Key Anti-Fibrosis Associated Long Noncoding RNAs Identified in Human Hepatic Stellate Cell via Transcriptome Sequencing Analysis.

Hepatic fibrosis is the main pathological basis for chronic cirrhosis, and activated hepatic stellate cells (HSCs) are the primary cells involved in liver fibrosis. Our study analyzed anti-fibrosis long noncoding RNAs (lncRNAs) in activated human HSCs (hHSCs). We performed RNA sequencing (RNA-seq) and bioinformatics analysis to determine whether lncRNA expression profile changes between hHSCs activation and quiescence. Eight differentially expressed (DE) lncRNAs and three pairs of co-expression lncRNAs-mRNAs were verified by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). A total of 34146 DE lncRNAs were identified in this study. Via gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, we found several DE lncRNAs regulated hHSC activation by participating in DNA bending/packaging complex, growth factor binding and the Hippo signaling pathway (p < 0.05). With lncRNA-mRNA co-expression analysis, three lncRNAs were identified to be associated with connective tissue growth factor (CTGF), fibroblast growth factor 2 (FGF2) and netrin-4 (NTN4). The quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) results of the eight DE lncRNAs and three pairs of co-expression lncRNAs-mRNAs were consistent with the RNA-seq data and previous reports. Several lncRNAs may serve as potential targets to reverse the progression of liver fibrosis. This study provides a first insight into lncRNA expression profile changes associated with activated human HSCs.

Transplantation with hypoxia-preconditioned mesenchymal stem cells suppresses brain injury caused by cardiac arrest-induced global cerebral ischemia in rats.

Cardiac arrest-induced global cerebral ischemia is a main cause of neurological dysfunction in emergency medicine. Transplantation with bone marrow mesenchymal stem cells (MSCs) has been used in stroke models to repair the ischemic brain injury, but it is little studied in models with global cerebral ischemia. In the present study, a hypoxia precondition was used to improve the efficacy of MSC transplantation, given the low survival and migration rates and limited differentiation capacities of MSCs. We found that hypoxia can increase the expansion and migration of MSCs by activating the PI3K/AKT and hypoxia-inducible factor-1α/CXC chemokine receptor-4 pathways. By using a cardiac arrest-induced global cerebral ischemic model in rats, we found that transplantation of hypoxia-preconditioned MSCs promoted the migration and integration of MSCs and decreased neuronal death and inflammation in the ischemic cortex. © 2017 Wiley Periodicals, Inc.

Mesenchymal stem cells transplantation suppresses inflammatory responses in global cerebral ischemia: contribution of TNF-α-induced protein 6.

AIM: To investigate the effects of mesenchymal stem cells (MSCs) transplantation on rat global cerebral ischemia and the underlying mechanisms. METHODS: Adult male SD rats underwent asphxial cardiac arrest to induce global cerebral ischemia, then received intravenous injection of 5×10(6) cultured MSCs of SD rats at 2 h after resuscitation. In another group of cardiac arrest rats, tumor necrosis factor-α-induced protein 6 (TSG-6, 6 µg) was injected into the right lateral ventricle. Functional outcome was assessed at 1, 3, and 7 d after resuscitation. Donor MSCs in the brains were detected at 3 d after resuscitation. The level of serum S-100B and proinflammatory cytokines in cerebral cortex were assayed using ELISA. The expression of TSG-6 and proinflammatory cytokines in cerebral cortex was assayed using RT-PCR. Western blot was performed to determine the levels of TSG-6 and neutrophil elastase in cerebral cortex. RESULTS: MSCs transplantation significantly reduced serum S-100B level, and improved neurological function after global cerebral ischemia compared to the PBS-treated group. The MSCs injected migrated into the ischemic brains, and were observed mainly in the cerebral cortex. Furthermore, MSCs transplantation significantly increased the expression of TSG-6, and reduced the expression of neutrophil elastase and proinflammatory cytokines in the cerebral cortex. Intracerebroventricular injection of TSG-6 reproduced the beneficial effects of MSCs transplantation in rats with global cerebral ischemia. CONCLUSION: MSCs transplantation improves functional recovery and reduces inflammatory responses in rats with global cerebral ischemia, maybe via upregulation of TSG-6 expression.

[Effects and mechanisms of heme oxygenase-1 on rats with postresuscitation myocardial dysfunction].

OBJECTIVE: To explore the effects and mechanisms of heme oxygenase-1 on rats with postresuscitation myocardial dysfunction. METHODS: Male Sprague-Dawley rats were asphyxiated for 9 minutes and resuscitated. They were randomly divided into 4 groups: sham-operated, cardiopulmonary resuscitation (CPR), hemin and hemin + ZnPP (zinc protoporphyrin IX). Resuscitated groups had 2 observation points: 6 and 24 hours post-CPR (n = 8 for each time point). And the sham-operated group of 12 rats were divided in two observation points, according to 6 or 24 hours post-operation (n = 6 each). Hemodynamic was observed. The expression of heme oxygenase-1 (HO-1) in cardiac tissue was detected by Western blot. And the activity of cardiac homogenate superoxide dismutase (SOD) was determined by xanthine oxidase method and the level of malondialdehyde (MDA) measured by the thiobarbituric acid method. Nitrotyrosine protein expression in cardiac tissue was analyzed by immunohistochemistry. RESULTS: (1) The mean blood pressure (MAP) significantly decreased in resuscitated groups after resuscitation (all P < 0.05). No difference existed between the subgroups. The scores of dP/dt40 and -dP/dt significantly decreased in CPR and hemin + ZnPP groups after resuscitation (all P < 0.05). But dP/dt40 in hemin group did not differ significantly after resuscitation and -dP/dt decreased only 0.5 hour and 1 hour post-resuscitation (3341.60 ± 524.85 and 3711.40 ± 502.39 vs 4284.20 ± 800.87, all P < 0.05). The scores of dP/dt40 and -dP/dt in hemin group at all time points post-resuscitation were significantly higher than those in CPR and hemin + ZnPP groups (all P < 0.05). (2) Compared with the sham-operated group, the HO-1 expression, MDA level and nitrotyrosine protein expression significantly increased while the activities of SOD decreased after resuscitation in the CPR, hemin and hemin + ZnPP groups (all P < 0.05). Compared with the CPR and hemin + ZnPP groups, the expression of HO-1 and the activity of SOD increased, while MDA level and nitrotyrosine protein expression were decreased in group hemin (all P < 0.05). No difference existed in the above indices between the CPR and hemin + ZnPP groups. CONCLUSION: HO-1 can reduce myocardial oxidative stress injury after cardiopulmonary resuscitation and effectively improve post-resuscitation myocardial function in rats.

The Effects of Patchouli Alcohol on Diarrhea-Predominant Irritable Bowel Syndrome are Correlated with Phenotypic Plasticity in Myenteric Neurons and the Targeted Regulation of Myosin Va.

Patchouli alcohol (PA) has been widely used for the treatment of diarrhea-predominant irritable bowel syndrome (IBS-D) in traditional Chinese medicine, and the related mechanism remains to be fully understood. Our previous study has indicated that PA significantly reduced visceral sensitivity and defecation area in IBS-D rats. In this study, we prepared an IBS-D rat model and observed the dynamic intestinal motility and colonic longitudinal muscle and myenteric plexus (LMMP) neurons, as well as their subtypes at D14, D21, and D28. After PA administration, we observed the effects on the changes in intestinal motility, colonic LMMP neurons, and LMMP Myosin Va in IBS-D rats and their co-localization with inhibitory neurotransmitter-related proteins. The results indicated that PA treatment could alleviate IBS-D symptoms, regulate the abnormal expression of LMMP neurons, increase Myosin Va expression, up-regulate co-localization levels of Myosin Va with neuronal nitric oxide synthase (nNOS), and promote co-localization levels of Myosin Va with vasoactive intestinal polypeptide (VIP). In conclusion, this study demonstrated the neuropathic alterations in the colon of chronic restraint stress-induced IBS-D rat model. PA reversed the neuropathological alteration by affecting the transport process of nNOS and VIP vesicles via Myosin Va and the function of LMMP inhibitory neurons, and these effects were related to the mechanism of enteric nervous system (ENS) remodeling.

[The epidemiological characteristic of 97,823 cases of pre-hospital medical care in Guangzhou city].

OBJECTIVE: To investigate the epidemiological information of patients in pre-hospital medical care in Guangzhou city, and to explore the characteristics of the patients. METHODS: The data in the year of 2008 were retrieved from the computer database of Guangzhou Emergency Medical Rescue Command Center. RESULTS: (1)In a total of 969 410 calls received, the time of distribution was found to be mainly between 16:00 and 18:00 [11.78% (114 224)], and least frequently between 04:00 and 06:00 [2.40% (23 237)]. (2)Among 109 682 dispatches of ambulances, Baiyun district received the most [26.77% (29 364)], and followed by Haizhu district [18.30% (20 069)], Tianhe district [18.20% (19 962)], respectively. (3)Among 97 823 cases of pre-hospital medical care, death rate of the male patients was higher than the female [amount: 57.65% (56 394) vs. 38.48% (37 641), mortality: 59.17% (3 269) vs. 33.95% (1 876)]. (4)In 9 7823 cases of pre-hospital medical care, trauma constituted the highest rate [34.57% (33 820)], especially traffic accidents [11.56% (11 307)], and the age of most of the patients ranged between 21 and 50. Disease of the nervous system ranged the second, followed by diseases of circulatory system, respiratory system and digestive system, and most of them were over 51 years old, and most frequently above 70. (5)In 97 823 cases of pre-hospital medical care, there were 5 525 deaths (5.65%), in whom the circulatory system diseases ranged first (especially sudden death) [33.07% (1 827)], followed by unclassified diseases [29.79% (1 646)], trauma [15.67% (866)], respiratory diseases [7.48% (413)], and neurological emergency illnesses [5.95% (329)]. The age of deceased was far older than 51, particularly 70. The age of most of the deceased was above 61, and age of traumatic death was 21-40. CONCLUSION: (1) It is very important to reduce the death rate of the middle-old aged patients by strengthening prevention and timely treatment of cardiovascular and cerebrovascular diseases, and improve the medical strategies in emergency care, in order to lower the death rate during emergency.(2)It is very important to emphasize safely in production lines and to strengthen traffic regulations in order to reduce the incidence of trauma, thus it is especially traffic accident, expect that the death rate of trauma could be lowered.

Isolation and Culture of Primary Neurons and Glia from Adult Rat Urinary Bladder.

The lower urinary tract has two main functions, namely, periodic urine storage and micturition; these functions are mediated through central and peripheral neuroregulation. Although extensive research on the lower urinary tract nervous system has been conducted, most studies have focused on primary culture. This protocol introduces a method for the isolation and culture of bladder neurons and glia from Sprague-Dawley rats. In this method, the neurons and glia were incubated in a 37 °C, 5% CO2 incubator for 5-7 days. As a result, they grew into mature shapes suitable for related subsequent immunofluorescence experiments. Cells were morphologically observed using an optical microscope. Neurons, synaptic vesicles, and glia were identified by ß-III-tubulin and MAP-2, Synapsin-1, and GFAP staining, respectively. Meanwhile, immunocytochemistry was performed on several neurotransmitter-related proteins, such as choline acetyltransferase, DYNLL2, and SLC17A9.

Characterization of SARS-CoV-specific memory T cells from recovered individuals 4 years after infection.

SARS-CoV infection of human results in antigen-specific cellular and humoral immune responses. However, it is critical to determine whether SARS-CoV-specific memory T cells can persist for long periods of time. In this study, we analyzed the cellular immune response from 21 SARS-recovered individuals who had been diagnosed with SARS in 2003 by using ELISA, CBA, ELISpot and multiparameter flow cytometry assays. Our results demonstrated that low levels of specific memory T cell responses to SARS-CoV S, M, E and N peptides were detected in a proportion of SARS-recovered patients, and IFN-gamma was the predominant cytokine produced by T cells after stimulation with peptides. Cytometry analysis indicated that the majority of memory CD8(+) T cells produced IFN-gamma, whereas memory CD4(+) T cells produced IFN-gamma, IL-2 or TNF-alpha. These results might provide valuable information on the cellular immune response in recovered SARS-CoV patients for the rational design of vaccines against SARS-CoV infection.

Inhibitory effects of patchouli alcohol on stress-induced diarrhea-predominant irritable bowel syndrome.

AIM: To elucidate the mechanism of patchouli alcohol (PA) in treatment of rat models of diarrhea-predominant irritable bowel syndrome (IBS-D). METHODS: We studied the effects of PA on colonic spontaneous motility using its cumulative log concentration (3 × 10-7 mol/L to 1 × 10-4 mol/L). We then determined the responses of the proximal and distal colon segments of rats to the following stimuli: (1) carbachol (1 × 10-9 mol/L to 1 × 10-5 mol/L); (2) neurotransmitter antagonists including Nω-nitro-L-arginine methyl ester hydrochloride (10 µmol/L) and (1R*, 2S*)-4-[2-Iodo-6-(methylamino)-9H-purin-9-yl]-2-(phosphonooxy)bicyclo[3.1.0]hexane-1-methanol dihydrogen phosphate ester tetraammonium salt (1 µmol/L); (3) agonist α,ß-methyleneadenosine 5'-triphosphate trisodium salt (100 µmol/L); and (4) single KCl doses (120 mmol/L). The effects of blockers against antagonist responses were also assessed by pretreatment with PA (100 µmol/L) for 1 min. Electrical-field stimulation (40 V, 2-30 Hz, 0.5 ms pulse duration, and 10 s) was performed to observe nonadrenergic, noncholinergic neurotransmitter release in IBS-D rat colon. The ATP level of Kreb's solution was also determined. RESULTS: PA exerted a concentration-dependent inhibitory effect on the spontaneous contraction of the colonic longitudinal smooth muscle, and the half maximal effective concentration (EC50) was 41.9 µmol/L. In comparison with the KCl-treated IBS-D group, the contractile response (mg contractions) in the PA + KCl-treated IBS-D group (11.87 ± 3.34) was significantly decreased in the peak tension (P < 0.01). Compared with CCh-treated IBS-D rat colon, the cholinergic contractile response of IBS-D rat colonic smooth muscle (EC50 = 0.94 µmol/L) was significantly decreased by PA (EC50 = 37.43 µmol/L) (P < 0.05). Lack of nitrergic neurotransmitter release in stress-induced IBS-D rats showed contraction effects on colonic smooth muscle. Pretreatment with PA resulted in inhibitory effect on L-NAME-induced (10 µmol/L) contraction (P < 0.05). ATP might not be the main neurotransmitter involved in inhibitory effects of PA in the colonic relaxation of stress-induced IBS-D rats. CONCLUSION: PA application may serve as a new therapeutic approach for IBS-D.

[Risk stratification and prognostic evaluation of patients with pulmonary thromboembolism].

OBJECTIVE: To explore the risk stratification and prognostic evaluation of pulmonary thromboembolism (PTE). METHODS: The clinical data of 46 patients suffering from PTE diagnosed by ventilation perfusion scan or spiral CT pulmonary angiography admitted to our hospital from January 2002 to December 2006 were analyzed retrospectively. RESULTS: The total mortality was 33% (15/46 cases). The mortality in the group whose cardiac troponin I was positive (n=11) was 82% (9/11 cases), 17% (6/35 cases)when troponin I was negative (n=35). The mortality in normal electrocardiogram (ECG) group (n=14) and abnormal group (n=32) was 7% (1/14 cases) and 44% (14/32 cases) respectively. The mortality in the group with right ventricular dilatation (right ventricular diastolic dimension/left ventricular diastolic dimension > or =0.6) as shown by echocardiography (n=20) and without right ventricular dilatation (n=26) right ventricular diastolic dimension/left ventricular diastolic dimension<0.6) was 55% (11/20 cases) and 15% (4/26 cases) respectively. The mortality in the group whose pulmonary arterial obstruction index shown by spiral CT pulmonary angiography <0.6 (n=19) and > or =0.6 (n=11) was 5% (1/19 cases) and 91% (10/11 cases) respectively. The mortality between above groups showed statically significant difference (all P<0.05). CONCLUSION: Cardiac troponin I, ECG, right ventricular dilatation by echocardiography and pulmonary arterial obstruction index by spiral CT pulmonary angiography may be taken as indices for risk stratification and prognostic evaluation of patients with PTE, and they may be helpful in optimizing treatment strategies.

[Effect of ulinastatin on apoptosis in ileal mucosa of rats with hemorrhagic shock].

OBJECTIVE: To investigate the effect of ulinastatin on apoptosis in ileal mucosa of rats with hemorrhagic shock. METHODS: A prospective, controlled animal study was performed. The rat model of hemorrhagic shock was replicated according to method described by Chaudry. After 60 minutes period of bleeding, rats were resuscitated by transfusion of shed blood and normal saline. A part of the animals were additionally treated with ulinastatin. The expression of tumor necrosis factor-alpha (TNF-alpha), malondialdehyde (MDA) content in serum, and expression of Bax, Bcl-2, caspase 3 protein in ileal mucosa were determined at different time points after reperfusion. RESULTS: Compared with the normal saline group, the expression levels of TNF-alpha, MDA content in serum, Bax and caspase 3 protein in ileal mucosa during hemorrhagic shock after resuscitation were significantly increased, while Bcl-2 protein was markedly decreased. After fluid resuscitation, obvious increase in MDA, Bcl-2 protein, significant decrease in the level of TNF-alpha, the expression of Bax and caspase 3 protein in ileal mucosa were observed in the ulinastatin group compared with normal saline group. CONCLUSION: Ulinastatin has protective effect on rats with hemorrhagic shock by suppressing the apoptosis in ileal mucosa.

Therapeutic effects of various methods of MSC transplantation on cerebral resuscitation following cardiac arrest in rats.

In the present study, mesenchymal stem cells (MSCs) were transplanted into the brain of rats following cardiopulmonary resuscitation (CPR) by three different methods: Direct stereotaxic injection into the lateral cerebral ventricle (LV), intra­carotid administration (A), and femoral venous infusion (V). The three different methods were compared by observing the effects of MSCs on neurological function following global cerebral hypoxia­ischemia, in order to determine the optimum method for MSC transplantation. MSCs were transplanted in groups A, V and LV following the restoration of spontaneous circulation. Neurological deficit scale scores were higher in the transplantation groups, as compared with the control group. Neuronal damage, brain water content and serum levels of S100 calcium­binding protein B were reduced in the hippocampus and temporal cortex of the transplantation groups, as compared with the control rats following resuscitation. MSCs were able to migrate inside the brain tissue following transplantation, and were predominantly distributed in the hippocampus and temporal cortex where the neurons were vulnerable during global cerebral ischemia. These results suggest that transplantation of MSCs may notably improve neurological function following CPR in a rat model. Of the three different methods of MSC transplantation tested in the present study, LV induced the highest concentration of MSCs in brain areas vulnerable to global cerebral ischemia, and therefore, produced the best neurological outcome.

Remote ischemic preconditioning improves post resuscitation cerebral function via overexpressing neuroglobin after cardiac arrest in rats.

In this study, we investigated the effects of remote ischemic preconditioning on post resuscitation cerebral function in a rat model of cardiac arrest and resuscitation. The animals were randomized into six groups: 1) sham operation, 2) lateral ventricle injection and sham operation, 3) cardiac arrest induced by ventricular fibrillation, 4) lateral ventricle injection and cardiac arrest, 5) remote ischemic preconditioning initiated 90min before induction of ventricular fibrillation, and 6) lateral ventricle injection and remote ischemic preconditioning before cardiac arrest. Reagent of Lateral ventricle injection is neuroglobin antisense oligodeoxynucleotides which initiated 24h before sham operation, cardiac arrest or remote ischemic preconditioning. Remote ischemic preconditioning was induced by four cycles of 5min of limb ischemia, followed by 5min of reperfusion. Ventricular fibrillation was induced by current and lasted for 6min. Defibrillation was attempted after 6min of cardiopulmonary resuscitation. The animals were then monitored for 2h and observed for an additionally maximum 70h. Post resuscitation cerebral function was evaluated by neurologic deficit score at 72h after return of spontaneous circulation. Results showed that remote ischemic preconditioning increased neurologic deficit scores. To investigate the neuroprotective effects of remote ischemic preconditioning, we observed neuronal injury at 48 and 72h after return of spontaneous circulation and found that remote ischemic preconditioning significantly decreased the occurrence of neuronal apoptosis and necrosis. To further comprehend mechanism of neuroprotection induced by remote ischemic preconditioning, we found expression of neuroglobin at 24h after return of spontaneous circulation was enhanced. Furthermore, administration of neuroglobin antisense oligodeoxynucleotides before induction of remote ischemic preconditioning showed that the level of neuroglobin was decreased then partly abrogated neuroprotection of remote ischemic preconditioning. These date suggested that neuroglobin involved in neuroprotective effect of remote ischemic preconditioning. In conclusion, remote ischemic preconditioning attenuated post resuscitation cerebral dysfunction and the neuroprotection was mediated partly by high level of neuroglobin in a rat model of cardiac arrest and resuscitation.

Carbon Monoxide Improves Neurologic Outcomes by Mitochondrial Biogenesis after Global Cerebral Ischemia Induced by Cardiac Arrest in Rats.

Mitochondrial dysfunction contributes to brain injury following global cerebral ischemia after cardiac arrest. Carbon monoxide treatment has shown potent cytoprotective effects in ischemia/reperfusion injury. This study aimed to investigate the effects of carbon monoxide-releasing molecules on brain mitochondrial dysfunction and brain injury following resuscitation after cardiac arrest in rats. A rat model of cardiac arrest was established by asphyxia. The animals were randomly divided into the following 3 groups: cardiac arrest and resuscitation group, cardiac arrest and resuscitation plus carbon monoxide intervention group, and sham control group (no cardiac arrest). After the return of spontaneous circulation, neurologic deficit scores (NDS) and S-100B levels were significantly decreased at 24, 48, and 72 h, but carbon monoxide treatment improved the NDS and S-100B levels at 24 h and the 3-day survival rates of the rats. This treatment also decreased the number of damaged neurons in the hippocampus CA1 area and increased the brain mitochondrial activity. In addition, it increased mitochondrial biogenesis by increasing the expression of biogenesis factors including peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor-1, nuclear respiratory factor-2 and mitochondrial transcription factor A. Thus, this study showed that carbon monoxide treatment alleviated brain injury after cardiac arrest in rats by increased brain mitochondrial biogenesis.

Functional and morphological changes of the gut barrier during the restitution process after hemorrhagic shock.

AIM: To investigate the functional, morphological changes of the gut barrier during the restitution process after hemorrhagic shock, and the regional differences of the large intestine and small intestine in response to ischemia/reperfusion injury. METHODS: Forty-seven Sprague-Dawley rats with body weight of 250-300 g were divided into two groups: control group (sham shock n = 5) and experimental group (n = 42). Experimental group was further divided into six groups (n = 7 each) according to different time points after the hemorrhagic shock, including 0(th) h group, 1st h group, 3rd h group, 6th h group, 12th h group and 24th h group. All the rats were gavaged with 2 mL of suspension of lactulose (L) (100 mg/2 mL) and mannitol (M) (50 mg/each) at the beginning and then an experimental rat model of hemorrhagic shock was set up. The specimens from jejunum, ileum and colon tissues and the blood samples from the portal vein were taken at 0, 1, 3, 6, 12 and 24 h after shock resuscitation, respectively. The morphological changes of the intestinal mucosa, including the histology of intestinal mucosa, the thickness of mucosa, the height of villi, the index of mucosal damage and the numbers of goblet cells, were determined by light microscope and/or electron microscope. The concentrations of the bacterial endotoxin lipopolysaccharides (LPS) from the portal vein blood, which reflected the gut barrier function, were examined by using Limulus test. At the same time point, to evaluate intestinal permeability, all urine was collected and the concentrations of the metabolically inactive markers such as L and M in urine were measured by using GC-9A gas chromatographic instrument. RESULTS: After the hemorrhagic shock, the mucosal epithelial injury was obvious in small intestine even at the 0(th) h, and it became more serious at the 1st and the 3rd h. The tissue restitution was also found after 3 h, though the injury was still serious. Most of the injured mucosal restitution was established after 6 h and completed in 24 h. Two distinct models of cell death-apoptosis and necrosis-were involved in the destruction of rat intestinal epithelial cells. The number of goblet cells on intestinal mucosa was reduced significantly from 0 to 24 h (the number from 243+/-13 to 157+/-9 for ileum, 310+/-19 to 248+/-18 for colon; r = -0.910 and -0.437 respectively, all P<0.001), which was the same with the large intestine, but the grade of injury was lighter with the values of mucosal damage index in 3 h for jejunum, ileum, and colon being 2.8, 2.6, 1.2, respectively. The mucosal thickness and the height of villi in jejunum and ileum diminished in 1 h (the average height decreased from 309+/-24 to 204+/-23 microm and 271+/-31 to 231+/-28 microm, r = -0.758 and -0.659, all P<0.001; the thickness from 547+/-23 to 418+/-28 microm and 483+/-45 to 364+/-35 microm, r = -0.898 and -0.829, all P<0.001), but there was no statistical difference in the colon (F = 0.296, P = 0.934). Compared with control group, the urine L/M ratio and the blood LPS concentration in the experimental groups raised significantly, reaching the peak in 3-6 h (L/M: control vs 3 h vs 6 h was 0.029+/-0.09 vs 0.063+/-0.012 vs 0.078+/-0.021, r = -0.786, P<0.001; LPS: control vs 3 h vs 6 h was 0.09+/-0.021 vs 0.063+/-0.012 vs 0.25+/-0.023, r = -0.623, P<0.001), and it kept increasing in 24 h. CONCLUSION: The gut barrier of the rats was seriously damaged at the early phase of ischemic reperfusion injury after hemorrhagic shock, which included the injury and atrophy in intestinal mucosa and the increasing of intestinal permeability. Simultaneously, the intestinal mucosa also showed its great repairing potentiality, such as the improvement of the intestinal permeability and the recovery of the morphology at different phases after ischemic reperfusion injury. The restitution of gut barrier function was obviously slower than that of the morphology and there was no direct correlation between them. Compared with the small intestine, the large intestine had stronger potentiality against injury. The reduction of the amount of intestinal goblet cells by injury did not influence the ability of intestinal mucosal restitution at a certain extent and it appeared to be intimately involved in the restitution of the epithelium.

[Clinical features of 96 patients with severe acute respiratory syndrome from a hospital outbreak].

OBJECTIVE: To describe a hospital outbreak of severe acute respiratory syndrome (SARS) and summarize the clinical features and therapeutic approaches. METHODS: Clinical data in this cohort were collected prospectively as they were identified. RESULTS: The outbreak started with a SARS patient from the community on 30 January 2003, followed by a total of 96 people [76 women and 20 men; mean age (29.5 +/- 10.3) years; 93.8% of whom were health care workers] infected in a short period of time after their exposure to this source patient. The incubation period ranged from 1 to 20 days, with a mean of (5.9 +/- 3.5) days. The initial temperature was (38.3 +/- 0.6) degrees C, while the highest was (39.2 +/- 0.6) degrees C (P < 0.001), with a mean fever duration of (9.0 +/- 4.2) days. Other common symptoms included fatigue, cough, mild sputum production, chills, headache, general malaise and myalgia. The radiographic changes were predominantly bilateral and in the middle or lower lung zones. Leukopenia was observed in 67.7% of this cohort. The mean lowest oxygen saturation was (94.8 +/- 3.1)% with supplementary oxygen through a nasal cannula. 68.8% of the patients were treated with methylprednisolone for a mean period l of (4.9 +/- 2.4) days. The initial dose was (67.3 +/- 28.2) mg/d and the maximal dose was (82.4 +/- 30.5) mg/d. Ninety-five patients (99.0%) had a complete clinical recovery, and 1 patient died of progressive acute respiratory distress syndrome. The mean hospitalized duration was (17.2 +/- 8.0) days. CONCLUSION: SARS appears to be highly contagious and potentially lethal among health care workers, characterized by acute onset and rapid progression. Corticosteroids, antibiotics, human gamma-globulin, interferon-alpha, and antiviral drugs, although used empirically, might be of some benefits in shortening the clinical course.

[Study on morphological change in intestinal mucosa from injury to repair after hemorrhagic shock].

OBJECTIVE: To study on morphological changes in mucosa of the small and large intestine mucosa after resuscitation of hemorrhagic shock. METHODS: The morphological changes in intestinal mucosa were observed under light and electron microscope, including the histology of intestinal mucosa, determination of height of villi and evaluation of mucosa damage index in the different phases after traumatic-hemorrhagic shock. RESULTS: Mucosa epithelial injury was obvious in small intestine were even at 0 hour, becoming more serious in 1 hour up to 3 hours. The tissue repair began after 3 hours, though the injury was still serious. Most of the inJured mucosa began to repair after 6 hours, and completed in 24 hours. The condition of the large intestine was similar to that of the small intestine, but the injury was less severe. The mucosal thickness and the height of villi were diminished after 1 hour of shock, but there was no obvious change in the colon. CONCLUSION: In the early phase after hemorrhagic shock, intestinal mucosal barrier are subJected to damage, but it could repair and recover in a short time. Compare with small intestine, large intestine have stronger potentiality against injury.

Changes of end-tidal carbon dioxide during cardiopulmonary resuscitation from ventricular fibrillation versus asphyxial cardiac arrest.

BACKGROUND: Partial pressure of end-tidal carbon dioxide (PETCO2) has been used to monitor the effectiveness of precordial compression (PC) and regarded as a prognostic value of outcomes in cardiopulmonary resuscitation (CPR). This study was to investigate changes of PETCO2 during CPR in rats with ventricular fibrillation (VF) versus asphyxial cardiac arrest. METHODS: Sixty-two male Sprague-Dawley (SD) rats were randomly divided into an asphyxial group (n=32) and a VF group (n=30). PETCO2 was measured during CPR from a 6-minute period of VF or asphyxial cardiac arrest. RESULTS: The initial values of PETCO2 immediately after PC in the VF group were significantly lower than those in the asphyxial group (12.8±4.87 mmHg vs. 49.2±8.13 mmHg, P=0.000). In the VF group, the values of PETCO2 after 6 minutes of PC were significantly higher in rats with return of spontaneous circulation (ROSC), compared with those in rats without ROSC (16.5±3.07 mmHg vs. 13.2±2.62 mmHg, P=0.004). In the asphyxial group, the values of PETCO2 after 2 minutes of PC in rats with ROSC were significantly higher than those in rats without ROSC (20.8±3.24 mmHg vs. 13.9±1.50 mmHg, P=0.000). Receiver operator characteristic (ROC) curves of PETCO2 showed significant sensitivity and specificity for predicting ROSC in VF versus asphyxial cardiac arrest. CONCLUSIONS: The initial values of PETCO2 immediately after CPR may be helpful in differentiating the causes of cardiac arrest. Changes of PETCO2 during CPR can predict outcomes of CPR.