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Biomedical subjects

Y L Yang

Publications and source records attributed to Y L Yang.

At least 55 records · Page 3Linked to original sources

Deficient cytokine signaling in mouse embryo fibroblasts with a targeted deletion in the PKR gene: role of IRF-1 and NF-kappaB.

The interferon (IFN)-induced double-stranded RNA (dsRNA)-activated Ser/Thr protein kinase (PKR) plays a role in the antiviral and antiproliferative effects of IFN. PKR phosphorylates initiation factor eIF2alpha, thereby inhibiting protein synthesis, and also activates the transcription factor, nuclear factor-kappaB (NF-kappaB), by phosphorylating the inhibitor of NF-kappaB, IkappaB. Mice devoid of functional PKR (Pkr(o/o)) derived by targeted gene disruption exhibit a diminished response to IFN-gamma and poly(rI:rC) (pIC). In embryo fibroblasts derived from Pkr(o/o) mice, interferon regulatory factor 1 (IRF-1) or guanylate binding protein (Gbp) promoter-reporter constructs were unresponsive to IFN-gamma or pIC but response could be restored by co-transfection with PKR. The lack of responsiveness could be attributed to a diminished activation of IRF-1 and/or NF-kappaB in response to IFN-gamma or pIC. Thus, PKR acts as a signal transducer for IFN-stimulated genes dependent on the transcription factors IRF-1 and NF-kappaB.

Animals↗

Captopril reverses high glucose-induced effects on LLC-PK1 cells partly by enhancing facilitative glucose transporter messenger RNA expressions.

One of the mechanisms of angiotensin-converting enzyme inhibitors in treating diabetic nephropathy is the reversal of renal hypertrophy. Hyperglycemia is the common denominator of all diabetic states. Thus, effects of captopril on high glucose (27.5 mM)-induced alterations in LLC-PK1 cells were studied as related to the facilitative glucose transporters. We found that high glucose (27.5 mM) inhibited mitogenesis and induced hypertrophy in these cells after 48 hours of culture concomitantly with decreased glucose transporter I messenger RNA expression. Captopril (1 mM) reversed the above effects concomitantly with enhancement of glucose transporter I and II messenger RNA expressions. We conclude that decreased expression of glucose transporter I may be associated with increased intracellular glucose and the resultant ill effects. Captopril reversed the above high glucose-induced effects partly by enhancing glucose transporter I and II messenger RNA expressions.

Angiotensin-Converting Enzyme Inhibitors↗

Involvement of interleukin-1 receptor mechanisms in development of arterial hypotension in rat heatstroke.

Rats, under urethan anesthesia, were exposed to a high ambient temperature (42 degrees C) to induce heatstroke and to assess the hemodynamic changes associated with heatstroke. Compared with normothermic controls, rats with heatstroke showed higher values of colonic temperature, heart rate, and plasma levels of interleukin (IL)-1 but lower values of R wave amplitude, P-R and Q-T intervals, systolic wave amplitude, diastolic and dicrotic wave duration, mean arterial pressure, stroke volume, and cardiac output. Animals injected intravenously with an IL-1-receptor antagonist at the time of heatstroke induction were protected from some of the cardiovascular effects of heatstroke, such as depressed ventricular depolarization, decreased stroke volume, decreased cardiac output, and arterial hypotension. The hemodynamic changes associated with heatstroke could be mimicked by IL-1beta administration. Other cardiovascular parameters such as total peripheral vascular resistance were unaffected by heatstroke induction or IL-1beta treatment. The results indicate that a selective decline in stroke volume or ventricular depolarization resulting from increased plasma levels of IL-1 may be an important mechanism signaling arterial hypotension or circulatory failure in rat heatstroke.

Animals↗

Effects of high glucose culture on EGF effects and EGF receptors in the LLC-PK1 cells.

We have shown that epidermal growth factor (EGF) may be important in diabetic renal hypertrophy. Since EGF is the most potent mitogen for the proximal tubule, it may be relevant to the cellular hyperplasia component in diabetic nephropathy. In order to further clarify the possible alterations of mitogenic effects of EGF on cultured renal cells in hyperglycemic states, the effects of high glucose culture on EGF-induced events and EGF receptors were studied in LLC-PK1 cells with equimolar mannitol being used as an osmotic control. The results showed that high glucose dose-dependently decreased mitogenesis while increasing cellular hypertrophy in LLC-PK1 cells. The dose-response curve of EGF-induced mitogenesis was similar in both normal (11 mM) and high (27.5 mM) glucose cultures. Meanwhile, EGF receptor number and affinity were not changed by high glucose in these cells. Furthermore, mannitol mimicked the growth-suppressive (but not hypertrophic) effects of high glucose cultures. Based upon these findings, we conclude that high glucose did not alter the mitogenic effects of EGF on the LLC-PK1 cells. This was associated with unchanged EGF receptor characteristics. Thus, concurrent with our previous studies, we speculate that it is the increased local EGF level, rather than an increased renal sensitivity to it, which is associated with hyperglycemic tubulopathy.

Animals↗

[The experience and adaptative behaviors of the infertile women who were suffering from in vitro fertilization failure].

The purposes of this study were to explore the women's experience and adaptative behaviors when they suffered from in vitro fertilization failure. Under a survey designed using purposive sampling, 30 IVF fertilization failure women were recrutied. A semi-structured interview guide was developed for data collection. When the subjects were informed for the IVF fertilization failure, they were interviewed and data were collected. All data were translated in a narrative form and analyzed by content analysis. The results showed there were four types of experience and each of them had different adaptative behaviors: (A) They were disappointed and confused to the fertilization failure; they coped by accepting the fate, decreasing the expectation, looking for the failing factors, and looking for the successful factors. (B) They felt painful during the treatment course; they coped by reviewing the treatment course, having a rest, doing something that they had delayed, and planning to go ahead. (C) They felt unfair to the outcome of the effort; they coped by blaming the fate, wanting to change the mode of treatment, or by refusing to accept the treatment again. (D) They did not know what to do next; they coped by avoiding the fact or searching for more consultation. The findings can be used to establish a nursing care standard for the IVF fertilization failure women. Accordingly, the nurses can help the infertile women to recover from their grief and restitute a positive prospect of their future lives.

Adaptation, Psychological↗

Long polymerase chain reaction amplification of heterogeneous HIV type 1 templates produces recombination at a relatively high frequency.

Studies of HIV molecular evolution and pathogenesis have relied on the polymerase chain reaction (PCR) to provide sequence information from infected tissues. Until recently, studies have been constrained by the limited length of fragments that can be reliably amplified. The addition of a thermostable 3'-exonuclease activity and altered cycling profiles has increased the length of target sequences that can be amplified by more than 10-fold. We have evaluated the fidelity of long PCR (LPCR). We determined that LPCR amplification maintains the distribution of sequences found in a heterogeneous sample and introduces nucleotide misincorporations at a rate comparable to that found with routine PCR. However, a significant proportion of the LPCR-amplified DNA fragments resulted from recombination events. This result suggests that LPCR amplification may have limited utility in the production and analysis of full-length HIV clones.

Base Sequence↗

In vivo sequence diversity of the protease of human immunodeficiency virus type 1: presence of protease inhibitor-resistant variants in untreated subjects.

We have evaluated the sequence diversity of the protease human immunodeficiency virus type 1 in vivo. Our analysis of 246 protease coding domain sequences obtained from 12 subjects indicates that amino acid substitutions predicted to give rise to protease inhibitor resistance may be present in patients who have not received protease inhibitors. In addition, we demonstrated that amino acid residues directly involved in enzyme-substrate interactions may be varied in infected individuals. Several of these substitutions occurred in combination either more or less frequently than would be expected if their appearance was independent, suggesting that one substitution may compensate for the effects of another. Taken together, our analysis indicates that the human immunodeficiency virus type 1 protease has flexibility sufficient to vary critical subsites in vivo, thereby retaining enzyme function and viral pathogenicity.

Amino Acid Sequence↗

Conditional human immunodeficiency virus type 1 protease mutants show no role for the viral protease early in virus replication.

The human immunodeficiency virus type 1 protease plays a critical role in the proteolytic processing of precursor polyproteins during virion maturation. Contradictory evidence has been obtained for a possible role for the protease early after infection, i.e., during DNA synthesis and/or integration. We have reexamined this question by using conditional mutants of the protease. In one set of experiments, protease mutants that confer a temperature-sensitive phenotype for processing were used to assess the need for protease activity early after infection. No significant difference from results with wild-type virus was seen when infections were carried out at either 35 or 40 degrees C. In a separate set of experiments, infections were carried out in the presence of a protease inhibitor. In this case, both wild-type virus and a drug-resistant variant were used, the latter as a control to ensure a specific effect of the inhibitor. Infection with either virus was not inhibited at drug concentrations that were up to 10-fold higher than those needed to inhibit intracellular processing by the viral protease. The results obtained by both of these experimental protocols provide evidence that the human immunodeficiency virus type 1 protease does not play a role early after infection.

Cell Line↗

Captopril reverses high-glucose-induced growth effects on LLC-PK1 cells partly by decreasing transforming growth factor-beta receptor protein expressions.

Transforming growth factor beta (TGF-beta) may be important in the pathogenesis of diabetic nephropathy, and captopril is effective in treating this disorder. However, the mechanisms of this therapeutic effect as related to TGF-beta and its receptors are not known. Thus, the effects of captopril on cellular growth, TGF-beta 1, and TGF-beta receptors were studied in LLC-PK1 cells cultured in normal (11 mM) or high glucose (27.5 mM). This study found that glucose dose-dependently inhibited cellular mitogenesis while inducing hypertrophy in these cells at 72 h of culture, concomitantly with enhanced TGF-beta 1 messenger RNA (mRNA) and TGF-beta receptor Types I and II protein expressions. Captopril dose-dependently (0.1 to 10 mM) increased cellular mitogenesis and inhibited hypertrophy in these cells. Moreover, captopril also decreased TGF-beta receptor Types I and II protein expressions dose-dependently. However, TGF-beta 1 mRNA was not affected by captopril. It was concluded that high glucose decreased cellular mitogenesis while increasing hypertrophy concomitantly with increased TGF-beta 1 mRNA and TGF-beta receptors in LLC-PK1 cells. Captopril can reverse high-glucose-induced growth effects by decreasing TGF-beta receptor protein expressions.

Angiotensin-Converting Enzyme Inhibitors↗

[The effect of air purification on 10,000 degree clean room in supply rooms].

This article introduced that purifying equipments were installed in the major operating departments of supply rooms in hospital, and that experimental tests were done on the packing department. In statil state, the air humidity and the number of bacteria in the room after purification was obviously lower than that before purification (P < 0.01). In trending conditions, the main technical index on 10,000 degree clean rooms were examined, all of the results were up to the national standards.

Air Microbiology↗

Deficient signaling in mice devoid of double-stranded RNA-dependent protein kinase.

Double-stranded RNA-dependent protein kinase (PKR) has been implicated in interferon (IFN) induction, antiviral response and tumor suppression. We have generated mice devoid of functional PKR (Pkr%). Although the mice are physically normal and the induction of type I IFN genes by poly(I).poly(C) (pIC) and virus is unimpaired, the antiviral response induced by IFN-gamma and pIC was diminished. However, in embryo fibroblasts from Pkr knockout mice, the induction of type I IFN as well as the activation of NF-kappa B by pIC, were strongly impaired but restored by priming with IFN. Thus, PKR is not directly essential for responses to pIC, and a pIC-responsive system independent of PKR is induced by IFN. No evidence of the tumor suppressor activity of PKR was demonstrated.

Animals↗

A new lunch box-type method in umbilical reconstruction.

A simple and easy technique for reconstruction of the umbilicus was devised, with emphasis on forming walls of the umbilicus and a depression in a caudal direction. A quite satisfactory result was obtained. A permanent and sufficient depression for the umbilicus can be expected as a result of three-dimensional formation of walls.

Abdominal Neoplasms↗

Interactions among deprenyl, clorgyline and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on catecholamines in mice.

The interactive effects of clorgyline, deprenyl and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on striatal dopamine (DA), serotonin (5HT) and hippocampal norepinephrine (NE) were examined in the present study. Results indicated that clorgyline did not have a preventive effect against MPTP's toxicity on DA and NE, but it had a partial therapeutic effect against subchronic MPTP-induced DA depletion when given with deprenyl together. However, this effect was not significantly different from the effect of deprenyl alone. Co-administration of clorgyline and deprenyl had a satisfactory effect in preventing MPTP-induced NE depletion. On the other hand, in all clorgyline-treated groups, there was a significant increase of 5HT in both the striatum and the hippocampus.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

[The effect of microinjection of AVP and AVP-antiserum into septal area on discharge activity of temperature-sensitive neurons in PO-AH of rabbits].

Arginine vasopress in (AVP) has been shown to have significant effects on thermoregulation. AVP-sensitive locus is located in the septal area of the limbic system. The present experiments were undertaken to investigate the effect of microinjecting AVP and AVP-antiserum into the septal area on the firing activity of temperature-sensitive neurons in preoptic-anterior hypothalamus (PO-AH) of rabbit. The results were as follows: (1) The firing rate of PO-AH warm-sensitive and cold-sensitive neurons were respectively increased and decreased by injection of AVP while that of temperature-insensitive neurons was unaffected. (2) Injection of AVP-antiserum decreased the firing rate of PO-AH warm-sensitive neurons but increased the firing rate of cold-sensitive neurons. (3) Injection of AVP increased the thermosensitivity of PO-AH warm-sensitive neurons and decreased the thermosensitivity of cold-sensitive neurons. The modulation action of AVP on PO-AH temperature-sensitive neurons was discussed.

Animals↗

Suppression of ColE1 high-copy-number mutants by mutations in the polA gene of Escherichia coli.

We isolated three Escherichia coli suppressor strains that reduce the copy number of a mutant ColE1 high-copy-number plasmid. These mutations lower the copy number of the mutant plasmid in vivo up to 15-fold; the wild-type plasmid copy number is reduced by two- to threefold. The suppressor strains do not affect the copy numbers of non-ColE1-type plasmids tested, suggesting that their effects are specific for ColE1-type plasmids. Two of the suppressor strains show ColE1 allele-specific suppression; i.e., certain plasmid copy number mutations are suppressed more efficiently than others, suggesting specificity in the interaction between the suppressor gene product and plasmid replication component(s). All of the mutations were genetically mapped to the chromosomal polA gene, which encodes DNA polymerase I. The suppressor mutational changes were identified by DNA sequencing and found to alter single nucleotides in the region encoding the Klenow fragment of DNA polymerase I. Two mutations map in the DNA-binding cleft of the polymerase region and are suggested to affect specific interactions of the enzyme with the replication primer RNA encoded by the plasmid. The third suppressor alters a residue in the 3'-5' exonuclease domain of the enzyme. Implications for the interaction of DNA polymerase I with the ColE1 primer RNA are discussed.

Amino Acid Sequence↗

Polymorphonuclear neutrophil chemotaxis in Chinese patients with post-juvenile periodontitis and rapidly progressive periodontitis.

The purpose of this study was to investigate polymorphonuclear neutrophil (PMN) chemotaxis in Chinese patients with post-juvenile periodontitis (post-JP) and rapidly progressive periodontitis (RPP). Peripheral blood PMNs were isolated from nine post-JP and 13 RPP patients. Eight patients with adult periodontitis (AP) and seven clinically healthy subjects were used for comparison. Clinical data, including the plaque index and gingival index, of each subject were recorded. The "modified Boyden chamber technique" was used for PMN chemotaxis assay. Our results showed that the PMN chemotaxis index in patients with post-JP and RPP were significantly depressed compared to that in healthy subjects or patients with AP. There was no significant difference in PMN chemotaxis between post-JP and RPP, or between AP and healthy subjects. There was also no significant correlation between the plaque index, or gingival index, and PMN chemotaxis in any group. These results suggest that there is a PMN chemotaxis defect in most Chinese patients affected by post-JP or RPP, and that the PMN chemotaxis defect is not associated with clinical parameters such as the plaque index or gingival index.

Adult↗