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Biomedical subjects

F Zhang

Publications and source records attributed to F Zhang.

At least 469 records · Page 26Linked to original sources

Mechanical evaluation of anastomotic tension and patency in arteries.

This study quantified arterial anastomotic tension, evaluated subsequent patency rates, and examined the degree of tension reduction with vessel mobilization. The study was divided into two components. In part I, a mechanical analysis was undertaken to evaluate tension, based on the determination of the force required to deflect a cable (vessel) laterally, and its resulting lateral displacement. Six Sprague-Dawley rats with 12 femoral arteries were divided into two subgroups: 1) no mobilization; and 2) axial mobilization by ligation and transection of superficial epigastric and gracilis muscular branches. The tension of femoral arterial anastomoses was calculated in vessels with no segmental defect and with 1.5-, 3-, 4.5-, 6-, and 7.5-mm defects. In part II, patency was evaluated. Fifty-five rats with 110 femoral arteries were divided into two sub-groups as defined in part I: 1) no mobilization; and 2) axial mobilization by ligation and transection of superficial epigastric and gracilis muscular branches. Microvascular anastomoses were performed with no segmental defect and with 1-, 2-, 3-, 4-, 5-, 6-, 7-, 8-, 9-, and 10-mm segmental vessel defects. Patency was evaluated 24 hr postoperatively. Part I of the study revealed that anastomotic tension gradually increased along with an increase in the length of the vessel defect, from 1.9 to 11.34 g in the no-mobilization group and from 1.97 to 8.44 g in the axial-mobilization group. Comparison of tension linear regression coefficient showed a significant difference between the two groups (p < 0.05). In part II of the study, the maximum length of femoral artery defects still able to maintain 100 percent patency of anastomoses was 4 mm (tension approximately 6 g) in the no-mobilization group and 6 mm in the axial-mobilization group (tension approximately 6.48 g). Microanastomotic tension was related to the size of the vessel defect, with increasing tension leading to thrombosis. Axial mobilization significantly reduced the tension in vessels with segmental defects and decreased thrombosis rates.

Anastomosis, Surgical↗

Permissive and obligatory roles of NO in cerebrovascular responses to hypercapnia and acetylcholine.

Inhibition of nitric oxide (NO) synthesis attenuates the hypercapnic cerebrovasodilation or the increases in cerebral blood flow (CBF) produced by acetylcholine (ACh), either topically applied or endogenously released in neocortex by stimulation of the basal forebrain cholinergic system. We investigated whether exogenous administration of NO, using NO donors, can reverse the attenuation of these responses by NO synthase (NOS) inhibitors. In halothane-anesthetized, ventilated rats the frontoparietal cortex was exposed and superfused with Ringer. CBF was monitored at the super fusion site by laser-Doppler flowmetry. The basal forebrain was stimulated (100 microA; 50 Hz) with microelectrodes stereotaxically implanted. Superfusion with the NOS inhibitor NG-nitro-L-arginine (L-NNA; 1 mM) reduced resting CBF (-38 +/- 2%; mean +/- SE) and attenuated the vasodilation elicited by hypercapnia (Pco2, 50-60 mmHg; -79 +/- 3%), ACh (10 microM; -83 +/- 7%), or basal forebrain stimulation (-44 +/- 2%) (P < 0.05, analysis of variance and Tukey's test). After L-NNA, topical application of 3-morpholinosydnonimine (SIN-1) (n = 7), S-nitroso-N-acetylpenicillamine (SNAP) (n = 6), or 8-bromoguanosine 3',5'-monophosphate (8-BrcGMP, n = 4) reestablished resting CBF (P > 0.05 from Ringer) and reversed the attenuation of the response to hypercapnia (P > 0.05 from Ringer). However, SIN-1 or SNAP failed to reverse the attenuation of the response to basal forebrain stimulation or topical ACh (P > 0.05 from L-NNA). After L-NNA, the NO-independent vasodilator papaverine (n = 4) reestablished resting CBF (P > 0.05 from Ringer) but failed to restore the hypercapnic vasodilation (P > 0.05 from L-NNA). The attenuation of hypercapnic response by the neuronal NOS inhibitor 7-nitroindazole was counteracted only partially by SIN-1 (n = 4) or 8-BrcGMP (n = 4). The data support the hypothesis that the vasodilation elicited by hypercapnia requires resting levels of NO for its expression, whereas the response to endogenous or exogenous ACh depends on agonist-induced NOS activation. In hypercapnia NO may act as a permissive factor by facilitating the action of other vasodilators, whereas in the vascular response initiated by ACh NO is likely to be the major mediator of smooth muscle relaxation.

8-Bromo Cyclic Adenosine Monophosphate↗

Anemia of chronic renal failure: characterization in the mouse and correction with human recombinant erythropoietin.

Anemia is a cardinal feature of chronic renal failure (CRF) which contributes significantly to the clinical syndrome of chronic uremia. We have conducted a detailed examination of the hematological changes in CRF in the inbred mouse strain C57BL/6J. As in the human situation, CRF mice presented major hematological changes affecting primarily the erythroid cell series. Despite the presence of abundant iron stores in the bone marrow, the CRF mice developed a hypoproliferative anemia of a severity commensurate with the degree of renal impairment. The levels of circulating erythropoietin (EPO) in CRF mice were not significantly different from those in normal control littermates and were therefore inappropriately low for the degree of anemia. In contrast acutely bled control mice with normal renal function showed a significant inverse correlation between the serum EPO level and hemoglobin concentration, indicating an appropriate response to anemia. The chronic administration of recombinant human EPO raised the hemoglobin concentration of CRF mice, a therapeutic effect which was independent of the initial degree of anemia. These observations suggest that this animal model has wide applicability for the study of anemia secondary to CRF.

Anemia↗

Aminoguanidine ameliorates and L-arginine worsens brain damage from intraluminal middle cerebral artery occlusion.

BACKGROUND AND PURPOSE: We studied whether the inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine reduces focal cerebral ischemic damage in a relatively noninvasive stroke model in which the rat middle cerebral artery (MCA) is occluded using an intravascular filament. METHODS: In rats anesthetized with halothane, a nylon filament was advanced into the internal carotid artery until its tip occluded the origin of the MCA. The filament was left in place for 2 hours and then withdrawn. Twenty-four hours later, rats received intraperitoneal injections of aminoguanidine (100 mg/kg BID; n = 7), aminoguanidine+L-arginine (300 mg/kg QID; n = 7), L-arginine alone (n = 6), D-arginine alone (n = 6), or vehicle (n = 10). Drugs were administered for 3 consecutive days. Infarct volume was determined by image analysis in thionin-stained brain sections 4 days after ischemia. iNOS mRNA was detected with the use of reverse transcription polymerase chain reaction. RESULTS: Cerebral ischemia led to iNOS mRNA expression in the affected brain 48 hours after induction of ischemia. Administration of aminoguanidine reduced neocortical infarct volume by 26% (P < .05 versus vehicle, ANOVA and Tukey's test), a reduction that was antagonized by coadministration of L-arginine (P > .05 versus vehicle). Administration of L-arginine alone, but not D-arginine, enlarged the infarct by 29% (P < .05). Aminoguanidine or L-arginine did not influence the increase in water content in the postischemic brain, indicating that the effect on infarct volume is not related to modulation of ischemic edema. CONCLUSIONS: These results demonstrate that cerebral ischemia is also associated with iNOS expression in a minimally invasive model of transient MCA occlusion and that iNOS inhibition reduces focal ischemic damage. The findings support the hypothesis that nitric oxide produced by iNOS contributes to ischemic brain damage and that inhibition of iNOS may be a valuable tool in the management of cerebral ischemia.

Animals↗

Inducible nitric oxide synthase gene expression in vascular cells after transient focal cerebral ischemia.

BACKGROUND AND PURPOSE: We investigated whether inducible nitric oxide synthase (iNOS) is expressed after transient cerebral ischemia and, if so, we sought to define the temporal profile and cellular localization of the expression and the role of iNOS in the mechanism of ischemic brain injury. METHODS: The middle cerebral artery in rats was occluded for 2 hours by an intraluminal filament. The occurrence of transient ischemia and reperfusion was confirmed by laser-Doppler flowmetry (n = 5). iNOS message in the ischemic neocortex was determined by reverse-transcription polymerase chain reaction. iNOS enzymatic activity was assessed by citrulline assay. The cellular localization of iNOS expression was determined by immunohistochemistry. RESULTS: iNOS mRNA was maximally expressed in postischemic brain at 12 hours and was not present at 4 days (n = 3 per time point). iNOS mRNA was not observed in the contralateral cerebral cortex. iNOS enzymatic activity developed in the postischemic brain between 12 and 24 hours (P < .05) and subsided at 4 days (n = 4 to 8 per time point). iNOS immunoreactivity in the ischemic region was restricted to the wall of capillaries and of larger blood vessels at 12 to 24 hours. In regions of early necrosis, inflammatory cells were iNOS positive. Treatment with the iNOS inhibitor aminoguanidine (n = 5; 100 mg/kg IP, BID for 4 days), starting 6 hours after ischemia, reduced infarct size in neocortex by 36 +/- 7% in comparison with vehicle-treated controls (n = 5) (P < .05). CONCLUSIONS: Transient focal ischemia leads to iNOS expression in postischemic brain. However, the spatial and temporal patterns of expression differ from those occurring in permanent ischemia: iNOS is induced earlier and predominantly in vascular cells rather than in neutrophils. Thus, the temporal profile and localization of postischemic iNOS expression depend on the nature of the ischemic insult. The finding that aminoguanidine reduces infarct size adds further support to the hypothesis that postischemic iNOS expression contributes to ischemic brain damage.

Animals↗

Occupational and Environmental Risk Factors for Asthma in Rural Communities in China.

Respiratory allergens such as dust, gases/fumes, and hay smoke, which are frequently present in agricultural settings, can cause or aggravate asthma. The purpose of this study was to examine the relationships between occupational and environmental exposures and asthma in Chinese rural communities. The study population consisted of 28,946 people 15 years old or older, living in rural areas of Anhui province, China. A modified Mandarin translation of the ATS-DLD questionnaire was administered by trained interviewers to request information about exposures to specific occupational/environmental agents and respiratory disorders. In Huaining, the prevalence of wheezing was 3.8% for men; 2.1% for women; the prevalence of asthma was 1.6% for men; 1.8% for women. In Zongyang, the prevalence of wheezing was 2.7% for men; 1.9% for women; the prevalence of asthma was 1.7% for men; 1.2% for women. With control for potential confounders such as gender, age, residential area, education level, and smoking status, the pooled adjusted odds ratios (ORs) of wheezing and asthma for the group exposed to wood/hay smoke were 1.36 (95% CI: 1.14-1.61) and 1.27 (95% CI: 1.02-1.58), respectively. For coal-stove users, the pooled adjusted ORs were 1.47 (95% CI: 1.09-1.98) for wheezing and 1.51 (95% CI: 1.05-2.17) for asthma. After stratification of the subjects by dust type, the estimated ORs for wheezing were 1.58 (95% CI: 1.02-2.44) among the group exposed to inorganic dust and 3.03 (95% CI: 1.25-7.33) among the group exposed to metal dust. Asthma was not shown to be significantly associated with any specific dust type. Findings of the present study are consistent with previously reported adverse respiratory health effects related to occupational/environmental exposures to wood/hay smoke and dust, and indicate the need for further occupational disease surveillance in rural communities.

Journal Article↗

Tamoxifen (estrogen antagonist) inhibits voltage-gated calcium current and contractility in vascular smooth muscle from rats.

Tamoxifen (Tx) has been used in breast cancer treatment and prophylaxis because of its antiestrogenic activity; however, Tx may also have beneficial cardiovascular effects and other actions mediated by mechanisms other than estrogen receptors. Previous studies showing interactions of Tx with Ca+(+)-channel blockers suggested that Tx may affect Ca++ channels, an hypothesis that was investigated using whole cell patch clamp techniques in vascular smooth muscle cells (cell line A7r5 and freshly dissociated cells) and by determining effects on contractions of isolated blood vessels. Tx reduced current through L-type Ca+2 channels, with an ID50 of 2 x 10(-6) M when applied by cumulative addition to A7r5 cells. With acute application, 10(-6) M Tx significantly reduced L-type current in A7r5 cells within 2 min to 88% of control (vehicle, 0.1% ethanol) in A7r5 cells, 67% of control in aortic vascular smooth muscle cells, and 60% of control in tail artery vascular smooth muscle cells. Tx also decreased the rate of inactivation of L-type current. Inhibition of T-type current by Tx was less than for L-type current but was significant at 10(-5) M Tx. Treatment of tail artery rings with Tx (10(-5) M, 15 min; 10(-6) M, 4 hr) reduced K+-elicited contractions. Since therapeutic concentrations of Tx during treatment may exceed 10(-6) M, these effects of Tx on vascular smooth muscle Ca++ channels and vessel contractions may have a role in the efficacy and side-effects of Tx treatment.

Animals↗

A systematic study of hypothermic lung preservation solutions: Euro-Collins solution.

BACKGROUND: Testing lung function after preservation is difficult because a suitable model is still lacking; thus, the effectiveness of different solutions for lung preservation has not been confirmed. This study tested the effectiveness of Euro-Collins solution alone for hypothermic preservation of rat lungs. METHODS: A living rat perfusion model was used, which allowed more than 5 hours of continuous perfusion for isolated lung function studies. Group 1 lungs (control, n = 8) were tested without preservation. In groups 2 through 6 (n = 8 lungs each), the lungs were flushed with 4 degrees C Euro-Collins solution and preserved for 4, 6, 8, 12, and 24 hours, respectively. Lung function studies were carried out after preservation. RESULTS: In groups 1 and 2, pulmonary arterial blood flow and pulmonary venous oxygen tension were higher and pulmonary resistance was lower than in the other groups. Airway pressure and resistance were lowest in group 1. Lungs in groups 5 and 6 demonstrated the worst function, but the lung tissue wet to dry ratio was higher only in group 6. CONCLUSIONS: At 4 degrees C, Euro-Collins solution can effectively preserve rat lungs for 4 hours. Six to 8 hours of preservation resulted in depressed lung function. More than 12 hours of preservation resulted in uniformly deficient lung function, rendering the lungs unsuitable for transplantation.

Airway Resistance↗

Intrinsic multidrug class 1 and 2 gene expression and localization in rat and human mammary tumors.

P-glycoproteins (P-gp), the protein products of the multidrug resistant (mdr) genes, are often overexpressed in tumors that are resistant to chemotherapy. In this study, we measured intrinsic (preexisting) mdr1a, -1b, and -2 gene expression in N-nitroso-N-methylurea-induced rat mammary tumors. Using immunohistochemistry and in situ hybridization, we determined the localization of mdr1b mRNA and P-gp. We compared these results with a similar morphologic analysis of untreated human breast carcinomas. The predominantly expressed member of the mdr gene family in normal rat mammary tissue was mdr2. In rat mammary tumors, mdr2 expression was only inconsistently and slightly increased (1.4-fold on average). In contrast, expression of the class 1 genes (mdr1a and mdr1b) were consistently increased to a much greater extent. The average increase of mdr1b gene expression was greater than that of mdr1a (on average, 12.9 compared with 2.4, respectively). This indicated a differential regulation of these two closely related genes in these tumors. Immunostaining and in situ analysis showed that mdr mRNA and P-gp were expressed in a minority of neoplastic epithelial cells located in defined areas of the tumor, often on the interface of the neoplastic epithelium and stroma. Single epithelial cells that had invaded the stroma also expressed P-gp. In human breast carcinomas, the patterns of mdr mRNA and P-gp expression were similar to those in rat N-nitroso-N-methylurea-induced mammary tumors.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Effect of chronic renal failure on the expression of erythropoietin message in a murine model.

The anemia of chronic renal failure (CRF) is largely due to decreased production of erythropoietin (EPO) by the kidney. A small amount of EPO also originates from extra-renal sources, and this would be expected to assume a more important role in maintaining erythropoiesis when renal production is impaired. In this study, we examined the production of EPO mRNA by RT-PCR in kidney, liver, and bone marrow tissues isolated from normal mice, mice rendered acutely anemic by phlebotomy, and from mice with surgically induced CRF. The induction of acute anemia results in an expected increase in the expression of EPO mRNA in renal and hepatic tissue. In contrast, while the expression of EPO mRNA was expectedly reduced in the kidney from CRF mice, it was completely absent in the liver of these same animals. EPO mRNA expression was also absent in the bone marrow in both states of acute anemia and CRF. These results show that CRF can directly or indirectly can suppress the extrarenal production of EPO by the liver and that this effect may further aggravate the anemia of CRF.

Anemia↗

[Influence factors in etiology of epithelial ovarian cancer].

OBJECTIVE: To investigate the role of genetic and psychosomatic factors in the development of epithelial ovarian cancer. METHODS: A hospital-based case-control study was conducted in 9 hospitals of Shandong province. 127 cases of epithelial ovarian cancer and 254 cases of non-malignant ovarian tumors were admitted for treatment during the same period of time. Data for single predictors and multivariants collected from hospital records were subjected to non-condition multivariate logistic analysis, in order to sort the protective factors and the high risk factors in the development of epithelial ovarian cancer. RESULTS: Adverse events in life, blood type A, mental depression or anger, family history of ovarian cancer and irregularity of bowel movements are the high risk factors. An open and cheerful disposition or optimism, hysterectomy with preservation of one or both ovaries and intrauterine device were shown to be the protective factors for the ovaries. CONCLUSION: Genetic and psychosomatic factors play an important role in the course of development of epithelial ovarian cancer.

Adolescent↗

[The bonding strength between plat castable ceramics and mild fusing alloy].

Plat castable ceramics (PCC) was bonded to SDA-I mild fusing alloy using three bonding agents, and the tensile bond strengths were tested respectively in order to select the best bonding agent and the best way of surface treatment. The results obtained with scanning electron microscope and X-ray energy spectrum showed that the bonding behavior of TF agent was the best one. The greatest tensille bond strength (24.37 MPa) was obtained with TF agent when the surface of PCC was etched by hydrofluoric acid and the alloy was painted with KH-570. Remarkable tensile bond strengths were noted in the group where EM agent was used with PCC etched by hydrofluoric acid and alloy treated with sandblasting (15.20 MPa), and in the group where Porcelite dual cure cement was applied with PCC painted by KH-570 and alloy treated with sandblasting (15.25 MPa).

Dental Bonding↗

[Expression of placental alkaline phosphatase in esophageal cancer cell line Eca109].

The expression and property of alkaline phosphatase (ALP) in Eca109 cells, a cell line derived from human esophageal carcinoma were studied with specific inhibition assay and poly-acrylamide gel electrophoresis. The results showed that ALP of Eca109 cells was heat stable and was strongly inhibited by L-phenyalanine, but slightly inhibited by urea. Prednisolone could cause dramatic increase in activity of ALP, but no change in ALP isozyme spectrum and concomitant increase in lactic dehydrogenase activity were found after prednisolone treatment. The results suggested that placental alkaline phosphatase as an oncofetal gene product could be expressed ectopically by Eca109 cells and prednisolone could specifically induce increase in its activity.

Alkaline Phosphatase↗

[Dynamic change of beta 2-microglobulin in hemodialysis].

In order to study the dynamic clearance of total beta 2-microglobulin in the body, two-compartment theory and perturbation solution were applied in our study. Based on the rate of formation of beta 2-microglobulin in the body and the mode of transmission and mass transfer resistance of solute, the concept of week clearance index of beta 2-microglobulin (R value) was suggested. Its theoretical value is more than 40%. Thirty-two patients undergoing dialysis with high-efficiency dialyzer were studied and data were processed in a computer. The results showed that when R value was more than 40%, the clinical manifestation of amyloidosis carpal tunnel syndrome induced by increase of beta 2-microglobulin was alleviated obviously. It makes up for the limitation of KT/V or TA Curea that were used only to estimate adequate dialysis of small molecules. It is shown that the concept of week cleacance index of beta 2-microglobulin improves the estimation of adequate dialysis.

Adult↗