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With the global warming, the incidence of heat stroke was significantly higher than before. Severe heat stroke has a high mortality, high morbidity and consolidated central nervous system injury characteristics. The main features of severe heat stroke cerebral injury include cognitive impairment, delirium, convulsions and coma. Its mechanism is related with heat shock induced cerebral tissue ischemia and hypoxia, vascular dysfunction, secondary cascade inflammation and so on. Currently, the main treatment of heat stroke cerebral injury is the hypothermia therapy, dehydration for the reduction of intracranial pressure, naloxone and other cerebral protection and nutrition treatments. Hyperbaric oxygen therapy (HBOT) is effective in treating brain injury. HBOT can alleviate tissue ischemia and hypoxia, improve circulation, reduce cerebral edema, and anti-inflammatory, anti-oxidative damage, anti-apoptosis and other molecular biological effects. HBOT also play a wake up-promoting effect of nerve repair in the cerebral injury. The treatment of cerebral injury has been the difficulty and weakness of heat stroke research. Therefore, this article reviewed the epidemiology, pathogenesis, the therapeutic effect and mechanism of hyperbaric oxygen on cerebral injury in severe heat stroke to clarify the advantages of HBOT and to provide experimental basis for further research.
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Objective To observe the effect of different temperatures on endoplasmic reticulum stress, calcium overload, mitochondria and cell damage in pulmonary microvascular endothelial cells (PMVEC) induced by heat stress, and clarify the mechanism of endothelial cell injury in the process of heat stress to provide experimental basis for clinical prevention and treatment of heat stree. Methods Heat stress model of PMVEC cell was set up. Control group cells were incubated at 37℃, 5%CO2, while heat stress group cells were incubated at 39℃, 41℃, 43℃ for 2h, respectively, then further incubated at 37℃, 5%CO2 for 6h. Pretreatment of cells with 20μmol/L BAPTA-AM or 50μmol/L CsA before heat stress at 43℃. The protein levels of p-PERK, PERK p-eIF2a, eIF2a, ATF4 and GRP78 were analyzed by Western blotting. Intracellular Ca2+, mitochondrial membrane potential and the changes in mitochondrial permeability transition pore were investigated by flow cytometry. The change of caspase-3 was detected by Caspase Assay Kit. Millicell-ERS Volt-Ohm Meter and Accessories was used for determining the changes of transepithelium electrical resistance (TER). Results Compared with the control group, with the increase of heat stress temperature (41-43℃), the phosphorylation of p-PERK and p-eIF2a protein and the expressions of ATF4 and GRP78 proteins were gradually activated, intracellular Ca2+ increased, MPTP pore was opened, mitochondrial membrane potential decreased, cell permeability increased and apoptosis occurred, and it was the most obvious in the 43℃ heat stress group, and the difference was statistically significant (P<0.05). Pretreatment with Ca2+ inhibitors promoted the recovery of the MPTP hole, mitochondrial membrane potential and cell permeability, and reduced the occurrence of apoptosis. While pretreatment with the mitochondrial protective agent did not reduce the release of Ca2+, but it could promote the recovery of cell permeability and reduce the occurrence of apoptosis. Conclusion Heat stress activates endoplasmic reticulum stress response, induces intracellular Ca2+ overload mediated cell and mitochondrial damages in PMVEC cells, which may be one of the important mechanisms of endothelial cell injury induced by heat stress.
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Objective To study the change of the contractile response of human umbilical artery smooth muscle cells (HUASMCs) during the heat stress, and explore the effect of the antioxidant on the changes. Methods HUASMCs were randomly divided into control group, heat stress group, antioxidant preprocessing group. Cells were stimulated by norepinephrine (NE) at a low concentration (0.05mg/L) and at a normal concentration (1.0mg/L) and cultured in the thermostatic water bath (41℃) for 0.5, 1, 1.5 or 2h, respectively. After stimulated by NE, proportion of the cell surface area contraction was measured to reflect the contractile response of each group. Results Compared with control group, regardless of the NE concentration: in heat stress group, contractile response at 1h increased significantly (P0.05), but in the antioxidant preprocessing group, the contractile response was more significant to the normal NE concentration than to the low NE concentration (P<0.05 or 0.01). Regardless of the NE concentration, the contractile response was lower in the antioxidant preprocessing group than in the heat stress group. Conclusions In the course of heat stress, the contractile response of HUASMCs presents as time-related change. The usage of antioxidant may correct the over-response of HUASMCs to NE in the early heat stress stage, but cannot correct the reduction of the contractile response in the middle and advanced stage.
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Objective To investigate the effect of gradient heat stress on phagocytosis of hepatic Kupffer cells (KCs) in vitro in rats. Methods Rat Kupffer cells were isolated in vitro and the temperature for gradient heat stress was set at 37, 39, 41 and 43℃. After thermal stimulation, cell injury was detected by PI and Hochest33342 staining. CCK-8 assay was used to investigate difference in cellular proliferation rate over 24h between the groups. Flow cytometry was used to investigate the influence of heat stress on the phagocytosis of KCs. Results Compared to the normal control group, cells in each heat stress group exhibited varying degrees of damage, especially cells in 43℃ group. The ratio of damage cells increased with the increase of heat stress severity (P<0.05). Proliferation assay indicated that the proliferation rate of cells in each heat stress group was significantly decreased in comparison with normal control group 6h after heat stress (P<0.05). After 12h recovery, decrease in proliferation rate was observed only in 43℃ group (P<0.001), and no difference in the rate of proliferation could be observed between the heat stress groups and normal control group after 24h recovery. Flow cytometry showed, that the phagocytosis of KCs decreased in heat stress groups compared with control group, especially in 43℃ group (P<0.05). This phenomenon disappeared after 24h recovery. Conclusion Heat stress can inhibit the phagocytosis of rat liver KCs through its cytotoxic effect on KCs, and subsequently inhibits its proliferative ability. Further investigation of the effect of heat stress on KCs may help understand the pathogenesis of heat stress.
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There exist a series of problems in heat stroke treatment,such as,pathogenesis is still unclear,clinical classification is too simple and has no intrinsic relation with pathophysiological process and prognosis,missing of indexes for hierarchical diagnosis and prognosis prediction,and lack of targeted therapeutic norms.All of these factors could lead to high mortality and disability by heat stroke.Our research team started an epidemiological investigation of heat stroke since 2002.On the basis of discovering organ injury rule,system info and treatment technology on critical medicine were applied to heat stroke treatment.Research on organ injury mechanism for heatstroke was carried out based on translational medicine idea,and periodic research results were also achieved.A series of key technologies for heat stroke treatment were obtained.These technologies were popularized in 30 hospitals across the country,thus improving ability of heat stroke treatment.
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Objective To investigate the role of oxidative stress in acute liver injury in a heat stroke model of conscious rats,and to explore its underlying mechanism.Methods Thirty-two rats were randomly (by using a random number table) assigned into a sham-heated control group (Sham group,n=8),a sham-heated group treated with NAC (Sham-NAC group,n=8),a heat stroke group (HS group,n=8) and a heat stoke group treated with NAC (HS-NAC,n=8).Rats were prepared with pre-warm chamber to initiate heat stoke.The change of rectum temperature (Tr),heart rate (HR) and systolic blood pressure (SBP) were monitored,and the time point of HS onset was recorded.Rats were sacrificed 12h after HS onset.ALT,serum TBIL,IL-6,IL-1β,TNF-α,MDA,T-SOD and GSH in the liver homogenates were measured.Liver tissues were harvested for determining the concentration of reactive oxygen species (ROS),neutrophil infiltration and the histological changes.Results During HS onset,no significant differences were observed in Tr,HR,SBP and heat exposure time between HS group and HS-NAC group (P＞0.05).However,the survival time was significantly longer in HS-NAC group than in HS group (P=0.039).12 hours after HS onset,the concentrations of ROS and MDA in the liver homogenates were significantly higher in HS group than in the other groups (P=0.000),while the concentrations of T-SOD and GSH were much lower than in the other groups (P=0.000).The serum concentrations of ALT and TBIL were significantly higher in HS group than in the other groups (P=0.000).Compare with HS group,the pathological injury was alleviated in HS-NAC group (P=0.000).The neutrophil infiltration level and the concentrations of IL-6,IL-1 β and TNF-α in liver tissue were significantly higher in HS group than in HS-NAC group (P=0.000).Conclusion Oxidative stress may play an important role in the pathogenesis of HS liver injury through its cytotoxic effect and by inducing inflammatory responses.
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Objective To investigate the protective effect of heat shock protein (HSP) 70 on the acute lung injury (ALI) of rats with heat stroke.Methods Sixty four rats were randomly (by employing a random number table) assigned into a sham-heated group (Sham group),heat stress group (HS group),and HS plus gluttamine treatment group (HS+GLN group) and HS plus quercet in treatment group (HS+QU group),16 each.All rats were housed in a artificial climate chamber,with the rats in the sham groups exposed to a temperature of 23 ℃ and humidity of 55％ ± 5％,while the rats of HS,HS+GLN and HS+QU groups to an ambient temperature of 39 ℃ and humidity of 65％.During heat stress or sham heating,rectal temperature (Tr),systolic blood pressure (SBP) and pulse rate (PR) were monitored to observe the difference in heat stress response among the groups.The time point at which the SBP started to drop from the peak level was taken as the point of HS onset.At the onset of HS,heat exposure was terminated,then the rats were immediately removed from the chamber,and returned to room temperature.The rats were scarified 0h and 6h after HS onset respectively.After bronchoalveolar lavage fluid (BALF) was collected,the lungs of all animals were harvested for pathological examination of lung injury.The concentrations of IL-1β,TNF-α and IL-6 in BALF and HSP70 in lung homogenate were measured by using an enzyme linked immunosorbent assay kit.Results Compared with HS and HS+QU groups,the rats in HS+GLN group required significantly greater heat load to induce HS (P＜0.001),and had longer survival time span after HS onset.Compared with Sham group,the concentration of HSP70 in lung homogenate in HS group increased in a time-dependent manner (P＜0.001).In comparison with HS group,the concentration of HSP70 in lung homogenate from HS+GLN group was significantly elevated at each time point (P＜0.001),while the treatment with QU significantly inhibited the expression of HSP70 (P＜0.001).The concentration of IL-1β,TNF-α and IL-6 in BALF significantly decreased in HS+GLN group compared with those in HS group and HS+QU group (P＜0.001).The pathological results showed that the lung injury was milder in HS+GLN group,while the opposite in HS+QU group.Conclusion HSP70 could protect HS rats against ALI by enhancing their thermo-tolerance and inhibiting inflammatory response.
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Objective To investigate the effect ofulinastatin on severe heat-stroke with acute lung injury induced by severe heat stroke.Methods Thirty severe heat stroke patients were divided into conventional group (n=15) and ulinastatin group (n=15) randomly,with another 80 healthy adults serving as controls.The baseline data such as age,gender,onset period and APACHE Ⅱ scores were recorded and compared between the two groups on admission.Peripheral leucocyte counts,oxygenation index and Murray scores were determined on the 1st,3rd and 5th day.The concentration of inflammatory mediators in bronchoalveolar lavage fluid (BALF) and alveolar macrophage supernatant were detected by enzyme-linked immunosorbent assay (ELISA).Western blotting and real-time PCR were used to measure expression of triggering receptor-1 on myeloid cells (TREM-1) on alveolar macrophages.Furthermore,comparison was made in terms of the ventilation period,ICU stay time and mortality in 28 days between the two groups.Results No differences were found in age,gender,onset period and APACHE Ⅱ scores between the two groups (P＞0.05).Compared with the conventional group,peripheral leucocyte counts and Murray scores in the ulinastatin group significantly decreased on the 3rd and 5th day (P＜0.05,P＜0.01).But oxygenation index was higher in the ulinastatin group than in the conventional group (P＜0.05).The concentration of TNF-α and IL-6 in BALF was lower in the ulinastatin group than in the conventional group (on the 3rd day:P＜0.05,P＜0.01;on the 5th day:P＜0.01,P＜0.01).The concentration of TNF-α and IL-6 in alveolar macrophage supernatant was lower in the ulinastatin group than in the conventional group (on the 3rd day:-P＜0.05,P＜0.01;on the 5th day:P＜0.01,P＜0.05).The expression of TREM-1 protein on alveolar macrophages were lower in the ulinastatin group than in the conventional group (on the 3rd day P＜0.01;on the 5rd day P＜0.05).TREM-1 mRNA was lower in the ulinastatin group than in the conventional group (on the 3rd day:P＜0.05;on the 5th day:P＜0.05).Eventually,the treatment of ulinastatin shorten ventilation period and ICU stay time (P＜0.01,P＜0.05).Nonetheless,it failed to show any improvement in terms of the mortality during 28 days (P＞0.05).Conclusion Our study exhibited that ulinastatin had good effect on the heat stroke patients with acute lung injury and it helped reduce the inflammatory reaction of pulmonary tissues.The underlying mechanism of these effects might lie in its ability to reduce heat stroke-induced inflammatory secretion and expression of TREM-1 on alveolar macrophage.
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Objective To investigate the effect of mitogen-activated protein kinases (MAPKs) activation on the heat stressinduced apoptosis of pulmonary microvascular endothelial cells (PMVECs).Methods A mouse model of severe heat stroke was made and TUNEL and immunohistochemistry were employed to detect lung tissue damage.MACS separation was used for isolation of neonatal PMVECs,and TUNEL was utilized to detect the apoptosis of PMVECs.Western blotting was used for determining the MAPKs activation during heat stress recovery (0,2,6h).The monolayer permeability of endothelial cells was detected in terms of transmembrane resistance (TEER) and horseradish peroxidase (HRP).Cells were pretreated with MAPKs activation inhibitors to examine the effect of heat stress on the monolayer cell permeability and apoptosis.Results In mice with severe heat stroke,extensive apoptosis of PMVECs was found in their pulmonary tissues.TUNEL revealed that the number of apoptotic cells increased over time during heat stress recovery period and heat stress could activate MAPKs in PMVECs.Compared with heat stress group,in the cells pretreated with p38 or ERK activation inhibitor PD98059 and SB203580,the monolayer permeability and apoptosis increased while in cells pretreated withJNK inhibitor SP600125,the cellular permeability and apoptosis decreased.Conclusion In mice with severe heat stoke,PMVECs might experience apoptosis and p38 and ERK could inhibit apoptosis while JNK could promote apoptosis.
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ObjectiveTo observe the effect of Xuebijing injection pretreatment on systemic inflammatory response induced by severe heat-stroke, and to investigate the mechanism of alleviation of intestinal injury in rats. Methods Thirty-six healthy adult male Wistar rats with grade SPF were randomly assigned into three groups with randomized number method, namely sham group, severe heat-stroke model group, and Xuebijing pretreatment group (XBJ group), with 12 rats in each group. The animals were placed in a pre-warm chamber [temperature (40±2)℃, humidity (65±5)%] in order to induce typical heat-stroke. The duration of heat-stress was 60 minutes, while the animals in sham group were exposed to ambient temperature of 25℃. Arterial blood samples were collected at the beginning and the end of heat-stress, the concentrations of tumor necrosis factor-α(TNF-α), interleukins (IL-1β, IL-6), and lipopolysaccharide (LPS) in peripheral blood were determined by enzyme linked immunosorbent assay (ELISA). The intestinal tissues were harvested after heat-stress, and the pathological changes in intestine tissues were observed after hematoxylin-eosin (HE) staining and under optical microscope. The pathological injury scores were calculated. Immunohistochemistry was performed to determine inducible nitric oxide synthase (iNOS) expression in intestinal tissue. Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Western Blot was used to measure the tight junction protein occludin expression.Results The concentrations of TNF-α, IL-1β, IL-6 and LPS in blood of the rats after heat-stress in model group were significantly higher than those of sham group [TNF-α (μg/L): 443.00±110.10 vs. 98.36±44.61, IL-1β (μg/L): 436.37±163.64 vs. 64.24±16.15, IL-6 (μg/L): 342.70±92.42 vs. 54.40±13.22, LPS (μg/L): 0.68±0.22 vs. 0.09±0.02, allP< 0.01], but the levels of these parameters in XBJ group were significantly lower than those of model group [TNF-α (μg/L):340.45±68.57 vs. 443.00±110.10, IL-1β (μg/L): 191.33±82.78 vs. 436.37±163.64, IL-6 (μg/L): 192.21±37.89 vs. 342.70±92.42, LPS (μg/L): 0.43±0.17 vs. 0.68±0.22, allP< 0.01]. Infiltration of inflammatory cells, necrosis and hemorrhage in intestinal mucosa were found in the intestine of heat-stroke animals in model group. The pathological lesions in XBJ group were milder than those of model group, with a decreased pathological injury score compared with model group (2.10±1.15 vs. 3.20±0.67,P< 0.01). The expression of iNOS and apoptosis of cells in intestinal tissue in model group were increased compared with that of sham group, but they were significantly less marked in XBJ group compared with model group [iNOS (adjustedA value): 0.32±0.15 vs. 0.74±0.17, apoptotic index: 0.23±0.08 vs. 0.56±0.07, bothP< 0.01]. The order of expression for occludin protein from high to low was sham group, XBJ group and model group (A value was 0.96±0.25, 0.62±0.20, 0.33±0.11, respectively). Furthermore, there was significant difference in the expression of occludin protein between model group and both XBJ group and sham group (bothP<0.01).Conclusions Xuebijing injection alleviates inflammation and endotoxemia produced by severe heat-stroke in rats. The mechanism may be related to amelioration of oxidative injury, apoptosis, and dysfunction of tight junction protein occludin expression.
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ObjectiveTo investigate the temporal features of renal injury in rats with severe heat stroke (SHS) and their relationship with inflammatory response.Methods Fifty-six male Wistar rats were randomly divided into normal control group and SHS for 0, 2, 6, 24, 48, 72 hours group (SHS-0, 2, 6, 24, 48, 72 h groups), with 8 rats in each group. Rats were placed in an artificial climate chamber [temperature (39.5±0.2)℃, humidity (60±5)%] to induce SHS model, and the criterion for successful model reproduction was the onset of lowering peak systolic blood pressure (SBP). Then the rats were transferred to room temperature (23.0±0.2)℃ after successful reproduction of the model. The rats of normal control group were kept in room temperature of (23.0±0.2)℃. Heart blood and renal tissue samples were harvested, and the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) were determined by automatic biochemistry analyzer. The levels of myeloperoxidase (MPO), tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) in renal tissue specimens were determined by enzyme linked immunosorbent assay (ELISA). The changes in histopathology in kidney were observed with light microscopy, and Paller scores were used to assess the degree of renal injury.Results Compared with normal control group, the levels of SCr and BUN in serum, and MPO, TNF-α and IL-6 in the renal tissue homogenate were significantly increased in SHS-6 h group [SCr (μmol/L): 174.0±27.0 vs.68.0±11.3, BUN (mmol/L): 12.6±2.3 vs. 4.3±1.2, MPO: (203.0±38.0)% vs. (100.0±1.4)%, TNF-α: (121.0±16.0)% vs. (100.0±1.4)%, IL-6: (118.0±19.0)% vs. (100.0±1.3)%, allP< 0.05], and they peaked at 24 hours [SCr (μmol/L): 489.0±96.0 vs. 68.0±11.3, BUN (mmol/L): 19.3±5.7 vs. 4.3±1.2, MPO: (511.0±41.0)% vs. (100.0± 1.4)%, TNF-α: (399.0±47.0)% vs. (100.0±1.4)%, IL-6: (473.0±56.0)% vs. (100.0±1.3)%, allP< 0.01], then declined to the normal levels at 72 hours. Under light microscopy, tissue edema and necrosis of renal tubules were found, and leukocyte infiltration was found to be most profuse at 24 hours, then they returned to normal levels at 72 hours. Paller scores in SHS-6 h group were significantly higher than those of the normal control group (75.45±9.70 vs. 14.23±3.26,P< 0.01), and it peaked at 24 hours (186.00±14.25 vs. 14.23±3.26,P< 0.01), followed by a gradual lowering, back to normal level at 72 hours.ConclusionThe results suggest that progressive renal damage occurred in the rats with SHS within 24 hours, and it was accompanied with elevated levels of MPO, TNF-α and IL-6 in the kidney homogenate, suggesting that inhibition of neutrophil activation and the release of IL-6, TNF-α may protect the SHS associated renal injury.
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Objective To investigate the effect of ulinastatin on acute lung injury in rats with severe heatstroke.Methods Fourty-eight rats were randomly (random number) assigned into control group (HS group,n =12),low dose Ulinastatin group (LUTI group,n =12),high dose Ulinastatin group (HUTI group,n =12) and non-thermal group (Sham group,n =12).Rats were prepared with pre-warm chamber to initiate heatstroke.The change of rectum temperature (Tc),heat-rate (HR) and mean arterial pressure (MAP) under heat-stress were recorded.The time-point of heatstroke onset and Tc ＞42 ℃ was observed.Arterial blood samples were draw at 0 min,20 min,40 min and 60 min for testing partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2).Bronchoalveolar lavage fluid (BALF) were collected at 60 min,and the concentrations of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-l β) and interleukin-6 (IL-6) in BALF were measured with enzyme linked immunosorbent assay kit.Lung tissues were harvested for observing pathological change and measuring the expression of iNOS with Western blot test.Results Compared with HS group,the time-point of Tc ＞ 42℃ (P =0.00),severe heat-stroke (P =0.00) and the median of survival time (P =0.00) in LUTI and HUTI groups were significantly increased.At 60min after heat-stress,the level of PaO2 in HS group was much lower than those in other groups (P =0.00).But there were no differences between LUTI and HUTI groups (P =0.91).The value of PaCO2 in HS group was much higher than those in other groups (P =0.00).And the differences between LUTI and HUTI groups were no significant (P =0.79).The concentrations of TNF-α,IL-1β and IL-6 in HS group was the highest in four groups (P =0.00,P =0.04 and P =0.04),followed by LUTI,HUTI and Sham group.The concentrations of proinflammatory cytokine in LUTI were higher than those in HUTI group (P =0.02,P =0.00,P =0.00).Compared with HS group,the pathological injuries were alleviated in LUTI and HUTI group (P =0.00).The expression of iNOS in lung tissue of HS group was strengthened than LUTI and HUTI group (P =0.00),and there was a significant difference between LUTI and HUTI group (P =0.03).Conclusion Ulinastatin improves respiratory dysfunction and the prognosis of severe heatstroke rats through reducing the inflammatory and oxidative injury in lung tissue.
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Objective To evaluate diagnostic value of Sonoclot in the diagnosis of heat stroke complicated with disseminated intravascular coagulation (DIC). Methods 43 patients with heat stroke and coagulation dysfunction were retrospectively included and divided into 2 groups according to scores by International Society of Thrombosis and Hemostasis (ISTH): DIC dominant group (22 case) and DIC non-dominant group (21case). Regular coagulation tests , routine blood test , D-dimer and Sonoclot tests were performed at admission and their clinical data were compared. Logistic regression analysis was applied to evaluate the relationships between DIC occurrence and Sonoclot parameters. ROC curves were used to evaluate diagnostic value of Sonoclot for the patients with DIC and heat stroke. Results There were no differences in age, sex, central temperature and total hospital stay between the 2 groups except ICU stay, DIC symptoms, outcome, ISTH scores and APACHEⅡscores (P <0.05). ACT and CR correlated with the occurrence of DIC (P < 0.05). The AUC of ACT and ACT combined with CR were 0.854 and 0.877 respectively. The specificity of ACT in predicting DIC was 69.2%with the sensitivity of 90.3%. When combined with CR, both the specificity and the sensitivity were increased to 80.2% and 93.5%, respectively. Conclusions Sonoclot can predict DIC quickly and is effective in the diagnosis of heat stroke patients with DIC.
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Objective To investigate the effect and safety of thoracic drainage by central venous catheter in critical patients with pleural effusion. Methods A prospective study was carried out,in which 46 critical patients with pleural effusion admitted to department of critical care medicine were included,and according to the types of their primary diseases to make matched pairs,and they were divided into two groups:conventional drainage control group and central venous catheter drainage observation group(each 23 cases). The drainage effect and complications were compared between the two groups,acute physiology and chronic health evaluation Ⅱ(APACHEⅡ)score, quantitative pleural effusion and the counts of white blood cells(WBC)and of platelets(PLT),the levels of prothrombin time(PT),procalcitonin(PCT)and C-reactive protein(CRP),etc. were measured on the baseline and 24 hours after the operation. Results There were no significant differences in the APACHEⅡ score,quantitative pleural effusion,amount and duration of drainage,as well as the levels of WBC,PLT,PT and PCT between group control and observation(all P>0.05). The post-drainage CRP(μg/L)level in group observation was much lower than that in group control(77.26±67.20 vs. 106.13±66.23,P0.05). Conclusions In the comparison between the conventional drainage and thoracic drainage with central venous catheter,the therapeutic effects for treatment of critical patients with pleural effusion were similar, but the stress was milder and the incidence of complications was lower in the latter group. Therefore,the thoracic drainage with central venous catheter is a safe,effective and alternative method to substitute the conventional drainage for critical patients with pleural effusion.
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Objective To prepare mouse model with heat stress and determine its pathological changes of the lung and brain during heat stress. Methods BALB/c mouse were randomly (random number) divided into two groups, control group and heat stress group. The animals in the control group were sham- heated at a temperature of ( 25 ± 0.5) ℃ and humidity of (35 ± 5 ) %. The animals of heat stress group were placed in a prewarmed incubator maintained at (35.5 ± 0.5) ℃ and relative humidity of (60 ± 5) %. Rectal temperature (Tc) was monitored, and when Tc respectively reached 39 ℃, 40 ℃ , 41 ℃ and 42 ℃, those study animals were killed. The other animals were removed from the incubator and allowed to cool at an ambient temperature of (25 ±0. 5)℃ and humidity of (35 ±5)% , respectirvely for 12 and 24 hrs when Tc reached 41 ℃ , and for 6 hrs when Tc reached 42 ℃. The lung and brain of all the animals were isolated. Hematoxylin and eosin stain and light microscope were used to detect their pathological changes. Results All the animals displayed uniform response to the heat stress. Low degree of heat stress could induced obviously pathological changes of the lung, progressively greater damage to lung with further congestion of lung matrix, asystematic hemorrhage of alveolar space, abscission of alveolar epithelial cell and disappear of pulmonary alveolus tissue structure were detected with the rise of Tc to 42 ℃. However, absorption of congestion and hemorrhage and recovery of pulmonary alveolus tissue structure could also be seen with cooling at ambient temperature. With low degree of heat stress, the brain only showed moderate edema. Neuronal denaturation and necrosis were detected when Tc reached to 42 ℃. Interestingly, the lesions of brain further aggravated even through cooling treatment after Tc reached to 42 ℃ , but recovery could been observed after cooling treatment followed with Tc of 41 ℃. Conclusions The pathological changes of the lung and brain showed distinctive lesions to heat stress and cooling treatment, and these changes were correlated with the timing and time of cooling treatment, which provide the experimental basis to further study the mechanisms between the heatstroke and multiple organ dysfunction syndrome (MODS).
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Objective To evaluate the curative effect of valsartan associated with low-dose amiodarone on the recurrence of atrial fibrillation (AF), the left atrial diameter (LAD), P wave dispersion (Pd) and the maximum P wave duration (Pmax) in patients with paroxysmal AF. Methods 76 patients with paroxysmal atrial fibrillation (PAF) were randomized to valsartan (test group) and placebo (placebo group), both associated with low-dose amiodarone, and were followed up for 18 months. The patients were asked to report any episode of symptomatic atrial fibrillation and to perform an ECG as early as possible. AF load, Pmax, Pd and LAD were measured before and at the 6th, 12th, and 18th month after the treatment. Results At least one ECG-documented episode of AF was reported in 16% of the patients in test group and in 41% in placebo group, the difference was significant (P
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Objective To analyze the differences in protein pro fi le between laterally spreading tumor (LST) cell line and SW480 cell line using t wo-dimensional electrophoresis (2-DE). Methods 2-DE was empl oyed to isolate the total proteins of the two cell lines.The gels were stained with silver, and the differential protein expressions were analyzed with Melanin e 3 software. Results The protein spots of the two cell lines w ere 1285?51(LST) and 1184?47(SW480) respectively,containing 96?7 differential protein spots with 50?6 expressed or obviously increased only in LST cell line and 47?5 in SW480 cell line. Conclusion The protein profiles between LST and SW480 cell lins are different and further analysis on the differ ent interested spots is required to acquire the biology-associated proteins spe cific LST.
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Objective To explore the endoscopic and histopathological features of serrated adenomas (SAs).Methods The data of patients with colorectal polyps diagnosed in the Digestive Endoscopy Center at Nanfang Hospital from January 2002 to July 2005 were reviewed and the detection rate, endoscopic appearances, pit patterns and histopathological features of SAs were analyzed.Results In 1928(16.21%) out of 11 894 patients undergoing colonscopy 2811 polyps were found.Among them 61 patients with 71 polyps were found,with a detection rate of 0.51%.The SAs,larger than hyperplastic polyps obviously,were found in patients 39.44% with diameter (larger than 1 cm).The incidence of pedunculated polyps in SAs (26.76%) was higher than that in hyperplastic polyps(13.25%),but less than in adenomatous polyps (43.95%).The pit patterns of SAs, were typeⅢ pit pattern (41.67%) and type Ⅳ pit pattern (18.33%), this result was similar to adenomatous polyps.The incidences of moderate and severe dysplasia of SAs were higher than those of tubular adenomas but lower than villous adenomas.The canceration rate of SA was 2.82%.Conclusion The endoscopic appearances,these of pit patterns and histopathological features of SAs,were different from hyperplastic polyps essentially, but similar to neoplastic polyps with potential malignancy,which should be emphasized in clinical practice.
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Objective To observe the changes of LoVo cell growth by galectin-1.Methods Eukaryotic expression vector of galectin-1 was constructed and transfected into LoVo cells using lipofectamineRM 2000.Immunochemistry was employed to detect galectin-1 expresson.LoVo cell proliferation and apoptosis were observed.Results Galectin-1 eukaryotic expression vector pEGFP-C1/GAL1 was successfully constructed.Three cell clones,p-GAL1-LoVo and p-LoVo,transfected with pEGFP-C1/GAL1 and pEGFP-C1 correspondingly,and LoVo were cultured successfully.Galectin-1 expression downregulated Bcl-2 level only occurring in p-GAL1-LoVo cells.p-GAL1-LoVo cell proliferation was similar to p-LoVo and LoVo cells,but p-GAL1-LoVo cell apoptosis was increased(9.61?0.56)%,as compared with p-LoVo and LoVo cells,[(3.56?0.53)% and(3.46?0.46)% respectively](P
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Objective To construct the RNA interference (RNAi) eukaryotic expression vectors of galectin-1, and establish the LST-R1 cell lines stably transfected by RNAi vectors. Methods Two pairs of small interfering RNAs (siRNA) targeting to galectin-1 mRNA (GenBank: NM002305) were designed. The corresponding single-strand short hairpin interfering RNAs (shRNA), containing BamH Ⅰ, Hind Ⅲ sites and a 9nt hairpin structure, was synthesized and annealed. The annealed product and the linear eukaryotic expression plasmid pSuperior-puro, which were digested with Bgl Ⅱ and Hind Ⅲ, were ligated by T4 ligase to set up the interfering system. The recombined plasmid was identified with EcoR Ⅰand Hind Ⅲ enzyme digestion and sequencing, and co-transfected to LST-R1 cells with pcDNA6/TR with Lipofectamine2000. Positive clones were selected with 0.8?g/ml puromycin. After incubated with 4?g/ml tetracyclin for 48 hours, RT-PCR, Western blotting and immunochemistry were employed to determine galectin-1 mRNA and protein levels. Results Sequencing results suggested that the nucleotide sequence and read frame of RNAi eukaryotic exprssion vector of galectin-1, p-shRNA1 and p-shRNA2 were perfect. Stably transfected LST-R1 cell lines of p-shRNA1-LST and p-shRNA2-LST were established. The relative values of galectin-1 expression in LST-R1 cells, p-shRNA1-LST cells, p-shRNA2-LST cells and p-LST cells by RT-PCR were 0.616, 0.298, 0.373 and 0.641, respectively, and 1.00, 0.07, 0.38 and 0.97 by Western blotting. The p-shRNA1 gave the best interfering effect, which was in conformity with the results of immunochemistry measurement. Conclusions RNAi eukaryotic expression vector of galectin-1 mRNA has been successfully constructed. Establishment of the stably transfected LST-R1 cell lines may lay a foundation to explore the roles of galectin-1 in laterally spreading tumor.