Dr. Yang Jiasan's experience in applying the back-shu points.
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Acupuncture Points↗
Biomedical subjects
T Yang
Publications and source records attributed to T Yang.
Epidemiology of anti-human T-cell leukemia virus type I antibody and characteristics of adult T-cell leukemia in China.
We analyzed the data from seroepidemiologic survey of anti-HTLV-I serum antibody (HTLV-1 Ab) and 16 adult cases of T-cell leukemia (ATL) in China (1984-1994). The results showed that the positive rate of HTLV-I Ab of the population of China was 0.54%, the birth or residence places of HTLV-I carriers and all the patients with ATL were mainly distributed in the coastal provinces and the northeast China, and a small endemic area of HTLV-I and ATl was found in Fujian Province (HTLV-I Ab positive rate, 2.1%). The HTLV-I in China may be transmitted from Japan or originated from China. The clinical characteristics of the cases included onset in adulthood; frequent skin lesions, lymphadenopathy and hepatosplenomegaly; no mediastinal mass; the ATL cells from peripheral blood with polymorphism nuclei and mature T cell immunophenotype HTLV-IAb positive in most of the cases tested (5/8); mostly acute type; with a median survival period of 3.5 months.
Adult↗
Mcl-1, a member of the Bcl-2 family, delays apoptosis induced by c-Myc overexpression in Chinese hamster ovary cells.
Mcl-1, a protein increased early in the differentiation of human myeloblastic ML-1 cells, has sequence similarity to Bcl-2. In the present study, we determined whether Mcl-1 has functional similarity to Bcl-2 by testing its ability to inhibit apoptosis induced by c-Myc overexpression. This was carried out using Chinese hamster ovary 5AHSmyc cells which contain the human c-myc proto-oncogene under the control of a heat shock promoter. Heat treatment induces c-Myc overexpression and thus apoptosis as determined by internucleosomal DNA fragmentation. We transfected 5AHSmyc cells with mcl-1 and found that clones expressing the introduced Mcl-1 protein exhibited reduced DNA fragmentation. Mcl-1 was also capable of delaying the onset of cell death as judged by loss of membrane integrity, although it could not provide complete protection from c-Myc overexpression. Thus, Mcl-1 has functional homology to Bcl-2 in that Mcl-1 can enhance cell viability under conditions that otherwise cause apoptosis.
Animals↗
Sequential activation of Raf-1 kinase, mitogen-activated protein (MAP) kinase kinase, MAP kinase, and S6 kinase by hyperosmolality in renal cells.
In the renal medulla during antidiuresis, the extracellular fluid becomes hyperosmotic. Madin-Darby canine kidney (MDCK) epithelial cells adapt in hyperosmotic conditions and serve as a useful tissue culture model for cellular responses to hyperosmolality. We demonstrate that hyperosmolality stimulates phospholipase C, Raf-1 kinase mitogen-activated protein (MAP) kinase kinase, MAP kinase, and S6 kinase activities and that it increases phosphorylation of Raf-1 kinase, and p42 MAP kinase in MDCK cells. Stimulation of these kinases is osmolality-dependent (from 300 to 600 mosm/kg H2O). The time course of activation is sequential; the peak stimulation for Raf-1 kinase is at 5 min, at 10 min for MAP kinase kinase and MAP kinase, and at 20 min for S6 kinase. The activation of Raf-1 kinase and MAP kinase is inhibited by phorbol 12-myristate 13-acetate pretreatment in the presence of calphostin C or H-7. Tyrosine kinase inhibitors (genistein, herbimycin) do not significantly suppress hyperosmolality-induced MAP kinase activity. The increase of Ins-1,4,5-P3 levels by hyperosmolality suggests that activation of these kinases is mediated at least partially via activation of phospholipase C. Thus, hyperosmolality stimulates the serine/threonine kinases, Raf-1 kinase, MAP kinase kinase, MAP kinase, and S6 kinase, via predominantly protein kinase C-dependent, tyrosine kinase-independent pathways in MDCK cells.
Amino Acid Sequence↗
Localization of cyclophilin A and cyclophilin C mRNA in murine kidney using RT-PCR.
Cyclosporin A (CsA), which is widely used as an immunosuppressant, has a nephrotoxic side effect. The mechanism of this nephrotoxicity is not well understood; however, recent studies suggest that cyclophilin (cyp) is responsible for mediating the immunosuppressive action of CsA through the interaction with the Ca(2+)- and calmodulin-dependent phosphatase, calcineurin. While cyp A mRNA is expressed ubiquitously, cyp C mRNA has been shown to be topically expressed, including in the kidney. We examined: (1) distribution of cyp A and cyp C mRNA in microdissected murine nephron segments, using a combination of reverse transcription and polymerase chain reaction (RT-PCR) techniques, and (2) the effect of CsA administration on cyp C mRNA expression in proximal convoluted tubule. Among the nephron segments examined, large signals for cyp C PCR product were detected in proximal convoluted tubule and proximal straight tubule. Our data showed that the distribution of cyp C mRNA was uneven, and it mainly existed in segments that are relatively sensitive to CsA toxicity. In contrast, cyp A mRNA was found to be distributed almost equally along the nephron segments examined. By CsA administration, the signal for cyp C mRNA PCR product was increased. These results suggest that cyp C may play some role in the renal tubular disorder observed in CsA nephrotoxicity.
Amino Acid Isomerases↗
Antecedent sympathetic stimulation alters time course of chronotropic response to vagal stimulation in dogs.
We determined the influence of antecedent sympathetic stimulation on the chronotropic responses of the heart to 10-s strains of vagal stimulation in anesthetized dogs. We used the reciprocal of the slope (m-1) of the initial portion of the vagal response as an index of the time required for the response to reach steady state. In one group of 11 animals, we found that the onset of the response to the vagal stimulation was progressively blunted as we increased the frequency and duration of the antecedent sympathetic stimulation; that is, m-1 increased from 0 to 8.13 +/- 2.75 (SE) and from 0 to 8.22 +/- 2.26, respectively. In three other animals, an antecedent infusion of norepinephrine had a blunting effect that resembled that of antecedent sympathetic stimulation. In 11 other animals, m-1 significantly decreased as we prolonged the elapsed time from the end of sympathetic stimulation to the beginning of vagal stimulation. In six other animals, m-1 was not affected by antecedent atrial pacing at frequencies that were equivalent to those elicited by antecedent sympathetic stimulations. The blunting effect of antecedent sympathetic stimulation was abolished by propranolol administration (1 mg/kg), but it was not affected appreciably by phentolamine administration (2 mg/kg). We conclude that the major blunting effect of antecedent sympathetic stimulation is mediated postjunctionally (i.e., at the level of the automatic cells in the heart.
Animals↗
PCR localization of C-type natriuretic peptide and B-type receptor mRNAs in rat nephron segments.
The present study was undertaken to investigate the presence of C-type natriuretic peptide (CNP) mRNA and its receptor, natriuretic peptide B-type receptor (ANPR-B) mRNA, in rat renal structures. The microlocalization of mRNAs coding for CNP and ANPR-B was carried out in the rat kidney, using an assay of reverse transcription and polymerase chain reaction (RT-PCR) in individual microdissected renal tubule segments, glomeruli, vasa recta bundle, and arcuate arteries. The PCR signal for CNP was detected in glomerulus, vasa recta bundle, and arcuate artery. The PCR product of ANPR-B was widely present in renal structures. Relatively large amounts of ANPR-B PCR product were detected in glomerulus, vasa recta bundle, arcuate artery, and distal nephron segments. A relatively high concentration of CNP (10(-7) M) stimulated guanosine 3',5'-cyclic monophosphate accumulation in glomerulus, medullary thick ascending limb, cortical collecting duct, and inner medullary collecting duct. Our data demonstrate that CNP can be produced locally in the glomerulus and renal vascular system and that ANPR-B is widely distributed in renal structures. Thus CNP may influence renal function and act in autocrine and paracrine fashions in the kidney.
Animals↗
Distribution of kallikrein-binding protein mRNA in kidneys and difference between SHR and WKY rats.
We investigated kallikrein-binding protein (KBP) mRNA distribution in the kidney of Sprague-Dawley (SD) rats, spontaneously hypertensive rats (SHR), and Wistar-Kyoto strain (WKY) rats. Northern blot analysis revealed that KBP mRNA was located mainly in the medulla and with lower amounts in SHR than in WKY rats. KBP mRNA in microdissected nephron segments was detected by reverse transcription and polymerase chain reaction (RT-PCR) followed by Southern blot analysis. In SD rats, the most abundant signals were consistently found in inner medullary collecting duct (IMCD), with small amounts in outer medullary collecting duct, proximal convoluted tubule, and glomerulus. No signals were found in connecting tubule and cortical collecting duct. The nephron distribution of KBP mRNA was similar in WKY and SD rats. Only a small amount of signal was found, however, in IMCD of SHR. In conclusion, 1) KBP mRNA was predominantly distributed in the medullary segments of the distal nephron, downstream from the known kallikrein activity site in the collecting duct, and 2) KBP mRNA expression was significantly decreased in the kidney of SHR.
Animals↗
K+ currents and K+ channel mRNA in cultured atrial cardiac myocytes (AT-1 cells).
Atrial tumor myocytes derived from transgenic mice (AT-1 cells) maintain a well-differentiated cardiac biochemical and histological phenotype. In addition, they beat spontaneously in culture and exhibit long action potentials whose repolarization resembles that observed in native mammalian myocytes. In this study, we identified the major depolarization-activated outward currents in AT-1 cells; also, the presence of mRNAs that encode outwardly conducting ion channels was determined by cloning from an AT-1 cDNA library or by Northern hybridization. Among K+ channel isoforms, Kv2.1, minK, and Kv1.4 were readily detected in tumors and at 1 day in culture. Their abundance remained relatively stable (twofold or less change) after 14 days. The major outward current in AT-1 cells is a delayed rectifier that displays prominent inward rectification, activates rapidly (eg, 182 +/- 27 milliseconds [mean +/- SEM] at + 20 mV, n = 12), exhibits biexponential deactivation kinetics, and is extremely sensitive to the methanesulfonanilide dofetilide (IC50, 12 nmol/L). These characteristics identify this current as IKr, a delayed rectifier observed only in cardiac cells. IKr in AT-1 cells displayed slow inactivation: dofetilide-sensitive deactivating tails were greater after 1-second than after 5-second pulses. When IKr was blocked by > or = 0.5 mumol/L dofetilide, time-independent current was usually recorded (50 of 65 experiments); rapidly inactivating (6 of 65) or slowly inactivating (9 of 65) outward currents were occasionally observed. We conclude that AT-1 cells express mRNAs encoding cardiac K+ channels and display a cardiac electrophysiological phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Enzymatic protection from autoxidation for crosslinked hemoglobins.
The autoxidation rates of hemoglobins crosslinked between the alpha subunits (alpha 99XLHb A) and between the beta subunits (beta 82XLHb A) were reduced in the presence of catalase and/or superoxide dismutase. In the presence of catalase the rate for alpha 99XLHb A decreased 2.3 fold and for beta 82XLHb A, 1.9 fold. Superoxide dismutase reduced the rate 1.6 fold for alpha 99XLHb A and 1.8 fold for beta 82XLHb A. In the presence of both catalase and superoxide dismutase the rate of autoxidation decreased by 3.0 fold in alpha 99XLHb A and 4.0 fold in beta 82XLHb A. The presence of catalase and superoxide dismutase or both in the crosslinked hemoglobin samples increases the autoxidation half-life of oxyhemoglobins. This suggests that crosslinked hemoglobins to be used as blood substitutes could be protected from oxidation in storage by these enzymes.
Aspirin↗
[Reconfirmation of golgiphobic dendrites of the motoneurons in rat spinal cord].
With CB-HRP method (injections into 5 muscles of anterior and posterior extremities) and Golgi technique, the corresponding sections of spinal cords were observed on same aged rats of the identical parent rats. Comparing the cell numbers of the lateral groups of anterior horns, the former (CB-HRP) revealed twice as many as the cell numbers of the latter (Golgi). As to the surface densities of the white matter dendrites (WMD) in the lateral funiculi from the neurons of the lateral groups of the anterior horns, the density revealed by injection of CB-HRP to the tibialis anterior is 2-9 times more than that in Golgi sections. All of WMD revealed in CB-HRP sections could extend into the peripheral portions of the lateral funiculi, and quite a few of them even form a subpial marginal plexus, that is one example of Golgiphobic dendrites (GBD). For labeled medial cell groups of the anterior horn with CB-HRP, their dendrites could reach to the ependymal layer of the central canal (another GBD). These two types of GBD were not present on the Golgi material. The significance of GBD was also discussed.
Animals↗
[Study of bronchoalveolar lavage fluid harvested from the dogs with steam inhalation injury].
The significances of analyzing bronchoalveolar lavage fluid (BALF) were studied using a steam inhalation injury model. Bronchoalveolar lavage was carried out at 1 and 5 h after steam inhalation injury. The parameters investigated included cellular analysis, the total protein content, malondialdehyde (MDA) content, the activity of superoxide dismutase (SOD), and the angiotensin converting enzyme (ACE) in the BALF, and pathologic examination of lungs. The study indicated that some informations of the pathophysiological changes in the lungs after inhalation injury could be acquired by the BALF analysis.
Animals↗
New limit on the rate-density of evaporating black holes.
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Journal Article↗
Calcium ATPase of sarcoplasmic reticulum has four binding sites for calcium.
The calcium-transporting ATPase of sarcoplasmic reticulum is known to bind two Ca2+ ions from the cytoplasm to the free enzyme and two Ca2+ ions from the lumen to the phosphoenzyme. The concentration of phosphoenzyme formed at equilibrium from Pi and Mg2+ increases with increasing concentration of calcium in the lumen, which binds to the phosphoenzyme to form Ca2.E approximately P.Mg. However, at subsaturating concentrations of Mg2+ increasing the concentration of lumenal Ca2+ does not drive phosphoenzyme formation to completion. The maximal levels of phosphoenzyme that are formed at saturating concentrations of lumenal Ca2+ increase with increasing concentrations of Mg2+. This result requires that Ca2+ can bind to low-affinity lumenal sites on both the free enzyme and the phosphoenzyme, as well as to the high-affinity cytoplasmic calcium-binding sites. If there were no lumenal binding sites for Ca2+ on the free enzyme, high concentrations of lumenal Ca2+ would convert all of the enzyme to the same maximal concentration of Ca2.E approximately P.Mg at subsaturating concentrations of Mg2+ and Pi. We conclude that there are two low-affinity lumenal sites as well as two high-affinity cytoplasmic sites for Ca2+ on the free enzyme. Phosphorylation by ATP results in translocation of Ca2+ from the high-affinity to the low-affinity sites.
Animals↗
Constitutive activation of opsin: influence of charge at position 134 and size at position 296.
In previous studies, mutation of Lys296 or Glu113 in opsin has been shown to result in constitutive activation of the protein--that is, these mutants can activate the G protein transducin in the absence of chromophore and in the absence of light. These and other data have led to the suggestion that a salt bridge between Lys296 and Glu113 helps to constrain opsin to an inactive conformation. It is shown here that of 12 different amino acids substituted at position 296, all, except Arg and the wild-type Lys, are constitutively active at neutral pH, lending further support to this suggestion. However, activation of opsin appears also to be influenced significantly by the size of amino acid side chain at position 296. Thus, there are multiple effects of the mutations. Wild-type opsin is also shown to be weakly active at pH 6.1. Five other charged amino acids in the membrane-embedded region of the protein (Asp83, Glu122, Glu134, Arg135, and Glu201) were mutated to see if they affect constitutive activity. Of these amino acids, only mutation of Glu134 results in an increase in the activity of opsin. Changing Glu134 to Gln increases the activity of opsin, while changing Glu134 to Asp inhibits activity. These results suggest that a negative charge on Glu134 is important in stabilizing the inactive state of opsin. Glu134 is highly conserved in all visual pigments and most of the other G protein-linked receptors.
Animals↗
MCL1, a gene expressed in programmed myeloid cell differentiation, has sequence similarity to BCL2.
During their lifespan, immature cells normally pass through sequential transitions to a differentiated state and eventually undergo cell death. This progression is aberrant in cancer, although the transition to differentiation can be reestablished in inducible leukemia cell lines. This report describes a gene, MCL1, that we isolated from the ML-1 human myeloid leukemia cell line during phorbol ester-induced differentiation along the monocyte/macrophage pathway. Our results demonstrate that expression of MCL1 increases early in the induction, or "programming," of differentiation in ML-1 (at 1-3 hr), before the appearance of differentiation markers and mature morphology (at 1-3 days). They further show that MCL1 has sequence similarity to BCL2, a gene involved in normal lymphoid development and in lymphomas with the t(14;18) chromosome translocation. MCL1 and BCL2 do not fall into previously known gene families. BCL2 differs from many oncogenes in that it inhibits programmed cell death, promoting viability rather than proliferation; this parallels the association of MCL1 with the programming of differentiation and concomitant maintenance of viability but not proliferation. Thus, in contrast to proliferation-associated genes, expression of MCL1 and BCL2 relates to the programming of differentiation and cell viability/death. The discovery of MCL1 broadens our perspective on an emerging MCL1/BCL2 gene family and will allow further comparison with oncogene families.
Amino Acid Sequence↗
Beta-actin mRNA-binding proteins associated with the cytoskeletal framework.
Association of mRNA with the cytoskeletal framework (CSK) is thought to play a strategic role in the placement of mRNA in the cytoplasm. However, the molecular determinants underlying mRNA/CSK association are completely unknown. To begin addressing this issue, we have employed a binding assay to identify proteins of the CSK compartment of NIH 3T3 cells that bind in-vitro-transcribed 32P-labelled beta-actin mRNA with high affinity. Three proteins, of approximate molecular masses 27, 50 and 97 kDa, were observed to exhibit strong binding. Binding to these proteins took place at physiological salt concentration and withstood washing in 0.5 M salt. Furthermore, binding was unaffected by heparin but was inhibited by unlabelled beta-actin mRNA. Treatment of isolated CSKs with the microfilament-severing agent DNase I abolished all beta-actin mRNA-binding activities, thus suggesting a possible association of beta-actin mRNA with the microfilament network in situ. Removal of the 3' untranslated region (UTR) significantly reduced beta-actin mRNA binding to all three CSK proteins but removal of the 5' UTR mainly affected binding to the 97-kDa species and that to a lesser extent. beta-Tubulin mRNA bound to the same three CSK proteins as did beta-actin mRNA, but with considerably less avidity. In contrast, vimentin mRNA strongly recognized these CSK proteins, and further bound to a group of smaller proteins (< 29 kDa). As beta-actin mRNA, beta-tubulin mRNA and vimentin mRNA have been observed to occupy separate cytoplasmic locales, the proteins detected here may be operative both in binding mRNAs to the CSK in situ, as well as in localizing mRNA in the cytoplasm.
3T3 Cells↗
Alterations in a voltage-gated K+ current during the differentiation of ML-1 human myeloblastic leukemia cells.
A voltage-gated K+ current has been identified in ML-1 human myeloid leukemia cells, with the use of the whole-cell patch-clamp technique. ML-1 cells proliferate in tissue culture as immature myeloblasts and can be induced to differentiate to nonproliferative monocyte/macrophages. In the myeloblastic cells, activation of the K+ current occurs upon depolarization of the membrane potential to above -40 mV; inactivation of this current is also voltage dependent and follows a simple exponential time course with a time constant (Ti) of 900 msec at 0 mV. The current is inhibited by 4-aminopyridine (IC50 of 80 microM at 0 mV), but is much less sensitive to tetraethylammonium of Ba2+. In cells exposed to the differentiation-inducer 12-O-tetradecanoylphorbol-13-acetate (TPA), dramatic alterations in the K+ current occur: upon exposure to 10 nM TPA during whole-cell recording, the amplitude of the voltage-activated current initially increases (within 4 min) and later decreases (at approximately 30-50 min). Upon addition of 0.5 nM TPA to cells in tissue culture, the current shows suppressed activation and accelerated inactivation in the early stages of differentiation (10-fold decrease in Ti at approximately 7 hr) and is completely suppressed in the later stages (3 days). Thus, this voltage-gated K+ current is suppressed early in the induction of differentiation and associated loss of proliferation in myeloid ML-1 cells exposed to TPA; this parallels the fact that channels of a similar type are activated upon the stimulation of proliferation in lymphoid cells exposed to mitogens.(ABSTRACT TRUNCATED AT 250 WORDS)
4-Aminopyridine↗