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T Yang

Publications and source records attributed to T Yang.

At least 217 records · Page 12Linked to original sources

SA gene expression in the proximal tubule of normotensive and hypertensive rats.

Previous studies have shown that the SA gene is expressed at higher levels in the kidney of genetically hypertensive rats than in control strains and that in hybrid crosses of genetically hypertensive rats and normotensive controls, markers in or close to the SA gene cosegregate with blood pressure. The present studies examine the localization of the SA gene product in the kidney by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). cDNA was prepared from microdissected nephron segments from Sprague-Dawley (SD) rats, spontaneously hypertensive rats (SHRs), and Wistar-Kyoto (WKY) rats, and RT-PCR was performed using specific primers. In all three strains, SA gene mRNA was found to be abundantly expressed in proximal tubules. SA PCR product was occasionally detected at approximately 100-fold lower abundance in glomeruli, while no signal was obtained from the collecting duct, thick ascending limb of the loop of Henle, or arcuate artery. Within the proximal tubule of normotensive rats, distribution of SA mRNA was found to be strain dependent: in SD rats it was expressed at high levels in the proximal convoluted tubule, whereas in WKY rats it was restricted to the proximal straight tubule. In SHRs, SA PCR product was detected along the entire proximal tubule. Induction of hypertension by renal artery clamping (two-kidney, one-clamp Goldblatt model) did not alter the pattern of expression observed in the SD rat. These results indicate that an extension of SA gene expression to the full length of the proximal tubule accompanies spontaneous hypertension and that in nonhypertensive animals the pattern of gene product expression is more restricted but shows substantial strain variability.

Animals↗

Regulation of endothelin production and secretion in cultured collecting duct cells by endogenous transforming growth factor-beta.

Confluent cultures of two renal collecting duct cell lines (M-1 and mIMCD-K2 cells derived from cortical and inner medullary collecting ducts, respectively) express endothelin1 (ET1), transforming growth factor-beta (TGF beta; both TGF beta 1 and TGF beta 2), and both types of the TGF beta receptor. Experiments were performed to test whether endogenous TGF beta may be a paracrine modulator of ET1 expression in these cells. Treatment of M-1 and mIMCD-K2 cells with TGF beta 2 antisense oligodeoxynucleotides (ODN) significantly reduced ET1 messenger RNA (mRNA) and ET secretion (as well as TGF beta 2 mRNA) in a concentration-dependent manner, whereas control ODN were without significant effects. To produce ET inhibition, antisense ODN had to be present in the basolateral medium, whereas its sole presence in the apical medium was without effect. In addition, a pan-specific TGF beta antibody caused a significant reduction of ET1 mRNA expression and ET1 secretion. M-1 cells were found to express high levels of the mRNA for plasminogen activator of both tissue and urokinase types. Addition of the nonspecific serine protease inhibitor aprotinin (50 micrograms/ml) to the medium for 24 h significantly reduced the secretion of ET1. These results suggest that secretion of endogenous TGF beta, at least in part activated by the plasminogen/plasmin system, participates in the regulation of ET1 synthesis and secretion by collecting duct cell lines.

Animals↗

[Detection of the mutational gene in phenylketonuria and prenatal diagnoses by using single strand conformation polymorphism methods].

OBJECTIVE: To establish rapid methods for the detection of gene mutations and prenatal diagnosis of phenylketonuria (PKU). METHODS: The single strand conformation polymorphism (SSCP) combined with silver staining technique were used to screen the mutations in the four exons of phenylalanine hydroxylase (PAH) gene. After the polymerase chain reaction, the DNA fragments were separated by electrophoresis on polyacrylamide gel containing glycerol and visualized by silver staining. RESULTS: Three known missense mutations which are R243Q (E7)[CGA(Arg243)-->CAA (Gln)], R413P(E12) [CGC(Arg413)-->CCC(Pro)] and Y356X(E11)[TAC(Tyr156)-->TAA(Ter)] were detected in 21 degrees C, 28 degrees C and 7 degrees C. Three kinds of unknown abnormal DNA bands in exon 10 were detected in 21 degrees C. The mutations of 13 PKU families have been detected. Prenatal gene diagnoses were successfully performed in 5 pregnancies at risk with PKU. CONCLUSION: The method is very useful for detecting the mutations and prenatal diagnoses of PKU families.

Exons↗

[CT scanning and treatment of intracranial tuberculoma].

OBJECTIVE: To evaluate the value of CT scanning and the efficacy of anti-tuberculosis short-course chemotherapy in intracranial tuberculoma patients. METHOD: The CT manifestations and the clinical characteristics of 55 intracranial tuberculoma patients were analysed. RESULTS: 44 out of 55 patients were cured. Among them, 40 patients' lesions were entirely resolved, while other 11 cases, clinical symptoms were subsided and still under treatment. In the contrast enhancing CT scanning, plate shaped or ring-form shadows were shown surrounding the lesions of tuberculoma. The characteristical features were more special for diagnosis and the positive rate was higher than that of other laboratory findings. The incidence of intracranial tuberculoma was found to be higher in children and juvenile patients who lived in rural areas. CONCLUSIONS: Enhancing CT scanning is valuable for diagnosis of intracranial tuberculoma. The anti-tuberculosis short-course chemotherapy used nowadays with which almost all the intracranial tuberculoma patients can be cured and only few of them need surgical operation.

Adolescent↗

[The secondary ossification center of fetus].

Most textbooks on human anatomy and human embryology state that the appearance of the secondary ossification center (SOC) of the fetus is considered to be after or around birth. In our study, while collecting the data on growth indexes from 346 fetuses in normal pregnancy with conceptional ages from 12 to 38 complete weeks, we investigated using B-ultrasonography the appearance of the secondary ossification center and compared them in part with the anatomically observed data collected from fetal specimens. The results of B-ultrasonic observation show that SOC can be seen at the distal end of femur after 29 complete weeks. From them on, the percentage of the appearance of SOC increases weekly, and it is almost 100% in 34 complete weeks.

Female↗

[Allotransplantation of fetal adrenal capsules for treating steroid deficiency].

A man suffering from bilateral adrenal carcinoma was treated by total adrenalectomy and steroids substitution. One and a half months later, two fetal adrenal capsules were grafted to his greater omentum. No immunosuppressive agent was given. From the fourth month exogenous steroid dose was gradually reduced. Five months after transplantation, substitution therapy was discontinued. The patient showed no signs of steroid deficiency and all laboratory studies were normal. Seven months later, the patient died of metastasis of the carcinoma. Pathological examination showed that much adrenal cortex had regenerated in the greater omentum. The findings suggest that this method for treating chronic steroid deficiency is simple and successful.

Adenocarcinoma↗

Ibutilide, a methanesulfonanilide antiarrhythmic, is a potent blocker of the rapidly activating delayed rectifier K+ current (IKr) in AT-1 cells. Concentration-, time-, voltage-, and use-dependent effects.

BACKGROUND: Ibutilide is an action potential-prolonging antiarrhythmic currently in clinical trials. The drug shares structural similarities with E-4031 and dofetilide, specific blockers of the rapidly activating delayed rectifier K+ current (IKr). However, previous in vitro studies in guinea pig myocytes have indicated that ibutilide does not block IKr but rather increases a slow inward sodium current. METHODS AND RESULTS: In this study, we compared the effects of ibutilide with those of dofetilide on outward current in mouse atrial tumor myocytes (AT-1 cells), a preparation in which, unlike guinea pig, a typical IKr is the major delayed rectifier and can be readily recorded in isolation from other currents. In AT-1 cells, ibutilide and dofetilide were both potent IKr blockers, with EC50 values of 20 (n = 12) and 12 (n = 8) nmol/L, respectively, at +20 mV. The time and voltage dependence of IKr inhibition by the two compounds were virtually identical. The following characteristics were most consistent with open channel block: (1) block increased with depolarizing pulses; (2) block increased with longer pulses; (3) currents deactivated more slowly in the presence of drug, resulting in a "crossover" typical of open channel block; and (4) with repetitive pulsing after drug wash-in, use-dependent block was observed. CONCLUSIONS: These data suggest that the clinical actions of ibutilide are mediated at least in part by block of IKr; an effect on inward currents is not excluded. AT-1 cells are a useful model system for the study of drug block of this important repolarizing current.

Animals↗

Sequential activation of MAP kinase cascade by angiotensin II in opossum kidney cells.

Angiotensin II (Ang II) is a potent regulator of proximal tubule functions, including transport, metabolism, and cell proliferation. The opossum kidney (OK) cell line is a useful model of renal proximal tubule. Mitogen-activated protein (MAP) kinases are rapidly phosphorylated and activated in response to various agonists. We investigated Ang II effects on serine/threonine kinase cascades in OK cells. The major findings of the present study are that Ang II stimulated MAP kinase kinase (MAPKK), MAP kinase (MAPK), and S6 kinase activities, and that it increased phosphorylation of Raf-1 kinase and p42 MAP kinase in OK cells. These stimulations of kinases were dose-dependent (from 10(-6) to 10(-11) M). The time course of activation was sequential; the peak stimulation was reached at 5 to 10 minutes for Raf-1 kinase, MAPKK and MAPK, and at 20 minutes for S6 kinase. The activation of MAPK was inhibited by approximately 70% with prolonged 24-hour PMA pretreatment or in the presence of calphostin C or H-7. Tyrosine kinase inhibitors (genistein and herbimycin) did not inhibit AngII-induced MAPK activity. This activation of MAPK was also inhibited via AT1 receptor antagonist, Dup753 and pertussis toxin. This evidence suggests that the activation of serine/threonine cascades by Ang II is largely dependent on PMA-sensitive PKC, and is not dependent on tyrosine kinase and pertussis toxin.

Angiotensin II↗

The intracellular distribution and pattern of expression of Mcl-1 overlap with, but are not identical to, those of Bcl-2.

A family of genes related to the bcl-2 protooncogene has recently emerged. One member of this family, mcl-1, was cloned from a human myeloblastic leukemia cell line (ML-1) undergoing differentiation. The intracellular localization of mcl-1, as well as the kinetics of its expression during differentiation, have now been studied. These studies show that the intracellular distribution of mcl-1 overlaps with, but is not identical to, that of bcl-2: mcl-1 is similar to bcl-2 in that the mcl-1 protein has a prominent mitochondrial localization, and in that it associates with membranes through its carboxyl hydrophobic tail. mcl-1 differs from bcl-2, however, in its relative distribution among other (nonmitochondrial/heavy membrane) compartments, mcl-1 also being abundant in the light membrane fraction of immature ML-1 cells while bcl-2 is abundant in the nuclear fraction. Similarly, in differentiating ML-1 cells, the timing of expression of mcl-1 overlaps with, but is not identical to, that of bcl-2: the mcl-1 protein increases rapidly as cells initiate differentiation, and mcl-1 is a labile protein. In contrast, bcl-2 decreases gradually as cells complete differentiation. Overall, the mcl-1 and bcl-2 proteins have some properties in common and others tht are distinct. A burst of expression of mcl-1, prominently associated with mitochondria, complements the continued expression of bcl-2 in ML-1 cells differentiating along the monocyte/macrophage pathway.

Cell Differentiation↗

Mechanism of block of a human cardiac potassium channel by terfenadine racemate and enantiomers.

1. The cardiac toxicity of racemic terfenadine (marked QT prolongation and polymorphic ventricular arrhythmias) is probably due to potassium channel blockade. To test whether one of its enantiomers would be a less efficient potassium channel blocker, we compared the mechanism of action of the racemate with that of the individual enantiomers. 2. We synthesized the individual enantiomers of terfenadine and examined under whole cell voltage-clamp conditions the mechanism of action of the racemate, both enantiomers and a major metabolite on a cloned human cardiac potassium channel, hKv1.5. This delayed rectifier is sensitive to quinidine, clofilium and other 'class III' antiarrhythmic drugs at clinically relevant concentrations. 3. Upon depolarization, racemic terfenadine and its enantiomers induced a fast decline of hKv1.5 current towards a reduced steady state current level. During subsequent repolarization the tail currents deactivated more slowly than the control, resulting in a 'crossover' phenomenon. 4. The voltage-dependence of block was biphasic with a steep increase in block over the voltage range of channel opening (-30 to 0 mV), and a more shallow phase positive to 0 mV (where the channel is fully open). The latter was consistent with a binding reaction sensing 21% of the transmembrane electrical field (with reference to the cell interior). 5. The EC50 for hKv1.5 block by racemic terfenadine was 0.88 microM, while the values for R- and S-terfenadine were 1.19 microM and 1.16 microM, respectively. In contrast, the acid metabolite reduced hKv1.5 current by only 5% at a concentration of 50 microM. 6. These findings suggest that terfenadine blocks the hKvl.5 channel after it opens by entering into the internal mouth of the channel. We have previously shown that quinidine blocks hKvl.5 in a similar manner but with an apparent affinity of ~6 micro M. Thus, terfenadine and its enantiomers are approximately equipotent open state blockers of this human K+ channel and about 6 times more potent than quinidine. The similar state-, time-, and voltage-dependence of hKvl.5 block by both enantiomers also indicates that the chiral centre does not significantly constrain the orientation of critical binding determinants of terfenadine with respect to the receptor site.

Animals↗

Effects of estrogen in vivo on coronary vascular resistance in perfused rabbit hearts.

Estrogen or its vehicle was given daily to three groups of ovariectomized rabbits for various lengths of time, after which coronary flow was measured in their isolated perfused hearts. In one group, intramuscular injections of estrogen (40 micrograms/kg) for 7 or 14 days increased coronary flow by 40-50% (P < 0.05). In rabbits given estrogen intramuscularly for 7 days, the coronary flow returned to the basal level within 7 days after the estrogen injections were discontinued. In a second group of animals, intravenous injections of estrogen (10 micrograms/kg) for 4 days increased the coronary flow by 45% (P < 0.01). In a third group, we administered the estrogen transdermally for 4 days, and we measured the plasma estrogen levels at the end of this period. The coronary flow in this group was increased by 52% (P < 0.001), and the plasma estrogen levels ranged from 39 to 800 pg/ml. In all groups of experiments, the increments in coronary flow evoked by estrogen were virtually abolished by NG-nitro-L-arginine, an inhibitor of nitric oxide synthase. We conclude that estrogen regulates coronary blood flow, in part by upregulating nitric oxide synthase in the coronary vasculature.

Administration, Cutaneous↗

Expression of mRNAs for different types of IP3 receptors in rat kidneys.

Cloning studies have extensively characterized two types of inositol 1,4,5-trisphosphate (IP3) receptors from the rat. An IP3 receptor from the cerebellum is referred to as type 1, and a second, recently described, receptor is referred to as the type 2 IP3 receptor. The significance of different types of IP3 receptors, especially in vivo in the kidney, is not fully understood. We investigated the localization of mRNAs encoding these two types of IP3 receptors in microdissected nephron segments of rats using reverse transcription and polymerase chain reaction (RT-PCR) followed by Southern blot analysis. Type 1 IP3 receptor mRNA displayed a widespread, although not uniform, distribution along the nephron. In contrast, type 2 IP3 receptor mRNA was confined almost exclusively to collecting ducts, suggesting specific expression of type 2 IP3 receptor in collecting ducts. We then detected mRNAs for the two types of IP3 receptors in collecting ducts in dehydrated rats. Dehydration downregulated type 2 IP3 receptor mRNA in cortical collecting duct, outer medullary collecting duct, and the initial part of inner medullary collecting duct (IMCD), but not in the terminal part of IMCD. It had no effect on type 1 IP3 receptor mRNA expression in collecting ducts. We propose that different types of IP3 receptors may have different functions in the rat kidney. the initial part of inner medullary collecting duct (IMCD), but not in the terminal part of IMCD. It had no effect on type 1 IP3 receptor mRNA expression in collecting ducts. We propose that different types of IP3 receptors may have different functions in the rat kidney.

Animals↗

Anti-minK antisense decreases the amplitude of the rapidly activating cardiac delayed rectifier K+ current.

The rapidly and slowly activating delayed rectifier K+ currents (IKr and IKs, respectively), which have different physiological properties have been identified in cardiac cells from several species, including humans. Although expression of the minimal K+ channel protein (minK) cDNA in some systems results in a current resembling IKs, the role of this gene product in channel function remains controversial. In atrial tumor myocytes (AT-1 cells), no IKs is recorded, but minK mRNA is detected, raising the possibility that expression of the minK gene serves an as-yet-unidentified function. In these experiments, AT-1 cells were exposed to antisense oligonucleotides targeting the 5' translation start site of the minK cDNA cloned from an AT-1 library. Cell size, IKr, and L-type and T-type Ca2+ currents were measured 24 to 48 hours after exposure and compared with data in cells exposed to the corresponding sense oligonucleotide or grown in medium only. Antisense oligonucleotide significantly reduced IKr compared with sense and medium-only control cells in 0 of 2 experiments (n = 3 to 6 cells per treatment in each experiment) at 50 nmol/L, 1 of 2 at 250 nmol/L, 6 of 6 at 1000 nmol/L, and 2 of 2 at 10,000 nmol/L. At 1000 nmol/L, maximum tail current in antisense-exposed cells was 2.5 +/- 0.1 pA/pF (mean +/- SEM, n = 28, 6 separate experiment), 6.6 +/- 0.4 pA/pF in sense-exposed cells (n = 27), 5.4 +/- 0.6 pA/pF in medium-only cells (n = 21), and 5.8 +/- 0.7 pA/pF in cells exposed to a random oligonucleotide (n = 9).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Message of nexin 1, a serine protease inhibitor, is accumulated in the follicular papilla during anagen of the hair cycle.

A group of specialized mesenchymal cells located at the root of the mammalian hair follicle, known as the follicular or dermal papillary cells, are involved in regulating the hair cycle, during which keratinocytes of the lower follicle undergo proliferation, degeneration and regrowth. Using the arbitrarily primed-PCR approach, we have identified a 1.3 kb messenger RNA that is present in large quantities in cultured rat follicular papillary cells, but not in skin fibroblasts. This mRNA encodes nexin 1, a potent protease inhibitor that can inactivate several growth-modulating serine proteases including thrombin, urokinase and tissue plasminogen activator. In situ hybridization showed that nexin 1 message is accumulated in the follicular papilla cells of anagen follicles, but is undetectable in keratinocytes or other skin mesenchymal cells. In addition, nexin 1 message level varies widely among several immortalized rat vibrissa papillary cell lines, and these levels correlate well with the reported abilities of these cell lines to support in vivo follicular reconstitution. These results suggest a possible role of nexin 1 in regulating hair follicular growth.

Amyloid beta-Protein Precursor↗

[The changes and clinical significance of interleukin 1 beta in pleural effusion].

An enzyme linked immunosorbent assay was set up by using anti-recombinant human interleukin 1 beta monoclonal antibodies. The interleukin 1 beta, anti-interleukin 1 beta autoantibody and interleukin 1 beta containing immune complex were detected in pleural effusion of 28 patients with bacterial infection cases pleurisy and 13 with lung cancer. The results showed that free interleukin 1 beta could be detectable in the early stage of pleurisy, and then transformed to the immune complex. The interleukin 1 beta containing immune complex were detectable in the pleeural effusions of all the 28 patients with pleurisy, but only two patients with lung cancer. The results suggested that this cytokine behaves differently in these two different kinds of diseases.

Antibodies, Monoclonal↗

[The human fetal development time table of the major limb bones-ultrasonic bone age].

B-ultrasonic technique was used to examine 297 Chinese fetuses in normal pregnancy woman of completed week age from 12 to 38 weeks. The lengths of the major limb bones were measured and statistical analysis showed that the positive linear correlation between the development of fetuses' limb bones and the completed fetal age is significant.

Bone Development↗

Metabolic approach for regulation of IL-1 beta in vivo.

IL-1 beta, the autoantibodies to IL-1 beta and IL-1 beta-containing immune complex in pleural effusion and cerebrospinal fluid were detected using anti-recombinant human IL-1 beta monoclonal antibody. The results indicate that IL-1 beta is detectable in some cases, and the amounts decrease gradually with the chemotherapy following the autoantibodies and the specific detectable immune complex. These autoantibodies may have a feedback effect, inhibiting the IL-1 beta activity, and forming the immune complex to speed the clearance of activated IL-1 beta.

Antibodies, Monoclonal↗