Biomedical subjects

H Xie

Publications and source records attributed to H Xie.

276 records · Page 16Linked to original sources

PubMedDate not supplied

Use of reconstructed small intestine submucosa for urinary tract replacement.

We used reconstructed SIS (ReSIS), a photocrosslinked biomaterial, to create grafts in various shapes and sizes. Sheets of ReSIS were placed in 14 swine to repair bladder defects, and ReSIS tubes were placed in six swine to replace a segment of excised ureter. Histologic analysis of the bladder repair revealed transitional urothelial cells lining the ReSIS by 1 week. After 2 weeks, fibroblasts and mononuclear cells had infiltrated the ReSIS, neovascularization had occurred, and the urothelial lining was more complex, containing multiple cell layers. After 4 weeks, a definite submucosa was present and the ReSIS was starting to degrade. An initial muscular regeneration was demonstrated at 12 weeks. No foreign body reaction, calcification, or sedimentation was noted in any animal. The ureteral implants showed identical histologic changes, without obstruction or leakage of the replaced segment. The ReSIS allowed rapid urothelial regeneration, ingrowth of new blood vessels, and the orderly deposition and organization of new collagen. Our study demonstrates that the photocrosslinking technique used to create larger sheets and tubes of this biomaterial (ReSIS) does not detract from the positive attributes of the SIS and should improve its usefulness in accomplishing larger bladder augmentations and ureter replacements.

Animals↗

PubMedDate not supplied

Use of a new elastin patch and glue for repair of a major duodenal injury.

Major duodenal injury with significant tissue loss causes high morbidity and mortality. Our new elastin based heterograft combined with small intestinal submucosa (SIS) and biodegradable glue could be used for repair of such defects. Twenty-four domestic pigs were anesthetized and underwent celiotomy. A 2 cm circular defect was created at the second portion of the duodenum with scissors, excising one-half of its circumference. Our elastin patch, combined with SIS, was applied to cover the defect using biodegradable cyanoacrylate glue and a few sutures. It was then covered with omentum. Animals were followed by weight gain, endoscopic evaluation, and upper GI barium studies. After 2-5 months, animals were sacrificed to obtain specimens. One failed in 3 days due to a technical problem, and one failed in 20 days due to an abdominal abscess. The other 22 animals (22/24, 91.7%) did well, gaining weight. Early endoscopic studies (5-14 d) showed an intact patch. Upper GI studies showed varying degrees of stenosis at the repair site at 3-4 months. Sacrifice after 2-5 months showed complete healing of the defect and a dissolved patch. Our new elastin patch material provides a reliable barrier for repair of duodenal injury, and the biodegradable glue provides quick and easy watertight tissue fusion for our patch.

Adhesives↗

PubMedDate not supplied

Barium and 4-aminopyridine inhibit flow-initiated endothelium-independent relaxation.

Although much is known about the underlying mechanism of endothelium-dependent flow-induced vasorelaxation, the cellular processes responsible for the endothelium-independent flow-induced relaxation observed in some vessels is unknown. As there is evidence for the participation of K+ channels in the endothelium-dependent response, the present study was designed to determine whether such channels are involved in the endothelium-independent response and if so, which ones. We examined the effects of various selective K+ channel blockers on endothelium-independent relaxation initiated by intraluminal flow (10-80 microl/min), and by an endothelium-independent vasodilator sodium nitroprusside (SNP, 1 nmol/l to 3 micromol/l) in segments of the rabbit facial vein under isometric conditions. Flow-initiated relaxation was abolished by 25 and 40 mmol/l K+ as well as 10 mmol/l tetraethylammonium (TEA), significantly inhibited by 100 micromol/l Ba2+, 5 mmol/l Cs+ and 7.5 mmol/l 4-aminopyridine (4-AP), but unaffected by 5 micromol/l glibenclamide and 50 nmol/l charybdotoxin. Relaxation induced by SNP was reduced by 7.5 mmol/l 4-AP, but not by any of the above drugs in their listed concentrations. The inhibitory effect of 100 micromol/l Ba2+ on the relaxation caused by low concentrations of K+ (15-20 mmol/l) supports the presence of inward rectifier K+ channels in the vascular smooth muscle cells of this tissue. We speculate that endothelium-independent flow-initiated relaxation of the rabbit facial vein may be associated with activation of inward rectifier and voltage-dependent K+ channels. The latter may also contribute to the vasorelaxation initiated by SNP.

4-Aminopyridine↗

PubMedDate not supplied

Chemosensitivity of human hepatocellular carcinoma cell line QGY-7703 is related to bcl-2 protein levels.

Bcl-2 protein is one of the major apoptosis regulators. The study examines the effect of Bcl-2 protein on the chemosensitivity of a human hepatocellular carcinoma cell line, QGY-7703. Western blot analysis showed that Bcl-2 and Bax proteins were expressed in QGY-7703 cells. Characteristic features of Taxol- and doxorubicin-induced apoptosis were evidenced by the Annexin-V binding assay, TUNEL and DAPI staining. At constant Bax protein levels, stable sense and antisense gene-transfected QGY-7703 cells showed that constitutive expression of Bcl-2 could render the cells more resistant to Taxol and doxorubicin. Contrarily, decreased Bcl-2 levels caused the cells to be more sensitive to the drugs. As Bcl-2 levels are directly proportional to the resistance of QGY-7703 cells to Taxol and doxorubicin, manipulation of Bcl-2 could be performed to enhance the sensitivity of liver cancer to chemotherapeutic agents.

Annexin A5↗

PubMedDate not supplied

Endothelium-independent relaxations to acetylcholine and A23187 in the human umbilical artery.

The effects of acetylcholine (ACh) and A23187 on ring preparations from the human umbilical artery (HUA) were investigated and compared with the rat aorta (RA). The results from the HUA demonstrate that: (1) At both high (pO2 > 600 mm Hg) and low O2 tension (pO2 < 55 mm Hg), ACh and A23187 relaxed precontracted rings in a concentration-dependent and endothelium-independent manner. Changes in pO2 did not influence the responses of the HUA to either relaxant. (2) Relaxation responses of the HUA to either ACh or A23187 were insensitive to methylene blue (50 microM), L-nitro-arginine methyl ester (100 microM), indomethacin (10 microM) and nordihydroguaiaretic acid (50 microM). Relaxations initiated by ACh were also atropine-resistant. (3) Meclofenamic acid (3 microM) suppressed the relaxations to A23187, but not ACh. (4) Regardless of pO2 superoxide dismutase (100 U/ml) potentiated the relaxant effects of ACh, whereas mannitol (60 mM) enhanced ACh-initiated relaxations at high but not low pO2. (5) Ouabain (30 nM), high potassium (HK+, 60 mM) and tetraethylammonium (20 mM) inhibited responses to ACh. (6) Na(+)-free physiological saline solution inhibited both relaxations and oscillations initiated by either ACh or A23187. (7) Both nitroglycerin and exogenous nitric oxide (NO) fully, and 8-bromoguanosine 3',5'-cyclic monophosphate partially, relaxed the HUA, and LY83583 (10 microM) reversed such relaxations. (8) In the RA, relaxation responses to ACh and A23187 were endothelium-dependent and sensitivity was reduced under high versus low pO2 conditions. We conclude that in the HUA, unlike in the RA, ACh and A23187 mediate their responses via an endothelium- and NO-independent process(es), perhaps involving the release of a muscle-derived relaxing factor. ACh-initiated relaxations are mediated by activation of Na+,K(+)-ATPase, and subsequent hyperpolarization via K+ efflux, whereas A23187-mediated relaxations result from the synthesis of an indomethacin-resistant cyclooxygenase product.

Acetylcholine↗

PubMedDate not supplied

Changes in serum ovotransferrin levels in chickens with experimentally induced inflammation and diseases.

A competitive enzyme immunoassay was developed to measure the changes in serum levels of ovotransferrin (OTF) during inflammation and infectious diseases in chickens. The assay is based on the competition of serum OTF with a fixed concentration of biotin-labeled OTF to bind to a rabbit anti-chicken transferrin antibody immobilized on microtiter wells. After several washing steps, the antibody-bound biotinylated OTF is probed with streptavidin-horseradish peroxidase conjugate (HRP) followed by a colorimetric detection of the HRP activity. The relative changes in the optical density of color are plotted against the competing concentrations of OTF with logarithmic regression to generate a standard curve that is used to determine the concentrations of OTF in unknown samples. Serum had no effect on the measurement of OTE By this method, the time course changes of serum OTF levels in 4-wk-old male broiler chickens that were subjected to inflammation by croton oil injection were measured. The results showed croton oil-induced inflammation elevated serum OTF levels at 16 hr postinjection. OTF levels reached a peak by 72 hr, remained high through 120 hr, and returned to a basal level of olive oil-injected controls by 240 hr. There were no changes in serum OTF levels at any of the above time points in olive oil-injected control chickens. For studies with poultry diseases, specific-pathogen-free (SPF) male chickens were challenged with known bacterial and viral pathogens, and serum was collected at the height of the infection, i.e., 7 days after the challenge. Compared with uninjected controls, the SPF chickens challenged with Escherichia coli, fowl poxvirus, respiratory enteric orphan virus, infectious bursal disease virus, infectious bronchitis virus, or infectious laryngotracheitis virus had higher levels of OTF in serum. Inflammation-induced changes in serum OTF levels were also evident in the changes in the density of a 65-kD band protein corresponding to OTF. These results demonstrate that serum OTF may be a nonspecific clinical marker of inflammation associated with traumatic or infectious avian diseases.

Animals↗