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Biomedical subjects

J Mao

Publications and source records attributed to J Mao.

At least 73 records · Page 4Linked to original sources

Pathology, isolation, and preliminary molecular characterization of a novel iridovirus from tiger salamanders in Saskatchewan.

All iridovirus was confirmed to be the cause of an epizootic in larval and adult tiger salamanders (Ambystoma tigrinum diaboli) from four separate ponds in southern Saskatchewan (Canada) during the summer of 1997. This organism also is suspected, based on electron microscopic findings, to be the cause of mortality of larval tiger salamanders in a pond over 200 km to the north during the same year. Salamanders developed a generalized viremia which resulted in various lesions including: necrotizing, vesicular and ulcerative dermatitis; gastrointestinal ulceration; and necrosis of hepatic, splenic, renal, lymphoid, and hematopoietic tissues. In cells associated with these lesions, large lightly basophilic cytoplasmic inclusions and vacuolated nuclei with marginated chromatin were consistently found. Virus was isolated from tissue homogenates of infected salamanders following inoculation of epithelioma papilloma cyprini (EPC) cells. The virus, provisionally designated Regina ranavirus (RRV), was initially identified as an iridovirus by electron microscopy. Subsequent molecular characterization, including partial sequence analysis of the major capsid protein (MCP) gene, confirmed this assignment and established that RRV was a ranavirus distinct from frog virus 3 (FV3) and other members of the genus Ranavirus. Intraperitoneal inoculation of 5 x 10(6.23) TCID50 of the field isolate caused mortality in inoculated salamanders at 13 days post infection. Field, clinical, and molecular studies jointly suggest that the etiological agent of recent salamander mortalities is a highly infectious novel ranavirus.

Ambystoma↗

[Multivariate analysis of clinical factors in restenosis after coronary interventional treatment].

OBJECTIVE: To found the independent predictors for restenosis after coronary interventional treatment. METHODS: Quantitative angiography was performed in 103 patients(128 successfully dilated lesions) at angioplasty and at 6-month follow-up, and then univariate analysis and multivariate logistic regression analysis were performed to identify correlates of restenosis with clinical factors. RESULTS: The total restenosis rate was 39.8% (51 of 128 lesions). According to univariate analysis, the patients who had undergone coronary tenting > or = 3.5 mm had a lower rate of restenosis(3/29 and 6/30) and the others with the ACC/AHA lesion type B and C(46/51 and 51/77), collateral circulation to the obstruction set(17/51 and 2/77), high percentage diameter stenosis before PTCA(86 +/- 14)% and (79 +/- 15)%, and high maximal inflation pressure(8.3 +/- 2.1) kPa and (7.4 +/- 1.7) kPa had a higher rate of restenosis (P < 0.01). Stable angina showed a low restenosis rate (3/29 and 6/30). The less minimal lumen diameter before(0.43 +/- 0.41) mm and (0.66 +/- 0.43) mm and after PTCA(2.56 +/- 0.55) mm and (2.85 +/- 0.59) mm, had the higher the restenosis rate (P < 0.05). Multivariate logistic regression analysis showed that coronary stenting had a low rate of restenosis, and that lesion type B and C, high percentage diameter stenosis before PTCA, high maximal inflation pressure, and male had a high rate of restenosis. CONCLUSION: Coronary stent, percentage diameter stenosis before PTCA, lesion type, maximal inflation pressure, and sex were independent predictors for restenosis.

Aged↗

[Evaluating retinal nerve fiber layer by scanning laser ophthalmoscopy].

OBJECTIVE: To evaluate the efficiency of scanning laser ophthalmoscopy (SLO) on detecting retinal nerve fiber layer defects (RNFLD). METHODS: 95 eyes with primary open angle glaucoma, 37 ocular hypertension, 83 glaucomatous suspect and 34 normal eyes were investigated by SLO to evaluate the retinal nerve fiber layer (RNFL). Recording tapes of 68 eyes were re-investigated by two investigators for estimating the intra- and inter-observer agreement. RESULTS: The intra- and inter-observer agreement of the presence and types of RNFLD was fairly good (Kappa values were 0.66 - 0.76 and 0.59 - 0.65 respectively). The sensitivity and specificity in detecting RNFLD by SLO were 80.0% and 94.1% respectively. CONCLUSION: The evaluation of RNFL by SLO is a quick, accurate and safe method. It may be clinically useful in the diagnosis of glaucoma.

Glaucoma↗

[Prevalence of blindness among adults aged 50 years or above in Shunyi county of Beijing].

OBJECTIVE: To estimate the prevalence of blindness among older adults aged >or= 50 years in Shunyi county of Beijing, China. METHODS: Cluster sampling was used in randomly selecting individuals aged >or= 50 years in 28 villages in Shunyi county in fall, 1996. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. RESULTS: 5,555 individuals were enumerated. The response rate was 91.5%. In this population, the prevalence of blindness was 1.7% defined as pinhole visual acuity < 0.05 in both eyes; or 2.8% were blind, defined as presenting visual acuity < 6/60 in both eyes. Blindness was associated with older age and female gender. The principal cause of blindness in eyes was cataract. CONCLUSIONS: The prevalence of blindness was decreased 35.8% after ten year active eye-care program in the survey area. However, cataract blindness continues as a significant problem among elderly, especially females, in this population sample of rural area.

Age Factors↗

Guanine nucleotide exchange factor GEF115 specifically mediates activation of Rho and serum response factor by the G protein alpha subunit Galpha13.

Signal transduction pathways that mediate activation of serum response factor (SRF) by heterotrimeric G protein alpha subunits were characterized in transfection systems. Galphaq, Galpha12, and Galpha13, but not Galphai, activate SRF through RhoA. When Galphaq, alpha12, or alpha13 were coexpressed with a Rho-specific guanine nucleotide exchange factor GEF115, Galpha13, but not Galphaq or Galpha12, showed synergistic activation of SRF with GEF115. The synergy between Galpha13 and GEF115 depends on the N-terminal part of GEF115, and there was no synergistic effect between Galpha13 and another Rho-specific exchange factor Lbc. In addition, the Dbl-homology (DH)-domain-deletion mutant of GEF115 inhibited Galpha13- and Galpha12-induced, but not GEF115 itself- or Galphaq-induced, SRF activation. The DH-domain-deletion mutant also suppressed thrombin- and lysophosphatidic acid-induced SRF activation in NIH 3T3 cells, probably by inhibition of Galpha12/13. The N-terminal part of GEF115 contains a sequence motif that is homologous to the regulator of G protein signaling (RGS) domain of RGS12. RGS12 can inhibit both Galpha12 and Galpha13. Thus, the inhibition of Galpha12/13 by the DH-deletion mutant may be due to the RGS activity of the mutant. The synergism between Galpha13 and GEF115 indicates that GEF115 mediates Galpha13-induced activation of Rho and SRF.

3T3 Cells↗

Specific involvement of G proteins in regulation of serum response factor-mediated gene transcription by different receptors.

Regulation of serum response factor (SRF)-mediated gene transcription by G protein subunits and G protein-coupled receptors was investigated in transfected NIH3T3 cells and in a cell line that was derived from mice lacking Galphaq and Galpha11. We found that the constitutively active forms of the alpha subunits of the Gq and G12 class of G proteins, including Galphaq, Galpha11, Galpha14, Galpha16, Galpha12, and Galpha13, can activate SRF in NIH3T3 cells. We also found that the type 1 muscarinic receptor (m1R) and alpha1-adrenergic receptor (AR)-mediated SRF activation is exclusively dependent on Galphaq/11, while the receptors for thrombin, lysophosphatidic acid (LPA), thromboxane A2, and endothelin can activate SRF in the absence of Galphaq/11. Moreover, RGS12 but not RGS2, RGS4, or Axin was able to inhibit Galpha12 and Galpha13-mediated SRF activation. And RGS12, but not other RGS proteins, blocked thrombin- and LPA-mediated SRF activation in the Galphaq/11-deficient cells. Therefore, the thrombin, LPA, thromboxane A2, and endothelin receptors may be able to couple to Galpha12/13. On the contrary, receptors including beta2- and alpha2-ARs, m2R, the dopamine receptors type 1 and 2, angiotensin receptors types 1 and 2, and interleukin-8 receptor could not activate SRF in the presence or absence of Galphaq/11, suggesting that these receptors cannot couple to endogenous G proteins of the G12 or Gq classes.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Tec/Bmx non-receptor tyrosine kinases are involved in regulation of Rho and serum response factor by Galpha12/13.

A transient transfection system was used to identify regulators and effectors for Tec and Bmx, members of the Tec non-receptor tyrosine kinase family. We found that Tec and Bmx activate serum response factor (SRF), in synergy with constitutively active alpha subunits of the G12 family of GTP-binding proteins, in transiently transfected NIH 3T3 cells. The SRF activation is sensitive to C3, suggesting the involvement of Rho. The kinase and Tec homology (TH) domains of the kinases are required for SRF activation. In addition, kinase-deficient mutants of Bmx are able to inhibit Galpha13- and Galpha12-induced SRF activation, and to suppress thrombin-induced SRF activation in cells lacking Galphaq/11, where thrombin's effect is mediated by G12/13 proteins. Moreover, expression of Galpha12 and Galpha13 stimulates autophosphorylation and transphosphorylation activities of Tec. Thus, the evidence indicates that Tec kinases are involved in Galpha12/13-induced, Rho-mediated activation of SRF. Furthermore, Src, which was previously shown to activate kinase activities of Tec kinases, activates SRF predominantly in Rho-independent pathways in 3T3 cells, as shown by the fact that C3 did not block Src-mediated SRF activation. However, the Rho-dependent pathway becomes significant when Tec is overexpressed.

3T3 Cells↗

Protein folding stability can determine the efficiency of escape from endoplasmic reticulum quality control.

A fraction of each secreted protein is retained and degraded by the endoplasmic reticulum (ER) quality control apparatus that restricts export to correctly folded proteins. The intrinsic biophysical attributes that determine efficiency of escape from this proofreading process have been examined by expressing mutants of bovine pancreatic trypsin inhibitor (BPTI) in yeast. Secretion efficiency is strongly correlated with thermodynamic stability for a series of six point mutations of BPTI. No correlation of secretion efficiency with either oxidative folding or refolding rates in vitro is found; both the rapidly folded Y35L BPTI mutant and the slowly unfolded G36D BPTI mutant exhibit low secretion efficiency. Elimination of cysteines 14 and 38 by mutagenesis does not increase secretion efficiency, indicating that intramolecular thiol/disulfide rearrangements are not primarily responsible for retention and degradation of destabilized BPTI variants. Mutant yeast strains with diminished ER-associated degradation do not secrete BPTI more efficiently, indicating that retention and degradation are separable processes. These data support a model for ER quality control, wherein protein folding is functionally reversible and the relative rates of folding, unfolding, vesicular export, and retention determine secretion efficiency.

Aprotinin↗

Antinociceptive tolerance to the mu-opioid agonist DAMGO is dose-dependently reduced by MK-801 in rats.

Morphine has been used in previous studies that investigate interactions between the spinal cord mu-opioid and N-methyl-D-aspartate (NMDA) receptors in mechanisms of antinociceptive tolerance. Although morphine acts primarily on the mu-receptor, it also activates other subtypes of opioid receptors. In the present study, the selective mu-opioid agonist, D-Ala2-N-Me-Phe4,Gly-ol5-enkephalin (DAMGO), was used to further test the hypothesis. Repeated intrathecal (i.t.) administration of 6 microg DAMGO (twice daily) in rats for 7 days resulted in an approximately 17-fold rightward shift of the cumulative dose-response curve (the tail-flick test) on Day 8 compared to that on Day 1. This rightward shift of the dose-response curve was prevented by the i.t. co-administration with DAMGO of the NMDA receptor antagonist MK-801 (10 = 5 > 2.5 >> 1.25 nmol > saline). Further, a lower dose range of MK-801 (2.5 > 1.25 nmol > 0.625 > 0.313 = saline) was effective to prevent the antinociceptive tolerance to a lower dose (1.5 microg) of DAMGO using the same i.t. administration regimen. Thus, the present results provide further evidence supporting a cellular and intracellular model of opioid tolerance involving interactions between the mu-opioid and the NMDA receptors in the spinal cord.

Analgesics↗

Molecular cloning and characterization of the porcine calcitonin gene-related peptide receptor.

Calcitonin gene-related peptide (CGRP) receptors (CGRP-Rs) are widely distributed throughout the central and peripheral nervous systems. A novel CGRP-R was identified from a porcine lung complementary DNA library. Sequence analysis indicated that the CGRP-R is 462 amino acids in length and shares 93% sequence identity with the human CGRP-R. Northern blot analysis indicated a messenger RNA species of 5.4 kilobases, which is abundantly expressed in the lung. Ligand binding studies of the cloned CGRP-R expressed in human embryonic kidney (HEK-293) cells showed the presence of high affinity receptor for CGRP with a Kd of 38.5 pM. The pharmacological profiles of various ligands competing for [125I]CGRP binding to the expressed receptor were in accordance with those for the natural receptor. Binding of [125I]CGRP to the expressed receptor was decreased in the presence of a nonhydrolyzable analog of GTP, guanosine 5' (gamma-thio)-triphosphate. In functional studies, CGRP stimulated the activation of adenylyl cyclase with an EC50 of 2.5 nM. The linear analog of CGRP, diacetoamidomethyl cysteine CGRP, did not affect adenylyl cyclase activity on its own or in the presence of CGRP. Furthermore, the CGRP receptor antagonists, CGRP-(8-37)alpha, inhibited the CGRP-mediated response in a competitive manner. Collectively, the binding and functional data demonstrate that we have cloned a porcine CGRP type 1 receptor. The availability of the CGRP-R complementary DNA will allow us to examine its participation in pathophysiological processes.

Amino Acid Sequence↗

Progesterone therapy during early pregnancy and embryonal survival in primiparous weaned sows.

The experiment was conducted in primiparous sows to determine whether progesterone supplementation during early pregnancy could improve embryonal survival and to confirm a functional relationship between progesterone concentrations in the postovulatory period and embryonal survival. Thirty-four primiparous sows were fed for ad libitum intake from farrowing to d 21 of lactation, restricted to 50% of ad libitum intakes between d 22 and 28, weaned on d 27, and then fed for ad libitum intake from weaning until d 28 of gestation. The number of pigs per litter was standardized to nine within 48 h after farrowing. After mating, sows were allocated either to be treated with ethyl oleate (control group) or to receive progesterone (P4) therapy (progesterone group) as 2 mg of P4/kg(.75) i.m., every 12 h from 36 to 96 h after onset of standing estrus. There was no difference in the weaning-to-estrus interval (123.5 +/- 5.7 vs 123.1 +/- 5.9 h) and number of corpora lutea (18.1 +/- .4 vs 18.3 +/- .5) between the control and progesterone sows (P > .05). Compared with a more gradual increase in control sows, plasma progesterone concentrations in progesterone sows increased immediately from .6 +/- .1 ng/mL at 36 h after onset of standing estrus to 6.3 +/- .5 ng/mL (P < .001) 12 h later and remained high. Total number of embryos, total embryonal survival rate, number of viable embryos, and viable embryonal survival rate on d 28 of gestation in control sows were greater than in progesterone sows (13.3 +/- 1.0 vs 8.5 +/- 1.1; 73.1 +/- 4.7 vs 47.3 +/- 5.4%, P < .005; 12.6 +/- .9 vs 7.1 +/- .9, and 69.5 +/- 4.2 vs 39.7 +/- 4.8%, P < .0005; respectively). Embryonal survival in control sows was comparable to that in previous experiments using the same primiparous sow model, and the relationship between plasma progesterone and embryonal survival seemed similar. However, using the treatment schedule adopted, progesterone not only failed to reverse the presumed detrimental effect of increased catabolism in the late lactation period on embryonal survival, but also adversely affected the number of embryos at d 28 in 7 out of 15 progesterone-treated sows.

Animals↗

[Mathematical diagnosis of idiopathic-hypoparathyroidism].

The present study devotes to diagnose idiopathic-hypoparathyroidism (IHP) by means of ratio of calcium and phosphorus and product of calcium and magnesium. Among 23 cases of IHP patients the coincidence of ratio (Ca/P) and low-calcium/high-phosphorus in blood was 95.7%. Among 17 cases of IHP patients the coincidence of product (Ca x Mg) low-calcium and low magnesium was 91.4%. It indicates that ratio (Ca/P) and product (Ca x Mg) are effective mathematical diagnosis of IHP.

Adolescent↗

Increased dopaminergic transmission mediates the wake-promoting effects of CNS stimulants.

Amphetamine-like stimulants are commonly used to treat sleepiness in narcolepsy. These compounds have little effect on rapid eye movement (REM) sleep-related symptoms such as cataplexy, and antidepressants (monoamine uptake inhibitors) are usually required to treat these symptoms. Although amphetamine-like stimulants and antidepressants enhance monoaminergic transmission, these compounds are non-selective for each monoamine, and the exact mechanisms mediating how these compounds induce wakefulness and modulate REM sleep are not known. In order to evaluate the relative importance of dopaminergic and noradrenergic transmission in the mediation of these effects, five dopamine (DA) uptake inhibitors (mazindol, GBR-12909, bupropion, nomifensine and amineptine), two norepinephrine (NE) uptake inhibitors (nisoxetine and desipramine), d-amphetamine, and modafinil, a non-amphetamine stimulant, were tested in control and narcoleptic canines. All stimulants and dopaminergic uptake inhibitors were found to dose-dependently increase wakefulness in control and narcoleptic animals. The in vivo potencies of DA uptake inhibitors and modafinil on wake significantly correlated with their in vitro affinities to the DA and not the NE transporter. DA uptake inhibitors also moderately reduced REM sleep, but this effect was most likely secondary to slow wave sleep (SWS) suppression, since selective DA uptake inhibitors reduced both REM sleep and SWS proportionally. In contrast, selective NE uptake inhibitors had little effect on wakefulness, but potently reduced REM sleep. These results suggest that presynaptic activation of DA transmission is critical for the pharmacological control of wakefulness, while that of the NE system is critical for REM sleep regulation. Our results also suggest that presynaptic activation of DA transmission is a key pharmacological property mediating the wake-promoting effects of currently available CNS stimulants.

Animals↗

[Clinical study on effect of concentrated xuefu zhuyu pill on restenosis of 43 cases coronary heart disease after intracoronary stenting].

OBJECTIVE: To explore the clinical effectiveness of concentrated Xuefu Zhuyu Pill (CXZP) on restenosis (RS) of coronary heart disease (CHD) after intracoronary stenting. METHODS: Eighty-four successful intracoronary stenting patients were randomly divided into conventional treatment group (control group, 41 cases) and conventional treatment plus CXZP group (treated group, 43 cases). The follow-up underwent for 6 months. Clinical symptom, change of blood stasis were observed. And occurrence of restenosis was estimated by ECG exercise treadmill testing, emission computed tomography (ECT) and coronary angiography (CAG). RESULTS: The symptoms of blood stasis of treated group improved in the follow-up significantly (P < 0.01), and the integral of blood stasis were decreased significantly in the treated group vs the conventional treatment group (P < 0.01). The recurrent angina pectoris rate of the treated group was lower than the conventional treatment group (P < 0.01). The 61.9% of 84 patients reexamined the CAG in the follow up, and the lower restenosis rate (25.8%) in the treated group than in the conventional treatment group (32.1%, P = 0.59). CONCLUSION: There is the trend that CXZP could prevent restenosis. Therefore, it is necessary to increase the cases for further study of CXZP on preventing restenosis.

Adult↗

[Pathophysiology and surgical treatment on Relaxed Pelvic Floor Syndrome].

OBJECTIVE: To study the pathophysiology of the "Relaxed Pelvic Floor Syndrome (RPFS)" and to assess the value of the "Pelvic Cavity Fixation Operation (PCFO)" for the syndrome. METHOD: 11 patients, who were diagnosed as having RPFS, underwent standardized PCFO. All the patients were followed for a mean time of 19 months (5 - 72 months). RESULT: The main syndromes and signs included difficulty in defecation, inability to empty the rectum properly, fullness of perineum, protrusion of perineum at bearing down, back-inclining uterus, relaxation of the rectum on digital examination. The anorectal dynamics showed that the sequence pressure and rest pressure of the anal cannel were lower and the time of contraction of the anal cannel decreased than that of the normal controls. The rectum sensation was damaged slightly. Defeacography showed that there were relaxing changes in several systems in the pelvic cavity. Operatively, it was easy to see the relaxation of the supporting structure of the colon, rectum, uterus and the lower position of the peritoneal cavity. PCFO has achieved good results. Seven patients were free of symptoms completely and 4 improved. CONCLUSION: The relaxing changes of the supporting tissue of many viscus fefer to several systems are the pathophysiologic of the RPFS. "Pelvic Cavity Fixation Operation" is useful in the treatment of the syndrome.

Adult↗

[Apraclonidine prevents the acute increase of intraocular pressure in brown eyes with Nd:YAG laser iridectomy].

OBJECTIVE: To investigate if apraclonidine can effectively prevent the acute increase of intraocular pressure (IOP) in brown eyes with Nd:YAG laser iridectomy. METHODS: 48 eyes with primary angle closure glaucoma were divided into treatment and control groups, which were matched by age and sex. One drop of apraclonidine was applied into the conjunctival sac at one hour before laser iridectomy and immediately after laser iridectomy in treatment group, whereas one drop of antibiotic as placebo was applied in control group at the same time. IOP, pupil diameter were measured at 0.5, 1, 1.5, 2, 3.5 hours after laser iridectomy. RESULTS: The maximum increase of IOP after laser iridectomy was 0.62 +/- 0.67 kPa and 1.13 +/- 0.87 kPa in treatment and control group respectively, there was a significant difference (P = 0.03). The obvious decrease of IOP occurred at 0.5, 1 and 1.5 hours after laser iridectomy in treatment group. No ocular and systemic side effects were found in treatment group, except pupil diameter was obviously larger in treatment group than that in control group. CONCLUSION: 1% apraclonidine effectively prevents the acute increase of IOP in brown eyes with Nd:YAG laser iridectomy.

Clonidine↗