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Biomedical subjects

Hong Shen

Publications and source records attributed to Hong Shen.

At least 91 records · Page 5Linked to original sources

The clinical pathology of severe acute respiratory syndrome (SARS): a report from China.

In order to investigate the clinical pathology of severe acute respiratory syndrome (SARS), the autopsies of three patients who died from SARS in Nan Fang Hospital Guangdong, China were studied retrospectively. Routine haematoxylin and eosin (H&E) staining was used to study all of the tissues from the three cases. The lung tissue specimens were studied further with Macchiavello staining, viral inclusion body staining, reticulin staining, PAS staining, immunohistochemistry, ultrathin sectioning and staining, light microscopy, and transmission electron microscopy. The first symptom was hyperpyrexia in all three cases, followed by progressive dyspnoea and lung field shadowing. The pulmonary lesions included bilateral extensive consolidation, localized haemorrhage and necrosis, desquamative pulmonary alveolitis and bronchitis, proliferation and desquamation of alveolar epithelial cells, exudation of protein and monocytes, lymphocytes and plasma cells in alveoli, hyaline membrane formation, and viral inclusion bodies in alveolar epithelial cells. There was also massive necrosis of splenic lymphoid tissue and localized necrosis in lymph nodes. Systemic vasculitis included oedema, localized fibrinoid necrosis, and infiltration of monocytes, lymphocytes, and plasma cells into vessel walls in the heart, lung, liver, kidney, adrenal gland, and the stroma of striated muscles. Thrombosis was present in small veins. Systemic toxic changes included degeneration and necrosis of the parenchyma cells in the lung, liver, kidney, heart, and adrenal gland. Electron microscopy demonstrated clusters of viral particles, consistent with coronavirus, in lung tissue. SARS is a systemic disease that injures many organs. The lungs, immune organs, and systemic small vessels are the main targets of virus attack, so that extensive consolidation of the lung, diffuse alveolar damage with hyaline membrane formation, respiratory distress, and decreased immune function are the main causes of death.

Adrenal Glands↗

Preliminary investigation into the expression of proton-coupled oligopeptide transporters in neural retina and retinal pigment epithelium (RPE): lack of functional activity in RPE plasma membranes.

PURPOSE: To determine the expression and functional activity of proton-coupled oligopeptide transporters (POT) in retinal pigment epithelial (RPE) cells. METHODS: RT-PCR was used to probe the presence of POT mRNA in freshly isolated bovine RPE (BRPE) and human RPE (HRPE) cells, a human RPE cell line (ARPE-19), and human and bovine neural retina. [14C]GlySar uptake was used to characterize POT activity in cultured ARPE-19 cells and freshly isolated BRPE cell sheet suspensions. RESULTS: PHT1 mRNA was expressed in BRPE, HRPE, ARPE-19, and bovine and human neural retina. In contrast, PEPT2 and PHT2 were expressed only in bovine and human retina, and PEPT1 could not be detected. GlySar exhibited a linear uptake over 6 h at pH values of 6.0 and 7.4, with greater uptake at pH 7.4 (p < 0.01). GlySar uptake did not exhibit saturability (5-2000 microM) and was unchanged when studied in the presence of 1 mM L-histidine. In contrast, GlySar uptake was significantly decreased when studied at 4 degrees C or in the presence of endocytic inhibitors at 37 degrees C (p < 0.01). Studies in BRPE cell sheet suspensions validated the results obtained in ARPE-19 cells and strongly suggested the absence of POT on the apical and basolateral membranes of RPE. CONCLUSIONS: PHT1 mRNA is present in native bovine and human RPE and a human RPE cell line. However, the data argue against PHT1 being expressed on plasma membranes of RPE. Overall, GlySar appears to be taken up by RPE cells via a low-affinity, endocytic process.

Animals↗

Hysteroscopy to detect Stage IA well-differentiated endometrioid adenocarcinoma of the endometrium.

BACKGROUND: Well-differentiated Stage IA endometrial carcinoma may be managed conservatively with progestin treatment. However, even advanced imaging methods cannot overcome limitations in the correct determination of the absence of early microscopic myometrial invasion by endometrial carcinoma. Hysteroscopy has not yet been investigated as a tool for this purpose. METHODS: Of 97 patients with well-differentiated endometrioid adenocarcinoma, 87 whose tumors were clinically confined to the uterine corpus were enrolled for inclusion in this study. The preoperative hysteroscopic appearance was correlated with the histological findings of the hysterectomy specimen. RESULTS: Post-surgical FIGO stage was Stage IA in 36 cases, IB in 29, IC in 16, IIA in one, and Stage IIIA/C in five cases. Before surgery, the growth pattern of the disease was hysteroscopically diagnosed as pedunculated in 69.0% and sessile nodular in 31.0%. Surface ulceration was observed in 23.3% of the pedunculated tumors and in 74.1% of the sessile tumors ( p < 0.0001), and in 39.1% of all tumors. The incidence of absent myometrial invasion was significantly higher in the pedunculated tumors (56.3%) than in the sessile tumors (3.7%) ( p < 0.0001) and was higher in the nonulcerated tumors (64.2%) than in the ulcerated tumors (5.9%) ( p < 0.0001). When the statistical parameters were calculated in combination with the tumor growth pattern and the absence or presence of ulceration, the nonulcerated pedunculated growth pattern had a sensitivity of 92% and a positive predictive value of 72% for correct selection of Stage IA disease with no myometrial invasion. CONCLUSION: Well-differentiated endometrioid adenocarcinoma was categorized by hysteroscopy into two growth patterns of pedunculated or sessile and with or without surface ulceration. This provided useful pretreatment diagnosis of Stage IA disease confined to the endometrium.

Carcinoma, Endometrioid↗

Effect of transforming growth factor beta and bone morphogenetic proteins on rat hepatic stellate cell proliferation and trans-differentiation.

AIM: To explore different roles of TGF-beta (transforming growth factor beta) and bone morphogenetic proteins (BMPs) in hepatic stellate cell proliferation and trans-differentiation. METHODS: Hepatic stellate cells were isolated from male Sprague-Dawley rats. Sub-cultured hepatic stellate cells were employed for cell proliferation assay with WST-1 reagent and Western blot analysis with antibody against smooth muscle alpha actin (SMA). RESULTS: The results indicated that TGF-beta1 significantly inhibited cell proliferation at concentration as low as 0.1 ng/ml, but both BMP-2 and BMP-4 did not affect cell proliferation at concentration as high as 10 ng/ml. The effect on hepatic stellate cell trans-differentiation was similar between TGF-beta1 and BMPs. However, BMPs was more potent at trans-differentiation of hepatic stellate cells than TGF-beta1. In addition, we observed that TGF-beta1 transient reduced the abundance of SMA in hepatic stellate cells. CONCLUSION: TGF-beta may be more important in regulation of hepatic stellate cell proliferation while BMPs may be the major cytokines regulating hepatic stellate cell trans-differentiation.

Animals↗

Microsatellite instability and loss of heterozygosity of fragile histidine triad gene in lung hyperplastic lesions.

OBJECTIVE: To ascertain weather there is any difference in the hyperplastic lesions in the bronchial endothelia between patients with lung cancer and those with pneumonia, so as to find reliable molecular marker for early diagnosis of "genuine" preneoplastic lesions. METHODS: With PCR-denaturing polyacrylamide gel electrophoresis and silver-staining, 82 specimens of bronchial hyperplastic lesions obtained from patients with squamous cell carcinoma (SCC) and 57 matched epithelial lesion specimens obtained from patients with pneumonia were examined for loss of heterozygosity (LOH) and microsatellite instability (MI) of fragile histidine triad (FHIT) gene. RESULTS: Allelic losses of FHIT were common in hyperplastic lesions from patients with SCC, and the frequencies of LOH and MI of the 4 microsatellite sites, D3S1234, D3S1300, D3S1481, and D3S1313 were significant higher in hyperplastic lesions from SCC patients than in those from pneumonia patients (P<0.01). The frequencies of LOH and MI of FHIT gene in cancerous and noncancerous squamous metaplasia were 54%(7/13) and 12%(2/16) respectively, and were 70%(7/10) and 18%(2/8) respectively in cancerous and noncancerous mild to moderate dysplastic lesions. No significant difference was observed between the frequencies of D3S1234, D3S1300, D3S1481, and D3S1313 in cancerous hyperplastic lesions, which were 41%(34/82), 37%(30/82), 38%(31/82), 34(28/82), respectively (P>0.05). CONCLUSION: Hyperplastic lesions showed higher frequency of LOH at the 4 microsatellite sites than MI (P<0.01). The fact that LOH of FHIT is prevalent in hyperplastic lesions in SCC patients but rare in pneumonic patients indicates the significant difference between cancerous and noncancerous hyperplastic lesions. LOH of FHIT may be an early event in the development of squamous cell carcinoma in the lungs and is crucial in the early stage of carcinogenesis, validating the use of FHIT as a molecular marker to identify "genuine" preneoplastic lesions.

Acid Anhydride Hydrolases↗

[Detection of nuclear factor kappa B by immunochemical staining and image analysis].

OBJECTIVE: To find a relatively simple and safe method for quantitative assay of nuclear factor (NF)-kappa B activity. METHODS: Immunochemical staining of NF-kappa B/p65 subunit with its antibody was performed in human umbilical vein endothelial cells stimulated with advanced glycation end products-modified human serum albumin (AGE-HSA). The ratio of p65 subunit staining in the nuclei and cytoplasm was determined by means of imaging analysis, and the results were compared with those of electrophoretic mobility shift assay (EMSA). RESULTS: NF-kappa B could be activated by AGE-HSA in a time- and dose-dependent manner, and the results obtained from immunochemical staining were consistent with those from EMSA. CONCLUSION: p65 immunochemical staining and subsequent image analysis is feasible in the quantitative detection of NF-kappa B activation.

Electrophoretic Mobility Shift Assay↗

[Quantitative study of bacteriological infections in dogs undergoing gunshot wound in seawater].

OBJECTIVE: To investigate the changes in bacterial proliferation and the time of infection occurrence in dogs wounded by gunshot in seawater. METHOD: Fourteen canine models of gunshot wound in seawater were established, with another 2 dogs receiving the wound without seawater immersion serving as control. Gross observation and quantitative bacterial analysis were performed at 0, 6, 12 and 24 h after the injury respectively, and two dynamic models for the bacterial growth were set up on the basis of statistical analysis of the results. RESULTS: Bacterial quantity in both of the two groups tended to increase with time, but at each time point after the injury, the seawater group had higher bacterial count than the other group. Within 6 h after the injury, the bacterial count reached the critical point for clinical infection in seawater group. The two bacterial growth dynamics models were (1) Y=9.12 x 10(3+0.247X) and (2) Y=1.35 x 10(3+0.227X) for the seawater group and land group respectively, with the variant X representing time after gunshot injury, and Y the bacterial count per gram tissue. Using the dynamic models, we found that to reach the same bacteria count, the land group needed 4 h more than the seawater group(4.2 h). CONCLUSIONS: Bacterial proliferation is accelerated in the wounds in seawater to result in earlier infection onset with more severity, suggesting that early debridement within 4 h after the injury, complete washing of the wound and early administration of the antibiotics are necessary for the wound management.

Animals↗

[Effect of oxidated low-density lipoprotein on early apoptosis of vascular smooth muscle cell].

OBJECTIVE: To investigate the apoptosis in vascular smooth muscle cell (VSMC) induced by oxidated low-density lipoprotein cholesterol (ox-LDL), and to discuss the relative mechanism of the apoptosis of VSMC. METHODS: The growth index of VSMC of Wistar rat was determined. By using trypan blue to count sustaining cells, the proliferative effect of ox-LDL on culturing VSMC was observed. With flow cytometer, the apoptosis of VSMC induced by ox-LDL and the inhibitory effect of cyclooxygenase-2 (COX-2) inhibitor NS-398 on apoptosis were determined. RESULTS: After VSMC grew normally in culture, ox-LDL in concentrations of 35 mg/L and 50 mg/L could advance the growth period of VSMC to between 12 and 24 hours, and the proliferation of VSMC were obvious. The proliferation of VSMC induced by ox-LDL were inhibited by NS-398. The rate of apoptosis of VSMC in ox-LDL and NS-398 groups were higher than that of normal control. CONCLUSION: ox-LDL could induce an obvious proliferation of VSMC in culture. Although NS-398 can decrease the proliferation of VSMC, it could enhance ox-LDL to induce apoptosis.

Animals↗

[Study on etiology and pathology of severe acute respiratory syndrome].

OBJECTIVE: To investigate the clinicopathologic characteristics of severe acute respiratory syndrome (SARS). METHODS: Three autopsy cases were studied retrospectively. Routine HE stain was used to study all the cases. Part of the lung tissue specimens were studied further with Macchiavello's stain, viral inclusion body stain, reticulin and PAS stains, immunohistochemistry, thin sections with staining, light microscopy and transmission electronic microscope investigation. RESULTS: The earliest symptom of all 3 cases was hyperpyrexia and followed by progressive dyspnea and appearance of lung field shadows in X rays findings. Pulmonary lesions included: bilateral and extensive consolidation, localized hemorrhage and necrosis, desquamative alveolitis and bronchitis, alveolar proliferation and desquamation, accumulation of protein exudates, mononuclear cells, lymphocytes, and plasma cells as well as hyaline membrane formation in alveoli and viral inclusion bodies were seen in the alveolus epithelial cells. The exudated organization tended to become glomeruloid organizing pneumonitis in a few avaoli. Lesions of the immune organs included: large patchy necrosis in the spleens and localized necrosis in the lymph nodes were seen. Bone marrow became restrained. There were lesions of systemic small vasculitis including edema of the perivascular tissue and vascular wall of the small veins with localized fibrinoid necrosis distributing in the heart, lungs, kidneys, adrenal glands and the striated muscles accompanying with mononuclear cells and lymphocytes infiltration. Thrombosis was seen in part of the small veins. In addition, there were also the systemic poisonous changes including: degeneration and necrosis of the parenchyma cells in lungs, liver, kidneys, heart and adrenals. Electronic microscopy demonstrated clusters of virus particles seen in the lung tissue. CONCLUSION: SARS is a systemic disease. Lungs, immune system and systemic small vessels are the main target organs attacked by the virus. Extensive consolidation of lungs, formation of hyaline membrane to a large extent, respiratory distress and decrease of immune function are the main causes of death.

Adult↗

[Role of kaliuretic peptide and molar ratio of kaliuretic peptide/atrial natriuretic peptide in atrial fibrillation].

OBJECTIVE: To investigate the role of kaliuretic peptide (KP) and molar ratio of KP/ atrial natriuretic peptide (ANP) in atrial fibrillation. METHODS: The levels of plasma KP and ANP in 23 patients with paroxysmal atrial fibrillation (group I), 24 patients with persistent atrial fibrillation (>1 year, group II) and 20 healthy humans (group III) were determined with radioimmunoassay. RESULTS: Compared with group III, the levels of plasma KP and ANP of the group I and group II were both higher (both P<0.01). Compared with group III, the level of KP/ANP of the group I was lower (P<0.01), while that of group II was no substantial change (P>0.05). CONCLUSION: The change of levels in ANP, KP and ANP/KP may play important role in atrial fibrillation.

Atrial Fibrillation↗