Biomedical subjects

C Qiu

Publications and source records attributed to C Qiu.

At least 73 records · Page 4Linked to original sources

PubMed1997

[Clinical use of bilateral cervico-thoracic skin flaps].

In order to study the clinical efficacy of bilateral cervico-thoracic skin flap on repairing the contracture of the burn scar of the neck, 66 flaps were used in 33 patients from 1983 to 1995. The size of the flap ranged from 5 cm x 6 cm to 8.5 cm x 15 cm. The donor site was covered with split skin graft. The ratio between the length and the width of the flaps should not exceed 3:1. Fifty-nine flaps survived completely, but 7 had necrosis of small area which was healed without any influence on the function and appearance. The operative technique of the bilateral cervico-thoracic skin flaps were reported. The advantages of this type of skin flap and its applied anatomy and the postoperative care were discussed. In the repair of the cicatritial contracture deformity of the neck, it was important to define whether the skin defect was located in the submandibular, anterior cervical or anterior thoracic region, thus appropriate type of repair could then be given accordingly.

Adolescent↗

PubMed1996

Importance of nitric oxide in the control of renal hemodynamics.

The kidney vasculature is under tonic control by nitric oxide (NO) and in cortex, NO controls RA and Kf. Systemic NO inhibition leads to systemic hypertension, increases in RE, mediated by Ang II and ET, and direct effects on RA and Kf. The relationship between NO and other vasoconstrictor systems is variable. In the conscious relaxed animal, vasoconstrictor activity is low, yet acute NO inhibition leads to pressor and renal vasoconstrictor responses. At physiologic levels, ET unexpectedly is a renal vasodilator, possibly via NO generation at RA. When vasoconstrictor activity is high, NO is very important in maintenance of renal perfusion. Chronic L-NAME produces dose dependent systemic and glomerular capillary hypertension and eventual proteinuria and glomerular damage. NO deficiency is key in this process, although the hypertension becomes refractory to L-arginine administration and dependent on Ang II and the SNS, by mechanisms not yet defined. In contrast, the renal vasculature remains fully responsive to L-arginine, suggesting that pressor and renal vascular responses to chronic NO inhibition are separately regulated. NO generated from iNOS does not normally control BP or renal hemodynamics. The relative contributions of NO from bNOS and eNOS, and importance of NOS in different locations in the kidney, remain to be determined.

Animals↗

PubMed1996

Phosphodiesterase inhibitors correct resistance to natriuretic peptides in rats with Heymann Nephritis.

Experimental nephrotic syndrome is characterized by abnormal sodium metabolism, reflected in a blunted natriuretic response both to volume expansion and to infused atrial natriuretic peptide (ANP). The studies presented here examined the relationships among plasma ANP concentration and urinary sodium (VNaV) and cyclic GMP excretion (UcGMPV) in vivo, and the responsiveness of isolated glomeruil and inner medullary collecting duct (IMCD) cells to ANP and urodilatin (renal natriuretic peptide; RNP) in vitro in rats with Heymann nephritis, an immunologically mediated model of nephrotic syndrome. Nine to 14 days after Ip injection of anti-Fx1A antiserum, rats were proteinuric and had a blunted natriuretic response to intravenous infusion of isotonic saline (2% body weight, given over 5 min). Thirty min after the onset of the infusion, plasma ANP concentration was increased to the same extent in both normal and nephritic rats, compared with their respective hydropenic controls. Despite this increase, UcGMPV was significantly less in nephritic rats after the saline infusion. Accumulation of cGMP by isolated glomeruil and IMCD cells from nephritic rats after incubation with ANP and RNP was also significantly reduced, compared with normal rats. This difference was not related to differences in either density or affinity of renal ANP receptors, but was abolished when accumulation of cGMP was measured in the presence of 10(-3) M isobutylmethylxanthine or Zaprinast, two different inhibitors of cyclic nucleotide phosphodiesterases (PDE). Infusion of Zaprinast into one renal artery in nephritic rats normalized both the natriuretic response to volume expansion and the increase in UcGMPV from the infused, but not the contralateral, kidney. Furthermore, cGMP-PDE activity was increased in IMCD cell homogenates from nephritic compared with normal rats (388 +/- 32 versus 198 +/- 93 pmol/min per mg protein, P < 0.03). These results indicate that blunted volume expansion natriuresis accompanied by cellular resistance to ANP in vitro occurs in an immunologic model of renal injury. The resistance is not related to an alteration in ANP release or binding to its renal receptors, but is suppressed by PDE inhibitors and is associated with increased renal cGMP. PDE activity, thus suggesting that enhanced cGMP-PDE activity may account for resistance to the natriuretic actions of ANP observed in vivo. This defect may represent the intrinsic sodium transport abnormality linked to sodium retention in nephrotic syndrome.

1-Methyl-3-isobutylxanthine↗

PubMed1996

The role of human leukocyte antigen in susceptibility and clinical manifestations of sarcoidosis.

OBJECTIVE: To investigate the correlation of human leukocyte antigen (HLA) with susceptibility and clinical manifestations of sarcoidosis. MATERIAL AND METHODS: Fifty-five patients with sarcoidosis and one hundred and six normal subjects were investigated. Genomic DNAs were purified using the proteinase K-phenol extraction method. DNA samples were amplified by the polymerase chain reaction (PCR) procedure using the DRB1 group specific primer pairs. RESULTS: The gene frequency of HLA-DR5 increased significantly in patients with sarcoidosis (P < 0.01), and HLA-DR7 decreased (P < 0.05). Gene frequencies of HLA-DR9 and HLA-DR5 increased remarkably in male patients and in patients with stage I and stage IIa, respectively (both P < 0.05). CONCLUSIONS: It is suggested that HLA-DR gene might contribute to the susceptibility as well as various clinical manifestations of sarcoidosis.

Adult↗

PubMed1996

[Induced-expression of MHC-DR molecules on mice islet cells].

The correlation of induced-expression of MHC-DR molecules with insulin release in cultured mice islet cells has been studied. The results showed that, (1) No detectable induced-expression of MHC-DR molecules by TNF-alpha alone at the concentration of 50-100 U/ml has been assayed, but the induced-expression of MHC-DR molecules has been identified in a few islet cells (8.5 +/- 2.9%) with IFN-r alone at concentration of 50-100 U/ml. (2) The induced-expression of MHC-DR molecules has been detected in as high as 80% of cultured islet cells with TNF-alpha and IFN-r combined at different concentrations. (3) Insulin released from cultured islet cells was enhanced by IFN-r and TNF-alpha either alone or combined at different concentrations. These results suggest that the induced-expression of MHC-DR molecules themselves does not damage the function for insulin release in cultured islet cells.

Animals↗

PubMed1996

HLA-DRB1 alleles genotyping in patients with rheumatoid arthritis in Chinese.

OBJECTIVE: To explore the role of HLA-DRB1 genes in the development of rheumatoid arthritis (RA) and the correlations between HLA-DR alleles and clinical manifestations of patients with RA. METHODS: 86 patients with rheumatoid arthritis and 106 race matched controls were studied in whom HLA-DR typing was performed by the method of DNA amplification with sequence-specific primers (PCR-SSP). The subtypes of HLA-DR4 were determined by the method of hybridization of PCR products with sequence-specific oligonucleotides (PCR-SSO). The absence or presence of HLA-DR4 and its subtypes was correlated with the clinical and serological characteristics of the patients. RESULTS: Compared with controls, an increased gene frequency of HLA-DR4 (48.8% vs 17.9%, P < 0.001) and a decreased frequency of HLA-DR7 (16.3% vs 27.4%, P = 0.06) were found. The DRB1* 0405 account for 61.9% of DR4+RA patients and 21.1% of DR4+ controls (P < 0.01). There was no difference between the DR4+ and DR4- patients with respect to age, sex, duration of disease, rheumatoid factor (RF), extra-articular manifestations including secondary Sjogren's syndrome. According to the wrist X-ray stage, the patients of DR4+ were more severe than that of DR4- (P < 0.05). CONCLUSION: HLA-DR4 and DR4 subtype of DRB1*0405 are related to the development of RA in Chinese. HLA-DR4 can be a useful prognostic marker in the patients with RA.

Alleles↗

PubMed1996

[Association of polymorphism in 5'-regulatory region of angiotensinogen gene with essential hypertension].

The association of the variant in the 5'-regulatory region of angiotensinogen gene with primary hypertension in the Han Nationality in China was studied by applying PCR-SSCP analysis and DNA cycle sequencing. The frequencies of three identified SSCP-patterns (pattern-A, B, C) in 73 hypertensive subjects were compared with those in 74 normal controls. It was found that the number of pattern-C was higher in the study group (5/73) than in the controls (1/74). The results of DNA sequencing showed that the difference of three SSCP-patterns was caused by a nucleotide substitution G-->A at -216 locus in the 5'-upstream region of angiotensinogen gene, and the subjects with pattern-C were homozygous for mutant A-allele (genotype A/A). These results suggest that the identified gene variant may be associated with primary hypertension.

Aged↗

PubMed1996

[Nucleotide sequence of HLA-DQA1 promoter region (QAP) in a lung cancer patient].

The HLA-DQA1 allele and nucleotide sequence of HLA-DQA1 promoter region (QAP) in a patient with IDDM complicated lung cancer have been identified by PCR/SSCP, PCR/SSCP and PCR/sequencing. The results showed that: (1) All of the lung cancer patient and his family members carried HLA-DQA1* 0301/0501 alleles. (2) a single base substitution G-->A at position -155 and deletion CAA at position -161 to -163 occurred in the patient. These results suggest that the mutation of HLA-DQA1 promoter region may modulate HLA-DQA1 gene expression by trans-acting factors binding to variant cis-acting elements and may be responsible for pathogenesis of lung cancer.

Alleles↗

PubMed1995

Acute changes in urinary excretion of nitrite + nitrate do not necessarily predict renal vascular NO production.

NO2 + NO3 (NOx), the stable oxidation products of NO, and cGMP are widely accepted as indices of in vivo NO production. Whether acute changes in urinary excretion of nitrite + nitrate (UNOXV) can be taken to reflect acute changes in renal and/or systemic NO production is not known. The present studies were conducted in the conscious rat to investigate the effect on acute changes in UNOxV, of maneuvers that (a) enhance NO production and (b) act as diuretics. L-arginine (L-arg) and acetylcholine (Ach) produce equivalent NO dependent falls in renal vascular resistance (RVR), but a much greater increase in UNOX V is seen with L-arg. D-arg does not stimulate NO and has no renal vasodilatory effect, but produces a large rise in UNOX V, and SNP lowers BP but not RVR and results in a reduced UNOX V. None of the diuretics employed should stimulate the NO system or lower RVR; however, the proximally acting agents, acetazolamide and D-arg increased UNOx V, while the loop diuretic furosemide had little effect. H2O diuresis (a distal event) led to a fall in UNOx V. These data suggest that NOx is reabsorbed extensively in the proximal tubule and that inhibition of proximal reabsorption leads to an increase in UNOx V. Also, our results show that the relationship between UNOx V and UcGMP V is unpredictable. Therefore, we conclude that measurements of acute changes in UNOxV and/or UcGMP V should be interpreted cautiously, since they may reflect altered tubular handling of NOx rather than the acute activity of the systemic and/or renal NO systems.

Acetylcholine↗

PubMed1995

Actions of endogenous endothelin on glomerular hemodynamics in the rat.

Both endothelin (ET) ETA/ETB receptors are distributed in the glomerular microcirculation, but their physiological functions, if any, are unknown. We used a nonpeptide mixed ETA/ETB receptor antagonist (Bosentan) and a selective ETA receptor antagonist (BQ-123) to investigate the glomerular hemodynamic actions of endogenous ET in the anesthetized euvolemic rat. Blockade of ETA and ETB receptors with Bosentan produced a small fall in systemic blood pressure and a large fall in glomerular blood pressure due to a significant increase in preglomerular (afferent) arteriolar resistance. Single-nephron glomerular filtration rate was not reduced because of an offsetting rise in the glomerular capillary ultrafiltration coefficient. Blockade of the selective ETA receptor with BQ-123 had no effect on blood pressure or glomerular hemodynamics. These observations indicate that endogenous ET is of physiological importance in control of glomerular hemodynamics. Surprisingly, endogenous ET tonically dilates rather than contracts the preglomerular arteriole, and it also tonically lowers the glomerular capillary ultrafiltration coefficient, probably by contracting the mesangial cell. All physiological glomerular actions of ET are mediated via the ETB receptor.

Animals↗

PubMed1995

Renal effects of acute amino acid infusion in hypertension induced by chronic nitric oxide blockade.

L-Arginine is the physiological substrate of nitric oxide, a vasodilator that controls blood pressure and renal hemodynamics in the basal state. In the present studies, we produced chronic nitric oxide blockade by oral administration of the L-arginine analogue NG-nitro-L-arginine methyl ester, which produced sustained hypertension and increased renal vascular resistance in conscious rats. Acute excess L-arginine had little effect on blood pressure but completely normalized renal vascular resistance and increased renal plasma flow in chronically nitric oxide-blocked hypertensive rats. In contrast to L-arginine, D-arginine had no renal hemodynamic effects in either normal or chronically nitric oxide-blocked rats. Acutely administered glycine was ineffective in vasodilating the chronically nitric oxide-blocked rat kidney, in a dose that produced renal vasodilation in normal rats. These findings indicate the following: (1) Hypertension induced by chronic nitric oxide blockade due to substituted L-arginine analogue cannot be acutely reversed with excess L-arginine, suggesting that the maintenance of the hypertension is not solely caused by competitive inhibition of nitric oxide production; (2) in contrast, the kidney remains responsive to L-arginine whereas the renal vasodilator response to glycine is abolished in this model of hypertension.

Animals↗

PubMed1995

Endothelin modulates the pressor actions of acute systemic nitric oxide blockade.

Acute nitric oxide blockade not only potentiates the vasoconstrictor actions of endothelin but also enhances the synthesis and release of endothelin. To investigate whether the vasoconstrictor actions of acute nitric oxide blockade are modulated by endothelin, studies were conducted in the conscious, chronically catheterized rat. Renal function was measured before and during acute nitric oxide blockade with nitro-L-arginine methylester (L-NAME), L-NAME + endothelin blockade with the endothelin-converting enzyme inhibitor phosphoramidon, or L-NAME + the nonpeptide ETA and ETB receptor antagonist Bosentan. The increases in blood pressure and RVR seen with acute nitric oxide blockade were attenuated by either method of concomitant endothelin blockade. The falls in RPF and GFR were not blunted because endothelin blockade produced parallel reductions of both pressor and renal vasoconstrictor responses to acute nitric oxide blockade. Endothelin blockade alone with either endothelin-converting enzyme inhibitor or the nonpeptide ETA and ETB receptor antagonist had little effect on blood pressure, RPF, or RVR, but increases in urinary sodium excretion and a small decline in GFR were observed with Bosentan. These observations indicate that endogenous endothelin exerts a tonic antinatriuretic action in the normal conscious rat and partially mediates the pressor actions of acute nitric oxide blockade.

Animals↗

PubMed1995

An association study between essential hypertension and HLA-DRB1 alleles.

It is well established that genetic and environmental factors are involved in the etiology of essential hypertension (EH). Previous studies have suggested that at least one of the HLA genes is responsible for the genetic susceptibility to EH. Our aim in the present study was to investigate this issue in China by the PCR-SSP HLA-DRB1 typing method. The results showed an increased frequency of HLA-DR2 and a decreased frequency of HLA-DR7 with EH patients compared with controls. We consider that HLA-DR2 may represent a marker for susceptibility to EH in the North Chinese population.

Alleles↗

PubMed1995

[Detection of mutation in insulin receptor gene in patients with essential hypertension].

We have analyzed single-stranded conformational polymorphism (SSCP) to screen for mutation in exon 17 of insulin receptor gene in 46 patients with hypertension and 49 normotensive controls. Three different SSCP patterns were detected in both patients and controls and the frequency of pattern I was 54.3% and 32.7% (chi 2 = 3.71, P = 0.05) in patients and controls respectively; The frequency of pattern II was 61.3% and 26.1% (chi 2 = 10.49, P = 0.001) in controls and patients respectively; the frequency of pattern III did not differ between controls and patients. Based on direct sequencing, the differences between pattern II and pattern I were explained by a mutation substituting at position 1040, GAG1040-->GAA1040, which suggests that codon GAA1040 may be a genetic marker for susceptibility to essential hypertension in Chinese.

Adult↗

PubMed1995

Modulation of ANP-dependent effects of endothelin by inhibitors of neutral endopeptidase and cGMP phosphodiesterase.

Endothelin 3 (ET3) infusion increases the concentration of atrial natriuretic peptide (ANP) in plasma, which in turn raises hematocrit (Hct) through a transcapillary shift of plasma fluid and proteins into the interstitium, thereby reducing plasma volume (PV). The level of ANP bioactivity in peripheral target tissues is a function of ANP secretory rate and the turnover rate of ANP and its intracellular effector mechanisms. Neutral endopeptidase (NEP) is a widely distributed enzyme that participates in ANP catabolism, whereas cGMP-phosphodiesterase (PDE) degrades the intracellular second messenger of ANP. Therefore, we examined the consequences of inhibition of NEP and PDE on the ANP-dependent activity described above using the NEP inhibitor SQ 28,603 and the cGMP-PDE inhibitor zaprinast (M&B 22,948). In anesthetized, bilaterally nephrectomized rats, infusion of SQ 28,603 alone reduced mean arterial pressure (MAP) by 2.5 +/- 0.5% and increased Hct by 4.6 +/- 0.3% (P < .01 for both), leading to a calculated decrease in PV of 7.5 +/- 0.6%. These changes were prevented by pretreatment with rabbit anti-rat ANP antiserum. Simultaneous infusion of ET3 (25 ng/kg/min) and SQ 28,603 caused MAP to increase by 12.8 +/- 2.2%, an effect identical with that observed after ET3 alone (12.7 +/- 2.3%), whereas the increase in Hct of 9.4 +/- 0.4% was greater (P < .05) than the 7.5 +/- 0.4% increase seen with ET3 alone. ET3 increased plasma ANP concentration (599 +/- 135 vs. 108 +/- 13 pg/ml in vehicle-infused rats; P < .0001); ET3 and SQ 28,603 infused simultaneously increased plasma ANP even further (810 +/- 166 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1995

Rapid HLA-DRB1 generic typing by PCR-SSP method.

We report a simple and rapid HLA-DRB1 generic typing method, PCR-SSP, which is practical and inexpensive. We use 9 sequence-specific primers and 2 group specific primers to define the HLA-DRB1 specificities DR1, DR2, DR3, DR4, DR5, DR6, DR7, DR8, DR9 and DR10. The HLA DR3, DR5, DR6 and DR8 can be amplified by the two primers of DR3568 and DRB1. The DR6 specificity can be identified by excluding the DR3, DR5 and DR8 when the DR3568 are positive. Any individuals can be typed with some exception: the three pairs of phenotype DR3/DR3 and DR3/DR6, DR5/DR5 and DR5/DR6, DR8/DR8 and DR8/DR6 cannot be discriminated from each other. We typed 106 unrelated healthy people from Beijing locations in two weeks. We think this typing method is suitable to replace the error-prone serologic HLA-DR tests in routine clinical practice, including the prospective typing of cadaveric organ donors.

Base Sequence↗

PubMed1995

[Analysis of HLA-DRB1 alleles in patients with IDDM].

HLA-DR association with IDDM in local population in Beijing was studied by PCR/SSP typing. The frequency of HLA-DR9 was significantly higher in diabetic patients (30.3% [45/148] vs 17.92% [38/212], chi 2 = 6.97, P < 8.3 x 10(-3)). DR3 was higher in diabetic patients in this study (7.0% [10/148] vs 2.36% [5/212], chi 2 = 3.19, P > 0.05) and DR2 was lower in patients with IDDM (7.4% [11/148] vs 19.8% [42/212], chi 2 = 9.67, P < 1.9 x 10(-3)). These results suggest that DR9 and DR3 both were positively associated with IDDM, but DR2 was negatively associated with IDDM.

Adolescent↗

PubMed1994

Angiotensin II and alpha 1-adrenergic tone in chronic nitric oxide blockade-induced hypertension.

Nitric oxide (NO) is a tonically produced vasodilator that maintains blood pressure (BP) in the normal animal. In these studies, we produced chronic NO blockade by oral administration of the NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME), which produced sustained hypertension and increased renal vascular resistance (RVR) in conscious rats. Acute blockade of the angiotensin II type 1 (AT1) receptor with losartan had little effect on BP and RVR in either chronically NO-blocked or normal conscious rats. Acute blockade of the alpha 1-adrenoceptor with prazosin produced moderate similar falls in BP in both chronically NO-blocked and normal rats. The combination of AT1 and alpha 1-adrenoceptor blockade was profoundly antihypertensive and was particularly effective in lowering BP in chronically NO-blocked rats where the hypertension was obliterated. In contrast, the increased RVR persisted in chronically NO-blocked rats receiving combined acute AT1 and alpha 1-adrenoceptor blockade. These observations indicate that, in the sustained phase of chronic NO blockade, the hypertension is largely due to the combined activities of alpha 1-adrenoceptor and AT1 stimulation.

Administration, Oral↗