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Biomedical subjects

Z Liu

Publications and source records attributed to Z Liu.

At least 865 records · Page 48Linked to original sources

Advances in the analysis of chromosome alterations in human lung carcinomas.

A review of chromosomal analyses of human lung carcinomas is presented. Karyotypic studies have revealed multiple cytogenetic changes in most small cell lung carcinomas (SCLCs) and non-small cell lung carcinomas (NSCLCs). In SCLCs, losses from 3p, 5q, 13q, and 17p predominate; double minutes associated with amplification of members of the MYC oncogene family may be common late in disease. In NSCLCs, deletions of 3p, 9p, and 17p, +7, i(5)(p10), and i(8)(q10) often are reported. The recurrent deletions encompass sites of tumor suppressor genes commonly inactivated in lung carcinomas, such as CDKN2 (9p21), RB1 (13q14), and TP53 (17p13). Despite technical advances in cell culture, the rate of successful karyotypic analysis of lung carcinomas has remained low. Alternative molecular cytogenetic methods to assess chromosome changes in lung cancer, particularly comparative genomic hybridization (CGH) analysis, are discussed. Initial CGH studies confirm the existence of many of the karyotypic imbalances identified earlier in lung cancer and have revealed several recurrent abnormalities, such as 10q- in SCLC, that had not been recognized previously. The further application of such molecular cytogenetic approaches should enable investigators to define more precisely the spectrum and clinical implications of chromosome alterations in lung cancer.

Carcinoma, Non-Small-Cell Lung↗

Mechanism of liver allograft rejection: the indirect recognition pathway.

Transplant rejection is mediated by the direct and indirect pathways. To explore the role of the indirect recognition pathway in the rejection of liver allografts, T cells obtained from peripheral blood were expanded in medium containing IL-2 and tested in LDA for reactivity to synthetic peptides corresponding to the hypervariable regions of the mismatched HLA-DR antigen(s) of the donor. Serial investigations of 17 recipients showed that T-cell reactivity to donor HLA-DR peptides was strongly associated with acute rejection episodes. In recipients carrying a graft that was mismatched by two HLA-DR alleles, a single donor antigen was targeted during primary rejection, although allopeptide reactivity against the second HLA-DR antigen was observed during subsequent episodes of acute rejection. The finding that allopeptide reactivity occurs early following transplantation and is predictive of rejection is consistent with the notion that processing of donor alloantigens by recipient APCs activates the indirect T-cell recognition pathway that plays a major role in initiating and amplifying allograft rejection.

Antigen Presentation↗

Basic fibroblast growth factor is highly neuroprotective against seizure-induced long-term behavioural deficits.

Basic fibroblast growth factor has been reported to protect neurons of various structures from excitotoxic damage. To study the effects of basic fibroblast growth factor on seizure-induced brain damage we infused the growth factor into the lateral ventricles of 35-day-old rats receiving convulsant dosages of kainic acid. Artificial cerebrospinal fluid or basic fibroblast growth factor at dosages of 0.5 ng/h or 2.5 ng/h was infused into the lateral ventricle continuously for seven days starting two days before and continuing for five days after the animals had kainic acid-induced status epilepticus. At age 80 days the animals underwent behavioural testing using the water maze, open field, and handling tests and at age 95 days were tested for seizure threshold using flurothyl inhalation. Neither artificial cerebrospinal fluid or basic fibroblast growth factor modified the latency or duration of the acute seizures following kainic acid. However, rats infused with 2.5 ng/h, but not 0.5 ng/h of basic fibroblast growth factor, had fewer spontaneous recurrent seizures, a higher seizure threshold, better performance in the handling, open field and water maze test, and less cell loss in the hippocampus when compared to rats receiving artificial cerebrospinal fluid or 0.5 ng/h of basic fibroblast growth factor. These results show that basic fibroblast growth factor has a dose-related neuroprotective effect against seizure-induced long-term behavioural deficits when administered by osmotic pump prior to seizure onset. This neuroprotective effect is not related to an anticonvulsant effect.

Aging↗

Acute effects of MK801 on kainic acid-induced seizures in neonatal rats.

Kainic acid (KA) causes behavioral and electrographic status epilepticus (SE) in rats of all ages. In adult rats, the noncompetitive N-methyl-D-aspartate (NMDA) channel blocker MK801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine ) is anticonvulsant against KA-induced seizures: it reduces their severity and protects against neuronal damage, although it may worsen electrographic seizures. Here we examined the effects of MK801 on KA seizures in the immature brain. Neonatal rats (P11-P12) were pretreated with MK801 (0.01, 0.1, 0.5 or 1.0 mg/kg, i.p.) or saline twenty minutes prior to KA (2 mg/kg, i.p.). Clinical seizure behavior was monitored for > 6 hrs, and in some rats the EEG was monitored with an intrahippocampal or intracortical electrode. MK801 caused immobility alternating with hyperactivity, ataxia, scratching and sometimes alternate limb cycling, which correlated with the appearance of spikes on the EEG. Compared to KA alone or KA preceded by 0.01 mg/kg MK801, the higher doses of MK801 (0.1, 0.5 and 1.0 mg/kg) significantly lowered the latency to electrographic seizures (P < 0.001), ictal scratching (P < 0.0001), and status epilepticus (P < 0.0001). MK801 pretreatment did not lower significantly the death rate due to KA seizures. No histologic damage was seen after MK801, KA or both agents together. These results suggest that MK801 exacerbates KA-induced seizures in the neonatal brain, and may even cause ictal behavioral and electrographic manifestations by itself. The findings point to an age-dependency of NMDA antagonist action, and suggest caution in considering the use of NMDA antagonists in neonates.

Animals↗

Inhibition of caspase proteases by CrmA enhances the resistance of human leukemic cells to multiple chemotherapeutic agents.

Proteases that are members of the caspase (or interleukin-1beta converting enzyme (ICE)) protease family have been shown to be important mediators of apoptosis induced by Fas activation, neurotrophic factor withdrawal, and detachment from extracellular matrix. In this report we have investigated the potential importance of caspase proteases in apoptosis induced by multiple chemotherapeutic agents. Human T leukemic cells engineered to overexpress the cowpox virus CrmA protein, a direct and specific inhibitor of caspase proteases, were studied for their resistance to 1-beta-D-arabinofurasosyl-cytosine (Ara-C), etoposide (VP-16), doxorubicin (DOX), and cis-dichlorodiammine platinum (CP). Overexpression of CrmA dramatically inhibited drug-induced activation of caspases, as measured by processing of the inactive precursor form of caspase-3 and cleavage of caspase substrate proteins poly(ADP-ribose) polymerase (PARP) and lamin B. CrmA also significantly inhibited the kinetics of cell death induced by each of the four drugs. Moreover, when examined several days or weeks after initial exposure to drug, cultures of CrmA-expressing cells were found to have recovered and repopulated, whereas vector-transfected control cells did not. These studies demonstrate that caspase proteases play an important role in conferring sensitivity to multiple chemotherapy drugs, and that constitutive downmodulation of caspase activities can enhance chemoresistance.

Antineoplastic Agents↗

Reproducibility and accuracy of interactive segmentation procedures for image analysis in cytology.

The segmentation of nuclear images is a crucial step in the development of procedures using image analysis for the cytological diagnosis of cancer. The purpose of this study is to evaluate the reproducibility and accuracy of several interactive segmentation methods which can be used in this context. Four methods were studied: a thresholding-based method enabling selection of intensity histogram contrast and brightness, manual tracing with a stylus, and arc- and ellipse-fitting routines. Features of nuclear size and shape were derived from nuclei segmented on repeated occasions by several individuals. Variance component models provided a statistical framework for evaluating the intraobserver and interobserver variability of these measurements in terms of their intraclass correlation coefficients. Of the methods tested, the arc-fitting segmentation method gave the most reproducible results, and thresholding the least. Reproducibility was generally very high both between individuals and for repeated segmentations by a single individual. Accuracies of area measurements for the various methods, as determined with respect to point counting, paralleled the reproducibilities of the methods. Sample size requirements were observed to be more dependent on the biological variability of the tissue sampled than on the particular segmentation method or on the number of individuals performing segmentation.

Cell Biology↗

Black tea constituents, theaflavins, inhibit 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in A/J mice.

The present study investigated the inhibitory activity against lung tumorigenesis by a group of characteristic black tea polyphenols, theaflavins. In a short-term study, female A/J mice were treated with a single dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; 103 mg/kg b.w., i.p.) on day 0, and 0.1 and 0.3% theaflavins were administered as the sole source of drinking fluid starting 24 h after NNK treatment. The proliferation index of the lung tissues was measured by the incorporation of bromodeoxyuridine (BrdU) immunohistochemically. The highest NNK-induced proliferation rate of bronchiolar cells, observed on day 5, was significantly decreased by 0.3% theaflavins (proliferation index, 1.51 +/- 0.08 versus 2.35 +/- 0.16). In a long-term lung tumorigenesis study, pulmonary adenomas were observed in 100% (30/30) of the mice at week 16 after NNK treatment. Administration of theaflavins (0.1%) as the sole source of drinking fluid, starting 2 days after the NNK treatment until the termination of the experiment, significantly reduced the tumor multiplicity and volume by 23% (8.5 +/- 0.6 versus 6.5 +/- 0.6 tumors/mouse) and 34% (0.08 versus 0.05 mm3 per tumor), respectively. The proliferation index in lung adenomas was also significantly inhibited by theaflavins. The present work demonstrates the inhibitory action of theaflavins against NNK-induced pulmonary hyperproliferation and tumorigenesis.

Animals↗

Tight clustering of extracellular BP180 epitopes recognized by bullous pemphigoid autoantibodies.

Bullous pemphigoid is a blistering skin disease associated with autoantibodies against the BP180 antigen, a transmembrane component of the hemidesmosome. Anti-BP180 antibodies have been demonstrated to be pathogenic in a passive transfer mouse model. One extracellular site on human BP180 (MCW-1) was previously shown to be recognized by 50-60% of bullous pemphigoid sera. To facilitate the identification of additional autoantibody-reactive epitopes, recombinant forms of the BP180 ectodomain were generated using both bacterial and mammalian expression systems. One recombinant protein, sec180e, that was expressed in COS-1 cells and that contained the entire BP180 ectodomain, provided us with a tool to detect conformational epitopes. Bullous pemphigoid sera immunoadsorbed against the major noncollagenous NC16A domain no longer reacted with sec180e, indicating that autoantibody reactivity to the BP180 ectodomain is restricted to the NC16A region. Immunoblot analysis of bullous pemphigoid sera immunoadsorbed with a series of recombinant NC16A peptides revealed the presence of three novel autoantigenic sites that, along with the MCW-1 epitope, are clustered within the N-terminal 45 amino acid stretch of NC16A. All 15 bullous pemphigoid sera tested reacted with a recombinant protein containing this BP180 segment. No disease-associated epitopes were detectable within the remaining 28 amino acids of NC16A. Thus, bullous pemphigoid patient autoantibodies react with a set of epitopes on the BP180 ectodomain that are highly clustered. This autoantibody-reactive region on human BP180 shows overlap with the corresponding murine BP180 site that is targeted by antibodies that are pathogenic in the mouse model of bullous pemphigoid. These findings suggest new directions for the development of diagnostic and therapeutic tools for this disease.

Amino Acid Sequence↗

A highly sensitive enzyme-linked immunosorbent assay for the detection of circulating anti-BP180 autoantibodies in patients with bullous pemphigoid.

The BP180 antigen, a component of the epidermal anchoring complex, has been identified as one of the major antigenic targets of autoantibodies associated with the blistering skin disease, bullous pemphigoid. Our research group has recently demonstrated that reactivity of bullous pemphigoid autoantibodies to the BP180 ectodomain is almost entirely restricted to a set of four antigenic sites clustered within the membrane-proximal noncollagenous stretch (NC16A). Using a passive transfer mouse model, antibodies to the corresponding noncollagenous region of murine BP180 were shown to trigger an inflammatory subepidermal blistering disease that closely mimics bullous pemphigoid. We now report the development of an enzyme-linked immunoabsorbent assay system that is extremely sensitive in detecting disease-specific autoantibodies in the sera of bullous pemphigoid patients. The target antigen in this assay is a recombinant form of the BP180 NC16A domain that contains all four of the well-defined bullous pemphigoid-associated antigenic sites. Of 50 randomly selected bullous pemphigoid sera tested, 47 (94%) were positive in this assay, whereas no specific reactivity was detected in any of the 107 controls. Interestingly, all three of the bullous pemphigoid sera that were negative in this assay had been obtained from patients who were already undergoing treatment. The NC16A enzyme-linked immunosorbent assay is more sensitive than any of the standard techniques for detecting circulating bullous pemphigoid autoantibodies, including other enzyme-linked immunosorbent assays, immunoblotting, and indirect immunofluorescence. Finally, the NC16A enzyme-linked immunosorbent assay provides immunologic information that cannot be obtained from direct immunofluorescence studies of skin biopsies, and that may well be relevant in the diagnosis and treatment of bullous pemphigoid.

Autoantibodies↗

Multiple kainic acid seizures in the immature and adult brain: ictal manifestations and long-term effects on learning and memory.

PURPOSE: While there is increasing evidence that the adverse effects of prolonged seizures are less pronounced in the immature than in the mature brain, there have been few investigations of the long-term effects of recurrent seizures during development. This study examined the effects of multiple administrations of the convulsant kainic acid (KA) on seizure characteristics and spatial learning as a function of brain development. METHODS: To determine the long-term effects of serial KA seizures during ontogeny, saline or convulsant doses of KA were given intraperitoneally 4 times, at 2-day intervals. Immature rats were given KA on P20, P22, P24 and P26; adult rats got KA on P60, P62, P64 and P66. Ictal characteristics and EEGs were recorded. To examine the effects of multiple KA seizures on the retention of spatial learning, water maze testing was performed before (immature group: from P16-19, adult group: from P56-P59) and after (immature: from P60-P63, adult: from P100-P103) KA injections. Finally, histology was performed to compare KA-induced damage at each age. RESULTS: In immature animals, serial KA administration resulted in seizures with a progressively longer onset latency and decreased severity. In contrast, KA serially administered to adult rats caused severe seizures after each of the 4 injections. In immature rats, epileptiform EEG changes were most prominent after the first KA injection, whereas in adults, prolonged paroxysmal EEG patterns were seen after all 4 KA injections. Before KA, both rat pups and adults acquired place learning in the water maze. One month after the final KA injection, there was no deficit in spatial learning retention in the immature group, whereas the adult group had profound impairment compared to age-matched, saline-injected controls. Histology revealed no lesions in immature rats treated multiple times with KA but profound cell loss in hippocampal fields CA4, CA3 and CA1 in rats treated serially with KA as adults. CONCLUSIONS: Previous studies have shown that a single KA injection causes prolonged status epilepticus (which persists for several hours), leading to severe histologic and behavioral sequelae in adult rats but not in pups. Our study extends those findings, demonstrating that immature rats are spared the cognitive and pathological sequelae of multiple injections of convulsant doses of KA as well.

Animals↗

O2-induced change in ventilation and ventilatory drive in COPD.

We examined the role of respiratory control during O2-induced hypercarbia in patients with chronic obstructive pulmonary disease (COPD), by comparing the observed change in ventilation (delta VEobs) with the delta VE predicted (delta VEpred) from the patients' ventilatory drive and the O2-induced delta PaCO2 and delta SaO2. Eleven stable hypoxemic COPD patients (mean +/- SD: FEV1 = 1.00 +/- 0.25 L, FVC = 2.33 +/- 0.38 L; room air PaCO2 = 52.7 +/- 7.9 mm Hg, SaO2 87.7 +/- 5.1%) were studied. Using standard rebreathing methods, we measured the ventilatory responses to hypercapnia (delta VE/PCO2 = 0.76 +/- 0.55 L/min/mm Hg) and to hypoxia (delta VE/delta SaO2 = -0.74 +/- 0.31 L/min/%). After breathing 100% O2 for 15 min, the mean delta VEobs was -0.08 +/- 0.62 (SEM) L/min (p = NS), the delta SaO2 was 7.6 +/- 3.6% (p < 0.001), and the delta PaCO2 was 6.6 +/- 3.3 mm Hg (p < 0.001). The delta VEpred was expressed as the sum of a decrease in ventilation due to suppression of hypoxic drive [calculated as the product (delta VE/SaO2) x delta SaO2] and an increase in ventilation due to the O2-induced hypercarbia [calculated as the production (delta VE/delta PCO2) x delta PaCO2]. The mean delta VEpred [-0.96 +/- 0.68 (SEM)] did not differ significantly from mean delta VEobs. We conclude that the O2-induced delta VEobs is equal to that expected from the ventilatory drives and the changes in PaCO2 and SaO2; and that O2-induced hypercarbia does not indicate a failure of respiratory control mechanisms in the maintenance of PaCO2 homeostasis.

Dose-Response Relationship, Drug↗

A putative binding site for Sp1 is involved in transcriptional regulation of CYP17 gene expression in bovine ovary.

In the bovine ovary, thecal cells are the only cell type capable of expressing the CYP17 gene in response to LH. With the onset of ovulation and luteinization in the cow, there is complete loss of P450c17alpha expression. To characterize the molecular mechanisms involved in tissue-specific regulation of the CYP17 gene in the bovine ovary, deletion mutations of the bovine CYP17 promoter were ligated into a promoterless luciferase expression vector, and reporter constructs were transiently transfected into primary cultures of bovine thecal and luteal cells. Deletion of the promoter sequences between -191 and 101 bp dramatically decreased the levels of reporter gene activity in both thecal and luteal cells. Computer-assisted analysis revealed the presence of a putative inverted Sp1-like binding site at -188/-180 bp. Deletion or mutation of this sequence caused a decrease in both basal and forskolin-stimulated reporter gene activity. In addition, mutation or deletion of this sequence also decreased reporter gene expression induced by overexpression of the protein kinase A catalytic subunit. Electrophoretic mobility shift assays showed that this sequence binds to a nuclear protein(s) from both thecal and luteal cells that is related to Sp1, as suggested by the results of gel mobility supershift assay employing an antibody raised against Sp1. DNA-binding activity was not increased by the addition of forskolin to thecal or luteal cells. We conclude that this inverted Sp1-like binding sequence is involved in constitutive as well as cAMP-dependent expression of the CYP17 gene in the bovine ovary.

Animals↗

Heat shock-induced inhibition of acute steroidogenesis in MA-10 cells is associated with inhibition of the synthesis of the steroidogenic acute regulatory protein.

The synthesis of heat shock proteins (HSPs) rapidly increases in cells under a broad range of stress conditions in addition to heat shock. Previous studies have shown that the induction of HSPs severely impairs the ability of steroidogenic cells to synthesize steroids in response to acute stimulation. De novo synthesis of the steroidogenic acute regulatory (StAR) protein has been shown to be indispensable for acute steroid hormone biosynthesis; however, the effect of HSP induction on the synthesis of the StAR protein has not yet been studied. In the present study we investigated whether HSP induction might influence the steroidogenic activity of MA-10 mouse Leydig tumor cells, and whether this effect may involve the synthesis of StAR protein. MA-10 cells exposed to 45 C for 10 min and allowed to recover for 2 h at 37 C displayed a 6-fold increase in HSP-70 at 3 h postrecovery and a 20-fold increase in this protein at 6 h postrecovery. This heat shock regimen also acutely inhibited both progesterone production and StAR protein synthesis in MA-10 cells in response to LH and cAMP analog stimulation. The activity and quantity of cytochrome P450 side-chain cleavage and 3beta-hydroxysteroid dehydrogenase were not affected by this heat shock treatment, indicating that the loss of steroidogenic capacity was not a result of inhibition of the enzymes involved in the conversion of cholesterol to progesterone. The results suggest that the previously observed antisteroidogenic effects of heat shock treatment may be due mainly to the acute inhibition of StAR protein synthesis.

17-Hydroxysteroid Dehydrogenases↗

Steroidogenic factor 1 (SF-1) and SP1 are required for regulation of bovine CYP11A gene expression in bovine luteal cells and adrenal Y1 cells.

Cholesterol side-chain cleavage cytochrome P450 (CYP11A; P450scc) gene expression is regulated by gonadotropins via cAMP in the ovary and by ACTH via cAMP in adrenal cortical cells. Previously, we have characterized a response element located at -118 to -101 bp in the 5'-flanking region of the bovine P450scc gene required for cAMP-stimulated transcription in both mouse adrenocortical Y1 cells and bovine ovarian cells in primary culture. It was shown that this region contains a binding site for the transcription factor Sp1. Deletion of this sequence abolished cAMP-stimulated transcription in both Y1 cells and bovine ovarian luteal cells. Another sequence element located at -57 to -32 bp upstream from the transcription initiation site, which is highly conserved in CYP11A of other species, contains the motif TAGCCTTG, similar to the consensus binding site of steroidogenic factor-1, SF-1 (or Ad4-BP), but in the inverted orientation. In the present study, gel shift analysis using nuclear extracts of either Y1 cells or bovine luteal cells demonstrated that the sequence between -57 and -32 bp bound SF-1. A mutation of the SF-1-binding site that abolished binding of the nuclear protein to DNA reduced markedly the basal transcription of the reporter gene as well as the responsiveness to cAMP, when the mutated fragments containing the region from -186 to +12 bp were cloned into a luciferase construct and transfected into mouse adrenal Y1 cells and bovine luteal cells. The role of SF-1 in P450scc transcription was further confirmed by transactivation of the -186/+12Luc construct employing an SF-1 expression vector after transfection into nonsteroidogenic COS-1 cells. In addition, results obtained employing a double mutation of the Sp1- and SF-1-binding sites, and from a construct containing both Sp1 and SF-1 elements upstream of the CYP11A TATA box, indicated that Sp1 and SF-1 function cooperatively in the transactivation of the bovine CYP11A promoter in both bovine luteal cells and Y1 cells. Finally, a mammalian two-hybrid system was employed to demonstrate that Sp1 and SF-1 can associate in vivo. These results establish that basal and cAMP-stimulated activity of the bovine P450scc promoter in both Y1 cells and bovine luteal cells requires the combined action of at least two transcription factors, Sp1 and SF-1.

Adrenal Gland Neoplasms↗

TSO1 functions in cell division during Arabidopsis flower development.

We describe an Arabidopsis mutant, tso1, which develops callus-like tissues in place of floral organs. The tso1 floral meristem lacks properly organized three cell layers, and the nuclei of these cells are irregular in size and shape. Further analyses reveal partially formed cell walls and increased DNA ploidy in tso1 floral meristem cells, indicating defects in mitosis and cytokinesis. Our finding that TSO1 is required for organ formation in floral tissues but not in other tissues indicates that TSO1 may encode a floral-specific cell division component, or that TSO1 function is redundant in nonfloral tissues.

Arabidopsis↗

Elevated cerebrospinal fluid substance P-like immunoreactivity in patients with painful osteoarthritis, but not in patients with rhizopatic pain from a herniated lumbar disc.

Cerebrospinal fluid (CSF) levels of substance P like immunoreactivity (SPLI) were determined in 11 patients with painful osteoarthritis in hip or knee, 9 patients with rhizopatic pain from a herniated lumbar disc, and in 9 healthy volunteers without pain. The patients with osteoarthritis had increased levels of SPLI in CSF (p < 0.001) compared to the controls. A positive correlation was also seen between the CSF SPLI and the degree of pain. At a second lumbar puncture 5 months after operation, SPLI had decreased, but was still significantly higher than in the controls. No difference in CSF SPLI was seen in the patients with herniated lumbar disc compared to the controls, neither before treatment, nor at follow up CSF postoperatively. The results suggest that nociceptive joint pain is consistent with increased SPLI in CSF. Differences in SPLI in CSF may be useful to differentiate pain from various origin, and may also increase our understanding of different pain mechanisms.

Chromatography, Gel↗

[Hemodynamic response to exercise in patients with chronic obstructive pulmonary disease (COPD)].

OBJECTIVE: The present study was undertaken to assess the cardiopulmonary response during the initial period of exercise. METHODS: Eight patients with COPD and 10 normal subjects were investigated during exercise (35W) in room air and oxygen breathing for 15 minutes, respectively. Pulmonary arterial mean pressure (mPAP), cardiac output (CO) and mixed venous oxygen saturation (SvO2) were measured by Swan-Ganz catheter during exercise. RESULTS: Compared with normal controls, mPAP in COPD patients was increased and SvO2 decreased markedly both in room air and oxygen breathing during exercise. And CO increased relative slowly than that of normal controls. Furthermore, in patients with COPD, the time to reach their steady state in mPAP and SvO2 during exercise were delayed compared with normal controls. Moreover, we found that the time to reach their steady state in mPAP and SvO2 were shortened when the patients were given oxygen breathing during exercise. CONCLUSIONS: The results indicate that the measurement of initial changes in mPAP and SvO2 during exercise have important clinical significance for evaluating the cardiopulmonary response in patients with COPD.

Blood Pressure↗

[The relationship between tumor necrosis factor and glomerular mesangial cells].

OBJECTIVE: To study the autocrine function of tumor necrosis factor (TNF) in glomerular mesangial cells (MC) and the action of TNF on MC. METHODS: Cultured rat and human MC were studied by RT-PCR, in situ hybridization and immunohistochemical methods. RESULTS: The expression of both TNF and TNF receptor mRNA and protein synthesis in MC were manifested. CONCLUSION: (1) MC is the target cell for TNF, MC have specific cell surface receptor to TNF. (2) TNF acts on MC through both autocrine and paracrine mechanism.

Animals↗