Search PubMed⌕ Search

Biomedical subjects

B Yang

Publications and source records attributed to B Yang.

At least 145 records · Page 8Linked to original sources
PubMed2000

[Application of extended high frequency audiometry in the early diagnosis of noise--induced hearing loss].

OBJECTIVE: To assess the application of 10-20 kHz audiometry in early diagnosis of noise-induced hearing loss and to explore the relationship between hearing loss and subjects' age, the exposure time as well as the noise level. METHODS: One thousand workers with noise exposure history were examined by pure tone audiometry(0.5-20 kHz). One hundred and twenty normal subjects served as the control group. RESULTS: The noise levels at working sites ranged from 95 to 115dB(A). Compared with the control group, noise-exposed subjects showed minor changes in the thresholds from 0.5 to 6 KHz, whereas the thresholds were elevated in the high frequency range of 10-16 kHz (P < 0.001). The incidence of ears without any response to the maximum output at the frequency range of 14 to 20 kHz was much higher (P < 0.01) than that of the control group. In the animals exposed to noise, the thresholds of 10-18 kHz increased with the aging and with increase of working time (6-10 years), but there were no significant differences among subjects exposed to the noises at different levels(P > 0.05). CONCLUSION: In noise-exposed ears, the occurrence of threshold changes in the high frequency range (10 to 20 kHz) is earlier than that in the low frequency range (0.5 to 6 kHz). Aging and working time also affect the 10-20 kHz hearing thresholds. The lack of responses to maximum output and the changes in thresholds in the high frequency range (10-20 kHz) can be used as indices for the diagnosis of early noise-induced hearing loss and for the assessment of the susceptibility of the subject to noise damage.

Adolescent↗
PubMed1999

Misfolding of mutant aquaporin-2 water channels in nephrogenic diabetes insipidus.

We reported that several aquaporin-2 (AQP2) point mutants that cause nephrogenic diabetes insipidus (NDI) are retained in the endoplasmic reticulum (ER) of transfected mammalian cells and degraded but can be rescued by chemical chaperones to function as plasma membrane water channels (Tamarappoo, B. K., and Verkman, A. S. (1998) J. Clin. Invest. 101, 2257-2267). To test whether mutant AQP2 proteins are misfolded, AQP2 folding was assessed by comparative detergent extractability and limited proteolysis, and AQP2 degradation kinetics was measured by label-pulse-chase and immunoprecipitation. In ER membranes from transfected CHO cells containing [(35)S]methionine-labeled AQP2, mutants T126M and A147T were remarkably detergent-resistant; for example wild-type AQP2 was >95% solubilized by 0.5% CHAPS whereas T126M was <10% solubilized. E258K, an NDI-causing AQP2 mutant which is retained in the Golgi, is highly detergent soluble like wild-type AQP2. The mutants and wild-type AQP2 were equally susceptible to digestion by trypsin, thermolysin, and proteinase K. Stopped-flow light scattering measurements indicated that T126M AQP2 at the ER was fully functional as a water channel. Pulse-chase studies indicated that the increased degradation rates for T126M (t((1)/(2)) 2.5 h) and A147T (2 h) compared with wild-type AQP2 (4 h) involve a brefeldin A-resistant, ER-dependent degradation mechanism. After growth of cells for 48 h in the chemical chaperone glycerol, AQP2 mutants T126M and A147T became properly targeted and relatively detergent-soluble. These results provide evidence that NDI-causing mutant AQP2 proteins are misfolded, but functional, and that chemical chaperones both correct the trafficking and folding defects. Strategies to facilitate protein folding might thus have therapeutic efficacy in NDI.

Animals↗
PubMed1999

False-positive findings on lumbar discography. Reliability of subjective concordance assessment during provocative disc injection.

STUDY DESIGN: Experimental disc injections in subjects with no history of low back symptoms. OBJECTIVE: To determine in an experimental model the reliability of patients' subjective interpretation of pain concordancy during provocative disc injection. BACKGROUND: Discography in the evaluation of low back pain relies on a patient's subjective assessment of pain magnitude and quality during disc injection. Reproduction of significant pain on disc injection, which is similar to patients' usual pain, is believed to prove that the disc injected is the source of the patient's low back pain. In the current study, this hypothesis was tested in a controlled setting on patients with known nonspinal pain in a common referral area of discogenic pain. METHODS: Patients with no history of low back pain were recruited to participate in a study of discography. Patients scheduled to undergo posterior iliac crest bone graft harvesting for nonthoracolumbar procedures were evaluated with lumbar radiography, magnetic resonance imaging, and psychometric testing. Two to 4 months after bone graft harvesting, patients underwent lumbar discography by strict blinded protocol. Patients were asked to compare the sensations elicited at discography to their usual back/buttock pain since bone graft harvesting. Pain was rated as 0-5 on a pain thermometer and concordancy was rated as none, dissimilar, similar, or exact. RESULTS: Eight subjects completed the study, and 24 discs were injected. Of the 14 disc injections causing some pain response, 5 were believed to be "different" (nonconcordant) pains (35.7%); 7 were "similar" (50.0%), and 2 were "exact" pain reproductions (14.3%). The presence of anular disruption predicted concordant pain reproduction (P < 0.05). Of 10 discs with anular tears, injection of 5 elicited pain that was similar to or an exact reproduction of pain at the iliac crest bone graft harvest sites. By the usual criteria for positive discography, 4 of the 8 patients (50%) would have been classified as positive. In these patients, the pain on a single disc injection was very painful, and the pain quality was noted to be exact or similar to the usual discomfort. All subjects had a negative control disc. CONCLUSIONS: The findings of this study demonstrate that patients with no history of low back pain who had undergone posterior iliac bone graft harvesting for nonlumbar procedures often experienced a concordant painful sensation on lumbar discography with their usual gluteal area pain. Thus, the ability of a patient to separate spinal from nonspinal sources of pain on discography is questioned, and a response of concordant pain on discography may be less meaningful than often assumed.

Adult↗
PubMed1999

Activity restrictions after posterior lumbar discectomy. A prospective study of outcomes in 152 cases with no postoperative restrictions.

STUDY DESIGN: A prospective clinical trial was conducted. OBJECTIVES: To determine the feasibility of removing activity restrictions after surgery and encouraging early return to work; to ascertain the clinical and behavioral response to such a strategy; and to identify factors predictive of early return to work, preparatory to possible randomized clinical trials. SUMMARY OF BACKGROUND INFORMATION: Current practice usually entails several weeks to several months of restricted activities after lumbar discectomy to avoid disc "reinjury." Earlier work has suggested these restrictions may not be necessary. METHODS: One hundred fifty-two consecutive working patients undergoing limited open discectomy for herniated lumbar intervertebral disc were treated postoperatively with no activity restrictions. Patients were encouraged to return to full activities as soon as possible. The patients were followed for a minimum of 2 years (average follow-up time = 4.8 years). At follow-up, an independent examiner evaluated each patient and collected further postoperative data. RESULTS: One hundred forty-nine of the 152 patients (98%) returned to work. The average work loss was 1.2 weeks and 148 of 149 patients had returned to full duty by 8 weeks. Approximately one-third of the group returned to work within 1 week of surgery (32%), many the next day. Statistical analysis demonstrated very early return to work did not correlate with either recurrent sciatica, reoperation for reherniation, or ultimate clinical outcome. Seventeen patients (11.2%) had possible reherniations (recurrent sciatica) and eight underwent reoperation (5.3%). CONCLUSION: Lifting of postoperative activity restrictions after limited discectomy allowed shortened time to return to work relative to the 4 to 16 weeks commonly recommended. Complication rates appear comparable to those reported in the literature for patients under postoperative restrictions. Postoperative restrictions may not be necessary in most patients.

Adult↗
PubMed1999

Two-dimensional freezing in the liquid-vapor interface of a dilute Pb:Ga alloy.

We report the results of x-ray reflectivity and grazing incidence x-ray diffraction studies of the liquid-vapor interface of a dilute alloy of Pb in Ga over the temperature range of 23-76 degrees C. Our data show that the liquid-vapor interface of this alloy is stratified for several atomic diameters into the bulk liquid and that a monolayer of Pb forms the outermost stratum of the interface. Over the temperature range of 23-56 degrees C, the monolayer of Pb is in an ordered hexagonal phase. At about 58 degrees C, this monolayer undergoes a first-order transition to a hexatic phase, which remains stable to 76 degrees C. An analogy between the observed transition and the first-order melting transition in a one-component classical plasma is suggested.

Journal Article↗
PubMed1999

Steric restrictions on the binding of large metal ions to serum transferrin.

Apotransferrin in 0.1 M N-(2-hydroxyethyl)piperazine-N'-2-ethanesulfonic acid at 25 degrees C and pH 7.4 was titrated with acidic solutions of Lu3+, Tb3+, and Eu3+. Metal binding at the two specific metal-binding sites of transferrin was followed from changes in the difference UV spectra at 245 nm. The binding of Tb3+ was also followed from changes in the fluorescence emission spectrum at 549 nm. Apotransferrin was titrated with solutions containing varying ratios of the metal ion and the competitive chelating agent nitrilotriacetic acid, and metal-transferrin binding constants were calculated by nonlinear least-squares fits of the absorbance as a function of titrant added. The sequential carbonate-independent equilibrium constants for the binding of two metal ions are log KM1 = 11.08 and log KM2 = 7.93 for Lu3+, log KM1 = 11.20 and log KM2 = 7.61 for Tb3+, and log KM1 = 9.66 and log KM2 = 7.27 for Eu3+. Titrations of both C-terminal and N-terminal monoferric transferrins indicate that all of these metal ions bind more strongly to the C-terminal binding site. The trend in log K values as a function of the lanthanide ionic radius has been evaluated both by plots of log K versus the metal ion charge/radius ratio and by linear free-energy relationships in which binding constants for complexes of the larger lanthanides are plotted versus the binding constants for complexes with the smallest lanthanide, Lu3+. Both methods indicate that there is a sharp drop in the binding constants for the C-terminal binding site for metals larger than Tb3+. This decrease is attributed to a steric hindrance to the binding of the larger cations. The steric effect is not as strong for metal binding at the N-terminal site. As a result, the selectivity for binding to the C-terminal site, which is quite high for the smaller lanthanides, drops sharply on going from Tb3+ to Nd3+.

Allosteric Site↗
PubMed1999

VAMP-7 mediates vesicular transport from endosomes to lysosomes.

A more complete picture of the molecules that are critical for the organization of membrane compartments is beginning to emerge through the characterization of proteins in the vesicle-associated membrane protein (also called synaptobrevin) family of membrane trafficking proteins. To better understand the mechanisms of membrane trafficking within the endocytic pathway, we generated a series of monoclonal and polyclonal antibodies against the cytoplasmic domain of vesicle-associated membrane protein 7 (VAMP-7). The antibodies recognize a 25-kD membrane-associated protein in multiple tissues and cell lines. Immunohistochemical analysis reveals colocalization with a marker of late endosomes and lysosomes, lysosome-associated membrane protein 1 (LAMP-1), but not with other membrane markers, including p115 and transferrin receptor. Treatment with nocodozole or brefeldin A does not disrupt the colocalization of VAMP-7 and LAMP-1. Immunoelectron microscopy analysis shows that VAMP-7 is most concentrated in the trans-Golgi network region of the cell as well as late endosomes and transport vesicles that do not contain the mannose-6 phosphate receptor. In streptolysin- O-permeabilized cells, antibodies against VAMP-7 inhibit the breakdown of epidermal growth factor but not the recycling of transferrin. These data are consistent with a role for VAMP-7 in the vesicular transport of proteins from the early endosome to the lysosome.

Animals↗
PubMed1999

Anti-inflammatory properties of cytochrome P450 epoxygenase-derived eicosanoids.

The epoxyeicosatrienoic acids (EETs) are products of cytochrome P450 epoxygenases that have vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor. The cytochrome P450 isoform CYP2J2 was cloned and identified as a potential source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytokine-induced endothelial cell adhesion molecule expression, and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-kappaB and IkappaB kinase. The inhibitory effects of EETs were independent of their membrane-hyperpolarizing effects, suggesting that these molecules play an important nonvasodilatory role in vascular inflammation.

8,11,14-Eicosatrienoic Acid↗
PubMed1999

Use of 5-HT3 receptor antagonists to prevent nausea and emesis caused by chemotherapy for patients with breast carcinoma in community practice settings.

BACKGROUND: Although 5-HT3 receptor antagonists are clinically more effective in controlling emesis, particularly that caused by high dose cisplatin, than previously available agents, they appear to be less effective against nausea. This report focuses on the effectiveness of these agents against nausea and emesis in patients receiving two moderately emetogenic combination chemotherapy regimens as treatment for breast carcinoma in community practice settings. METHODS: Six hundred ninety-two breast carcinoma patients (688 female, 4 male; mean age, 51 years) enrolled in a nonrandomized study completed the Morrow Assessment of Nausea and Emesis (MANE) following 4 consecutive chemotherapy treatments. The frequency, duration, and severity of postchemotherapy nausea (PN) and postchemotherapy emesis (PE) were compared by type of antiemetic (5-HT3 receptor antagonist vs. other) and chemotherapy regimen (cyclophosphamide and doxorubicin with or without 5-fluorouracil [CA/CAF] vs. cyclophosphamide, methrotrexate, and 5-fluorouracil [CMF]). RESULTS: Within each regimen, the mean duration of PN was significantly longer for patients who received a 5-HT3 receptor antagonist than for those who were not given an antiemetic of that type (CA: 40.3 hours vs. 29.6 hours, P < 0.05; CMF: 37.6 hours vs. 30.2 hours, P < 0.05). There were no significant differences in the frequency or severity of nausea or in the frequency, severity, or duration of emesis by type of antiemetic for patients receiving either regimen. CONCLUSIONS: The results of this observational study suggest that 5-HT3 receptor antagonists are no more effective than other commonly used medications in controlling postchemotherapy nausea and emesis in women with breast carcinoma who are treated with moderately emetogenic chemotherapy in community practice settings. In fact, they may be associated with significant prolongation of the course of postchemotherapy nausea.

Adult↗
PubMed1999

Choline modulates cardiac membrane repolarization by activating an M3 muscarinic receptor and its coupled K+ channel.

Choline is a necessary substrate of the lipid membrane and for acetylcholine synthesis. Accumulating evidence indicates that besides being a structural component, choline is also a functional modulator of the membrane. It has been shown to be a muscarinic acetylcholine receptor (mAChR) agonist and can induce a novel K+ current in cardiac cells. However, the potential role of choline in modulating cardiac functions remained unstudied despite that mAChRs are known to be important in regulating heart functions. With microelectrode techniques, we found that choline produced concentration-dependent (0.1 approximately 10 mm) decreases in sinus rhythm and action potential duration in isolated guinea pig atria. The effects were reversed by 2 nm 4DAMP (an M3-selective antagonist). Whole-cell patch-clamp recordings in dispersed myocytes from guinea pig and canine atria revealed that choline is able to induce a K+ current with delayed rectifying properties. The choline-induced current was suppressed by low concentrations of 4DAMP (2 approximately 10 nm). Antagonists toward other subtypes (M1, M2 or M4) all failed to alter the current. The affinity of choline (Kd) at mAChRs derived from displacement binding of [3H]-NMS in the homogenates from dog atria was 0.9 mm, consistent with the concentration needed for the current induction and for the HR and APD modulation. Our data indicate that choline modulates the cellular electrical properties of the hearts, likely by activating a K+ current via stimulation of M3 receptors.

Animals↗
PubMed1999

cDNA and genomic cloning of mouse aquaporin-2: functional analysis of an orthologous mutant causing nephrogenic diabetes insipidus.

As the first step in generating a transgenic mouse model of nephrogenic diabetes insipidus (NDI), we have analyzed the mouse aquaporin-2 (Aqp2) cDNA and gene and generated a mutated Aqp2 orthologous to NDI-causing human AQP2-T126M. Aqp2 cDNA was isolated from mouse kidney and encoded a 271-amino-acid protein with 90.4% identity to human AQP2. Expression in Xenopus oocytes indicated that Aqp2 encoded a mercurial-sensitive, water-selective channel. Northern blot analysis showed a single 1.7-kb Aqp2 transcript expressed only in kidney (medulla > cortex); transcript expression was increased approximately 20-fold in 48-h water-deprived mice. Immunoblot analysis revealed a 29-kDa glycoprotein in mouse kidney. Sequence comparison of the Aqp2 cDNA with a 5.5-kb mouse genomic DNA indicated three introns (lengths 2.4, 0.9, and 0.6 kb) separating four exons with boundaries at amino acids 120, 175, and 202. Genomic Southern blot analysis revealed a single-copy Aqp2 gene. The mutant Aqp2-T126M was water permeable when expressed in Xenopus oocytes, but was retained at the endoplasmic reticulum (ER) in transfected mammalian cells. The chemical chaperone glycerol produced a redistribution of Aqp2-T126M from ER to plasma membrane/endosomes. These results establish a basis for an Aqp2-T126M transgenic knock-in model of NDI.

Amino Acid Sequence↗
PubMed1999

Interaction of Diphenylamine Diazonium Salt with Sodium Dodecyl Sulfate in Aqueous Solution.

The interaction of diphenylamine-4-diazonium salt (DDS) with sodium dodecyl sulfate (SDS) in aqueous solution was investigated. The results show that in a 2.1-2.3 molar ratio of SDS/DDS, the solution viscosity increases suddenly to a thousand times the original and then drops rapidly as the ratio beyond the region. The dramatic increase in the viscosity was proposed to be due to aggregated micelles that form in solution due to the interaction of diphenylamine diazonium salt and micelles formed from SDS, and when further SDS was added drops rapidly, because the aggregated micelles were separated by the electrostatic repulsion force originated from the overfeeding of SDS. It is interesting that the viscosity of the solution is very susceptible to UV light, i.e., the increased viscosity decreases gradually when the solution was exposed under UV light because the irradiation decomposes the diazonium group. The influence of [SDS] and the ratio of SDS/DDS on the viscosity of the solution were also investigated. Copyright 1999 Academic Press.

Journal Article↗
PubMed1999

SNARE interactions are not selective. Implications for membrane fusion specificity.

The SNARE hypothesis proposes that membrane trafficking specificity is mediated by preferential high affinity interactions between particular v (vesicle membrane)- and t (target membrane)-SNARE combinations. The specificity of interactions among a diverse set of SNAREs, however, is unknown. We have tested the SNARE hypothesis by analyzing potential SNARE complexes between five proteins of the vesicle-associated membrane protein (VAMP) family, three members of the synaptosome-associated protein-25 (SNAP-25) family and three members of the syntaxin family. All of the 21 combinations of SNAREs tested formed stable complexes. Sixteen were resistant to SDS denaturation, and most complexes thermally denatured between 70 and 90 degreesC. These results suggest that the specificity of membrane fusion is not encoded by the interactions between SNAREs.

Cell Membrane↗
PubMed1999

Disruption of the beta subunit of the epithelial Na+ channel in mice: hyperkalemia and neonatal death associated with a pseudohypoaldosteronism phenotype.

The epithelial Na+ channel (ENaC) is composed of three homologous subunits: alpha, beta and gamma. We used gene targeting to disrupt the beta subunit gene of ENaC in mice. The betaENaC-deficient mice showed normal prenatal development but died within 2 days after birth, most likely of hyperkalemia. In the -/- mice, we found an increased urine Na+ concentration despite hyponatremia and a decreased urine K+ concentration despite hyperkalemia. Moreover, serum aldosterone levels were increased. In contrast to alphaENaC-deficient mice, which die because of defective lung liquid clearance, neonatal betaENaC deficient mice did not die of respiratory failure and showed only a small increase in wet lung weight that had little, if any, adverse physiologic consequence. The results indicate that, in vivo, the beta subunit is required for ENaC function in the renal collecting duct, but, in contrast to the alpha subunit, the beta subunit is not required for the transition from a liquid-filled to an air-filled lung. The phenotype of the betaENaC-deficient mice is similar to that of humans with pseudohypoaldosteronism type 1 and may provide a useful model to study the pathogenesis and treatment of this disorder.

Aldosterone↗
PubMed1999

Molecular cloning of a full-length cDNA for human type 3 adenylyl cyclase and its expression in human islets.

The GK (Goto-Kakizaki) rat is a lean model of type 2 diabetes in which the diabetic state was spontaneously induced. We recently demonstrated the presence in GK rats of two functional point mutations in the promoter region of the type 3 adenylyl cyclase (AC3) gene that resulted in overexpression of AC3 mRNA associated with increased cAMP generation. The AC3 gene promoter mutations are the first molecular changes to be described in any specific gene in the GK rat. Here we report cloning of a full-length cDNA encoding human AC3 from a human fetal brain cDNA library using a PCR-based screening method. This 4142-bp cDNA predicts an open reading frame encoding 1144 amino acids containing putative 12 transmembrane-spanning domains which are typically found in other mammalian AC isoforms. Comparison of the translated amino acid sequence of the AC3 gene between human and rat shows 95% homology. Using RT-PCR, clear AC3 expression was detected in isolated human islets as well as a cDNA panel containing templates from eight different tissues (brain, heart, kidney, liver, lung, pancreas, placenta, and skeletal muscle). This wide distribution of AC3 expression may involve a number of physiological and pathophysiological metabolic processes.

Adenylyl Cyclases↗
PubMed1999

Modulation of constitutive nitric oxide synthase, bcl-2 and Fas expression in cultured human coronary endothelial cells exposed to anoxia-reoxygenation and angiotensin II: role of AT1 receptor activation.

BACKGROUND: Angiotensin II (Ang II) plays a critical role in the pathophysiology of myocardial ischemia-reperfusion injury. We have recently shown that reoxygenation following a period of anoxia causes apoptosis of cultured human coronary artery endothelial cells (HCAECs). Ang II further enhances apoptosis of HCAECs via Ang II type 1 receptor (AT1R) activation. Recent studies suggest an important role of constitutive nitric oxide synthase (cNOS), Fas and bcl-2 proteins in apoptosis. This study was designed to examine the modulation of cNOS, and Fas and bcl-2 expression in HCAECs during exposure to anoxia-reoxygenation and Ang II. METHODS AND RESULTS: HCAECs were exposed to anoxia-reoxygenation and Ang II. Anoxia-reoxygenation significantly decreased cNOS mRNA, protein and activity in cultured HCAECs (P < 0.05 vs. control). Anoxia-reoxygenation also caused an increase in Fas and a decrease in bcl-2 protein expression in cultured HCAECs (both P < 0.05 vs. control). The presence of Ang II (0.3 microM) further enhanced these effects of anoxia-reoxygenation on cNOS, Fas and bcl-2 expression. The effects of Ang II were significantly attenuated by the AT1R inhibitor losartan (10 microM). CONCLUSION: During exposure of HCAECs to anoxia-reoxygenation and Ang II, AT1R activation induces important changes in cNOS mRNA, protein expression and activity, as well as bcl-2 and Fas protein expression which may have a bearing on the development of apoptosis.

Analysis of Variance↗
PubMed1999

Tumor necrosis factor-alpha enhances hypoxia-reoxygenation-mediated apoptosis in cultured human coronary artery endothelial cells: critical role of protein kinase C.

BACKGROUND: Ischemia and tumor necrosis factor-alpha (TNF alpha) released during ischemia both cause apoptosis and necrosis of myocardial tissues. Since endothelium may be critically important in determination of cardiac function, we examined the interaction between TNF alpha and hypoxia-reoxygenation with regard to induction of apoptosis and underlying signaling pathway in cultured human coronary artery endothelial cells (HCAECs). METHODS AND RESULTS: HCAECs were cultured and exposed to hypoxia alone, hypoxia-reoxygenation, TNF alpha alone, TNF alpha plus hypoxia-reoxygenation, or TNF alpha only during the period of reoxygenation. Apoptosis was evaluated by transmission electron microscopy, DNA nick-end labeling and DNA laddering. Hypoxia alone caused modest time-dependent apoptosis of cultured HCAECs, and reoxygenation increased the number of apoptotic cells (P < 0.01 vs. hypoxia alone). TNF alpha induced concentration-dependent apoptosis, and enhanced reoxygenation-mediated apoptosis in cultured HCAECs (P < 0.01 vs. hypoxia-reoxygenation alone). As expected, monoclonal antibody to TNF alpha significantly blocked the pro-apoptotic effect of TNF alpha-induced apoptosis (P < 0.01). TNF alpha-induced apoptosis was found to be associated with marked activation of protein kinase C (PKC), and pretreatment of cells with a specific PKC inhibitor markedly reduced TNF alpha-mediated PKC activity and apoptosis. CONCLUSION: These observations indicate that hypoxia alone causes modest apoptosis, reoxygenation increases apoptosis beyond that caused by hypoxia in cultured HCAECs. TNF alpha alone causes apoptosis, and further enhances apoptosis caused by hypoxia-reoxygenation. The activation of PKC plays a critical role in TNF alpha-induced apoptosis of cultured HCAECs.

Antibodies, Monoclonal↗