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Biomedical subjects

M Yu

Publications and source records attributed to M Yu.

At least 73 records · Page 4Linked to original sources
PubMed2001

Leucokinin and the modulation of the shunt pathway in Malpighian tubules.

Transepithelial secretion in Malpighian tubules of the yellow fever mosquito (Aedes aegypti) is mediated by active transport of Na(+) and K(+) through principal cells and passive Cl(-) transport through the shunt. Permeation through the shunt was assessed by measuring transepithelial halide diffusion potentials in isolated perfused Malpighian tubules, after first inhibiting active transport with dinitrophenol. Diffusion potentials were small under control conditions, revealing Eisenman selectivity sequence I (I(-)>Br(-)>Cl(-)>F(-)) which is the halide mobility sequence in free solution. Accordingly, electrical field strengths of the shunt are small, selecting halides for passage on the basis of hydrated size. Leucokinin-VIII (LK-VIII) significantly increased the shunt conductance from 57.1 µS/cm to 250.0 µS/cm. In parallel, the shunt selectivity sequence shifted to Eisenman sequence III (Br(-)>Cl(-)>I(-)>F(-)), revealing increased electrical field strengths in the shunt, now capable of selecting small, dehydrated halides for passage. High concentrations of peritubular F(-) (142.5 mM) duplicated the effects of LK-VIII on shunt conductance and selectivity, suggesting a role for G-protein. In the presence of LK-VIII (or F(-)), coulombic interactions between the shunt and I(-) and F(-) may be strong enough to cause binding, thereby blocking the passage of Cl(-). Thus, LK-VIII increases both shunt conductance and selectivity, presumably via G-protein.

Journal Article↗
PubMed2001

Abnormal pressure-natriuresis in hypertension: role of cytochrome P450 metabolites of arachidonic acid.

The pressure-natriuresis relationship is shifted to higher pressures in genetic and experimental models of hypertension; however, the factors responsible for altering kidney function remain to be determined. In spontaneously hypertensive (SHR) and Lyon hypertensive rats, the resetting of pressure-natriuresis results from increased preglomerular renal vascular tone, whereas sodium reabsorption is elevated in the thick ascending loop of Henle (TALH) of Dahl S rats. Recently, a new route for the renal metabolism of arachidonic acid (AA) has been described, and there is evidence that this pathway contributes to the resetting of renal function in hypertension. In the kidney, cytochrome P450 (CYP) enzymes metabolize AA primarily to 20-HETE and EETs. 20-HETE is a potent constrictor of renal arterioles that has an important role in autoregulation of renal blood flow and tubuloglomerular feedback. 20-HETE and EETS also inhibit sodium reabsorption in the proximal tubule and TALH. In the SHR, the renal production of 20-HETE is elevated and inhibitors of the formation of 20-HETE decrease arterial pressure. Blockade of 20-HETE formation also reduces blood pressure or improves renal function in deoxycorticosterone acetate (DOCA)-salt, angiotensin II--infused, and Lyon hypertensive rats. In contrast, 20-HETE formation is reduced in the TALH of Dahl S rats and this contributes to elevated sodium reabsorption. Induction of 20-HETE synthesis improves pressure-natriuresis and lowers blood pressure in Dahl S rats, whereas inhibitors of the synthesis of 20-HETE promote the development of hypertension in Lewis rats. These findings indicate that the renal production of CYP metabolites of AA is altered in genetic and experimental models of hypertension and that this system contributes to the resetting of pressure-natriuresis and the development of hypertension in some models.

Animals↗
PubMed2001

Molecular biology of Hendra and Nipah viruses.

The structure and genetic organization of Hendra and Nipah viruses places them in the subfamily Paramyxovirinae. However, low homology with other subfamily members and several novel biological and molecular features such as genome length and F(0 )cleavage site suggest classification in a new genus within the Paramyxovirinae.

Amino Acid Sequence↗
PubMed2001

Pre-clinical validation of a novel, highly sensitive assay to detect PML-RARalpha mRNA using real-time reverse-transcription polymerase chain reaction.

We have developed a sensitive and quantitative reverse-transcription polymerase chain reaction (RT-PCR) assay for detection of PML-RARalpha, the fusion oncogene present as a specific marker in >99% of cases of acute promyelocytic leukemia (APL). The assay is linear over at least 5 orders of magnitude of input DNA or RNA, and detects as few as 4 copies of PML-RARalpha plasmid DNA. PML-RARalpha transcripts could be detected in mixtures containing 2 to 5 pg of RNA from fusion-containing cells in a background of 1 microg of RNA from PML-RARalpha-negative cells. Using 1.0 to 2.5 microg of input RNA, the sensitivity of the assay was between 10(-5) and 10(-6). Furthermore, determination of GAPDH copy number in each reaction allowed an accurate assessment of sample-to-sample variation in RNA quality and reaction efficiency, with consequent definition of a detection limit for each sample assayed. Using an internal calibrator, assay precision was high, with coefficients of variation between 10 and 20%. An interlaboratory study using coded samples demonstrated excellent reproducibility and high concordance between laboratories. This assay will be used to test the hypothesis that sensitive and quantitative measurement of leukemic burden, during or after therapy of APL, can stratify patients into discrete risk groups, and thereby serve as a basis for risk-adapted therapy in APL.

Biomarkers, Tumor↗
PubMed2001

Transcriptional and translational regulation of calpain in the rat heart after myocardial infarction--effects of AT(1) and AT(2) receptor antagonists and ACE inhibitor.

1. Recent studies demonstrated that the cardiac calpain system is activated during ischaemic events and is involved in cardiomyocyte injury. The aim of this study was to investigate the contribution of AT(1) and AT(2) receptors in the regulation of calpain-mediated myocardial damage following myocardial infarction (MI). 2. Infarcted animals were treated either with placebo, the ACE inhibitor ramipril (1 mg kg(-1) d(-1)), the AT(1) receptor antagonist valsartan (10 mg kg(-1) d(-1)) or the AT(2) receptor antagonist PD 123319 (30 mg kg(-1) d(-1)). Treatment was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, gene expression and protein levels of calpain I, II and calpastatin were determined in left ventricular free wall (LVFW) and interventricular septum (IS). At day 3 and 14 post MI, morphological investigations were performed. 3. Calpain I mRNA expression and protein levels were increased in IS 14 days post MI, whereas mRNA expression and protein levels of calpain II were maximally increased in LVFW 3 days post MI. Ramipril and valsartan decreased mRNA and protein up-regulation of calpain I and II, and reduced infarct size and interstitial fibrosis. PD 123319 did not affect calpain I or II up-regulation in the infarcted myocardium, but decreased interstitial fibrosis. Calpastatin expression and translation were not affected by AT receptor antagonists or ACE inhibitor. 4. Our data demonstrate a distinct, temporary-spatial up-regulation of calpain I and II following MI confer with the hypothesis of calpain I being involved in cardiac remodelling in the late and calpain II contributing to cardiac tissue damage in the early phase of MI. The up-regulation of calpain I and II is partly mediated via the AT(1) receptor and can be reduced by ACE inhibitors and AT(1) receptor antagonists.

Angiotensin II↗
PubMed2001

Role of endothelin and vasopressin in DOCA-salt hypertension.

1. The relative roles of endothelin (ET) and vasopressin (AVP) in the regulation of blood pressure (BP), cardiac output (CO) and total peripheral resistance (TPR) were investigated in the early stages (24 - 31 days) of development of hypertension in the conscious deoxycorticosterone acetate (DOCA)-salt hypertensive rat model. 2. BP was recorded with radiotelemetry devices and CO with ultrasonic transit-time probes. TPR was calculated from the BP and CO recordings. The contributions of endogenous ET and AVP were studied by infusing [d(CH(2))(5)(1),O-Me_Tyr(2),Arg(8)]-vasopressin, a V(1)-receptor antagonist, and bosentan, a mixed ET(A)/ET(B) receptor antagonist (Study 1). Vascular responsiveness was estimated from the changes in TPR evoked by i.v. infusions of ET-1 and AVP (Study 2). 3. In study 1, infusion of bosentan reduced TPR and BP dramatically in DOCA-salt hypertensive rats but not in SHAM control rats, and this effect was greater when the AVP system had been blocked. In contrast, the V(1) receptor antagonist alone failed to change TPR and BP in DOCA-salt hypertensive rats. However, subsequent infusion of the V(1) receptor antagonist during the plateau phase of the response in bosentan pretreated DOCA-salt hypertensive rats led to significant decreases in both BP and TPR. 4. In study 2, TPR and BP responses to ET-1, but not AVP, were greater in DOCA-salt rats than in control rats. CO responses to ET-1 or AVP were similar in the two groups. 5. The results suggest that both ET and AVP play a role in the maintenance of TPR and BP; when one system is blocked the other compensates. However, the magnitude of the contribution to the hypertensive state appears greater for ET than for AVP. Enhanced vascular responses to ET appear to contribute to this greater role.

Animals↗
PubMed2001

T7 single strand DNA binding protein but not T7 helicase is required for DNA double strand break repair.

An in vitro system based on Escherichia coli infected with bacteriophage T7 was used to test for involvement of host and phage recombination proteins in the repair of double strand breaks in the T7 genome. Double strand breaks were placed in a unique XhoI site located approximately 17% from the left end of the T7 genome. In one assay, repair of these breaks was followed by packaging DNA recovered from repair reactions and determining the yield of infective phage. In a second assay, the product of the reactions was visualized after electrophoresis to estimate the extent to which the double strand breaks had been closed. Earlier work demonstrated that in this system double strand break repair takes place via incorporation of a patch of DNA into a gap formed at the break site. In the present study, it was found that extracts prepared from uninfected E. coli were unable to repair broken T7 genomes in this in vitro system, thus implying that phage rather than host enzymes are the primary participants in the predominant repair mechanism. Extracts prepared from an E. coli recA mutant were as capable of double strand break repair as extracts from a wild-type host, arguing that the E. coli recombinase is not essential to the recombinational events required for double strand break repair. In T7 strand exchange during recombination is mediated by the combined action of the helicase encoded by gene 4 and the annealing function of the gene 2.5 single strand binding protein. Although a deficiency in the gene 2.5 protein blocked double strand break repair, a gene 4 deficiency had no effect. This argues that a strand transfer step is not required during recombinational repair of double strand breaks in T7 but that the ability of the gene 2.5 protein to facilitate annealing of complementary single strands of DNA is critical to repair of double strand breaks in T7.

Bacteriophage T7↗
PubMed2001

Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension.

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

Angiotensin II↗
PubMed2001

Exercise-associated differences in an array of proteins involved in signal transduction and glucose transport.

Vastus lateralis muscle biopsies were obtained from endurance-trained (running approximately 50 km/wk) and untrained (no regular physical exercise) men, and the expression of an array of insulin-signaling intermediates was determined. Expression of insulin receptor and insulin receptor substrate-1 and -2 was decreased 44% (P < 0.05), 57% (P < 0.001), and 77% (P < 0.001), respectively, in trained vs. untrained muscle. The downstream signaling target, Akt kinase, was not altered in trained subjects. Components of the mitogenic signaling cascade were also assessed. Extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase expression was 190% greater (P < 0.05), whereas p38 mitogen-activated protein kinase expression was 32% lower (P < 0.05), in trained vs. untrained muscle. GLUT-4 protein expression was twofold higher (P < 0.05), and the GLUT-4 vesicle-associated protein, the insulin-regulated aminopeptidase, was increased 4.7-fold (P < 0. 05) in trained muscle. In conclusion, the expression of proteins involved in signal transduction is altered in skeletal muscle from well-trained athletes. Downregulation of early components of the insulin-signaling cascade may occur in response to increased insulin sensitivity associated with endurance training.

Adult↗
PubMed2001

Health-related quality of life after stroke a comprehensive review.

BACKGROUND AND PURPOSE: We performed a comprehensive review of all quality-of-life (QOL) estimates for stroke appearing in the peer-reviewed literature between 1985 and 2000. We examine variation in QOL weights and the rigor of methods used to assess QOL and discuss the implications for cost-utility assessment and resource allocation decisions. METHODS: Through a systematic search, we identified 67 articles that met our inclusion criteria. A team of trained researchers read each article and followed detailed guidelines to extract QOL weights and other parameters. This effort yielded 161 QOL estimates for stroke-related health states. All estimates were measured on a 0 to 1 scale, with 0 representing the worst outcome and 1 representing the best. RESULTS: QOL estimates range from -0.02 to 0.71 (n=67) for major stroke, from 0.12 to 0.81 (n=14) for moderate stroke, from 0.45 to 0.92 (n=38) for minor stroke, and from 0.29 to 0.903 (n=42) for general stroke. Although QOL should decrease with severity, there were many instances in which the QOL for major stroke as reported by one study exceeded the QOL for moderate stroke as reported by another. The same reversal was found for moderate and minor stroke, and it occurred even when both authors used similar assessment methods and subject populations. Authors of cost-utility and decision analyses rarely base their choice of QOL weights on their own primary data (19%). When obtaining weights from secondary sources, some authors (23%) chose QOL weights for a severity of stroke that did not match the severity for which they sought data. CONCLUSIONS: QOL estimates for stroke vary greatly and are not always estimated in sound fashion. This impedes the comparability and quality of the cost-effectiveness studies that use these QOL weights and hampers good resource allocation decisions.

Cost-Benefit Analysis↗
PubMed2001

Isomer-specific antidiabetic properties of conjugated linoleic acid. Improved glucose tolerance, skeletal muscle insulin action, and UCP-2 gene expression.

Conjugated linoleic acid (CLA) isomers have a number of beneficial health effects, as shown in biomedical studies with animal models. Previously, we reported that a mixture of CLA isomers improved glucose tolerance in ZDF rats and activated peroxisome proliferator-activated receptor (PPAR)-gamma response elements in vitro. Here, our aim was to elucidate the effect(s) of specific CLA isomers on whole-body glucose tolerance, insulin action in skeletal muscle, and expression of genes important in glucose and lipid metabolism. ZDF rats were fed either a control diet (CON), one of two CLA supplemented diets (1.5% CLA) containing differing isoforms of CLA (47% c9,t11; 47.9% c10,t12, 50:50; or 91% c9,t11, c9,t11 isomers), or were pair-fed CON diet to match the intake of 50:50. The 50:50 diet reduced adiposity and improved glucose tolerance compared with all other ZDF treatments. Insulin-stimulated glucose transport and glycogen synthase activity in skeletal muscle were improved with 50:50 compared with all other treatments. Neither phosphatidlyinositol 3-kinase activity nor Akt activity in muscle was affected by treatment. Uncoupling protein 2 in muscle and adipose tissue was upregulated by c9,t11 and 50:50 compared with ZDF controls. PPAR-gamma mRNA was downregulated in liver of c9,t11 and pair-fed ZDF rats. Thus, the improved glucose tolerance in 50:50 rats is attributable to, at least in part, improved insulin action in muscle, and CLA effects cannot be explained simply by reduced food intake.

Adipose Tissue↗
PubMed2001

[Isolation and characterization of the porcine glial fibrillary acidic protein (GFAP) gene by CATS].

Primers for the glial fibrillary acidic protein (GFAP) gene were designed from a human cDNA sequence aligned with the mouse GFAP gene on the principle of comparative anchor tagged sequence (CATS). The 412 bp PCR product isolated from Chinese Erhualian pig genome was characterized as the porcine GFAP gene by comparing the sequence with the GenBank database. The chromosomal location of the GFAP gene is on pig Chr: 12(p11-(2/3)p13) using pig x rodent somatic cell hybrid panel.

Animals↗
PubMed2001

Genetic approach to insight into the immunobiology of human dendritic cells and identification of CD84-H1, a novel CD84 homologue.

To better understand the immunobiology of dendritic cells (DCs), we took the expressed sequence tag (EST) approach to describe their transcript profile and discovered novel genes. ESTs (n = 25,668) were generated from monocyte-derived DCs, and 15,863 ESTs (61.8%) represented unique genes in GenBank. Integration of ESTs allowed for the generation of a profile of 4,367 known genes and identification of > 100 novel genes. HLA-DR invariant chain p33, cathepsin D, HLA-DR alpha chain, beta2-microglobulin, HLA-DP beta chain, CD11a, and mannose receptor were in the top 30 transcripts, and 451 known genes were potentially associated with the immunobiology of DCs. This transcript profile was consistent with the unique antigen-presenting capacity of DCs and provided invaluable information to better understand the immunobiology of DCs. On the basis of the EST database, a full-length novel gene was identified that exhibited close homology with CD84; it was designated CD84-H1. The full-length cDNA of CD84-H1 contained an open reading frame of 870 bp encoding a type I transmembrane protein of 289 amino acids. Consistent with the structural feature of the CD2 family, the predicted 270-amino acid mature protein of CD84-H1 contained two extracellular immunoglobulin-like domains that shared homology with CD2 family members, e.g., CD84, Ly-9, CD48, and signaling lymphocyte activation molecule. Its intracellular domain was short and contained no putative signaling structure. Northern blot analysis revealed that CD84-H1 expression was predominantly restricted in hematopoietic tissues. Reverse transcription-PCR analysis showed that it was widely expressed in the immune cells, including monocytes, DCs, B cells, and T cells. These data indicate that CD84-H1 may be relevant to immune responses.

Adult↗
PubMed2001

CT virtual endoscopy of the auditory ossicular chain: clinical applications.

OBJECTIVE: To evaluate the clinical applications and limitations of CT virtual endoscopy (CTVE) in the auditory ossicular chain. METHODS: CTVE of the auditory ossicular chain was performed with 1.0 mm collimation at pitch 1.0, bone algorithm, 9.6 cm field of view, and 0.1-0.2 mm reconstruction interval in 40 patients with middle ear diseases. 30 cases were confirmed by surgery. Results were compared with the findings of axial high resolution CT (HRCT) and multiplanar reformation (MPR) images and surgery. RESULTS: The accuracy of CTVE images in detecting ossicular destruction was 92.6%, significantly higher than that of axial HRCT (83.9%) and multiplanar reformation (76.5%) images. CTVE could also clearly reveal the postoperative condition and congenital dysplasia of the auditory ossicular chain. CONCLUSIONS: CTVE can clearly demonstrate a three-dimensional image of the auditory ossicular chain and is useful in evaluating diseases of the ear, especially the auditory ossicles. CTVE could not clearly demonstrate abnormal soft tissue within the tympanic cavity, abnormal changes of the tympanic membrane and tympanic walls, and could be easily influenced by artificial factors.

Adolescent↗
PubMed2001

[A clinical analysis of 112 cases with glucocorticoid glaucoma].

OBJECTIVE: To investigate the etiology, clinical characteristics, treatment and prevention of glucocorticoid glaucoma (GIG). METHODS: Retrospectively, 112 cases (215 eyes) with GIG including 79 males and 33 females in the age range 6-69 years were studied. RESULTS: One hundred and ten cases used glucocorticoid locally, 2 cases used it systemically, and the mean therapeutic time was (27.5 +/- 23.18) months. Conjunctivitis of various causes was the main disease to use glucocorticoid, all 215 eyes had the defect of visual field caused by hypertension, damage of optic disc and retinal nerve fiber layers, just like primary open-angle glaucoma. The degree of injury was related to the therapeutic time. The IOP was decreased after the use of glucocorticoid was stopped, but it could not get to the normal level. There were 162 eyes (75.4%) with characteristic posterior subcapsular cataract and 76 cases combined with myopia. CONCLUSION: The important cause leading to GIG is the abuse of glucocorticoid. The history of using glucocorticoid and the posterior subcapsular cataract are the main bases in the diagnosis and differential diagnosis of GIG.

Adolescent↗