Imaging characteristics and prognostic factors of Behcet's disease with arterial involvement: A long-term follow-up study.

PURPOSE: To investigate the imaging characteristics and prognostic factors for the long-term survival of Behcet's disease (BD) with arterial involvement. METHODS: In this retrospective study, BD patients with arterial involvement were identified from January 2003 to January 2020. Arterial lesions were detected by ultrasonography, traditional arteriography, and/or computed tomography angiography (CTA). Cox proportional hazards regression analyses were performed to identify the prognostic factors. RESULTS: Totally, 84 BD patients with arterial involvement were identified (73.8 % males). The mean age at BD diagnosis was 39.1 ± 13.1 years. Arterial involvement was the initial manifestation in 33.3 % of the patients, and the median time from BD diagnosis to arterial involvement was 6 (IQR 1-15.5) years for the rest of patients. Systemic artery involvement and pulmonary artery involvement (PAI) were found in 64 and 27 patients, respectively. Approximately 94.0 % (79/84) of the patients had more than one artery involved concurrently or successively during the course of BD. Aneurysm/dilation was the most prevalent lesion in the aorta (76.0 %), while stenosis/occlusion was the main lesion of the coronary artery (90.9 %) and other aortic branches (74.5 %). Pulmonary hypertension was found in 70.4 % (19/27) of patients with PAI. The 5- and 10-year survival rates of BD patients with arterial involvement were 87.4 % and 84.1 %, respectively. Cardiac involvement (HR: 4.34) and pulmonary artery aneurysm/dilation (HR: 4.89) were independently associated with mortality. CONCLUSIONS: Arterial lesions associated with BD usually involve multiple arteries and manifest differently in different types of arteries. Cardiac involvement and pulmonary artery aneurysm/dilation are independent prognostic factors of BD patients with arterial involvement.

Meta-analysis reveals variations in microbial communities from diverse stony coral taxa at different geographical distances.

Coral-associated microbial communities play a vital role in underpinning the health and resilience of reef ecosystems. Previous studies have demonstrated that the microbial communities of corals are affected by multiple factors, mainly focusing on host species and geolocation. However, up-to-date, insight into how the coral microbiota is structured by vast geographic distance with rich taxa is deficient. In the present study, the coral microbiota in six stony coral species collected from the coastal area of three countries, including United States of America (USA), Australia and Fiji, was used for analysis. It was found that the geographic influence on the coral microbiota was stronger than the coral host influence, even though both were significant. Interestingly, the contribution of the deterministic process to bacterial community composition increased as geographical distance grew. A total of 65 differentially abundant features of functions in coral microbial communities were identified to be associated with three geolocations. While in the same coastal area of USA, the similar relationship of coral microbiota was consistent with the phylogenetic relationship of coral hosts. In contrast to the phylum Proteobacteria, which was most abundant in other coral species in USA, Cyanobacteria was the most abundant phylum in Orbicella faveolata. The above findings may help to better understand the multiple natural driving forces shaping the coral microbial community to contribute to defining the healthy baseline of the coral microbiome.

Nestin represents a potential marker of pulmonary vascular remodeling in pulmonary arterial hypertension associated with congenital heart disease.

OBJECTIVE: Reportedly, nestin was re-expressed in proliferative synthetic-type pulmonary artery smooth muscle cells (PASMCs) and obligatory for PASMC proliferation in pulmonary arterial hypertension (PAH). Accordingly, nestin is increased in pulmonary vascular lesions of congenital heart disease (CHD)-associated PAH patients. We tested the hypothesis whether nestin was re-expressed in proliferative synthetic-type PASMCs and associated with pulmonary vascular remodeling in CHD-PAH. MATERIALS AND METHODS: Nestin expression was tested using lung tissues from CHD-PAH patients and monocrotaline (MCT) plus aortocaval (AV) shunt-induced PAH rats, human PASMCs (HPASMCs), and pulmonary artery endothelial cells (PAECs) and PASMCs from MCT-AV-induced PAH rats. The role and possible mechanism of nestin on HPASMC proliferation, apoptosis, cell cycle and migration were investigated by assays of CCK-8, EdU, TUNEL, flow cytometry, transwell chamber and immunoblotting assays. RESULTS: Nestin was solely expressed in proliferative synthetic-type PASMCs, but rarely detected in PAECs. Nestin was barely detected in normal pulmonary arterioles and occlusive pulmonary vascular lesions. Its expression was robustly increased in developing pulmonary vasculature, but returned to normal levels at the late stage of pulmonary vascular remodeling in lung tissues from CHD-PAH patients and MCT-AV-induced PAH rats. Besides, nestin peaks were consistent with the histological features in lung tissues of MCT-AV-induced PAH rats. Moreover, nestin overexpression effectively promoted HPASMC phenotypic transformation, proliferation, apoptosis resistance and migration via enhancing Wnt/ß-catenin activation. CONCLUSIONS: These data indicated that nestin was re-expressed in proliferative synthetic-type PASMCs and might represent a potential marker of pulmonary vascular remodeling in CHD-PAH.

Study on the development and usage of a cardiopulmonary resuscitation time point recorder.

BACKGROUND: To invent a novel cardiopulmonary resuscitation (CPR) time point recorder to synchronously and automatically record the time and to identify its effectiveness in humans. METHODS: A CPR time point recorder was invented after the doctors were familiar with the traditional Utstein recovery registration mode and mastered the registration time points required. The progress of CPR was simulated. The standard and correct times were recorded, and the doctors performing the recovery collected the data about the times using our CPR time point recorder or the memory registration mode. RESULTS: The deviation times were 21.4±24.7 seconds for the memory group and 3.57±4.58 seconds for CPR time point recorder group. The deviation of times increased significantly depending on the increase of the operation items in the memory group. A similar phenomenon was found in the timer group but with a smaller difference (P<0.01). CONCLUSION: A CPR time point recorder could reduce the deviation of operate-time, especially after a long-time operation, and for procedures with more operating items, compared with the memory mode. It was a more advantageous and accurate method for the Utstein registration.

Activation of autophagy improved the neurologic outcome after cardiopulmonary resuscitation in rats.

OBJECTIVE: Recent studies have shown the existence of autophagy in cerebral ischemia; however, there has been no research on the role of autophagy in cerebral injury after cardiopulmonary resuscitation (CPR). This study was conducted to determine the role of autophagy in an animal model of ventricular fibrillation (VF)/CPR. METHODS: Experiment 1: A total of 48 adult Wistar rats were untreated for 7 minutes after induction of VF using an external transthoracic alternating current, and subsequent CPR was performed to observe the existence of autophagy after the return of spontaneous circulation (ROSC). Experiment 2: A total of 72 rats were pretreated with intracerebroventricular injection of physiologic saline (control group), the autophagy inducer (rapamycin group), or the autophagy inhibitor 3-methyladenine (3-methyladenine group) before ROSC to evaluate the contribution of autophagy to neuronal injury after ROSC. RESULTS: The activation of autophagy was attenuated 2 to 4 hours after ROSC, which was related to the activity decrease of 5'-adenosine monophosphate-activated protein kinase after ROSC. Rapamycin treatment significantly increased the expressions of LC3-II and Beclin-1 after ROSC, attenuated the activation of caspase-3, promoted neuronal survival and decreased neuronal apoptosis, and improved the neurologic deficit score after CPR. CONCLUSIONS: The activation of autophagy after ROSC offered a remarkable tolerance to VF/CPR ischemic insult and improved the neurologic outcomes.

[Relationship between PMI and ATR-FTIR Spectral Changes in Swine Costal Cartilages and Ribs].

OBJECTIVE: To analyze postmortem chemical changes in Landrace costal cartilages and ribs using attenuated total reflection-Fourier transform infrared (ATR-FTIR) spectroscopy, and to provide a novel technique for estimation of postmortem interval (PMI). METHODS: The swines were sacrificed by hemorrhage and their costal cartilages and ribs were kept in 20 degrees C. The chemical analysis of the costal cartilages and ribs were performed using ATR-FTIR every 72 h. The correlation between the certain spectral parameters and PMI was also analyzed. The time-dependent changes of costal cartilages were more significant than ribs. RESULTS: There were no obvious changes for the main absorbance bands position, and some absorbance band ratios showed time-dependent changes and significant correlations with the PMI. CONCLUSION: ATR-FTIR has the ability to analyze postmortem chemical changes of the swine costal cartilages and ribs, and it can be a new method to estimate PMI based on spectroscopy.

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation.

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, IL-6, Myeloperoxidase, and Malondialdehyde.

Ulinastatin attenuates oxidation, inflammation and neural apoptosis in the cerebral cortex of adult rats with ventricular fibrillation after cardiopulmonary resuscitation

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, ...

Ulinastatin improved cardiac dysfunction after cardiac arrest in New Zealand rabbits.

OBJECTIVE: The present study was designed to evaluate the effects of ulinastatin (UTI) on cardiac dysfunction after cardiopulmonary resuscitation (CPR). METHODS: A total of 48 healthy adult male New Zealand rabbits were untreated for 8 minutes after the induction of ventricular fibrillation (VF) by an external transthoracic alternating current and then treated by CPR. These rabbits were then randomly divided into the control and UTI groups after the return of spontaneous circulation (ROSC) and were observed for 8 hours after the ROSC. Before CPR and after ROSC at 2, 4, and 8 hours, blood samples were collected to determine the levels of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), cardiac troponin I (cTnI), and N-terminal probrain natriuretic peptide (NT-proBNP), and the left ventricular ejection fraction (EF) was measured by echocardiography. RESULTS: Nineteen of 24 rabbits in the control group and 18 of 24 in the UTI group were successfully resuscitated. The plasma levels of TNF-α, IL-6, MDA, cTnI, and NT-proBNP were significantly increased, accompanying a deceased EF in the control group, but the cotreatment with UTI decreased the plasma levels of TNF-α, IL-6, MDA, cTnI, and NT-proBNP (P < .05), attenuating the myocardial injury and improving the EF in the UTI group. Only 9 of 19 animals in the control group but 14 of 18 animals in the UTI group survived longer than 8 hours (P = .011). CONCLUSIONS: The progression of proinflammatory responses, oxidative stress, and myocardial injury have been linked to the reduced EF after VF/CPR, and the administration of UTI at a cardioprotective dosage preserved the cardiac function after VF/CPR.

Early enhanced external counter pulsation improves neurological recovery after the return of spontaneous circulation in a mongrel dog cardiac arrest model*.

OBJECTIVES: The aim of this study was to investigate whether early enhanced external counter pulsation therapy after cardiopulmonary resuscitation improved neurological outcome in a mongrel dog cardiac arrest model. DESIGN: Randomized, animal study. SETTING: Assisted circulation laboratory. SUBJECTS: Twenty-four healthy male adult dogs (12-14 kg). INTERVENTIONS: After minutes of untreated ventricular fibrillation followed by 2 minutes of cardiopulmonary resuscitation, the dogs were randomized to receive 4 hours of enhanced external counter pulsation therapy, to receive 4 hours of hypertension with over 140 mm Hg or to be a control. MEASUREMENTS: Blood pressure and left ventricular ejection fraction were recorded. Cerebral flow was assessed using magnetic resonance imaging. Arterial blood gases and endothelium-derived vasoactive substances were assessed before cardiac arrest and 4 hours after the return of spontaneous circulation. Neurological outcome was assessed by the neurologic deficit score and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. RESULTS: Enhanced external counter pulsation significantly improved the left ventricular ejection fraction and increased common carotid artery blood flow and shear stress. Enhanced external counter pulsation increased both relative cerebral blood volume (RCBV, p = 0.043) and relative cerebral blood flow (RCBF, p = 0.012) in animals 4 hours after return of spontaneous circulation. Enhanced external counter pulsation therapy promoted the production of nitric oxide and tissue plasminogen activator and decreased the release of endothelin-1 (p = 0.013) after return of spontaneous circulation. Treatment with norepinephrine in the high mean artery pressure also increased common carotid artery blood flow and shear stress. However, no effects on the left ventricular ejection fraction, the production of nitric oxide and tissue plasminogen activator, or the release of endothelin-1 were found. The neurologic deficit scores of the animals were significantly lower at 24, 48, 72, and 96 hours in the enhanced external counter pulsation group, as well as at 24, 72, and 96 hours compared with animals in the control group after return of spontaneous circulation. Fewer apoptotic neurons were observed in the animals in the enhanced external counter pulsation group compared with the animals in the control and hypertension groups. CONCLUSIONS: These data indicated that the treatment of early enhanced external counter pulsation improved neurological outcome by both increasing cerebral blood flow and improving the recovery of microcirculation after return of spontaneous circulation. The treatment of early enhanced external counter pulsation can be a good option for protecting the brain after return of spontaneous circulation.

Changes in expression of Nogo receptor 1 in hippocampus and cortex after cardiopulmonary resuscitation in rats.

The aim of this study was to investigate changes in Nogo receptor 1 (NgR(1)) expression in the cerebrum after cardiopulmonary resuscitation (CPR) in rats. Cardiac arrest was induced by alternating current in 50 SD rats through transcutaneous electrical epicardium stimulation, and CPR was performed with the Utstein mode 6 minutes after cardiac arrest. Rats were killed 1, 3, and 7 days after CPR. We performed immunofluorescence with antibodies against NgR(1) to map the distribution of NgR(1) in the rat cerebrum, whereas quantitative polymerase chain reaction was performed for quantitative analysis of NgR(1) messenger RNA (mRNA). There was a striking transient up-regulation of the NgR(1) protein and mRNA in both the hippocampus and cortex in response to CPR. Nogo receptor 1 proteins were strongly expressed in hippocampal neurons 1 and 3 days after CPR (P < .001 for 1 day and P < .05 for 3 days, vs the control group, respectively), which returned to the basal level 7 days after CPR. In the cortex, staining moderately increased 1 day after CPR and got the peak level after 3 days (P < .001), returning to normal expression levels on day 7. The levels of NgR(1) mRNA in the hippocampus and cerebral cortical cortex showed the same trend with staining. The changes were significantly different between day 3 and baseline in both the hippocampus and cortex (P < .05, respectively). Furthermore, there were significant differences between the hippocampus and cerebral cortical cortex at 1 day and 3 days after the CPR (P < .05, respectively). There was a transient increase in NgR(1) in the vulnerable areas of the rat brain after CPR. Blockade of NgR(1) may be important in maintaining the high regenerative capacity of neurons during the time window when NgR(1) expression increases.

Drug associated vanishing bile duct syndrome combined with hemophagocytic lymphohistiocytosis.

A 28-year-old woman with untreated autoimmune disorder, demonstrated skin rash and fever after taking Amoxicillin-clavulanate and developed progressive jaundice. A bone marrow aspiration indicated an increased number of macrophages with hemophagocytosis and liver biopsy showed pure centrilobular cholestasis with necrosis and some absence of portal bile ducts. Furthermore, a serological test for Epstein-Barr virus was positive. Under treatment by liver dialysis and administration of steroids led to rapidly defervescence and clinical improvement. However, liver enzymes were still markedly elevated with persistent anemia, even after immunosuppressive treatment. The patient is currently waiting for liver transplantation. This is the first description of vanishing bile duct syndrome combined with hemophagocytic lymphohistiocytosis, with underlying causes including infection, drug-induced factors and untreated autoimmune disorder.

Investigation of the relationship between venticular fibrillation duration and cardiac/neurological damage in a rabbit model of electrically induced arrhythmia.

BACKGROUND: To establish a simple, economic, and reliable alternating current (AC)-induced cardiac arrest (ACCA) model in rabbits for cardiopulmonary cerebral resuscitation research. METHODS: Ventricular fibrillation was induced in 27 New Zealand rabbits by external transthoracic AC, which were randomly divided into three groups according to the duration of untreated ACCA (ACCA-3 minutes, ACCA-5 minutes, and ACCA-8 minutes). After ACCA, all animals received cardiopulmonary resuscitation for 2 minutes and subsequent defibrillation until return of spontaneous circulation (ROSC). The troponin I levels were measured at 4 hours after ROSC. Animals died spontaneously or were killed at 72 hours after ROSC. The hippocampus were removed and fixed in 3% formalin. TdT-mediated dUTP-biotin nick end labeling and Nissl stainings were performed in 10-µm thickness coronal sections. Furthermore, two rabbits (without induction of ventricular fibrillation, cardiopulmonary resuscitation, and defibrillation) served as normal control group. RESULTS: Mean survival times after ROSC were 48.57 hours ± 24.70 hours, 18.0 hours ± 15.13 hours, and 3.88 hours ± 2.39 hours for groups ACCA-3 minutes, ACCA-5 minutes, and ACCA-8 minutes, respectively. Survival was significantly different between ACCA-3 minutes and other two groups (p = 0.002 and p = 0.01). Neuronal necrosis and apoptosis were found in the hippocampus CA1, CA2, and CA3 areas of group ACCA-3 minutes. In contrast, neuronal necrosis and TdT-mediated dUTP-biotin nick end labeling positive cells were fewer in control animals. CONCLUSIONS: The rabbits in group ACCA-3 minutes had significant neuronal damage with apoptosis in hippocampus CA1, CA2, and CA3 areas at 72 hours after ROSC and survived longer than those in other groups. The model we describe may be a simple, economic, and reliable model for experimental investigation on cardiopulmonary cerebral resuscitation.

Myelin-associated glycoprotein inhibits the neuronal differentiation of neural progenitors.

Nogo-66, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein, possess axon growth-inhibiting properties by binding with the Nogo-66 receptor. Recent studies have shown that Nogo-66 inhibits neuronal differentiation of neural progenitor cells (NPCs) and the neurite outgrowth of the neurons differentiated from NPCs. However, the effects of MAG on the differentiation and proliferation of NPCs are unclear. We found that NPCs derived from the hippocampus of embryonic rats expressed Nogo-66 receptor and MAG-Fc, which mimics the function of MAG, inhibited the differentiation of NPCs into neurons but promoted differentiation of NPCs into astrocytes. Furthermore, MAG-Fc inhibited the neurite outgrowth of the neurons differentiated from NPCs. Our results suggest that MAG can inhibit the neuronal differentiation of NPCs.

[The expression and clinical implication of advanced oxidized protein products in patients with multiple organ dysfunction syndrome].

OBJECTIVE: To investigate the expression and clinical implication of advanced oxidized protein products (AOPP) in patients with multiple organ dysfunction syndrome (MODS). METHODS: Serum concentrations of C-reactive protein (CRP) and AOPP were determined in 180 patients with systemic inflammatory response syndrome (SIRS) or MODS (90 patients, respectively). The acute physiology and chronic health evaluation III (APACHE III) scoring system was applied to assess severity of patients' condition. The contents of serum CRP and AOPP in MODS group, SIRS group and normal control group, and also in survivor and dead patients in MODS group were determined and compared. The correlation between CRP and AOPP levels and the correlation between AOPP levels and severity of MODS were also observed. Ninety healthy volunteers who matched with study subjects in age and gender comprised the normal control group. RESULTS: The CRP [(22.22+/-4.32) mg/L] and AOPP [(130.66+/-18.08) micromol/L] levels in patients with MODS were significantly higher than those in normal control group [(2.38+/-0.89) mg/L and (33.20+/-5.32) micromol/L, respectively] and SIRS group [(5.32+/-1.22) mg/L and (48.58+/-6.03) micromol/L, respectively, all P < 0.05], and were positively correlated with APACHE III scores [(98.66+/-20.87) scores] of the patient (r1 = 0.469, r2 = 0.528, both P < 0.01). However, there was no significant difference between SIRS group and normal control group. The CRP and AOPP levels were found to be significantly higher in the patients who eventually died (47 cases) as compared to those in the patients who survived (43 cases, both P < 0.05). Positive correlations were noted between AOPP and CRP level (r = 0.448, P < 0.01). The serum concentrations of CRP and AOPP levels were elevated with the increase of the number of failed organs in MODS patients(all P < 0.05). CONCLUSION: The data show that AOPP might participate in the process of pathogenesis of MODS. The serum AOPP level may be taken as a diagnostic and prognostic indicator for MODS.

[Expression of brain natriuretic peptide and c-fos gene in rat after acute myocardial ischemia and its medicolegal significance].

OBJECTIVE: To study the mRNA expression of BNP and c-fos gene in rat heart after acute myocardial ischemia (AMI) and to provide a marker for its medicolegal diagnosis. METHODS: AMI animal model of rat was made by ligating LAD. mRNA expression of BNP and c-fos gene were studied with RT-qPCR and ordinary PCR at 10 min, 30 min, 60 min and 3h after the successful ligation. The H&E staining was also used. Changes of the mRNA expression in different time groups were compared. RESULTS: There was significant difference in BNP mRNA expression of the 3 h group by RT-qPCR compared with normal control group, 10 min, 30 min, and 60 min groups (P < 0.05). There were dramatic differences in c-fos mRNA expression between every two groups (P < 0.05) except between the normal group and the 10 min group, between the 30 min group and the 3 h group. The peak of c-fos expression was in 60 min group. No difference was shown between groups by the ordinary PCR. Myocardial fiber acidophilia staining and wavy changes could be seen occasionally at 3 h experimental group by H&E staining. CONCLUSIONS: C-fos gene probably be used as an auxiliary test for myocardial ischemia of duration of 30 minutes or longer. RT-qPCR may be suitable for diagnosis of early AMI.

[Study of relationship between cyclooxygenase and platelet-activating factor on peripheral blood mononuclear cells in patients with systemic inflammatory response syndrome and multiple organ dysfunction syndrome].

OBJECTIVE: To study the role of cyclooxygenase (COX) and platelet-activating factor (PAF) in pathophysiologic mechanisms of patients with systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). METHODS: Twenty-eight adult patients whose diagnosis met American college of chest physicians/society of critical care medicine (ACCP/SCCM) criteria for SIRS and MODS were enrolled for study including 13 cases for SIRS group and 15 cases for MODS group. The normal control group consisted of 11 healthy volunteers who matched with study subjects for age and gender. Enzyme linked immunoadsorbent assay (ELISA) was used to measure the content of COX-2 and the activity of platelet-activating factor acetylhydrolase (PAF-AH) of peripheral blood mononuclear cells (PBMCs). Reverse transcription polymerase chain reaction (RT-PCR) was used to measure the COX-2 mRNA and PAF-AH mRNA expression of PBMCs. RESULTS: The content of COX-2 and the activity of PAF-AH of PBMCs and the expression of their mRNA in MODS group were higher than those in SIRS group and control group (all P<0.05). There was no significant difference between SIRS group and control group. The content of COX-2 and the activity of PAF-AH and the expression of their mRNA of PBMCs in non-survivors were higher than those in survived patients (all P<0.05). In 3 groups, positive correlation was found between the COX-2 content and PAF-AH activity (r=0.329, P<0.05). The leukocyte count, lymphocyte count, and PaO(2)/FiO(2) of peripheral blood in non-survivors showed no significant difference with those of survived patients (all P>0.05). The blood glucose and creatinine of non-survivors were higher than those of survived patients (P<0.05 and P<0.01). The total CO(2) content (TCO(2)) and pH value of non-survivors were lower than those of survived patients (both P<0.01). CONCLUSION: This study shows that COX-2 and PAF-AH play a role in the occurrence of MODS and they can be used as indexes to judge the prognosis of SIRS and MODS. Blood glucose, creatinine, TCO(2) and pH value of blood can be used as other indexes for judging the state and the prognosis of the illness.

A meta-analysis of cardiopulmonary resuscitation with and without the administration of thrombolytic agents.

OBJECTIVE: To pool data on the role of thrombolytic agents in cardiopulmonary resuscitation (CPR) and evaluate the efficacy and safety of thrombolysis. MATERIALS AND METHODS: The clinical studies in MEDLINE database from 1966 to August 2004 that studied the efficacy and safety in CPR with and without treatment with thrombolytic agents were assessed by a meta-analysis performed to evaluate the effect of the treatment. RESULTS: A total of eight papers evaluating the effect of thrombolysis in CPR were identified. This meta-analysis showed that thrombolytic agents significantly improved the rate of return of spontaneous circulation, 24 h survival rate, survival to discharge and long-term neurological function in patients treated with CPR (p < 0.01). However, the patients receiving thrombolysis had a risk of severe bleeding (p < 0.01). CONCLUSION: Thrombolytic agents during CPR can improve the survival rate to discharge and neurological function.

[Protective effect of p38 mitogen activated protein kinase inhibitor on organs in sepsis in rats].

OBJECTIVE: To investigate the pathogenesis of multiorgan injury and the protective of p38 mitogen activated protein kinase(p38MAPK) inhibitor on organs in sepsis. METHODS: Cecal ligation and puncture was adopted to reproduce sepsis model. The levels of serum biochemical parameters [including alanine aminotransferase (ALT), blood urea nitrogen(BUN), creatinine(Cr), MB isoenzyme of creatine phosphokinase (CPK-MB), tumor necrosis factor-alpha(TNF-alpha) and interleukin-1beta(IL-1beta) were determined at different time points. RESULTS: The levels of ALT, BUN, Cr, CPK-MB, TNF-alpha and IL-beta rose progressively after the cecal ligation operation. The levels of TNF-alpha and IL-1beta showed a significant correlation with levels of ALT, BUN, Cr, CPK-MB. After the administration of p38MAPK inhibitor, SB203580, the level of TNF-alpha and IL-1beta were found to decrease evidently, and the injury to multiple organs was alleviated. CONCLUSION: Excessive secretion of TNF-alpha and IL-beta may be the main cause of multiorgan injury in sepsis. Modulation of the p38MAPK pathway may protect multiorgan injury in sepsis.

[Analysis of the status of diagnosis of acute pulmonary embolism and a study of further strategy to improve the diagnostic level].

OBJECTIVE: To analyze the present status of diagnosis of pulmonary embolism (PE) by analyzing the clinical data of patients admitted during last 10 years to our hospital, in order to look for a significant diagnostic strategy to improve the diagnostic level. METHODS: The data of patients diagnosed to have PE in last 10 years were analyzed. In the last 5 months, the patients suspected to have PE were diagnosed by a comprehensive approach including clinical manifestations, lung scan and/or spirals computer tomography (SCT) in our emergency department. RESULTS: The diagnostic rate, the final diagnostic rate within 3 days and the diagnostic rate by lung scan or/and SCT were all higher in the last 3 months than ever. The proportions of angiograms and the overall 3-month PE risk were 2.8% and 0. CONCLUSION: The comprehensive approach which includes clinical manifestations, lung scan and/or SCT can obviously improve the diagnostic level of PE.