Biomedical subjects

S Hou

Publications and source records attributed to S Hou.

At least 127 records · Page 7Linked to original sources

PubMed1995

[The role of endothelin the development of hypoxic pulmonary hypertension].

To evaluate the role of endothelin in the development of hypoxic pulmonary hypertension, seven pigs (50 +/- 5kg) models with hypoxia induced pulmonary hypertension were established. Swan-Ganz catheter and arterial catheter were inserted into the pulmonary artery and aorta, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO) and arterial blood gases were monitored before and during hypoxia and 5 min, 30 min, 60 min, 120 min after nitrendipine injected (100 micrograms/kg). Plasma endothelin concentration was measured by RIA. It was found that plasma ET concentration was significantly increased, from 5.5 +/- 1.1 ng/L during normoxia to 11.9 +/- 1.2 ng/L during hypoxia (PaO2 = 5.55 +/- 0.24 kPa) (P < 0.002), while PAP increased from 3.88 +/- 0.10 kPa to 5.92 +/- 0.19 kPa. After nitrendipine injection, PAP and ET level were decreased by 1.03 kPa (P < 0.05) and 40% (P < 0.02) respectively compared with those with pure hypoxia. Our results indicate that ET may play an important role in the development of hypoxia induced pulmonary hypertension. Ca++-channel blocker nitrendipine not only relieves hypoxic pulmonary hypertension, but also inhibits the release of endothelin.

Animals↗

PubMed1994

Virus-specific CD8+ T-cell memory determined by clonal burst size.

Although some viruses, particularly the herpes viruses, may never be eliminated from the body, others like influenza A, regularly reinfect humans and boost waning crossreactive CD8+ T-cell immunity. Prolonged T-cell memory is found for viruses that are unlikely to be re-encountered and which do not persist in the host genome, indicating that CD8+ T-cell memory might be independent of continued (or sporadic) antigenic exposure. A feature of virus-specific CD8+ T-cell memory is that antigen-specific cytotoxic T-lymphocyte precursors (CTLp) are greatly increased and remain high throughout life. The idea that persistence of the inducing antigen is essential is based on experiments in which adoptively transferred CD8+ memory T cells could not be detected for more than a few weeks in naive recipient mice without secondary challenge. Here we show that restimulation of such chimaeric mice with an inducing Sendai virus antigen increases the clonal burst size more than 7-fold within 8 days, making memory CTLp easier to detect in the longer term. We find that Sendai-virus-specific CTLp are maintained for > 250 days in irradiated uninfected recipients, including reconstituted beta 2-microglobulin-/- mice. To determine whether a source of viral peptide can persist after primary infection, we gave Sendai-virus-specific Thy1.1+ memory spleen cells to naive mice that had been minimally depleted of Thy1.2+ T cells, or to comparable recipients that had recovered from infection with Sendai virus or influenza virus. Although antibody against Sendai virus was never found in the naive recipients, Sendai-virus-specific CD8+ memory T cells were maintained equally well in each case for > 100 days after cell transfer. We find no evidence for persisting depots of viral protein that might feed into the endogenous processing pathway and maintain virus-specific CD8+ T-cell memory.

Animals↗

PubMed1994

Mice lacking CD8+ T cells develop greater numbers of IgA-producing cells in response to a respiratory virus infection.

Antibody production profiles have been compared for Sendai virus infection of normal mice and mice that lack CD8+ T cells as a consequence of treatment with a lymphocyte subset-specific monoclonal antibody or homozygous disruption of the beta 2-microglobulin (beta 2-m(-/-)) gene encoding the light chain of the class I major histocompatibility complex glycoprotein. Using the single-cell ELISPOT assay, we show a relative increase in IgA antibody forming cell (AFC) numbers in the mediastinal lymph node (MLN), spleen, and bone marrow of the CD8-depleted mice. This is reflected in higher serum IgA titers. Similarly, secondary infection with a large dose of Sendai virus leads to greater prevalence of virus-specific IgA AFCs as early as Day 5 postinfection in the beta 2-m(-/-) mice. Also, in primed beta 2-m(-/-) mice challenged with vaccinia constructs containing the genes for the hemagglutinin-neuraminidase (HN), nuclear protein, or the fusion protein of Sendai virus, the majority of the virus-specific AFCs in the MLN are specific for HN and secrete IgA.

Animals↗

PubMed1994

Limiting the available T cell receptor repertoire modifies acute lymphocytic choriomeningitis virus-induced immunopathology.

The invariably fatal immunopathological disease that follows intracerebral injection of CBA/Ca (H-2k) mice with 1000 PFU of lymphocytic choriomeningitis virus (LCMV) generally fails to develop in congenic mice transgenic for a V beta 8.1D beta 2J beta 2.3C beta 2 T cell receptor (TCR) gene. The majority of these LCMV-infected TCR-transgenic mice show a substantial meningitis of delayed onset, that resolves without causing any obvious clinical impairment. This inflammatory process depends on the involvement of V beta 8+ T cells, but does not require the participation of the CD4+ subset. The cytotoxic effectors that develop in both the transgenic mice and the CBA/Ca controls are lytic for target cells infected with a vaccinia construct expressing genes encoding the putative polymerase protein of LCMV. Limiting the available TCR repertoire to lymphocytes with a single V beta phenotype (not required for the generation of potent effectors in wild-type mice) thus modifies the development of the lethal neuropathology characteristic of LCMV infection, although the CD8+ cytotoxic T lymphocyte response is not greatly compromised.

Acute Disease↗

PubMed1994

CD8+ T-cell memory to viruses.

Recent experiments show that laboratory mice infected once with an influenza A virus or with the murine parainfluenza type 1 virus, called the Sendai virus, have enhanced numbers of cytotoxic T-lymphocyte precursors ( > 20x background) for life. Neither virus persists at the genome level, and the mice are maintained under conditions where there is no possibility of re-infection. These observations are highly relevant to any understanding of CD8+ cell memory and suggest that the clonal burst size associated with the primary challenge is a key determining factor.

Animals↗

PubMed1994

Virus-specific CD8+ T-cell responses in mice transgenic for a T-cell receptor beta chain selected at random.

The consequences of severely limiting the T-cell receptor (TCR) repertoire available for the response to intranasal infection with an influenza A virus or with Sendai virus have been analyzed by using H-2k mice (TG8.1) transgenic for a TCR beta-chain gene (V beta 8.1D beta 2J beta 2.3C beta 2). Analyzing the prevalence of V beta 8.1+ CD8+ T cells in lymph node cultures from nontransgenic (non-TG) H-2k controls primed with either virus and then stimulated in vitro with the homologous virus or with anti-CD3 epsilon showed that this TCR is not normally selected from the CD8+ T-cell repertoire during these infections. However, the TG8.1 mice cleared both viruses and generated virus-specific effector cytotoxic T lymphocytes (CTL) and memory CTL precursors, though the responses were delayed compared with the non-TG controls. Depletion of the CD4+ T-cell subset had little effect on the course of influenza virus infection but substantially slowed the development of the Sendai virus-specific CTL response and virus elimination in both the TG8.1 and non-TG mice, indicating that CD4+ helpers are promoting the CD8+ T-cell response in the Sendai virus model. Even so, restricting the available T-cell repertoire to lymphocytes expressing a single TCR beta chain still allows sufficient TCR diversity for CD8+ T cells (acting in the presence or absence of the CD4+ subset) to limit infection with an influenza A virus and a parainfluenza type 1 virus.

Animals↗

PubMed1994

Protection against lethal lymphocytic choriomeningitis virus (LCMV) infection by immunization of mice with an influenza virus containing an LCMV epitope recognized by cytotoxic T lymphocytes.

The reverse genetics system has made it possible to modify the influenza virus genome. By this method, we were able to assess influenza virus as a vaccine vector for protecting BALB/c mice against otherwise lethal lymphocytic choriomeningitis virus (LCMV) infection. A single dose of influenza virus [A/WSN/33 (H1N1)] bearing a cytotoxic T-lymphocyte-specific epitope of the LCMV nucleoprotein (residues 116 to 127) in the neuraminidase stalk protected mice against LCMV challenge for at least 4 months. The immunity was mediated by cytotoxic T lymphocytes and was haplotype specific, indicating that the observed protective response was solely a consequence of prior priming with the H-2d LCMV nucleoprotein epitope expressed in the recombinant influenza virus. We also found that as many as 58 amino acids could be inserted into the neuraminidase stalk without loss of viral function. These findings demonstrate the potential of influenza virus as a vaccine vector, with the neuraminidase stalk as a repository for foreign epitopes.

Amino Acid Sequence↗

PubMed1994

[The distribution and pharmacokinetics in lung of bovine serum albumin microspheres for pulmonary targeting in mice].

125I-labeled bovine serum albumin microspheres loaded cisplatinum (CDDP-125I-BSA-MS) with the size range of 7-25 microns were prepared and injected into the tail vein of mice. The results showed that the microspheres were accumulated almost entirely in the lung after i.v. injection (about 97.52% injected dose at the highest concentration). While in blood and other organs almost no accumulation was found. Photomicrographs showed that microspheres reached the lung and lodged in precapillary arteriols and capillaries of lung. The microspheres in lung were eliminated gradually. The pharmacokinetics of microspheres in lung of mice was also studied with "practical pharmacokinetic program-version 87", and was fitted by two-compartment model with i.v. injection or one-compartment model with 1st order absorption, but the meaning of some parameters changed. Based on the analysis of the models and parameters, it was concluded that the pharmacokinetics of microspheres in lungs can be described by the model of "one-compartment of first-order intake and first-order elimination".

Animals↗

PubMed1993

Pedicle morphology of the lower thoracic and lumbar spine in a Chinese population.

Knowledge of pedicle diameter and surface landmarks is crucial for safe placement of screws. Little attention has been paid to variations of entrance points for pedicle screws, differentiation of male and female pedicle sizes and pedicle size differences in nonwhite populations. Forty thoracolumbar spinal columns from T9 to L5 were measured using vernier calipers. Cephalad-caudad and medial-lateral diameter of the pedicle, length of the pedicle from posterior cortex to anterior cortex at the midline and parallel to midline was measured. Relation of the centre of the pedicle to the transverse process (TP) and to the superior facet joint was noted. Twenty-five male and 15 female specimens were measured. Average pedicle width in the female was 5.2 mm at T9 (SD 0.9) to 13 mm at L5 (SD 2.7) and in the male 6.0 mm at T9 (SD 1.1) to 12.8 mm at L5 (SD 2.7). Cephalad caudad diameter was 12.5 mm (SD 1.2) at T9 to 20.5 mm (SD 3.6) at L5 in the male and in the female 12.2 mm (SD 1.3) at T9 to 18.7 mm (SD 3.9) at L5. All specimens had starting points cephalad to the midpoint of the TP at T9. At L5, 37 of 40 specimens had starting points at the midpoint of the TP. Starting points were parallel to the middle or lateral third of the superior facet joint at T9. At L5 starting points were at least one third of the facet joint lateral to the lateral border of the facet. Female pedicle width was smaller than male at T9 (P = 0.03) and T12 (P = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Asian People↗

PubMed1993

Partitioning of responder CD8+ T cells in lymph node and lung of mice with Sendai virus pneumonia by LECAM-1 and CD45RB phenotype.

Patterns of LECAM-1 and CD45RB expression have been analysed for mediastinal lymph node (MLN) and bronchoalveolar lavage (BAL) populations from C57BL/6J mice with primary Sendai virus pneumonia. The findings indicate that virus-specific CD8+ CTL precursors differentiate in the regional lymph node and become effector CTL after localization to the virus-infected respiratory tract. Relatively few of the MLN CD8+ T cells were LECAM-1-, and all were CD45RB-hi throughout the acute and recovery phases of this disease process. The CD8+ CD45RB-hi and LECAM-1+ T cells characteristic of the MLN were more apparent in the BAL during the 1st wk after exposure to virus, with this shifting to a predominant CD8+ LECAM-1- CD45RB-lo phenotype from day 10 after infection. In contrast, the CD4+ set was generally CD45RB-lo LECAM-1- in the BAL, although CD4+ CD45RB-lo and LECAM-1- cells maintained at relatively high levels in the MLN. The virus-specific CD8+ effectors found in the BAL from day 8 after infection were uniformly LECAM-1-, but varied in the level of CD45RB expression. Evidence of CTL activity was minimal for the MLN, though virus-specific CTLp were present from day 5 after infection and reached maximum numbers within a further 2 days. The ratio of LECAM-1-:LECAM-1+ CTLp in the MLN ranged from 25:1 to > 200:1, with this pattern being maintained for memory spleen cells recovered 3 mo later. Lack of expression of LECAM-1 is thus characteristic of the great majority of Sendai-virus-specific CD8+ T cells, identified either as effector CTL or as precursors that can be stimulated in vitro under limiting dilution conditions. These lymphocyte populations cannot be discriminated on the basis of hi or lo CD45RB expression.

Animals↗

PubMed1993

Lymphocytic choriomeningitis virus induces a chronic wasting disease in mice lacking class I major histocompatibility complex glycoproteins.

Lymphocytic choriomeningitis virus (LCMV) induces a chronic, wasting syndrome when injected intracerebrally into H-2b mice homozygous for a beta 2-microglobulin (beta 2-m (-/-)) gene disruption. These mice have very few CD8+ T cells and express little class I MHC glycoprotein, though minimal levels of the H-2Db molecule have been detected on in vitro cultured beta 2-m (-/-) cells. The underlying immunopathological process in these beta 2-m (-/-) mice is mediated by virus immune CD4+ effectors. However, adoptively transferred CD8+ T cells from normal, LCMV-infected H-2Db compatible donors induce significant (but low level) meningitis in beta 2-m (-/-) recipients. Such mice develop neither the neurological disease characteristic of LCM nor the persistent, though generally non-fatal, debility that occurs when only the CD4+ T cell subset is involved.

Animals↗

PubMed1993

Pregnancy in women with end-stage renal disease: treatment of anemia and premature labor.

There is little experience with the use of various therapies in the end-stage renal disease patient who becomes pregnant. Erythropoietin for the treatment of anemia has become part of the standard treatment regimen of dialysis patients, but experience with its use in pregnancy is limited. We report five cases of its use in dialysis patients during pregnancy. We found no evidence that it crossed the placenta or that it made blood pressure control more difficult. We found that patients required a higher dose of erythropoietin to maintain hematocrit levels than they had before pregnancy. Another therapy involves the treatment for premature labor, which is the most common cause of pregnancy loss in dialysis patients. Two of our patients were successfully treated with indomethacin for premature labor. Both drugs are useful tools in the management of pregnant dialysis patients.

Abnormalities, Drug-Induced↗

PubMed1993

Divergence between cytotoxic effector function and tumor necrosis factor alpha production for inflammatory CD4+ T cells from mice with Sendai virus pneumonia.

Sendai virus pneumonia in beta 2-microglobulin-deficient [beta 2-m(-/-)] mice lacking CD8+ T cells is characterized by the development of CD4+ cytotoxic T lymphocytes that can be recovered directly from the respiratory tract. These CD4+ cytotoxic T lymphocytes are not found in beta 2-m (+/+) mice, though inflammatory CD4+ T cells from both beta 2-m (-/-) and beta 2-m (+/+) mice produce substantial amounts of tumor necrosis factor alpha. Blocking experiments with a monoclonal antibody that also inhibits tumor necrosis factor beta show that the secreted forms of these two cytokines are not responsible for virus-specific killing of class II major histocompatibility complex-compatible targets. Comparison of electron micrographs indicates that the CD4+ effectors from the beta 2-m (-/-) mice are potent inducers of apoptosis, while this is not the case for the beta 2-m (+/+) CD4+ set. These experiments further define the functional status of virus-specific CD4+ T cells responding in vivo in the presence or absence of CD8+ effectors.

Animals↗

PubMed1993

Pregnancy and birth control in CAPD patients.

This report summarizes the experience with 17 pregnancies in 16 continuous ambulatory peritoneal dialysis (CAPD) patients. Early experience suggests that the outcome of pregnancy in CAPD patients may be better than in hemodialysis patients. Catheter placement can be undertaken during pregnancy with little increased risk. Peritonitis can precipitate premature labor. Blood-tinged dialysate may herald serious obstetric problems. Hypertension, anemia, and prematurity are serious problems in CAPD patients. Cesarean section can be done, with only a brief interruption in CAPD. The major modification of the usual regimen is the need for smaller exchange volumes and increased frequency.

Birth Weight↗

PubMed1993

[An observation of the anticarcinogenic effect of mitoxantrone-polybutylcyanoacrylate-nanosperes].

This paper reports the result of an experiment on the anticarcinogenic effect of liver targeted drug delivery system-mitoxantrone-polybutylcyanoacrylate-nanospheres (DHAQ-PBCA-NS) by using a model of heterotopic and orthotopic transplantation of human hepatocellular carcinoma (HCC) in nude mice. No significant difference was noted between the anti-HCC effects of mitoxantrone and dexerubicin, but the anti-orthotopic transplanting HCC effect of mitoxantrone-nanospheres was obviously higher than that of mitoxantrone and dexerubicin by comparison of tumor inhibition rates and proliferating cell nuclear antigen (PCNA). The result showed the applicability of mitoxantrone-nanospheres.

Animals↗

PubMed1993

[Determination of apparent pharmacokinetic parameters of shengfu injection by acute mortality of mice].

Apparent pharmacokinetic parameters of Shengfu injection, a first-aid traditional Chinese medicine, were determined by acute mortality of animals. The results suggested that the pharmacokinetics of Shengfu injection accords with the two compartment open model, and t1/2 alpha = 0.063h, t1/2 beta = 2.70h. The process of distribution was quite rapid, and the process of elimination was slow.

Animals↗

PubMed1993

[A model of orthotopic transplantation of human hepatoma established in nude mice tumor inhibition studies].

We established a model of orthotopic transplantation of human hepato-carcinoma. The tissues from human hepatoma LTNM4 were surgically implanted into the livers of 32 BALB/c nu/nu nude mice. These led to the development of tum or masses in the livers of 31 nude mice; the rate of success was about 96.8% (31/32). Furthermore, this model was applied to the studies on the tumor inhibitory action of DHAQ-PBCA-NS, a hepatic targeting preparation for anticarcinoma. Satisfactory effect was attained. The result has proved the applicability of this animal model to researches on hepatic targeting preparations against carcinoma.

Animals↗

PubMed1992

Delayed clearance of Sendai virus in mice lacking class I MHC-restricted CD8+ T cells.

The role and interdependence of CD8+ and CD4+ alpha beta-T cells in the acute response after respiratory infection with the murine parainfluenza type 1 virus, Sendai virus, has been analyzed for H-2b mice. Enrichment of CD8+ virus-specific CTL effectors in the lungs of immunologically intact C57BL/6 animals coincided with the clearance of the virus from this site by day 10 after infection. Removal of the CD4+ T cells by in vivo mAb treatment did not affect appreciably either the recruitment of CD8+ T cells to the infected lung, or their development into virus-specific cytotoxic effectors. In contrast, depletion of the CD8+ subset delayed virus clearance, although most mice survived the infection. Transgenic H-2b F3 mice homozygous (-/-) for a beta 2 microglobulin (beta 2-m) gene disruption, which lack both class I MHC glycoproteins and mature CD8+ alpha beta-T cells, showed a comparable, delayed clearance of Sendai virus from the lung. Virus-specific, class II MHC-restricted CTL were demonstrated in both freshly isolated bronchoalveolar lavage populations and cultured lymph node and spleen tissue from the beta 2-m (-/-) transgenics. Treatment of the beta 2-m (-/-) mice with the mAb to CD4 led to delayed virus clearance and death, which was also the case for normal mice that were depleted simultaneously of the CD4+ and CD8+ subsets. These results indicate that, although classical class I MHC-restricted CD8+ cytotoxic T cells normally play a dominant role in the recovery of mice acutely infected with Sendai virus, alternative mechanisms involving CD4+ T cells exist and can compensate, in time, for the loss of CD8+ T cell function.

Animals↗