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Biomedical subjects

J Jiang

Publications and source records attributed to J Jiang.

At least 325 records · Page 18Linked to original sources
PubMed1997

Growth hormone induces detergent insolubility of GH receptors in IM-9 cells.

In this study, we examined human growth hormone (hGH)-induced changes in nonionic detergent solubility characteristics of its receptor (hGHR). Exposure of IM-9 cells to hGH caused a time- and concentration-dependent loss of immunoblottable detergent-extractable hGHRs and a corresponding accumulation of receptors in a detergent-insoluble pool. At 37 degrees C, the loss of detergent-soluble and the accumulation of detergent-insoluble hGHRs both preceded hGH-induced loss of total cell hGHRs. The detergent-insoluble receptor pool was progressively enriched in an apparent disulfide-linked form of the hGHR. Exposure to hGH at 4 degrees C allowed hGH-induced hGHR disulfide linkage but did not promote changes in receptor detergent solubility, indicating that hGHR detergent insolubility cannot be explained solely by the formation of that linkage. Experiments carried out with hGH at 20 degrees C and with the phorbol ester, phorbol-12,13-myristate acetate, at 37 degrees C indicated that loss of detergent-soluble hGHRs can be uncoupled from accumulation of detergent-insoluble receptors. From these data, we envision at least two related, but separable, trafficking pathways taken by hGHRs after their surface interaction with hGH:1) ligand-mediated endocytosis and degradation (accounting for only some of the receptors lost from the detergent-soluble fraction) and 2) ligand-mediated accumulation in a detergent-insoluble subcellular fraction (arising largely from receptors redistributed from the detergent-soluble fraction).

Cell Line↗
PubMed1997

Transfer of a salt-resistant renin allele raises blood pressure in Dahl salt-sensitive rats.

To evaluate the role of the renin gene in the development of hypertension in Dahl salt-sensitive rats (SS/Jr/Hsd), we derived a congenic strain of rats homozygous for the salt-resistant renin allele (S/renrr) and compared them with a control strain homozygous for the salt-sensitive renin allele (S/ren(ss). Mean arterial pressure was significantly higher in 12-week-old S/renrr rats fed a high salt (8.0%) diet for 3 weeks than in S/ren(ss) rats or in SS/Jr/Hsd rats rederived from the foundation colony we used to generate the cogenic strain (195 +/- 3 [n = 49] versus 168 +/- 3 [n = 17] or 161 +/- 3 [n = 16] mm Hg). Mean arterial pressure was also higher in S/renrr rats than in S/ren(ss) rats raised from birth on either a very low salt (0.1%) diet (119 +/- 9 [n = 6] versus 100 +/- 7 [n = 7] mm Hg) or a low salt (0.4%) diet (143 +/- 1 [n = 22] versus 117 +/- 3 [n = 10] mm Hg). Plasma renin activity of S/renrr rats was significantly higher than that of S/ren(ss) rats fed a very low salt diet (5.7 +/- 2.0 versus 1.8 +/- 0.3) ng angiotensin l/mL per hour), a low salt diet (4.4 +/- 1.0 versus 1.1 +/- 0.3), or a high salt diet (1.5 +/- 0.2 versus 0.9 +/- 0.1). Urinary protein excretion was greater in S/renrr rats than in S/ren(ss) rats fed a high salt diet (244.2 +/- 48.5 versus 43.6 +/- 19.5 mg/24 h), and this was associated with significant reductions in renal blood flow (3.3 +/- 0.6 versus 4.6 +/- 0.5 mL/min per gram kidney weight) and glomerular filtration rate (0.49 +/- 0.11 versus 0.82 +/- 0.08 mL/min per gram kidney weight). Captopril (20 mg/kg i.v.) had no effect on blood pressure in S/ren(ss) rats fed a low salt diet, but it lowered blood pressure by 20 mm Hg in S/ren(rr) rats to the same level seen in untreated S/ren(ss) rats. Chronic administration of captopril (5 mg/100 mL drinking water) reduced blood pressure in S/renrr rats fed a high salt diet (170 +/- 5 mm Hg) to the same level seen in untreated S/ren(ss) rats, whereas it had no significant effect on blood pressure in S/ren(ss) rats. These results indicate that transfer of a salt-resistant renin allele to SS/Jr/Hsd rats raises plasma renin activity and augments the severity of hypertension and renal disease.

Alleles↗
PubMed1997

Lovastatin prevents development of hypertension in spontaneously hypertensive rats.

The present study evaluated the effects of lovastatin on renal function and the development of hypertension in spontaneously hypertensive rats (SHR). Four-week-old SHR were given lovastatin (10 mg/kg) or vehicle twice daily by gavage. After 4 weeks of treatment, mean arterial pressure was significantly lower in lovastatin-treated SHR (131 +/- 4 mm Hg, n=5) than in control animals (160 +/- 4 mm Hg, n=12) (P<.05). The fall in arterial pressure in lovastatin-treated rats was accompanied by changes in renal function. The slope of the relationship between arterial pressure and sodium excretion was threefold greater in lovastatin-treated SHR (n=6) than in control rats (n=6), and this was associated with significant elevations in renal medullary blood flow and renal interstitial hydrostatic pressure. Glomerular filtration rate was 17% higher in lovastatin-treated SHR (n=6) than in control rats (n=6) (0.94 +/- 0.05 versus 0.81 +/- 0.07 mL/min per g of kidney weight, P<.05). The wall-to-lumen area ratio of renal arterioles was significantly reduced in lovastatin-treated SHR compared with vehicle-treated rats (0.86 +/- 0.05 versus 1.08 +/- 0.04 for vessels with inner diameters <50 microm and 0.62 +/- 0.02 versus 0.75 +/- 0.04 for vessels with inner diameters of 50 to 100 microm, P<.05). These results indicate that chronic treatment with lovastatin shifts the relations between renal medullary blood flow, renal interstitial pressure, sodium excretion, and renal perfusion pressure to lower levels of arterial pressure and attenuates the development of hypertension and renal vascular hypertrophy in SHR.

Animals↗
PubMed1997

[Biomechanical observation on unstable intertrochanteric fracture fixed by 130 degrees angled-plate].

We examined the stability of unstable intertrochanteric fracture fixed by 130 degrees angled-plate biomechanically, and the stress distribution of the plate. The results showed that after 300 times circle-loading test, the fracture stability was destroied. Stress concentration was observed on the plate, which was aggravated by circle-loading test. These confirmed the inproper biomechanical stature of the plate. Referring to the clinical review, we conclude that using angled-plate to fix unstable intertrochanteric fracture hardly yields satisfactory results, at least, early wight-bearing exercise should not be promoted.

Biomechanical Phenomena↗
PubMed1997

[Phacoemulsification and foldable intraocular lens implantation through a small sutureless incision].

OBJECTIVE: To evaluate the therapeutic effects of phacoemulsification and the foldable intraocular lens implantation. METHODS: The surgery was performed through a 3.2 mm incision on 72 eyes of 65 patients with senile, complicated, congenital and traumatic cataracts. RESULTS: Post-operatively, the visual acuities with spherical correction or without correction were 0.5 or better in 94.4% at one day, and 1.0 or better in 70.8%, 75.8%, and 76.5% at one week, one month and three months respectively. The mean post-operative astigmatism was 0.89 +/- 0.83 D at one week and 0.73 +/- 0.76 D at one month which was respectively less than that in the control group with a 6.5 mm incision (P < 0.001), but no statistical difference between them at three months (P > 0.05). CONCLUSION: The foldable intraocular lens implantation through a small sutureless incision could reduce early post-operative astigmatism and shorten the period of visual rehabilitation.

Adult↗
PubMed1997

Clinical observation on 41 cases of threatened and habitual abortion treated by blood activation and stasis removal.

41 cases of pregnancy diagnosed as belonging to 4 subtypes of blood stasis, namely, qi stagnant, qi deficient, pernicious cold condensing and heat accumulating, suffering from womb leak, stirred fetus and fetal slip (threatened and habitual abortion) were treated by the method of blood activation and stasis removal in accordance with diagnostic typing. The treatment proved effective in 34 cases, the effective rate reaching 82.9%, with no significant differences either between threatened and habitual abortions or among the groups of cases with different syndromes. The treatment resulted in varying degrees of improvement in blood rheology and the level of serum (human) chorionic gonadotropin (HCG). Follow-up examination of 28 patients who had reacted favorably to the treatment and whose pregnancy had ended in normal deliveries revealed that none of the newborns differed significantly from the normal.

Abortion, Habitual↗
PubMed1997

Effects of superoxide anion, B(alpha)P and TPA on the membrane fluidity of NIH3T3 cells.

The membrane fluidity of NIH3T3 cells treated with low and high concentration of cell stimulatives (extracellular generated superoxide anion(O2-.),12-O-tetra-decanoyl-phorbol-13-acetate(TPA), and benzo(alpha)-pyrene[B(alpha)P]) was investigated by means of fluorescence labels 1,6-diphenyl-1,3,5 hexatriene (DPH) and N-(3-pyrene) maleimide (N(3p)M). The high concentration of O2-., TPA, B(alpha)P greatly increased the fluidity of cell membrane lipid domain. No changes of the florescence polarization of DPH was found in membrane lipid domain treated with low concentration of O2-., TPA, and B(alpha)P. However, decrease in the fluoresence polarization of N(3p)M on the cell membrane protein domain damaged by low concentration of cell stimulatives was observed, showing that these treatment could influence the conformation of membrane protein. The possible relationship between the changes of the conformation of membrane protein and the cell transformation and its carcinogenic machenisms were discussed.

3T3 Cells↗
PubMed1997

[Changes of plasma cytokines in patients with severe trauma and their relationship with organ damage].

We investigated kinetics of plasma TNF, IL-6 and IL-8 and their relationship with organ dysfunction and endotoxemia in 17 patients with severe trauma in order to further elucidate the role of cytokines in the development of organ damage and their production mechanism after trauma. Plasma cytokine levels significantly increased in trauma patients, and their plasma TNF was increased earlier. The cytokines were positively correlated with ISS, cardiac and hepatic enzyme activities, index of renal function, and plasma endotoxin levels. It is suggested that TNF, IL-6 and IL-8 may participate in the development of organ damage after trauma, and its release might be related to massive endotoxin translocation into body at the early stage of trauma.

Adolescent↗
PubMed1997

Expression of TNF alpha, IL-1 beta, IL-6 mRNA, release of TNF alpha in vital organs and their relationship with endotoxin translocation following hemorrhagic shock.

This study was designed to systematically investigate expression of TNF alpha, IL-1 beta, Il-6 mRNA in the liver, lungs and kidneys, release of TNF alpha in the above tissues, their relationship with hepatic, pulmonary and renal dysfunction, and distribution of endogenous endotoxin in tissues after hemorrhagic shock in mice and rats, with reverse-transcription-polymerase chain reaction, ELISA, etc, to elucidate the kinetics of expression and release of major cytokines in vital organs, their role and mechanism of production in shock. The results were: 1. expression of TNF alpha, IL-1 beta, IL-6 mRNA in vital organs successively increased after hemorrhagic shock and resuscitation, and TNF alpha expression was the first to appear followed by IL-1 beta. Though expression of IL-6 mRNA appeared late, it persisted longer; 2. TNF alpha levels in the liver, lungs and kidneys were all elevated but to different degrees after shock and resuscitation. At 3 hours after resuscitation, TNF alpha levels in the three above tissues were still significantly high, while plasma TNF alpha levels were already decreased to control levels; 3. hepatic, pulmonary and renal functions were damaged to different degrees after hemorrhagic shock, with hepatic dysfunction being the most severe; 4. endotoxin levels in the liver, lungs and kidneys were markedly increased after shock and resuscitation, and paralleled the expression of cytokine genes. In addition, there was significant correlation between changes in endotoxin level in tissues and TNF alpha release in tissues during early shock. It is suggested that expression and release of cytokines in vital organs might play an important role in local organ damage after hemorrhagic shock, and production of cytokines is related to endotoxin translocation.

Animals↗
PubMed1997

[Experimental study on erythrocyte of obstructive jaundice patient: its changes of membrane protein and mechanical properties].

The component of the erythrocyte membrane protein under three states obstruction, after surgical relief of obstruction, and normal) were analyzed qualitatively by using SDS-PAGE and the method of thin scanning. The result revealed that the membrane protein band 4.2 was absent under the state of obstruction and it recovered after surgical relief of obstruction. Then the mechanical properties of the above three cases of erythrocytes were tested by the micropipette aspiration system and the data were analyzed by Voigt model. The result showed that the elastic modulus and the coefficient of viscosity of the erythrocytes under the state of obstruction were greater than those of the normal; thus the deformability decreased, but "overcorrection" appeared after surgical relief of obstruction. The possible relations between the mechanical properties and the change of membrane protein were discussed.

Adult↗
PubMed1997

Effect of hemorrhagic shock on endotoxin-induced TNF production and its molecular mechanism in rats.

The present study was designed to investigate the production of tumor necrosis factor alpha (TNF alpha) induced by low-dose (1 microgram/kg) lipopolysaccharide (LPS) and its cellular source after hemorrhagic shock (HS) in rats, and to further analyze the mechanism for increased sensitivity to LPS through looking at expression of lipopolysaccharide-binding protein (LBP) mRNA in the liver, lungs and kidneys. It was found in vivo that plasma TNF alpha levels in the HS + LPS group were 20-fold higher than that in the HS group (P < 0.01), and 2.7-fold higher than that in the LPS group (P < 0.05). It was shown in vitro that the capacity of peripheral white blood cells to produce TNF alpha in response to LPS stimulation was significantly decreased by 126% (P < 0.01) and 57% (P < 0.05) compared with pre-shock levels and the sham group respectively at the end of resuscitation following shock, and was still markedly decreased 3 hours after resuscitation, while the capacity of Kupffer cells was significantly increased by 110% compared with the sham group (P < 0.01) after shock and resuscitation. Results from RT-PCR showed that expression of LBP mRNA in the liver, lungs and kidneys was increased after shock and resuscitation. It is suggested that hemorrhagic shock could significantly enhance endotoxin-induced TNF alpha production, which might be due to up-regulation of LBP expression in tissues after shock, and tissue macrophages might be the main source of cytokine production.

Acute-Phase Proteins↗
PubMed1997

[Human tolerance to landing impact (+Gz) in sitting position].

The study showed that macaca mulatta selected can be used as a substitute for human in studying tolerance to landing impact. Based on the data of the experiments, the revisional coefficient from macaca mulatta to humans was calculated, and curves of human tolerance to landing impact in sitting position were given. Tolerance limits for different injuries such as safe, slight injury, medium injury and serious injury are also given in this paper. The results might be useful for setting human tolerance standards to landing impact in sitting position.

Acceleration↗
PubMed1997

Measurement of cerebrospinal fluid pressure in conscious rats.

We describe a method of using a micro-tip transducer to measure cerebrospinal fluid pressure (CSFp) through a lateral ventricular cannula in unanesthetized, restrained, non-stressed rats. The mean value of CSFp under the anesthesia was 4.2 +/- 0.9 (mean +/- SEM, n = 6), ranging from 1.3 to 7.5 mmHg. Measurements were made daily in conscious state for 7 consecutive days after the operation. Mean value of CSFp was 9.1 +/- 0.5 mmHg (n = 42), ranging between 8.0 +/- 1.4 and 10.4 +/- 1.3 mmHg (n = 6) from day to day (P > 0.05). The permanent intraventricular cannula did not cause any detectable changes in behavior, arterial pressure, arterial blood gas, arterial blood acid-base chemistry, and water content of the punctured hemisphere. The results indicated that the method is a reliable alternative for CSFp measurement in a conscious, restrained, non-stressed rat which can be used under a variety of experimental conditions.

Animals↗
PubMed1997

Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats.

Based on a model of acute carbon monoxide (CO) poisoning in rats with an occluded left carotid artery, we have evaluated the effects of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2) on mortality and morbidity. After exposure to 2,700 ppm CO in air for 1 h, the rats were grouped and treated with air (group 1, untreated controls, in a previous study), 100 kPa O2 for 4 h (group 2), 300 kPa normoxia (group 3, pressure controls), and 300 kPa O2 (group 4) for 1 h, respectively. NBO2 started immediately, whereas HBO2 began 35 min after the end of the CO exposure. At the termination of the exposure, the four groups suffered identical levels of poisoning as indicated by the degrees of hypothermia, hypocapnia, drop in mean arterial pressure, and acidosis. Up to 48 h after the end of the CO exposure, mortalities were 76, 58, 75, and 17 in groups 1-4, respectively. The neurologic morbidities, indicated by abnormal motor behaviors and edema in the left cerebral hemispheres, were 84, 67, 83, and 42% in groups 1-4, respectively. Compared to the normoxic treatments, the HBO2, but not the NBO2, significantly reduced the mortality and the neurologic morbidity. HBO2 was also significantly better than NBO2 in increasing surviving time and survival rate. The results support the value of HBO2 in improving short-term outcome of acute CO poisoning in this rat model.

Acute Disease↗
PubMed1997

Cerebrospinal fluid pressure changes after acute carbon monoxide poisoning and therapeutic effects of normobaric and hyperbaric oxygen in conscious rats.

This study on conscious rats with occluded left carotid artery investigates the influence of cerebral edema after acute carbon monoxide (CO) poisoning on cerebrospinal fluid pressure (CSFp) and evaluates the therapeutic effectiveness of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2). The CSFp was continuously recorded via a cannula placed in the left cerebral ventricle before, during, and for up to 6 h after exposure to 0.27% CO for 1 h. A non-sustained small increase in the CSFp and identical degrees of hypoxemia, hypocapnia, arterial hypotension, and acidosis were found during the exposure in all rats. After the CO exposure, all non-edema control rats without carotid artery ligation (n = 7) recovered completely with normal CSFp, behavior, and brain water content. All untreated (n = 7) and NBO2-treated rats (n = 7) developed a severely increased CSFp (> 50 mmHg) with neurologic motor dysfunction, and died of a severely increased CSFp (> 100 mmHg) with considerable cerebellar herniation. Except in one rat, the CSFp did not reach a dangerous level (> 25 mmHg) after the HBO2 session (300 kPa O2 for 1 h, beginning at 20 min post CO). All HBO-treated rats (n = 7) survived with less neurologic motor dysfunction and less left hemispheric edema than those in untreated and NBO2-treated rats. The results demonstrated that the increase in the CSFp was related to the left hemispheric edema, and that the cerebellar herniation was the predominant cause of death after the CO exposure. HBO2, but not NBO2, prevented the severe increase in the CSFp and thus saved the life after the CO exposure.

Acute Disease↗
PubMed1997

[Increased sensitivity to endotoxin and its molecular mechanism after hemorrhagic shock].

OBJECTIVE: To study the increasing sensitivity to endotoxin induced by hemorrhagic shock and its mechanism. METHODS: Routine biochemical assay, reverse transcription-polymerase chain reaction. (RT-PCR) and cell in situ hybridization were used to investigate the effects of low-level endotoxin under hemorrhagic shock and its possible mechanism. RESULTS: In rabbits, blood pressure levels were significantly decreased, and plasma lactate and beta-glucuronidase (beta-G) levels increased in hemorrhagic shock (HS) + LPS group, all of which were significantly different from those in the LPS or HS group. All of the animals in the HS + LPS group were dead while those in the LPS or HS group survived 24 hours after shock. The results of RT-PCR showed that expression of lipopolysaccharide-binding protein (LBP) mRNA in the liver, lungs and kidneys was increased in rats after shock and resuscitation. The expression of CD144 mRNA in the peritoneal macrophages in mice was also enhanced after hemorrhagic shock and subsequent resuscitation showed by cell in situ hybridization. CONCLUSION: Hemorrhagic shock can significantly increase the sensitivity to endotoxin possibly because of up-regulation of LBP/CD14 after shock.

Acute-Phase Proteins↗
PubMed1997

Kinetics of plasma cytokines and its clinical significance in patients with severe trauma.

OBJECTIVE: To examine the kinetics of plasma tumor necrosis factor alpha (TNF alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8) in patients with severe trauma and to discuss their relationship with organ damage and endotoxemia. METHODS: Seventeen patients (10 men and 7 women) with severe trauma were selected in this study. Their mean age was 37.9 +/- 11.9 years. All patients were divided into two groups according to injury severity score (ISS): group I with ISS from 16-25 (18.8 +/- 2.9, n = 10) and group II with ISS more than 25 (34.3 +/- 8.3, n = 7). Ten young healthy volunteers (6 men and 4 women) were used as controls. Plasma TNF alpha and IL-8 levels were assayed with enzyme-linked immunosorbent assay. IL-6 activity in the plasma was determined by bioassay with IL-6-dependent cell-line 7TD1. Limulus amebocyte lysate chromogenic test was used for plasma endotoxin assay. RESULTS: Plasma cytokine levels in patients with trauma had a successively significant increase. Plasma TNF level increased earlier. Increases in plasma IL-6 and IL-8 occurred later. All the increases were significantly correlated with the severity of trauma and organ damage after trauma. In addition, obvious endotoxemia occurred at the early stage of trauma and was significantly correlated with the severity of trauma and the levels of plasma TNF alpha, IL-6 and IL-8. CONCLUSIONS: Release of TNF alpha, IL-6 and IL-8 can be significantly increased in patients with severe trauma. The increase may be related to massive endotoxin translocation and may play an important role in the development of organ damage after trauma.

Adolescent↗