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H C Yan

Publications and source records attributed to H C Yan.

At least 37 records · Page 2Linked to original sources

Involvement of platelet-endothelial cell adhesion molecule-1 in neutrophil recruitment in vivo.

During inflammation, neutrophils migrate from the vascular lumen into extravascular sites. In vitro assays have suggested that platelet-endothelial cell adhesion molecule-1 [PECAM-1 (CD31)], a member of the immunoglobulin superfamily, is required for the transmigration of neutrophils across endothelial monolayers. Antibody to human PECAM-1, which cross-reacts with rat PECAM-1, was found to block not only in vivo accumulation of rat neutrophils into the peritoneal cavity and the alveolar compartment of the lung but also neutrophil accumulation in human skin grafts transplanted onto immunodeficient mice. On the basis of these findings in three different models of inflammation, it appears that PECAM-1 is required for neutrophil transmigration in vivo and may thus be a potential therapeutic target.

Animals↗

Platelet/endothelial cell adhesion molecule-1 (CD31)-mediated cellular aggregation involves cell surface glycosaminoglycans.

Platelet/endothelial cell adhesion molecule-1 (PECAM-1, CD31) is a 130-kDa integral membrane glycoprotein expressed on endothelial cells, platelets, and leukocytes. Experiments analyzing the aggregation of mouse L-cells stably transfected with full-length PECAM-1 cDNA have demonstrated that PECAM-1 is capable of mediating calcium-dependent heterophilic aggregation. In this report the ligand interactions involved in the aggregation process were studied. This aggregation was inhibited by heparin and chondroitin sulfate, but not by other glycosaminoglycans. Enzymatic removal of cell surface glycosaminoglycans confirmed a PECAM-1-glycosaminoglycan interaction and suggested that this interaction involved glycosaminoglycans on adjacent cells. PECAM-1 contains a glycosaminoglycan consensus binding sequence in the second immunoglobulin-like domain of the molecule's extracellular domain. A comparable region in the related adhesion protein N-CAM has been shown to mediate the adhesive properties of N-CAM. Cells expressing mutant PECAM-1 protein missing the second domain failed to aggregate. Synthetic peptides mimicking the consensus glycosaminoglycan binding sequence, L-K-R-E-K-N, inhibited aggregation. These results demonstrate that PECAM-1-mediated aggregation is dependent on the binding of PECAM-1 to specific glycosaminoglycans on adjacent cells via a glycosaminoglycan consensus binding sequence in the second immunoglobulin-like homology domain.

3T3 Cells↗

Prevalence and type of anaemia in female cotton mill workers in Beijing, China.

The present study investigates the prevalence and type of anaemia in Chinese female cotton mill workers. The prevalence of anaemia is reported in 447 non-pregnant female workers aged between 19 and 45 years. The mean value for haemoglobin (Hb) was 123 (SD 15) g/l and 150 of the total 447 subjects had Hb values below 120 g/l; thus 34% of the population was anaemic according to World Health Organization (WHO, 1975) criteria. The mean value for free erythrocyte protoporphyrin (FEP) was 419 (SD 215) micrograms/l; 55% of the total population had FEP values higher than 350 micrograms/l and 72% among the anaemic subjects. Serum ferritin (SF) was tested in all the women with a Hb value less than 120 g/l and 71% of them had SF values below 12.0 micrograms/l. Eighty women diagnosed as either Fe deficient or with Fe-deficient anaemia were selected for a diagnostic supplementation trial. They were randomly assigned to FeSO4 (60 or 120 mg Fe/d) or placebo treatment for 12 weeks. Fe supplementation increased mean Hb values from 114 to 127 g/l (P < 0.001) and SF levels from 9.7 to 30.0 micrograms/l (P < 0.001), and decreased mean FEP values from 570 to 277 micrograms/l (P < 0.001). The response rate of Hb in the whole Fe-treated group or Fe-treated subjects with an Hb level less than 120 g/l was 90% or 92% respectively. These findings indicate that the type of anaemia in this population was mainly Fe deficiency. It was also found that in this population the severity of anaemia, not the prevalence, was significantly related to the use of intra-uterine devices (IUD).

Adult↗

Human/severe combined immunodeficient mouse chimeras. An experimental in vivo model system to study the regulation of human endothelial cell-leukocyte adhesion molecules.

The ability of circulating white blood cells to enter inflamed tissues is mediated by specific cell adhesion molecules thought to be expressed in a programmed and sequential manner to form an "adhesion cascade." Because of the complexity of this process, it is becoming increasingly important to develop in vivo models. Two major problems have limited the utility of current animal models. The first is the inability of many of the antibodies developed against cell adhesion molecules in human cell culture models to cross-react in animals. The second is the uncertainty in extrapolating animal (particularly rodent) findings to humans. To circumvent these problems, full thickness human skin grafts were transplanted onto immunodeficient (severe combined immunodeficient) mice. After 4-6 wk, the transplanted skin grafts closely resembled normal skin histologically and maintained their human vasculature as determined by immunohistochemical staining with human-specific endothelial cell markers. Intradermal injection of tumor necrosis factor-alpha resulted in the reversible upregulation of the leukocyte-endothelial adhesion molecules E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1, and in an active inflammatory reaction with migration of murine leukocytes into cytokine-injected areas. These results indicate that the severe combined immunodeficient mouse/human skin transplant model provides a useful in vivo system in which to study human endothelium during the process of inflammation.

Adult↗

Regulation of extracellular matrix proteins and integrin cell substratum adhesion receptors on epithelium during cutaneous human wound healing in vivo.

Although changes in extracellular matrix proteins during wound healing have been well documented, little is known about the regulation of corresponding extracellular matrix adhesion receptors (integrins). To study this process in a human in vivo model, full thickness human skin grafts were transplanted onto severe combined immunodeficient mice and deep excisional wounds involving both the epidermal and dermal layers were then made. The changes in the expression of cell matrix proteins and epithelial integrins over time were analyzed with specific antibodies using immunohistochemistry. Wounding was associated with alterations in extracellular matrix proteins, namely, loss of laminin and type IV collagen in the region of the wound and expression of tenascin and fibronectin. Changes were also noted in the integrins on the migrating keratinocytes. There was marked up-regulation of the alpha v subunit and de novo expression of the fibronectin receptor (alpha 5 beta 1) during the stage of active migration (days 1 to 3 after wounding). In the later stages of wound healing, after epithelial integrity had been established, redistribution of the alpha 2, alpha 3, alpha 6, and beta 4 collagen/laminin-binding integrin subunits to suprabasal epidermal layers was noted. Thus, during cutaneous wound healing, keratinocytes up-regulate fibronectin/fibrinogen-binding integrins and redistribute collagen/laminin-binding integrins. This study demonstrates that the human skin/severe combined immunodeficient chimera provides a useful model to study events during human wound repair.

Animals↗

Platelet endothelial cell adhesion molecule, PECAM-1, modulates cell migration.

Cell migration is an important process in such phenomena as growth, development, and wound healing. The control of cell migration is orchestrated in part by cell surface adhesion molecules. These molecules fall into two major categories: those that bind to extracellular matrix and those that bind to adjacent cells. Here, we report on the role of a cell-cell adhesion molecule, platelet-endothelial cell adhesion molecule-1, (PECAM-1), a member of the lg superfamily, in the modulation of cell migration and cell-cell adhesion. PECAM-1 is a 120-130 kDa integral membrane protein that resides on endothelial cells and localizes at sites of cell-cell contact. Since endothelial cells express PECAM-1 constitutively, we studied the effects of PECAM-1 on cell-cell adhesion and migration in a null-cell population. Specifically, we transfected NIH/3T3 cells with the full length PECAM-1 molecule (two independent clones). Transfected cells containing only the neomycin resistance gene, cells expressing a construct coding for the extracellular domain of the molecule, and cells expressing the neu oncogene were used as controls. The PECAM-1 transfectants appeared smaller and more polygonal and tended to grow in clusters. Indirect immunofluorescence of PECAM-1 transfectants showed peripheral staining at sites of cell-cell contact, while the extracellular domain transfectants and the control cells did not. In two quantitative migration assays, the full-length PECAM-1 transfectants migrated more slowly than control cells. Thus, PECAM-1 transfected into a null cell appears to localize to sites of cell-cell contact, promote cell-cell adhesion, and diminish the rate of migration. These findings suggest a role for this cell-cell adhesion molecule in the process of endothelial cell migration.

Animals↗

Pleomorphic adenoma of the trachea: report of two cases.

Two unusual cases of pleomorphic adenoma (benign mixed tumor) of the trachea were found in a 56-year-old woman and a 20-year-old man. Both patients had been initially treated for presumed bronchial asthma for 5 years and 4 years, respectively. Pulmonary function tests in each showed typical extrathoracic obstruction. The diagnosis of tracheal lesions in both cases was based principally on the following: 1) dyspnea without complete remission over an extended period of time following initial examination; 2) marked retraction of the supraclavicular and suprasternal notches during inspiration with stridor on physical examination; and 3) a high degree of suspicion. Large tumors were found within the air column of the trachea by soft tissue density X-ray films and electroradiographs of the neck, CT scans of the neck and mediastinum in each patient revealed that the tumor originated from the membranous layers of the trachea in the woman and the posterolateral wall of the trachea in the man. Fiberoptic bronchoscopy confirmed the clinical diagnosis. Both cases were successfully treated by segmental resection of the trachea with end-to-end anastomosis.

Adult↗

Intercostal arteriovenous fistula due to pleural biopsy.

A 32 year old woman had a pleural biopsy for a left pleural effusion, which showed caseating granuloma typical of tuberculosis. When the fourth biopsy specimen was removed considerable bleeding occurred from the puncture site. Four days later a bruit was audible over the punctured area, radiating to the back. Eight days after the procedure the patient had a massive bleed into the left pleural space. Selective aortic angiography showed an arteriovenous fistula between the 9th intercostal artery and vein and a pseudoaneurysm in the intercostal punctured area. Thoracotomy showed bleeding from the site of the pleural biopsy. The intercostal vessels were ligated and pleural decortication was performed, and the patient recovered uneventfully.

Adult↗

[Survival of lung cancer patients of different histologic types].

The survival curves of primary lung cancers are significantly different by histologic type. The purpose of this study was to analyze the survival curves and prognostic factors of primary lung cancers according to the histologic type at the Tri-Service General Hospital for the years from 1983 to 1988. All records of new patients admitted to TSGH with primary lung malignancies were retrieved from the tumor registry. The survival curve was estimated by Kaplan-Meier Limit Estimate. The prognostic significance of 6 clinical and pathologic factors (sex, age, stage of disease, primary location, histologic differentiation and treatment) were analyzed by single variable analysis and by Cox multivariate regression. There were 448 male and 199 female patients with a mean age of 61.5 years. Adenocarcinoma was the most common histologic type found in both sexes, 37.9% in the men and 72.8% in the women. Patients in the advanced stage with distant metastasis comprised 52.8%. The most frequent location was the upper lobe (37.8%). Methods of treatment were: a) no therapy (39.7%), b) radiotherapy (34.7%), c) surgery with radiotherapy (8.7%), and d) other treatment (16.9%). The median survival of the 647 patients was 6.8 months after diagnosis. The overall one-year, three-year, and five-year survival rates were 26%, 10% and 5%, respectively. Survival curves according to the histopathologic type demonstrated that patients with small cell carcinoma had the lowest cumulative survival and patients with adenocarcinoma had a lower cumulative survival than those with squamous cell carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Protective effect of pentoxifylline on phorbol myristate acetate-induced acute lung injury in rats.

The pathogenesis of adult respiratory distress syndrome (ARDS) is not clear, and its therapy is still a problem. Pentoxifylline, a methylxanthine derivative, can inhibit phosphodiesterase activity and thus increase the intracellular cAMP. There are also some hypotheses that pentoxifylline can attenuate pulmonary edema. In order to evaluate the protective effect of pentoxifylline in acute lung injury, we set up an isolated lung perfusion model in rats and induced experimental acute lung injury similar to ARDS by intravenously infused phorbol myristate acetate (PMA) 7.5 micrograms/300 g body weight. Four groups of experimental rats were studied: group 1, normal control group, neither PMA nor pentoxifylline was used in 6 rats; group 2 (acute lung injury group), only PMA was infused in 8 rats; group 3 (protective group), pentoxifylline 100 mg/300 g body weight was given intravenously before PMA infusion in 6 rats; group 4, only pentoxifylline was given in 6 rats. Pulmonary arterial pressure (PAP) as well as lung weight changes were recorded before and 5, 10, 15, 20 and 25 minutes after drug injection. Bronchial lavage fluids were then measured for albumin concentration. We found that PAP was strikingly increased in group 2 (54.0 +/- 8.8 mmHg), but the increase was significantly reduced in group 3 (29.8 +/- 5.8 mmHg, p less than 0.001). Similarly, the lung weight gain was markedly increased in group 2 (4.69 +/- 1.28 g), but was significantly attenuated in group 3 (1.25 +/- 1.60 g, p less than 0.001). There was no apparent change in PAP and lung weight gain throughout the entire procedure in groups 1 and 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[The adverse effect of catheter ablation on the AV junction in experimental dogs].

The purpose of this study was to assess the adverse effects of catheter electrical ablation. Eighteen anesthetized mongrel dogs received 10-400 J of DC countershocks one to five times in each of them near the region of AVJ. Complete AV block was established, no pacemaker was implanted. Electrical unstability was seen nearly in all. Among the date of observation (1-547 days), 16 dogs died spontaneously and the other two were killed. Gross and microscopic examination revealed that cardiac damage produced by DC shock was diffusely spread over the endocardium/valve, myocardium and epicardial layers. The prominent lesions of the acute stage were myocytolysis and/or necrosis of myocardium/endocardium. In chronic stage, diffuse fibrosis and other types of tissue degeneration were revealed, some dogs had both acute and chronic lesions at the same time. Two dogs with perforated aortic valve revealed an elevation of PAEDP, one of them developed marked right heart failure and ascites. We proposed that the acute submicroscopic injury induced by DC shock may progress to a diffuse and irreversible pathologic changes. Therefore, the chronic adverse effects of catheter ablation should be evaluated carefully.

Animals↗

The provocative test and their diagnostic value in sinus node failure.

Exercise and pharmacologic tests were used for evaluation of the sinus node and S-A function. In all 10 normal persons, the heart rate raised above 90/min without development of cardiac arrhythmia. Among 13 patients with sinus node failure, only 1 had the heart rate raised to 90/min after exercise test and 7 above 90/min after medicinal induction. Cardiac arrhythmia, which is characteristic in sinus node failure, may appear during the test, provide an important clue in making a diagnosis. Criteria for the provocative tests are described. During the test, it is necessary to be on guard against any untoward effects. The patients in this study have been all uneventful throughout.

Adult↗

Wenckebach phenomenon (W.P.) at sites other than A-V junctional area.

W.P. occurring at sites other than A-V junctional area are reported. Some of the cases are rather rare. His bundle electrography may be the best method in discovering the site of block, but the using of conventional ECG is also able to detect a correct diagnosis. Clinical significance are discussed, some are innocent, some are related to serious heart disease. Thorough examination is necessary before arriving at any conclusion.

Arrhythmias, Cardiac↗

Case reports of phase 4 paroxysmal atrioventricular block.

Four cases of PAVB were reported, 3 of which manifested third-degree AV block, while one exhibited first-degree AV block, while one exhibited first-degree AV block. The location and mechanism of establishment and disappearance of PAVB was discussed. It was speculated that, in some cases, concealed conduction of P waves could promote depolarization of the injured area which displayed Phase 4 block and thus temporarily restore 1.1 AV conduction.

Adult↗