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Biomedical subjects

J Guan

Publications and source records attributed to J Guan.

At least 91 records · Page 5Linked to original sources
PubMed1998

Glucose turnover and insulin sensitivity in rats with pancreatic islet transplants.

To study the metabolic effects of insulin derived from islet grafts, oral glucose tolerance (OGT) and glucose turnover were examined in streptozotocin-induced diabetic Lewis rats rendered normoglycemic by syngeneic islet grafts in the renal subcapsular space (REN), in REN with renal vein-to-mesenteric vein anastomosis (REN-RMA), in the liver (intrahepatic [IH]), or in a parahepatic omental pouch (POP) and compared with normal rats. Normal OGT was found at 1 month posttransplant in all animals receiving approximately 3,000 islets, with hyperinsulinemic responses in the REN group compared with the other groups, and with higher C-peptide responses in the IH group than in the other groups (P < 0.05 by one-way analysis of variance). Glucose turnover studies in the insulin-stimulated steady state (INS-SS; infusion of insulin at 10 pmol x kg(-1) x min(-1)) at 2 months posttransplant showed that whole body glucose disappearance rates (Rd) were similar in all groups, but the REN group had higher steady-state insulin levels than the other groups. Glucose infusion rates (GIRs) were lower in the REN and IH groups than in the other groups. Apparent endogenous glucose production (EGP) was not completely inhibited in the REN and IH groups, while complete inhibition was observed in the other groups. When INS-SS insulin levels were matched to the level in REN rats by increasing the insulin infusion rate to 20 pmol x kg(-1) x min(-1) in REN-RMA, IH, and normal rats, GIR and Rd were elevated, exceeding those values in REN rats, but GIR in IH rats was still lower than in REN-RMA and normal rats. Thus, 1) in the REN group, impairment of inhibition of EGP and of stimulation of Rd by exogenous insulin contribute to insulin resistance; 2) in the IH group, incomplete inhibition of EGP is the major determinant of insulin resistance; and 3) with portal delivery of insulin in the REN-RMA and POP groups, normal insulin sensitivity is preserved. The present study confirms that hepatic portal delivery of islet secretions is necessary for physiological regulation of glucose metabolism. The study also suggests the IH grafts do not provide physiological regulation of glucose metabolism, raising the question of whether the liver is an appropriate site for insulin-secreting tissue replacement therapy in diabetes.

Anastomosis, Surgical↗
PubMed1998

[Retrospective study on the risk factors in patients with nosocomial bacterial L-form infection].

To survey the risk factors of nosocomial bacterial L-form infections, 22 risk factors were investigated and analysed with nonconditional logistic regression. Resutts showed through single factor regression that cancer, chronic disease, primary infection, longer than 3-week hospitalization before the onset of nosocomial infection, preventive use of antibiotics longer than 7 days, preventive use of cell wall depressive antibiotics, steroid use, anti-tumor drugs and urine guide technique were significant factors. Multiple factor regression demonstrated that two models including cell wall depressive antibiotics, primary infection, urine guide technique cell wall depressive antibiotics, primary infection, anti-tumor drugs and longer than 3-week hospitalization before the development of nosocomial infection were conjugated properly. It suggested that the surveillance of risk factors of nosocomial bacterial L-form infections was helpful to control nosocomial infections.

Adolescent↗
PubMed1998

[P16 expression in lung cancer and its significance].

OBJECTIVE: To study the relationship of suppressor gene p16 and lung cancer for prognosis evaluation. METHODS: Immunohistochemical method was used to detect and analyse the expression of P16 protein of CDKN2 suppressor gene of 76 cases in formalin-fixed, paraffin-embedded tissue specimens of human lung cancer. RESULTS: P16 positive rate was 45%: 52% for 23 of 44 cases of squamous carcinoma and 29% for 7 of 24 cases of adenocarcinoma. Differentiation degree and prognosis of lung cancer were associated significantly with P16 expression. P16 expression was somewhat related to clinical stage. CONCLUSION: P16 gene plays a key role in the prognosis of patients with lung cancer.

Adenocarcinoma↗
PubMed1998

[Apoptosis in multiple organs of rats in early stage of polytrauma combined with shock].

OBJECTIVE: To discuss Apoptosis in multiple organs of rats in early stage of polytrauma combined with shock. METHODS: DNA agarose gel electrophoresis, in situ end labeling (ISEL), light microscope and electron microscope were used and DNA fragmentation percentage (ap%) was detected. RESULTS: The special ladder pattern for apoptosis was seen in thymus, spleen, liver, lung and intestine, but not in heart, kidney and brain. At 6 hours after resuscitation, the ap% of thymus, spleen, liver, lung and intestine increased together with the severity of trauma. In six-site trauma combined with hemorrhagic shock group, the ap% of these five organs increased significantly at 1 hour after resuscitation and most significantly at 3 hours. At this point, the ap% of spleen, liver, lung and intestine reached peak, and declined gradually afterward. But the ap% of thymus continued to increase after 3 hours and kept stable from 6 hours to 24 hours ISEL showed that there were positive responses of different degrees in these eight organs. It was feand Morphologically most apoptotic cells in the thymus were positioned in the cortex, and those in spleen in the growing center of white pulp, and those in liver in the border area of hepatic lobule and portal area, and apoptosis of multiple kinds of cells including alveolar epithelial cells, vascular endothelial cells and polymorphonuclear neutrophils was induced in lung, and intestinal apoptotic cells laid in the epithelium and lamina propria of mucosa. CONCLUSION: Apoptosis was really induced in thymus, spleen, liver, lung and intestine in early stage of polytrauma combined with shock, which may play a role in early organ injury and late multiple organ failure.

Animals↗
PubMed1998

[Collagen sponge and its hemostatic properties].

Soluble collagen was extracted from bovine tendon in acid solution. Collagen sponge hemostatics were prepared by means of lyophibization. The amino acid and UV spectrum analyses were made to confirm the composition of the soluble collagen. The results of experiments on rabbits indicated the collagen sponge prepared in the authors' lab had excellent hemostatic and adhesive properties in vivo surgical tests.

Amino Acids↗
PubMed1997

Mouse extracellular superoxide dismutase: primary structure, tissue-specific gene expression, chromosomal localization, and lung in situ hybridization.

Extracellular superoxide dismutase (EC-SOD) is the major extracellular antioxidant enzyme. We have determined the primary structure of mouse EC-SOD by characterization of complementary DNA (cDNA) clones and by amino-acid sequence analysis of purified protein. cDNA sequence analysis indicates that mouse EC-SOD is synthesized as a 251-amino-acid precursor protein with a predicted molecular weight of 27,400 D. Amino-terminal micro sequence analysis of purified mature mouse lung EC-SOD demonstrated the sequence to begin with SSFDLADRLDPV-. These results indicate that EC-SOD as initially synthesized contains a 24-amino-acid precursor peptide, and that the mature protein is 227 amino acids in length. Computer algorithms that predict the most likely site of cotranslational signal peptidase cleavage suggest that processing will occur between amino acids 18 and 19 or 20 and 21, which implies that EC-SOD may be initially synthesized as a pre-pro-protein. Like human EC-SOD, mature mouse EC-SOD is glycosylated. The full-length mouse EC-SOD cDNA is 1,834 base pairs long and is 82% (79% for protein) identical to rat EC-SOD, but only 60% (60% for protein) identical to human EC-SOD. The mouse EC-SOD gene locus (Sod3) was mapped by interspecific backcross haplotype analysis as being 0.9 +/- 0.9 centimorgans distal to the Qdpr locus on mouse Chromosome 5, a position suggesting that the human homologue of EC-SOD will map close to the human QDPR locus (4p15.3). Of nine tissues examined by Northern blot analysis, those of the kidney and lung are by far the major tissues that express EC-SOD messenger RNA. Using in situ hybridization in the mouse lung, we demonstrate EC-SOD gene expression to be highly localized to alveolar Type II epithelial cells. These data suggest that alveolar Type II cells play a central role in mediating EC-SOD antioxidant function in the lung.

Amino Acid Sequence↗
PubMed1997

Insulin resistance prevented by portal delivery of insulin in rats with renal subcapsular islet grafts.

We determined the metabolic effects of insulin derived from renal subcapsular islet grafts, either with systemic delivery of insulin through renal venous drainage (REN) or with portal delivery of insulin after renal vein-to-superior mesenteric vein anastomosis (RMA), in streptozotocin-induced diabetic Lewis rats, in comparison with normal rats. After gavage glucose, the plasma glucose responses were similar to normal in REN and RMA rats; however, hyperinsulinemia occurred in REN rats (area under the concentration curves [AUCs] of insulin, 27 +/- 3 nmol x 1(-l) min) in comparison with RMA (14 +/- 2) and normal rats (19 +/- 2), P < 0.003, with no difference in C-peptide responses. The ratio of AUC C-peptide to AUC insulin was lower in REN (2.0 +/- 0.2) than in RMA (3.4 +/- 0.3) and normal animals (3.2 +/- 0.3), P < 0.0005. In euglycemic-hyperinsulinemic clamp studies using the same insulin infusion rate (10 pmol x kg(-1) x min(-1), insulin resistance was found in REN animals (mean glucose infusion rate [GIR], REN: 7.5 +/- 1.2; RMA: 12.0 +/- 1.2; normal: 12.7 +/- 1.0 mg x kg(-1) x min(-1); P < 0.008), with higher steady-state insulin levels in REN (554 +/- 63 pmol/l) than in RMA (291 +/- 26) and normal rats (269 +/- 60), P < 0.0001. With matching steady-state insulin levels in RMA and REN rats during infusion of insulin at 20 pmol x kg(-1) x min(-1) in RMA rats (steady-state insulin 623 +/- 64 pmol/l), GIR was 15.7 +/- 0.7 mg x kg(-1) x min(-1). Thus, systemic delivery of insulin from islet grafts is associated with hyperinsulinemia, insulin resistance, and decreased metabolic clearance of insulin. These abnormalities are prevented by portal delivery of insulin from islet grafts in the same site. The findings are consistent with the hypothesis that portal delivery of insulin is important in maintenance of normal whole-body insulin sensitivity.

Anastomosis, Surgical↗
PubMed1997

[An experimental study on effect of atrial natriuretic peptide on intraocular pressure of white rabbits].

OBJECTIVE: To study the therapeutic effect of atrial natriuretic peptide (ANP) on glaucoma. METHODS: Various doses of ANP were injected subconjunctivally in albino rabbits, and their effects on intraocular pressures (IOPs) were observed. RESULTS: The IOPs were significantly decreased by the subconjunctival injection of 20, 30, 40 micrograms of ANP, and with a dose of 40 micrograms, the maximum effect of IOP lowering of 0.88-0.15 kPa maintaining for the longest time 7.5 hours was obtained. Generally, one hour after the injection, the maximum effect could be seen. A dose-effect relationship that is the degree of the reduction of IOP increasing with the dose increase of ANP could be observed. CONCLUSION: This study indicates that ANP might play an effective therapeutic role in glaucoma.

Animals↗
PubMed1997

[Protective effects of exogenous superoxide dismutase on rabbit retinal injury by acute intraocular hypertension].

OBJECTIVE: To study active oxygen and free radical injury in rabbit retina during elevated intraocular pressure and the protective effect of exogenous superoxide dismutase (SOD) on the retinal damage by the hypertension. METHODS: Lipid peroxidative product, malondialdehyde (MDA), activity of SOD and glutathione peroxidase (GSH-Px), reduced GSH in the retinal tissue were measured during 24 h after the release of an ocular hypertension, 6.67 kPa (1 kPa = 7.5 mmHg) maintaining for 1.5 h, and the effects of retrobulbarly injected Cu-Zn-SOD on the level of MDA and the activity of SOD in the retinal tissue after the release of ocular hypertension for 12 h were observed. RESULTS: MDA increased gradually during 0-12 h after the release of ocular hypertension and maintained at a relatively high level in 12-24 h. The activity of SOD and GSH-Px was lower than normal level immediately after the release, and then increased to a certain different extent. But the activity of SOD began to decrease gradually 4 h after the release. GSH had no significant changes during 24 h after the release. Retrobulbar injection of Cu-Zn-SOD reduced the production of MDA in the retinal tissue and enhanced SOD activity. CONCLUSIONS: Active oxygen and free radicals participate the rabbit retinal injury by elevated intraocular pressure. A high dose of Cu-Zn-SOD retrobulbar injection plays a beneficial role in enhancing the antioxidative ability of the retina.

Animals↗
PubMed1997

[Effects of iron deficiency on expression of transferrin receptor in human lymphocytes].

Cell culture in vitro, ABC-ELISA,RNA dot blot and atom absorption spectrum analysis were used to study biological effects of low concentration of iron citrate (Fe-cit) on the expression of transferrin receptor (TfR) in healthy human peripheral lymphocytes. Results showed that TfR increased by 36%, 50%, and 67% in groups with 1.25 x 10(-5), 5 x 10(-6) Fe-cit and without it, respectively as compared with a control group with 2.5 x 10(-5) mol/L Fe-cit. Levels of TfR-mRNA also increased with decrease of iron in substrate. Iron concentration within cells correlated inversely to the change in the number of TfR. It indicated that iron deficiency could regulate the number of TfR in lymphocytes and its gene expression.

Gene Expression↗
PubMed1996

The movement of IGF-I into the brain parenchyma after hypoxic-ischaemic injury.

The movement of peptides from CSF into the parenchyma is thought to be slow and diffusion limited. However IGF-I can reduce neuronal loss at distal sites when given centrally 2 h after hypoxic-ischaemic (HI) injury. The present study determined the distribution of [3H]IGF-I given into the lateral ventricle after unilateral HI injury in adult rats. Radioactivity in the injured cortex peaked immediately after administration then rapidly declined. Autoradiography demonstrated radioactivity in the perivascular spaces and in the corpus callosum and external capsule of the injured hemisphere. HPLC and radioimmunoassay confirmed a rise in intracerebral IGF-I levels (from 159 +/- 9 to 401 +/- 88 ng g-1). These data suggest that injury can enhance the movement of IGF-I into the cerebrum via the white matter tracts and perivascular spaces.

Adult↗
PubMed1996

Rats with portal-caval vein transposition show hyperinsulinemia and insulin resistance.

To compare the metabolic effects of portal and systemic delivery of insulin, we used portal-caval transposition (PCT) in rats to provide total systemic diversion of splanchnic venous blood. PCT rats exhibited normal weight gain, liver histology, liver-function tests, glycosylated hemoglobin, arterial blood pressure, and hepatic blood flow. Mean liver weight relative to body weight was 12% lower in PCT rats than in sham-operated control (CTR) rats 30 days following transposition. Indwelling venous catheters were established to facilitate metabolic studies in conscious, minimally restrained animals. Postabsorptive plasma glucose and C-peptide (CPEP) levels were similar in PCT and CTR rats; however, postabsorptive immunoreactive insulin (IRI) levels were elevated in PCT rats (67 +/- 3.1 v 49 +/- 3.5 pmol.L-1, P < .002, n = 11 v 11), as were postabsorptive plasma glucagon levels (570 +/- 67 v 240 +/- 11 ng.L-1, P < .001, n = 11 v 16) at similar body weights. The postabsorptive CPEP/IRI concentration ratio was lower in PCT than in CTR rats (4.0 +/- 0.3 v 6.0 +/- 0.6, P < .02), suggesting reduced hepatic extraction of insulin. Insulin sensitivity (IS), determined by minimal model analysis of frequently sampled intravenous glucose tolerance tests yielding the sensitivity index (SI), was reduced in PCT compared with CTR (61 +/- 5.6 v 86 +/- 9.0 (mumol.L-1)-1.min-1, P < .04, n = 9 v 10). During euglycemic-hyperinsulinemic clamps, glucose infusion rates (GIRs) from 60 to 120 minutes were lower in PCT than in CTR rats (6.0 +/- 0.3 v 8.0 +/- 0.4 g.kg-1.min-1, P < .002, n = 9 v 7) with matching plasma IRI levels, confirming the reduced IS in PCT rats. Areas under the concentration curves ([AUCs] 0 to 150 minutes) for glucose tolerance tests (gavage) indicated that plasma glucose excursion was similar in PCT and CTR rats whereas AUC IRI was significantly higher in PCT than in CTR rats (23 +/- 1.3 v 18 +/- 0.6 nmol.L-1.min, P < .009, n = 11 v 11). However, AUC CPEP for oral glucose tolerance tests was lower in PCT than in CTR rats (55 +/- 3.4 v 68 +/- 4.8 nmol.L-1.min, P < .05), indicating decreased insulin secretion. Thus, the mean ratio AUC CPEP/AUC IRI was significantly lower in PCT rats (2.5 +/- 0.2 v 3.8 +/- 0.3, P < .002), again suggesting reduced hepatic extraction of insulin. Thus, euglycemia after PCT was accompanied by elevated postabsorptive and glucose-stimulated levels of IRI in systemic blood, postabsorptive hyperglucagonemia, and decreased insulin secretion in response to glucose challenge (gavage), with diminished hepatic extraction of insulin and decreased IS. The PCT model illustrates the insulin-resistant adaptive state that results from systemic delivery of insulin, and indicates the importance of hepatic portal delivery of insulin and possibly of other gastroenteropancreatic hormones in the maintenance of IS and physiological metabolic control.

Animals↗
PubMed1996

Increased renal tubular expression of transforming growth factor beta in human allografts correlates with cyclosporine toxicity.

Cyclosporine A (CsA) is a potent immunosuppressive drug that inhibits the transcription of several proinflammatory cytokines including interleukin-2. In contrast, CsA stimulates transcription of the pleuripotent cytokine, transforming growth factor-beta (TGF beta). Since the effect of CsA in transplant recipients is unpredictable, we examined whether tissue levels of TGF beta protein in renal allografts correlate with in vivo CsA responsiveness. Intra-allograft TGF beta protein content was assessed in renal biopsies by immunohistochemical means using the mouse anti-TGF beta monoclonal antibody (Mab), 1D11. We studied 68 specimens: 21 with acute CsA toxicity (ACT), 11 with acute tubular necrosis (ATN) and 36 with acute cellular rejection (ACR). Intensity of TGF beta immunostaining was evaluated in a blinded fashion using a scale from 0 to 3+. In biopsies with histological evidence of CsA toxicity, 77% demonstrated intense (2 to 3+) TGF beta immunostaining. TGF beta protein was detected in both proximal and distal tubules but was either absent or present in low levels within glomeruli and interstitium. In contrast, only one of the 11 biopsies with ATN had minimal staining (1+) for TGF beta. The remaining 10 biopsies with ATN were negative for TGF beta immunostaining. In biopsies with ACR, the levels of renal TGF beta were more variable with 36% showing intense (2 to 3+) staining and 64% having minimal or no (0 to 1+) tubular TGF beta. Within the first 18 months post-transplantation, patients with intense TGF beta staining and ACR underwent an average of 4.1 +/- 1.8 allograft biopsies and suffered 33% graft losses. During the same period of time, the patients with ACR and absent or low (0 to 1+) TGF beta levels underwent only 2.1 +/- 1.2 biopsies, maintained better late renal function and suffered 4% graft losses. In conclusion, we demonstrate that TGF beta protein levels in renal allografts correlate with CsA effect and differentiate ACT from ATN. In CsA treated patients who develop ACR, TGF beta levels predict the subsequent clinical course and graft function. Therefore, evaluating tissue levels of TGF beta may offer unique diagnostic and prognostic benefits in the care of patients receiving CsA based immunosuppression.

Adult↗
PubMed1996

The effects of insulin-like growth factor (IGF)-1, IGF-2, and des-IGF-1 on neuronal loss after hypoxic-ischemic brain injury in adult rats: evidence for a role for IGF binding proteins.

Insulin-like growth factor (IGF)-1, IGF binding protein (IGFBP)-2, and IGFBP-3 are expressed in the rat brain in regions of neuronal loss by 3 days after hypoxic- ischemic (HI) brain injury and IGF-2 somewhat later. Central administration of rh-IGF-1 after HI injury reduces neuronal loss in vivo. To clarify the mode of action of IGF-1 and the potential role of IGFBPs, the effects of IGF-1, IGF-2, des(1-3)-N-IGF-1 (des-IGF-1), an analogue of IGF-1 with low affinity for IGFBPs, and IGF-1 combined with IGF-2 were compared 2 h after administration into the lateral cerebral ventricle after an HI injury. Unilateral HI was induced in adult rats by right carotid artery ligation followed by 10- min exposure to 6%O2. The extent of neuronal loss was determined in the cortex, striatum, hippocampus, dentate gyrus, and thalamus 5 days later. Central administration of 20 micrograms IGF-1 (n = 17) reduced neuronal loss in all regions (P < 0.01). Neither 20 micrograms IGF-2 (n = 17), 2 micrograms des-IGF-1 (n = 10), nor 20 micrograms des-IGF-1 (n = 17) reduced neuronal loss. There was a trend towards a reduction in neuronal loss after 150 micrograms des-IGF-1 (n = 20). IGF-2 alone increased neuronal loss in the hippocampus and dentate gyrus compared with the same regions in vehicle-treated animals (P < 0.05). Coadministration of 30 micrograms IGF-2 blocked the neuroprotective effects of 20 micrograms IGF-1 (n = 18, P < 0.05) and reduced the accumulation of [3H]IGF-1 in the injured hemisphere (n = 4) (P < 0.05). These observations suggest a role for IGFBPs in targeting the neuroprotective actions of IGF-1. IGF-2 may antagonize the protective effect of IGF-1 by displacing it from IGFBPs.

Animals↗
PubMed1996

[Reversion of malignant phenotypes of human lung squamous carcinoma cells by ornithine decarboxylase antisense RNA].

Abnormally elevated activity of ornithine decarboxylase (ODC), with subsequent polyamine accumulation are intimately associated with the genesis, development and metastasis of cancer. Therefore, ODC antisense RNA was used to transfect human lung squmous carcinoma cell line LTEP-78. Compared with the parental cells, growth of the antisense transfected LTEP-78 cells arrested in G0/G1 phase and colony formation in soft agar and tumorigenicity in nude mice were significantly reduced. Nucleic acid hybridization demonstrated the expression of ODC antisense RNA and the content of ODC mRNA was markedly reduced. The results suggest that the reversion of malignant phenotypes of human lung squamous carcinoma cells is associated with the control of polyamine biosynthesis.

Animals↗
PubMed1996

[Measures combating pre-hospital sudden death].

OBJECTIVE: To study pre-hospital sudden death so as to reduce the death rate. METHOD: 814 pre-hospital deaths were randomly selected from January 1990 to May 1994 for a retrospective study. RESULTS: 616 deaths (75.7%) showed a history of cardiac disease and hypertension. The age for high sudden death rate ranged from 50 to 69 years (53.9%). Most of the cases (87.8%) were found in their homes. 21 cases (2.58%) successfully recovered. CONCLUSIONS: The key points to improve the success rate of pre-hospital sudden death are: completing Beijing Emergency Medical Center's emergency care network so as to decrease the emergency care radium and shorten the emergency care time; disseminating emergency care knowledge on CPR and CPR technique.

Adolescent↗
PubMed1996

[Apparent accommodation in pseudophakic eyes after implantation of posterior chamber intraocular lenses].

OBJECTIVE: To study the question about apparent accommodation in pseudophakic eyes after implantation of posterior chamber intraocular lens (IOL). METHODS: The distant and near vision, refraction, pupillary size and shape, the depth of anterior chamber before and after mydriasis of 68 patients (73 eyes) with rigid posterior chamber IOL implantation were examined when the correcting lenses were worn, their powers of apparent accommodation were measured by HS-9D Accommod-Polyrecorder. RESULTS: The mean value of apparent accommodation was 1.53 +/- 0.59D. There was a negative correlation between apparent accommodation of pupillary diameter (r = -0.62). The apparent accommodation in the group with normal pupillary movement is greater than that in the group with abnormal one. A mean change of anterior chamber depth, 0.4 mm, before and after mydriasis was found. It appears that rigid posterior chamber implants do move backward on ciliary muscle relaxation. There was a positive correlation between apparent accommodation and the degree of IOL movement (r = 0.47). No significant correlation was found between apparent accommodation and the anterior chamber depth before mydriasis and age (r = 0.26, r = 0.22), etc. CONCLUSION: The apparent accommodation is the result of the change of focus depth in the eye which is caused by the cooperation of several factors such as corneal astigmatism, pupillary size and movement, etc. So optimal postoperative myopic astigmatism and good pupillary movement are beneficial to apparent accommodation in an eye with posterior chamber IOL implantation.

Accommodation, Ocular↗