Seborrheic verruca and intraepidermal basal cell epithelioma of Jadassohn.
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Dermatitis, Seborrheic↗
Biomedical subjects
F Hu
Publications and source records attributed to F Hu.
The developmental cycle of B16 melanoma cell in culture.
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Animals↗
Increased reactivity to endothelin of pulmonary arteries in long-term post-obstructive pulmonary vasculopathy in rats.
Post-obstructive pulmonary vasculopathy (POPV) describes the constellation of findings following chronic ligation of one pulmonary artery, including bronchial angiogenesis, pulmonary vasculopathy and increased vasoreactivity to pharmacologic agents. Previously, we found in rats with POPV of 28 days duration that maximal responses to endothelin-1 (ET-1) and ET-3 of pulmonary arteries but not veins were increased, and that relaxation of arteries to ET-1 was reduced, attributable to an elevated proportion of ETA over ETB receptors. To determine the reactivity of pulmonary vessels and airways to ET in protracted POPV, we ligated the left main pulmonary artery of nine rats. Eleven months later, using a lung explant technique, we compared contractile responses of pulmonary vessels and airways to ET-1 and ET-3 in POPV lungs with controls. Morphometric measurements were made on the vessels, and immunoreactivity to ET-1 and endothelin converting enzyme (ECE-1) studied. We found contractile responses to ET-1 and ET-3 significantly increased in arteries, but not veins or airways. Morphometry showed arteries and veins had reduced diameters with muscle thickening only in veins. Expression of ET-1 and ET-3 in vascular endothelial cells and airway epithelial cells were not altered significantly. Our data suggest that protracted POPV selectively enhanced the contractility of pulmonary arteries to ET, and is not attributable to medial muscle thickening.
Animals↗
Somatic cell hybrids derived from terminally differentiated rhesus cells and established mouse cell lines.
The mechanisms of normal cell differentiation in vivo may be related to some features of cellular aging in vitro in that both are considered to be under genetic control. Diploid rhesus choroidal melanocytes and purified peripheral lymphocytes were fused by means of inactivated Sendai virus with three long-term murine cell lines which lacked either hypoxanthine-guanine phosphoribosyl transferase or thymidine kinase. Cell hybrids were selected by their growth in medium containing hypoxanthine, aminopterin, thymidine, and glycine. G-banded chromosomes were analyzed and elements from both the rhesus and the established mouse cell lines were identified in all metaphases. Hybrids derived from choroid X mouse cells contained more than one chromosome set from the mouse, but those between lymphocytes and established cell lines had only one. However, in every combination continuously replicating hybrids were produced; most of them have undergone more than 40 subculture passages. Our results demonstrate not only that DNA synthesis can be re-initiated in postreplicative cells, but also that DNA continues to replicate in a manner consistent with the life span of the long-term cell line parent.
Adenocarcinoma↗
Myoendothelial junctional complexes in postobstructive pulmonary vasculopathy: a quantitative electron microscopic study.
Postobstructive pulmonary vasculopathy (POPV), produced by chronic unilateral ligation of one pulmonary artery, is characterized by (1) marked proliferation of bronchial collateral vessels, (2) increased pulmonary vascular resistance, and (3) hyperreactivity of arteries to serotonin and of veins to histamine. Electron microscopic examination of the vessels in POPV suggested an increase in myoendothelial junctional complexes (MEJC). To quantitate this change, the number of MEJC in the vessel walls of the left lung was compared with that of the right lung in 16 dogs after ligation of the left main pulmonary artery for 8.4 +/- 1.6 (SE) months. The lungs were fixed by airway instillation of 3% glutaraldehyde. Electron micrographs were taken of pulmonary arteries, capillaries, and veins and of bronchial vessels, and their external diameter and length of endothelial basal lamina were measured. The MEJC were counted and expressed as number per length of basal lamina and typed: Type I consisted of endothelial processes, type II of smooth muscle or pericyte processes, and type III of processes from each cell type. The results demonstrated that the vasculature from the control lung had the smallest number of MEJC and the majority were type I. With ligation, there was a significant increase (p < .01) in the number of MEJC for each type of vessel examined, but no significant change in the distribution of the type. In addition, no correlation was found between the number of MEJC and vascular diameter. It can be concluded that MEJC are increased in each region of the lung's vasculature in POPV and that they may play a role in the proliferative response of the bronchial vasculature, the remodeling of the pulmonary vasculature, and the pulmonary vascular hyperreactivity of this model.
Animals↗
Detection of p53 protein accumulation in sputum and lung adenocarcinoma associated with indoor exposure to unvented coal smoke in China.
Lung cancer in Xuan Wei (XW), China has been linked to exposure to unvented coal smoke and adenocarcinoma, especially bronchioloalveolar carcinoma, is most common. p53 mutations occur commonly in lung cancers and usually generate detectable levels of p53 protein accumulation. Sputum is noninvasive to collect and ideal for screening p53 abnormalities. p53 protein accumulation was detected by immunohistochemistry in lung tumors and sputa from XW lung cancer patients to determine (1) the role of p53 in lung pathogenesis, and (2) feasibility of detecting p53 protein accumulation in sputum, p53 protein accumulation was detected in 73% (22/30) of lung adenocarcinomas from XW females exposed to coal emissions and significantly higher than the control cases (33%, p < 0.05). In sputum, we detected p53 overexpression in tumor cells in 54% (13/24) of XW cases and also in dysplastic cells (50% or 4/8). These findings suggest that p53 abnormalities is important in XW lung cancer etiology.
Adenocarcinoma↗