The histological lesions of toxic hepatitis of wistar rat induced by carbon tetrachloride (CCl_4) were observed with electron microscope. We found that in sinusoids or inflamatory infiltrated areas. there were classical matured plasma cells and 4 typesof plasmablast cells with characteris tic morphological criteria. cccrrrsss,,,According to the direct injuring effect of CCl_4 on liver, we deduced that the humoral immunological reaction was the result of toxic hepatitis and not its cause.

Hepatic fibrsosis was induced by carbon tetrachloride in mice C 57.Then the feed containing Dangshen pollen was given to the animals. It was demonstrated under the electron microscope that the Dangshen pollen lowered the activity of the fibroblasts around the central vein and the fatstoring ceils of sinusoids, and lowered the grade of collagenous fibers of Disse's spaces (P

It was observed under an electron microscope that in the hepatic piecemeal necrotic area of CAH patients,there were T lymphocytes,plasma cells,monocytes,fatstoring cells and proliferating Hering's tubules.The more severe the patient's condition was,the much more the sorts and numbers of these cells were.We consider that the above observations by electron microscopy afford valuable morphological information about the severity of CAH.

It has been repored that the Biopsy positive rate of HBsAg in the liver specimens of the patients of hepatitis B was only 70% or so.We have observed with electron miroscopy the liv- er biopsy tissues and found that its positive rate was as high as 93.8%.Under electron microscopy,we could identify the HBsAg filaments as tubular,branching-tubular and tubu- lar-vesicular.We have also found that it was not easy to find the HBsAg filaments in the pa- tients of CAH(only 9% was found)and it was easy to be found(78.9%)in the patients of CPH or CLH. It had a high significant difference in the two groups.

Specimens from 12 cases of pancreatic endocrine tumors were investigated by light and electron microscopy and immunohistochemical staining. Pancreatic stem cell-like cells with special characteristics of pancreatic stem cell were found in the proliferating small ductules and dispersed at the margins of pancreatic endocrine tumors in all the cases studied.

By electron microscopic observation,we found few pit cells in liver,spleen.lungs,and small intestine in Wistar rat.The pit cells show several morphologicalcharacteristics as follows:1.electron dense granules in cytoplasm,which aresurrounded by a limiting membrane;2.vesicles with rod shaped bodies incytoplasm;3.eccentric nucleus with marginal heterochromatin;4.well developedpseudopodia.In addition,the pit cells have also been found in breast carcinoma in3 patients.According to their distribution and morphology,we preliminarilydeduced they probably belong to natural killer cells and may act as a cytotoxicagent and an immunological defender against carcinoma.

Objective To investigate the protective effects of HTD4010 against lipopolysaccharide(LPS)-induced septic cardiomyopathy(SCM)in mice and explore the mechanisms mediating its effect.Methods Forty-five male ICR mice were randomized equally into control group,LPS(10 mg/kg)group,and LPS+HTD4010 group(in which 2.5 mg/kg HTD4010 was injected subcutaneously at 1 h and 6 h after LPS injection).Cardiac function of the mice was evaluated by ultrasound,and pathological changes in the myocardial tissues were observed with HE staining.The levels of IL-6 and TNF-α in serum and myocardial tissues were detected using ELISA,and apoptosis of the cardiomyocytes was detected with TUNEL staining.The expression levels of the key proteins associated with apoptosis,autophagy and the AMPK/mTOR pathway in the myocardial tissues were detected using Western blotting.The ultrastructural changes of cardiac myocardial mitochondria was observed with transmission electron microscopy.Results LPS exposure caused severe myocardial damage in mice,characterized by myocardial fiber rupture,structural disorder,inflammatory cell infiltration,and mitochondrial damage.The LPS-treated mice exhibited significantly decreased cardiac LVEF and FS values,elevated IL-6 and TNF-αlevels in serum and myocardial tissue,and an increased myocardial cell apoptosis rate with enhanced expressions of Bax,p-62 and p-mTOR and lowered expressions of Bcl-2,LC3 Ⅱ/I,Beclin-1 and p-AMPK(P<0.05 or 0.01).Treatment of the septic mice with HTD4010 significantly alleviated myocardial damage,increased LVEF and FS values,reduced IL-6 and TNF-α levels in serum and myocardial tissue,decreased cardiomyocyte apoptosis,lowered myocardial expressions of Bax,p-62 and p-mTOR,and increased Bcl-2,LC3 Ⅱ/I,Beclin-1 and p-AMPK expressions(P<0.05 or 0.01).Conclusion HTD4010 can attenuate myocardial injury in SCM mice possibly by promoting autophagy via modulating the AMPK/mTOR signaling pathway.

Objective To investigate the protective effects of HTD4010 against lipopolysaccharide(LPS)-induced septic cardiomyopathy(SCM)in mice and explore the mechanisms mediating its effect.Methods Forty-five male ICR mice were randomized equally into control group,LPS(10 mg/kg)group,and LPS+HTD4010 group(in which 2.5 mg/kg HTD4010 was injected subcutaneously at 1 h and 6 h after LPS injection).Cardiac function of the mice was evaluated by ultrasound,and pathological changes in the myocardial tissues were observed with HE staining.The levels of IL-6 and TNF-α in serum and myocardial tissues were detected using ELISA,and apoptosis of the cardiomyocytes was detected with TUNEL staining.The expression levels of the key proteins associated with apoptosis,autophagy and the AMPK/mTOR pathway in the myocardial tissues were detected using Western blotting.The ultrastructural changes of cardiac myocardial mitochondria was observed with transmission electron microscopy.Results LPS exposure caused severe myocardial damage in mice,characterized by myocardial fiber rupture,structural disorder,inflammatory cell infiltration,and mitochondrial damage.The LPS-treated mice exhibited significantly decreased cardiac LVEF and FS values,elevated IL-6 and TNF-αlevels in serum and myocardial tissue,and an increased myocardial cell apoptosis rate with enhanced expressions of Bax,p-62 and p-mTOR and lowered expressions of Bcl-2,LC3 Ⅱ/I,Beclin-1 and p-AMPK(P<0.05 or 0.01).Treatment of the septic mice with HTD4010 significantly alleviated myocardial damage,increased LVEF and FS values,reduced IL-6 and TNF-α levels in serum and myocardial tissue,decreased cardiomyocyte apoptosis,lowered myocardial expressions of Bax,p-62 and p-mTOR,and increased Bcl-2,LC3 Ⅱ/I,Beclin-1 and p-AMPK expressions(P<0.05 or 0.01).Conclusion HTD4010 can attenuate myocardial injury in SCM mice possibly by promoting autophagy via modulating the AMPK/mTOR signaling pathway.

【Objective】 To establish a method for detecting human immunoglobulin Fc function based on surface plasmon resonance technology. 【Methods】 Based on the characteristic that FcγRI can be binded to the Fc segment of IgG, the affinity constant of the sample was detected by surface plasmon resonance, and its Fc function was the KD ratio of the sample to the standard. The method was validated for specificity/specificity, precision and robustness. The method and the pharmacopoeia method were used to detect the Fc function of 30 human immunoglobulins, and the correlation and consistency of the detection results were analyzed. 【Results】 The method validation results showed that this method has strong specificity/specificity (t values were 0.15, 0.22, both P>0.05), good precision (CV value 5.37%~10.69%) and good robustness (CV value 10.06%). The detection results of this method and the pharmacopoeia method have high correlation (r=0.96, P<0.05) and high consistency (Bias-2.060, 95% Limits of Agreement-5.628~1.508). 【Conclusion】 A method for detecting human immunoglobulin Fc function based on surface plasmon resonance has been successfully established.