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Biomedical subjects

S Yan

Publications and source records attributed to S Yan.

At least 109 records · Page 6Linked to original sources
PubMed1996

[Confirming the cause of inherited chronic chorea in Chinese patients].

OBJECTIVE: Huntington's disease (HD, known as inherited chronic chorea in China) is an autosomal dominant disorder. Almost all of the cases of inherited chronic chorea reported in the chinese literature were sporadic while about one-third of the HD families in foreign reports were related. To find out whether the gene defect responsible for inherited chronic chorea in Chinese is the same as that for Huntington's disease in Caucasians. METHOD: PCR method was employed to amplify the (CAG)n repeat sequence of the IT15 gene in normal Chinese and members of the families suffering from inherited chronic chorea in Chinese. RESULTS: The copy number of the repeats varied from 16 to 26 in 25 normal Chinese and increased significantly from 44 to 53 in 7 affected members from 4 families. CONCLUSION: It was confirmed for the first time at the gene level that the mechanism for inherited chronic chorea in Chinese is the same as that for Huntington's disease in Caucasians.

Adult↗
PubMed1996

[Function of the diaphragm during exercise].

We examined the control of respiratory muscles with emphasis on the diaphragm during exercise at 30%, 60% and 90% of maximal working capacity in normal subjects. Control of the diaphragm was quantified by plotting transdiaphragmatic pressure (Pdi), its electromyographic activity (Edi) and its power (Wdi = Pdi x Dab/Ti) vs. workload and Pdi, an index of shortening velocity of diaphragmatic fibres (Dab/Ti) and Wdi vs. Edi. We observed that increase in Pdi (approximately 2-fold) from rest to heavy exercise was inadequately small comparing to increases in minute ventilation (approximately 9-fold) and Edi (approximately 4.5-fold). We hypothesized and confirmed that Wdi might increase even though Pdi decreased due to increasing Dab/Ti and expresses more closely diaphragmatic contribution to inspiratory effort during exercise than Pdi. Significantly augmented shortening velocity of the diaphragm suggests that it acts predominantly as a flow generator during exercise. It is strongly assisted in this task by abdominal muscles. The responsibility for generating inspiratory pressures falls on the inspiratory rib cage muscles. This arrangement may however impair diaphragm's performance even in healthy subjects as indicated by reduced Pdi twitch after exercise.

Adult↗
PubMed1996

[Effect of respiratory muscle fatigue on their function during exercise].

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30%, 60%, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Respiratory pressures, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. The respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.

Abdominal Muscles↗
PubMed1996

[Changes in intracellular K+ concentration and ATPase activity of myocardiocytes in early stage of burn injury].

In this experiment, intracellular K+ concentration ([K+]i) and ATPase activity of myocardiocytes were measured in early stage of burn injury. Comparing with control group, it was found that, 1. [K+]i were decreased after burn injury, [K+]i of 1st, 3rd, 8th and 24th hours were decreased to 96.2 +/- 1.3%, 85.8 +/- 1.3%, 65.9 +/- 1.0% and 73.7 +/- 1.1% of normal, respectively. 2. Cardiac sarcolemma total ATPase, Mg(2+)-ATPase and Na(+)-K(+)-ATPase activities were all reduced significantly at 8th hour after injury. These results suggest that, burn injury accelerates K+ efflux current, but inhibits K+ influx current, and the reduction of Na(+)-K(+)-ATPase activity is one reason of decrease of [K+]i after injury.

Animals↗
PubMed1996

[Effects of intermittent short-course chemotherapy under full-course supervision on the treatment of smear positive pulmonary tuberculosis].

OBJECTIVE: To evaluate the effects of intermittent short-course chemotherapy under full-course supervision on the treatment of smear positive pulmonary tuberculosis. METHOD: The regimens of 2H3R3Z3S3(E3)/4H3R3 and 2H3R3Z3S3E3/6H3R3E3 were respectively used in 125 initial and 249 relapse smear positive pulmonary tuberculosis cases under full-course supervision and management. RESULTS: The total rate of treatment completion was 99.7%, and the rates of sputum negative conversion in initial and relapse cases were 96.7% and 84.8% respectively. During three-year follow-up, the bacteriological relapse rates were found to be 1.8% in initial cases and 10.2% in relapse cases. CONCLUSIONS: The regimen was proved to be convenient, economical and effective in tuberculosis control programme.

Antitubercular Agents↗
PubMed1995

Met-enkephalin-like immunoreactivity in microdialysates from nucleus tractus solitarii in piglets during normoxia and hypoxia.

Met-enkephalin-like immunoreactivity in microdialysates from the respiratory-related nucleus tractus solitarii was determined simultaneously with ventilatory responses in seven, spontaneously breathing, developing swine under conditions of normoxia, hypoxia and recovery from hypoxia for 30 min each. Assayed levels of Met-enkephalin-like immunoreactivity in normoxia were 0.89 +/- 0.23 pg/microliters. These levels increased to 203.6 +/- 32.2% and 283.1 +/- 55.8% of control during hypoxia and recovery, respectively. Hyperventilation during hypoxia was not sustained, comprising brief stimulation followed by return to near-control level. Taken together, these results provide further evidence that opioid release may contribute to the suppression of ventilation in hypoxia during development.

Animals↗
PubMed1995

Transforming growth factor beta-induced activation of cyclin E-cdk2 kinase and down-regulation of p27Kip1 in C3H 10T1/2 mouse fibroblasts.

Transforming growth factor (TGF-beta)-stimulated induction of DNA synthesis is preceded by the activation of cyclin E/cyclin-dependent kinase (cdk)2 kinase in late G1 in C3H 10T1/2 mouse fibroblasts. TGF-beta has no effect on the steady-state level of cdk4, while having only a modest inductive effect on cyclin D1 expression. TGF-beta stimulation does, however, lead to the striking down-regulation of p27Kip1 expression during G1 in a manner consistent with the timing of cyclin E-cdk2 activation. Coimmunoprecipitation analysis reveals that the amount of p27Kip1 in complexes with the cdk2 catalytic subunit is drastically reduced at the time in late G1 when cyclin E-cdk2 activity is maximal. These data indicate that cyclin E-cdk2 is inhibited by p27Kip1 in the growth-arrested state and that TGF-beta relieves this inhibition by down-regulating the steady-state level of the p27Kip1 inhibitor protein, thus reducing the level of inhibitor present in complexes with cdk2.

Animals↗
PubMed1995

Malignant and normal T cells show random use of T-cell receptor alpha chain variable regions in patients with cutaneous T-cell lymphoma.

Cutaneous T-cell lymphoma (CTCL) is a malignancy of mature T lymphocytes, most of which express alpha/beta type T-cell receptors (TCRs). The cause of CTCL is unknown, but hypotheses postulating chronic stimulation of TCRs by superantigen or by a leukemogenic virus have been proposed. Either mechanism might produce bias in the TCR variable (V) region types used by the malignant cells. To determine if TCR alpha use is restricted in CTCL, we used reverse transcription and the polymerase chain reaction to determine V alpha and V beta usage by malignant cells purified from the peripheral blood of leukemic patients with CTCL. Usage of alpha chain V region segments appeared totally random; malignant lymphocytes isolated from each of six patients used different V alpha regions. As has been previously reported, no bias was found in beta chain V region usage either. In addition to productive (in frame) TCR V region mRNAs in malignant cells from each patient, we detected non-productive (out of frame) beta chain transcripts in these cells in two of six patients, and non-productive alpha chain transcripts in five of six. Residual normal peripheral blood lymphocytes from these patients showed a random, polyclonal or oligoclonal pattern of V region usage. We conclude that there is no bias in V region usage in CTCL, making it unlikely that interactions between superantigen or virus and the TCR V regions play a role in the pathogenesis of CTCL.

Aged↗
PubMed1995

Microdialyzed adenosine in nucleus tractus solitarii and ventilatory response to hypoxia in piglets.

Levels of adenosine, inosine, and hypoxanthine from the interstitial space at the nucleus tractus solitarii were measured by microdialysis in eight 20- to 25-day-old anesthetized spontaneously breathing piglets. Microdialyzed samples were collected every 30 min for 2 h after the insertion of the probe to ensure stability of purine levels and then during 30 min each of normoxia, hypoxia (10% O2-90% N2), and normoxia. The purines were separated by high-pressure liquid chromatography with ultraviolet detection and quantified at 254-nm wavelength. Tidal volume, breathing frequency, minute ventilation, mean arterial blood pressure, pH, and gas tensions were measured. Compared with control, adenosine levels during hypoxia increased by 40.7 +/- 5.5% and then tended to decline during the recovery from hypoxia, but the levels remained higher than in control. Ventilatory measures exhibited a modest biphasic pattern during hypoxia and resumed control values by 10 min after the removal of the hypoxia. The increased adenosine release during hypoxia provides additional evidence for the possible participation of adenosine in the central suppression of breathing during hypoxia.

Adenosine↗
PubMed1995

Effects of fatigue, fiber length, and aminophylline on human diaphragm contractility.

The clinical relevance of methylxanthines as therapeutic agents for improving diaphragmatic contractility is controversial. In a double-blind, placebo-controlled trial, we investigated the effect of aminophylline on the contractility of fresh and fatigued human diaphragm at different lung volumes, and therefore as a function of fiber length. The diaphragmatic contractility of normal subjects was assessed by measurements of transdiaphragmatic pressure changes (Pdi,T) in response to single, bilateral, supramaximal phrenic-nerve shocks during relaxation from total lung capacity (TLC) to functional residual capacity (FRC). Fatigue was induced by resistive breathing. Therapeutic levels of theophylline were reached in all subjects. Under fresh (i.e., nonfatigue) conditions, aminophylline significantly increased Pdi,T at lung volumes above 75% of the inspiratory capacity (IC). Fatigue in the absence of aminophylline caused a disproportionately greater reduction of Pdi,T at high than at low lung volume (J. Appl. Physiol. 1992; 72:1064), which was rapidly reversible with rest. With aminophylline, the disproportionate decrease in diaphragmatic contractility at short fiber lengths was not observed. Aminophylline potentiates diaphragmatic contractility to a proportionately greater extent at short than at long fiber lengths, under both fresh and fatigued conditions. We explain these findings by known effects of muscle shortening, fatigue, and methylxanthines on excitation-contraction coupling mechanisms.

Adult↗
PubMed1995

[Study on Bian Que's tomb and temple].

The historical archives and records and the existed Bian Que's tombs and temples in over a dozen of locations, including Hebei, Shandong, Henan, Shanxi, have aroused controversies as to which is the authentic one. So far, no conclusion can be drawn. By combining the burial and offering customs and rituals at the end of Spring-Autumn period, analyses are made on Bian Que's tombs, temples, former residence, Bian Que Village, Bian Que town, historical remains of Prince Guo and legends on location of Bian Que's activity for making immortal pills etc., it is claimed by the authors that, besides a few places related to Bian Que's life, all the others are tombs and temples built by local people where Bian Que's visited for his memory, and his merits, reflecting the historical facts about Bian Que's activities. All these historical and cultural remains are precious evidences for the historic appraisal of Bian Que by modern scholars.

China↗
PubMed1995

Abrupt reduction of c-myc expression by antisense RNA inducing terminal differentiation and apoptosis of a human esophageal cancer cell line.

A human esophageal cancer cell line (EC8712) expressing high-level Myc protein was infected with recombinant retroviral particles (pA-BD9) at a multiplicity of infection (MOI) 1:1. This viral particle contains a neomycin-resistant gene and a 1.53-kb antisense RNA spanning the 2nd exon and its flanking sequences of the human c-myc oncogene. The G418-resistant EC8712 clones showed an 86% inhibition of growth rate and morphological changes characteristic of terminal differentiation and apoptosis. A decrease of about 80% of Myc protein was also observed in these infected cells by ABC-ELISA assay. 12-24 h after the infection of EC8712 cells with pA-BD9 at a high viral particle concentration (MOI = 1:10), the integration of the extrinsic 1.53-kb antisense c-myc fragment into the cancer cell genome was evidenced by the Southern blot analysis. Northern blot analyses showed the expression of this antisense fragment and a decrease of the intrinsic c-myc expression by 74% in comparison with that of the parental EC8712 cells. Heterotransplants of the infected EC8712 cells into the nude mice revealed a substantial decrease in tumorigenicity and morphological changes characteristic of terminal differentiation and apoptosis. Primary monolayer cell cultures of normal epithelia derived from the fetal and adult esophagus mucosa were set as controls. No noticeable increase in c-myc expression was found in these cultures. Infection of these cells with the same recombinant viral particles neither affected the growth rate of the cells nor their normal morphology. Our experiments indicate that the drastic decrease of the over-expressed Myc protein in cancer cells may also be an entrance to one of many pathways leading to the terminal differentiation and programmed cell death.

Animals↗
PubMed1995

[Effects of nitroglycerin, prostaglandin E1, trimetaphan and nicardipine on systemic vascular resistance, pulmonary vascular resistance and pulmonary-systemic vascular resistance ratio in dogs].

Effects of the experimentally induced hypotension with 4 vasodilators; nitroglycerin (TNG), prostaglandin E1 (PGE1), trimetaphan (TMP) and nicardipine (NCP) on systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and pulmonary-systemic vascular resistance ratio (PVR/SVR ratio) were studied in dogs. The SVR values were significantly reduced by TNG, PGE1 and NCP, and not affected by TMP. The PVR values were significantly reduced by TNG and PGE1, and not affected by TMP and NCP. The PVR/SVR ratio values were significantly reduced by TNG, and significantly increased by NCP, and not affected by PGE1 and TMP. We concluded that TNG reduced PVR and SVR but it affected PVR more; PGE1 reduced PVR and SVR equivalently; TMP did not affect PVR and SVR remarkably; NCP reduced SVR but did not affect PVR.

Alprostadil↗
PubMed1994

Persistent acylation of high-molecular-weight penicillin-binding proteins by penicillin induces the postantibiotic effect in Streptococcus pyogenes.

Penicillin at 10X MIC induced a postantibiotic effect (PAE) of 2.1 h in Streptococcus pyogenes. Progressive increases in the densities of penicillin-binding proteins (PBPs) 1-3 of the bacterium were detected at 30, 60, and 90 min during the postantibiotic phase. The increase in colony-forming units during this phase paralleled the kinetics of incorporation of lysine into proteins, suggesting that growth was triggered by de novo synthesis of PBPs. The question was raised as to whether the progressive increases in densities of PBPs were due to the restoration of preexisting PBPs or to synthesis of new PBPs. With 10X MIC of clindamycin to inhibit PBP synthesis during the postantibiotic phase, the temporal increase in densities of PBPs 1-3 were totally inhibited. These results suggest that the PAE of penicillin in S. pyogenes is caused by irreversible binding of penicillin to PBPs 1-3 and represents the time necessary for synthesis of new PBPs required for normal growth.

Acylation↗
PubMed1993

The in vitro antibacterial activity of ceftriaxone against Streptococcus pyogenes is unrelated to penicillin-binding protein 4.

The in vitro activities of penicillin and ceftriaxone were compared against 29 strains of Streptococcus pyogenes with the result that ceftriaxone showed greater activity than penicillin. The morphological changes induced by 1/2 and 1x MIC concentrations of penicillin and ceftriaxone, respectively, were very similar using scanning electron microscopy. Competitive binding studies using 'cold' penicillin or ceftriaxone as inhibitors of radiolabeled penicillin binding demonstrated that ceftriaxone had a very low affinity for penicillin binding protein (PBP) 4 compared to that of penicillin. Since ceftriaxone had greater antibacterial activity, this suggests that PBP 4 may not be important to the in vitro activity of ceftriaxone. In contrast, the IC50 for ceftriaxone was much lower (> 200 fold) for PBPs 2 and 3 compared to PBP 4, suggesting greater avidity of these high molecular mass PBPs for ceftriaxone. These data may at least in part explain the superior in vitro activity of ceftriaxone compared to penicillin against S. pyogenes. These data, together with the observation that PBP 1 was saturated at a lower concentration of penicillin than any of the other PBPs, suggest that the inhibition of PBPs 1, 2, and 3 mediates the bactericidal activity of beta-lactam antibiotics against group A streptococci.

Bacterial Proteins↗
PubMed1993

Penicillin-binding protein expression at different growth stages determines penicillin efficacy in vitro and in vivo: an explanation for the inoculum effect.

Mechanisms to explain the "inoculum effect" have not been elucidated in gram-positive infections. A mouse model of group A streptococcal myositis was used to compare the efficacies of two beta-lactams, penicillin and ceftriaxone, and a protein synthesis inhibitor, clindamycin, at three different inoculum sizes. beta-lactams were more susceptible to inoculum effects than was clindamycin both in vivo and in vitro (P < .05). The large inocula were hypothesized to reach stationary phase of growth sooner than smaller inocula both in vitro and in vivo. The penicillin-binding protein (PBP) patterns from membrane proteins isolated from mid-log-phase and stationary-phase cultures of Streptococcus pyogenes were compared. Binding of radiolabeled penicillin by all PBPs was decreased in stationary cells; however, PBPs 1 and 4 were undetectable at 36 h. Thus, the loss of certain PBPs during stationary-phase growth in vitro may be responsible for the inoculum effect observed in vivo and may account for the failure of penicillin in both experimental and human cases of severe streptococcal infection.

Animals↗