[Focus on cardiopulmonary resuscitation in China in 2004].
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Biomedical subjects
Publications and source records attributed to Hong Shen.
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OBJECTIVE: To investigate the therapeutic effect of mild hypothermia on severe traumatic brain injury. METHODS: Eighty-six in-patients with severe traumatic brain injury treated ordinarily were consecutively randomized into two groups: a hypothermia group (n=43) and a normothermia group (the control group, n=43). In the hypothermia group, the core temperature (i.e., nasopharyngeal or brain temperature) of the patient was reduced to and maintained at 33-35 degrees C with a systemic cooling blanket. Natural rewarming began after 3-5 days (mean: 4.3 days) of hypothermia treatment. In the control group, the patient received no hypothermia treatment. The vital sign, extradural pressure and serum superoxide dismutase were observed and measured during treatment, and the complications as well as the Glasgow outcome scale were evaluated at 2 years after injury. RESULTS: The mean extradural pressure in the hypothermia group (27.38 mm Hg +/- 4.88 mm Hg at 24 hours, 29.40 mm Hg +/- 4.50 mm Hg at 48 hours and 26.40 mm Hg +/- 4.13 mm Hg at 72 hours after injury) was much lower than that in the control group (32.63 mm Hg +/- 3.00 mm Hg, 34.80 mm Hg +/- 6.00 mm Hg and 31.81 mm Hg +/- 4.50 mm Hg respectively at 24, 48 and 72 hours, P<0.05). The mean serum superoxide dismutase levels in the hypothermia group on days 3 and 7 (583.7 microg/L +/- 99.6 microg/L and 699.4 microg/L +/- 217.3 microg/L, respectively) were much higher than those in the control group at the same time period (446.6 microg/L +/- 79.5 microg/L and 497.1 microg/L +/- 101.2 microg/L, respectively, P<0.01). The recovery rates at 2 years after injury were 65.1% in the hypothermia group and 37.2% in the control group (P<0.05). The mortality rates were 25.6% in the hypothermia group and 51.2% in the control group (P<0.05). The complications, including pulmonary infections, thrombocytopenia (platelet count < 100 x 10(9)/L), hemorrhage in the digestive tract, electrolyte disorders and renal malfunction, were managed without severe sequelae. CONCLUSIONS: Mild hypothermia is a safe and effective therapeutic method, which can lower the extradural pressure, increase the serum superoxide dismutase and improve the neurological outcomes without severe complications in the patients with severe traumatic brain injury.
OBJECTIVE: To investigate the effect of arterial elongation on the arteries and to set up a new method for vessel repair. METHODS: This study was performed in 24 arteries that underwent different traumatic deficit and acute intra-operative elongation repair. The vessels were harvested and studied by histology, electron microscopy, and immunohistochemistry on day 1, 7 and 28 after operation. RESULTS: The total unobstructed rate was 100% for deficit group as well as control experimental group. The content of collagen and elastin at various intervals showed no significant difference, the ratio of them also had no significant difference. Following anastomosis, the compliance of arteries was decreased, the peak value of proliferative cell nuclear antigen (PCNA) positive cell percentage was less than 20%, the internal diameter of elongation and anastomosis edge had no significant difference between deficit group and control group. There were no marked differences in pathological changes between deficit group and control group. CONCLUSION: Acute intraoperative artery elongation after balloon dilatation is a simple, safe, and effective alternative to vein interposition in the repair of traumatic arterial injuries. It appears to be a useful method in the emergency treatment.
Hepatic stellate cells (HSCs) are now considered the major cell type in the liver mediating the development of liver fibrosis. Recently it was demonstrated that HSCs express membrane proteins involved in antigen presentation. We further evaluate immunological properties of HSCs by examining the expression and function of the Fc fragment of immunoglobulin G (IgG) in HSCs. In this study, we document the presence of mRNAs for three Fc gammaRs in HSCs. Ligand binding assay indicated the existence of Fc gammaRs with different binding affinities on membranes of HSCs. We also documented that the abundance of the three Fc gammaR mRNAs increased upon activation of HSCs in vitro. Moreover, an examination of the biological activities of IgG revealed that exposure to IgG significantly stimulated HSC differentiation and proliferation. Furthermore, we studied the intracellular signaling protein, LcK, in HSCs and regulation of Lck expression and phosphorylation by IgG. Although IgG did not regulate Lck abundance and phosphorylation in HSCs, highly phosphorylated Lck was present in these cells. In conclusion, we provided evidence that HSCs expresses receptors for the Fc fragment of IgG, and IgG regulates HSC differentiation and proliferation. Therefore, immunoglobulin G may play a role in HSC activation.
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OBJECTIVE: To evaluate the efficacy and the safety of emergent primary percutaneous coronary intervention (PCI) in the saphenous vein bypass graft (SVBG) of acute myocardial infarction (AMI), and compare the results between aged -patients with non-aged patients. METHODS: Three hundred and nine consecutive AMI patients with culprit SVBG vessels, were analysed, including aged patients 213 cases(>or=70 years old), non-aged patients 96 cases(<70 years old), underwent the emergent primary PCI after confirmed below TIMI III perfusion(TIMI 0-TIMI II) in coronary angiographies. The immediate results and in-hospital outcomes were compared between two groups. RESULTS: Procedural successful rate, re-occlusion rate, and emergency re-CABG had no significant differences between two groups. The rate of slow-flow/no-reflow and in-hospital mortality rate were significantly higher in elderly group (19.7% vs 10.4%, 9.4% vs 4.2%, both P<0.05), with no difference in the rate of the using of distal protection devices between two groups. The comparison of the rate of direct stenting in slow-flow/no-reflow subgroup with normal-flow subgroup, had not showed statistic difference (73.5% vs 67.3%, P>0.05). There was no statistic difference of heavy hemorrhage between two different age groups. CONCLUSION: The primary PCI for the elderly AMI patients with infarction-related SVBG vessels, has higher risks in slow-flow/no-reflow and the mortality, even with using the distal protection devises and direct stents implantation.
OBJECTIVE: To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI). METHODS: In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain. RESULTS: Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP. CONCLUSIONS: In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.
OBJECTIVE: To investigate the biological changes of the epithelia of benign prostate hyperplasia under heating at different temperatures and at different points of time after heating. METHODS: Cell morphology, MTT, flow cytometer, and the immunocytochemical method for detecting heat shock protein 70 and prostate specific antigen were used to observe the effect of heating on the primarily cultured epithelia of benign prostate hyperplasia at 45 degrees C and 60 degrees C and at 1 hour and 12 hours after heating. RESULTS: Heating at 45 degrees C for 15 min resulted in apoptosis, and at 60 degrees C, necrosis in most of the cells. The inhibiting effect of heating on the growth of cells was observed, more significant in the 60 degrees C group than in the 45 degrees C group. The cell phase arrest induced by heat, mainly G0/G1 arrest, was more significant in the 12 h group than in the 1 h group. Heating up-regulated the expressions of heat shock protein 70 and prostate specific antigen in cells. CONCLUSION: Heating can induce apoptosis, necrosis and growth suppression of the epithelia of benign prostate hyperplasia. Its process and mechanism are correlated with the cell phase arrest and the up-regulation of the expressions of heat shock protein 70 and prostate specific antigen.
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OBJECTIVE: To investigate the effects of a combination of naloxone and methylprednisolone on nuclear factor-kappaB (NF-kappaB) p65 expression in the lung tissue in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. METHODS: ALI models were reproduced by intratracheal instillation of LPS (3 mg/kg). Four hours after LPS instillation, rats were randomly divided into five groups: normal saline group, LPS group, methylprednisolone group, naloxone group (LPS+naloxone) and combined drug group (LPS+naloxone+methylprednisolone). The level of interleukin-8 (IL-8) in serum was measured by immunoassay. Meanwhile, the expression of NF-kappaB p65 in the lung tissue was determined with immunohistochemical staining. RESULTS: Naloxone and methylprednisolone significantly reduced the LPS-induced increase in IL-8 concentrations in serum in vivo, and suppressed the activation of NF-kappaB p65 in the lung tissue. CONCLUSION: NF-kappaB activation is involved in the LPS-induced ALI in rats. Combination of naloxone and methylprednisolone could suppress the increase of IL-8 content and NF-kappaB activation in the lung tissue of rat in vivo in our experiment.
The measure analysis and QA system for gamma knife dose field and its pivotal techniques are described in this paper. By using our own measuring tools and analysis software, we have made a testing analysis about the HuaYuan Gamma Knife dose field with a satisfactory result.
AIM: Cyclooxygenase (COX)-2 is over expressed in gastrointestinal neoplasm. Helicobacter pylori (H pylori) infection is causally linked to gastric cancer. However, the expression of COX-2 in various stages of H pylori-associated gastric carcinogenesis pathway has not been elucidated. Therefore, the aim of this study was to clarify the role of H pylori induced COX-2 expression during carcinogenesis in the stomach. METHODS: Gastric biopsies from 138 subjects (30 cases of chronic superficial gastritis (CSG), 28 cases of gastric glandular atrophy (GA), 45 cases of gastric mucosal intestinal metaplasia (IM), 12 cases of moderate gastric epithelial dysplasia and 23 cases of gastric cancer) were enrolled. H pylori infection was assessed by a rapid urease test and histological examination (modified Giemsa staining). The expression of COX-1 and COX-2 in human gastric mucosa was detected by immunohistochemical staining. RESULTS: H pylori infection rate was 64.3% in GA and 69.5% in gastric cancer, which was significantly higher than that (36.7%) in CSG (P<0.05). The positive expression rates of COX-2 were 10.0%, 35.7%, 37.8%, 41.7% and 69.5% in CSG, GA, IM, dysplasia and gastric cancer, respectively. From CSG to GA, IM, dysplasia and finally to gastric cancer, expression of COX-2 showed an ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. The level of COX-2 expression in IM and dysplasia was significantly higher in H pylori-positive than in H pylori-negative subjects (P<0.01). CONCLUSION: COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.
Safe and efficient gene delivery would have great potential in gene therapy and tissue engineering, but synthetic biomaterial surfaces endowed with efficient gene-transferring functions do not yet exist. Inspired by naturally occurring biomineralization processes, we co-precipitated DNA with inorganic minerals onto cell-culture surfaces. The DNA/mineral nanocomposite surfaces obtained not only supported cell growth but also provided high concentrations of DNA in the immediate microenvironment of the cultured cells. Gene transfer from the engineered surfaces was as efficient as an optimized commercial lipid transfection reagent; in addition, the extent of gene transfer was adjustable by varying the mineral composition. DNA/mineral nanocomposite surfaces represent a promising system for enhancing gene transfer and controlling the extent of gene transfer for various biomedical applications, including tissue engineering or gene therapy of bone.
An extension of the stoichiometric displacement (SD) model for the ion-exchange adsorption of dilute proteins is developed which accounts for the effects of hydrogen ion Donnan equilibrium on the protein charge. The ability of the new model to fit retention data when the fluid phase pH is near the protein pI and the effects of hydrogen ion Donnan equilibrium are important is examined using four different proteins and four different column packings. The results indicate that the model is able to fit retention data using values for the protein pI and the change in protein charge with pH at the pI, i.e., (dz/dpH)pI, that are significantly closer to the values of these parameters determined by isoelectric focusing and acid-base titrametry in free solution, respectively, as compared to the values obtained by determining the characteristic binding change as a function of pH using the traditional stoichiometric displacement model. This suggests that when the fluid phase pH is near the protein pI, charge regulation is an important cause of the discrepancy between the electrical charge of a protein in free solution and the characteristic binding charge from the stoichiometric displacement model. The results also indicate that for the case where the fluid phase pH is near the protein pI, the new model accounts for the effect of charge regulation during protein ion-exchange adsorption more accurately than previous models in the literature.
The Al-induced release of organic acid has been suggested as an important mechanism for Al resistance in plants. In this study, the effect of K-252a and abscisic acid (ABA) on the efflux of citrate was investigated in soybean (Glycine max L.) roots. Al initiated citrate efflux from the root apices 30 min after the addition of Al. The Al-triggered efflux of citrate was sensitive to metabolic inhibitors and anion channel inhibitors. Pretreatment or treatment with K-252a, an inhibitor of protein kinase, severely inhibited the Al-induced efflux of citrate accompanying an increase in Al accumulation and intensified Al-induced root growth inhibition. Al-treatment increased the endogenous level of abscisic acid (ABA) in soybean roots in a dose- and time-dependent manner, while K-252a failed to inhibit the Al-induced increase in endogenous ABA. Exogenous application of ABA increased the activity of citrate synthase (EC 4.1.3.7) by 26.2%, and decreased Al accumulation by 32.3%, respectively. ABA-induced increases in citrate efflux and root elongation were suppressed by K-252a, while ABA could not reverse the K-252a effects. Taken together, these results suggest that ABA is probably involved in the early response, after which K-252a-sensitive protein kinases play a key step in regulating the activity of an anion channel, through which citrate is released from the apical cells of soybean roots.
We previously identified the major pathological changes in the respiratory and immune systems of patients who died of severe acute respiratory syndrome (SARS) but gained little information on the organ distribution of SARS-associated coronavirus (SARS-CoV). In the present study, we used a murine monoclonal antibody specific for SARS-CoV nucleoprotein, and probes specific for a SARS-CoV RNA polymerase gene fragment, for immunohistochemistry and in situ hybridization, respectively, to detect SARS-CoV systematically in tissues from patients who died of SARS. SARS-CoV was found in lung, trachea/bronchus, stomach, small intestine, distal convoluted renal tubule, sweat gland, parathyroid, pituitary, pancreas, adrenal gland, liver and cerebrum, but was not detected in oesophagus, spleen, lymph node, bone marrow, heart, aorta, cerebellum, thyroid, testis, ovary, uterus or muscle. These results suggest that, in addition to the respiratory system, the gastrointestinal tract and other organs with detectable SARS-CoV may also be targets of SARS-CoV infection. The pathological changes in these organs may be caused directly by the cytopathic effect mediated by local replication of the SARS-CoV; or indirectly as a result of systemic responses to respiratory failure or the harmful immune response induced by viral infection. In addition to viral spread through a respiratory route, SARS-CoV in the intestinal tract, kidney and sweat glands may be excreted via faeces, urine and sweat, thereby leading to virus transmission. This study provides important information for understanding the pathogenesis of SARS-CoV infection and sheds light on possible virus transmission pathways. This data will be useful for designing new strategies for prevention and treatment of SARS.