUSION</b>Redundant prepuce had direct or indirect relationship with premature ejaculation. The circumcision is one of the effective methods to treat premature ejaculation.</p>

Detection of hepatic progenitor cells in patients with severe hepatitis and their distribution / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To identify hepatic progenitor cells (HPCs) in patients with severe hepatitis (SH) by detecting their markers and investigate the features of their distribution and location.</p><p><b>METHODS</b>Liver tissues taken from 59 SH patients were tested for the receptor of stem cell factor (c-kit), pi-class glutathione S-transferase (GST-pi), cluster of differentiation 34 (CD34), cytokeratin 19 (CK19), cytokeratin 18 (CK18) and alpha fetoprotein (AFP) by immunohistochemistry (IHC). Meanwhile, 58 patients with acute or chronic hepatitis were also detected to act as controls.</p><p><b>RESULTS</b>Hepatic progenitor cells could be seen in SH patients. Most of them existed as ductular cells that had been called "typical ductular proliferation (ADP)" or "typical ductular reaction" in previous research. These ductular cells were mainly located at the portal areas, fibro septa, periportal parenchyma and the border of the pseudolobuli and inflammatory foci. Further, c-kit, GST-pi, CK19 and CK18, but not CD34 and AFP could be detected in these cells. Another kind of HPC was the small hepatocyte-like cell (SHLC), which could express c-kit, GST-pi, and CK18, but not CK19, CD34 and AFP. The semi-quantitative analysis showed that the scope of ADP in SH patients was significantly larger than that in acute and chronic hepatitis patients (chi2= 63.62, P<0.05), and the scope of ADP in subacute severe hepatitis and chronic severe hepatitis patients was also significantly larger than that in acute severe hepatitis patients.</p><p><b>CONCLUSION</b>In the course of regeneration of viral hepatitis, different types of pathology have different features. In acute and chronic hepatitis (G1-2), the regeneration is mainly owing to the proliferation of mature hepatocytes, and in chronic hepatitis (G3-4), there is the participation of HPCs, although they are limited. In severe hepatitis, however, since the replicative capacity of normal hepatocytes is impaired or prohibited, liver regenerates and restores mainly by the means of hepatic stem cells activation and proliferation. But the hepatic stem cells don't differentiate into their mature functional compartments directly at all. There are several intermediary or transition populations. In human severe hepatitis, they are mainly ductular cells, and parts of them are small hepatocyte-like cells.</p>

A clinicopathological study on 3 cases of severe acute respiratory syndrome / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the pathological characteristics of severe acute respiratory syndrome (SARS) and its relationship to clinical manifestation.</p><p><b>METHODS</b>Tissue specimens from 3 autopsy cases of diagnosed SARS were studied under microscopy and the clinical data were reviewed.</p><p><b>RESULTS</b>The typical pathological changes of lungs were diffuse hemorrhage on surface. A mixture features of serous, fibrinous and hemorrhagic inflammation were seen in most pulmonary alveoli with engorgement of capillary and there were microthrombosis in some capillary. Pulmonary alveoli became thick with interstitial mononuclear inflammatory infiltration, diffused alveoli damage, desquamation of pneumocytes and hyaline-membrane formation. Fibrinoid materials and erythrocytes could be found in alveolar spaces. There were thrombo-embolisms in some bronchial artery. Meanwhile, haemorrhagic necrosis was showed in lymph nodes and spleen with attenuation of lymphocytes. Other atypical pathological changes, such as hydropic degeneration, fatty degeneration, interstitial cell proliferation and some lesions observed in liver, heart, kidney, pancreas may have existed before the hospitalization.</p><p><b>CONCLUSION</b>Severe damages of pulmonary and immunological system damage are responsible for clinical features of SARS and may lead to death of patients.</p>