[Long non-coding RNA PCAT-1 expression in oral squamous cell carcinoma and its clinical significance].

PURPOSE: To investigate the correlation between the expression of lncRNA PCAT-1 and clinicopathological features of oral squamous cell carcinoma. METHODS: In this study, 112 oral tissue specimens, including 60 oral squamous cell carcinoma, and 52 non-cancer oral tissues were collected from Department of Stomatology in Anhui Provincial Hospital during 2013 to 2016. Reverse transcription quantitative PCR (RT-PCR) was performed to detect the expression of PCAT-1 and c-Myc. The correlation between the levels of PCAT-1 and clinical features (age, gender, high risk habit, histological stage, cervical lymphatic metastasis, differentiation) were analyzed. Graphpad Prism 7.0 software package was used for statistical analysis. RESULTS: Significant different levels of PCAT-1 were found between the high risk habit (alcohol and tobacco) group and low risk habit group, between patients with cervical lymphnode metastasis and patients without cervical lymphnode metastasis. The expression of PCAT-1 and c-Myc were up-regulated in OSCC, and there were positive correlation between the expression of PCAT-1 and c-Myc; up-regulated expression of PCAT-1 may be associated with higher morbidity of OSCC. CONCLUSIONS: PCAT-1 is overexpressed in oral squamous cell carcinoma and is associated with higher morbidity of OSCC.

HSP70 protects intestinal epithelial cells from hypoxia/reoxygenation injury via a mechanism that involves the mitochondrial pathways.

Though recent studies have reported the importance of several endogenous cytoprotective factors including heat shock protein 70 (HSP70) that protect intestinal epithelial cells (IECs) from the effects of stress and injury, the exact mechanism of HSP70 underlying cytoprotection against hypoxia/reoxygenation induced IEC injury remains unclear. The present study was designed to investigate the possible mechanisms by which HSP70 protected IECs against hypoxia/reoxygenation injury and focused on the effects of HSP70 on IEC apoptosis induced by hypoxia/reoxygenation injury. Recombinant adenoviruses (Ad-HSP70) were transfected into the intestinal epithelial cell line in vitro and then suffered from 90 min of hypoxia followed by 60 min of reoxygenation. The LDH leaking, apoptosis, and mitochondrial membrane potential (Psi(m)) were evaluated after hypoxia/reoxygenation. The expression of HSP70, cytochrome c and Bcl-2 protein was determined by Western blot or immunofluorescence analysis. The results show that HSP70 protein was highly expressed in the IECs at 48h following Ad-HSP70 transfection. HSP70 overexpression could reduce LDH leakage and cell apoptosis in IECs following hypoxia/reoxygenation injury. Furthermore, the overexpression of HSP70 significantly reversed the decrease of mitochondrial membrane potential and the release of mitochondrial cytochrome c in IECs during hypoxia/reoxygenation. HSP70 overexpression was also associated with the increasing expression of Bcl-2 protein in IECs during hypoxia/reoxygenation. We conclude that HSP70 protects IECs against hypoxia/reoxygenation induced apoptosis through increasing Bcl-2 expression, which in turn could inhibit the mitochondria-related apoptotic pathway that involves the disruption of the Psi(m) and release of cytochrome c from mitochondria.

[Subcellular localization of human endothelial-overexpressed lipopolysaccharide-associated factor 1 protein].

OBJECTIVE: To study the subcellular localization of human endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1) protein in endothelial cells. METHODS: Human umbilical vein endothelial cell strain ECV304 were cultured in vitro. The fusion protein of enhanced green fluorescent protein (EGFP)-EOLA1 expressing plasmid was constructed. Empty plasmid with EGFP at N side (pEGFP-N2) and fusion protein expressing plasmid EGFP-EOLA1 was respectively transfected into ECV304 cells with liposome. After being cultured for 48 hours, the expression levels of EGFP and fusion protein EGFP-EOLA1 in cells were detected with Western blot. The subcellular localization of EOLA1 protein was detected by laser scanning confocal microscope and immunoelectron microscopy. RESULTS: The EGFP-EOLA1 coexpression plasmid was verified to be successfully constructed by enzyme cutting and gene sequencing. The fusion protein of EGFP-EOLA1 was observed to express in transfected cells through Western blot. Green fluorescence scattered all over the ECV304 cells transfected with empty plasmid and cells transfected with fusion protein expressing plasmid, and it gathered obviously in the nuclei in the latter cells. Immune deposits were observed in the matrix of cells transfected with fusion protein expressing plasmid but not in the cells transfected with empty plasmid. CONCLUSIONS: EOLA1 protein is localized in the nucleus and the matrix of ECV304 cell, and it plays its role as a signal transduction factor.

[Relationship between learning and memory ability and expression of hippocampal N-methyl-D-aspartic acid (NMDA) in burn rats with depression].

OBJECTIVE: To observe changes of learning and memory ability (LMA) in burn rats with depression, and study the relationship between LMA and expression of hippocampal NMDA. METHODS: According to simple random method, 46 Wistar rats were divided into burn group (B, with 30% TBSA deep partial-thickness burn, n = 10), depression group (D, with moderate stress stimulation in chronic and unpredictable, n = 12), B + D group (with the same stress stimulation inflicted to B group after burn, n = 12), healthy control group ( HC, without treatment, n = 12). Changes in escape latency was examined in water maze test. Expression of hippocampal NMDA in CA1, CA2 regions and dentate gyrus were observed with immunohistochemistry. RESULTS: Compared with that of HC group (22 +/- 20 s), water maze escape latency in B, D, B + D groups on 2 day after training prolonged (38 +/- 31, 41 +/- 36, 42 +/- 33 s, respectively, P < 0.05 or P < 0.01). Water maze escape latency in B + D group on 4th day after training was longer than that of other groups (P < 0.01). There was no obvious difference in positive expression of NMDA in CA1, CA2 regions among groups (P > 0.05). The positive count of NMDA in dentate gyrus in D group (198 +/- 14) and B + D group (191 +/- 6) were lower than that of HC group (224 +/- 23, P < 0.05 or P < 0.01), but there was no obvious difference between HC group and B group (219 +/- 25, P > 0.05). CONCLUSIONS: Burn complicated with depression can reduce LMA, which may be due to a decrease in NMDA in dentate gyrus.

Analysis of the early adaptive response of endothelial cells to hypoxia via a long serial analysis of gene expression.

Activation of endothelial cells in humans is an early event in the response to hypoxia that may contribute to the endothelium's endogenous capacity to reduce tissue injury. To better understand the mechanism underlying this process, we utilized Long Serial Analysis of Gene Expression to study the transcriptome of human vein umbilical endothelial cells (EA.hy926) shortly after the induction of hypoxia. Of over 13,000 genes detected in each pool, 112 showed obvious differences in expression. Metabolic processes such as protein biosynthesis and proteolysis, aminoglycan metabolism, ribonucleotide biosynthesis, adenosine salvage, and lipid metabolism were reinforced. Pro-proliferation and pro-apoptotic states suggest the co-existence of pro- and anti-injury forces in endothelium shortly after the induction of hypoxia. Other adaptive responses include reinforced angiogenesis and vasodilation. Additionally, gene transcription in the endothelium shortly after the induction of hypoxia was regulated independently of HIF-1alpha. Our efforts to elucidate the adaptive response at an early post-hypoxia stage should contribute to further investigation of the protective processes that occur in the endothelium and has potential clinical implications.

[Pay great attention to research on monitoring burn shock].

Improvement in early burn treatment has been realized, the mortality of burn shock has been decreased. However, the treatment of burn shock is still inadequate and occult hypoperfusion is usually occurred. This may be difficult to identify the appropriate resuscitation endpoint. The goal in management of burn shock is restoration of adequate tissue perfusion and normalization of cellular metabolism. Traditional endpoints, such as blood pressure, urine output are useful in managing mild and moderate burn shock. Additional endpoints that evaluate the adequacy of global and regional perfusion and oxygenation at the tissue level should be used in treatment of severe burn injury. Now the most useful parameters may be blood pressure, urine output, serum lactate, BE and CVP, SCVO2.

[Achievements in burn surgery over the past 50 years in China].

This paper reflects briefly the main advancements of clinical and scientific research in the field of burn surgery over the past 50 years in China. It includes emergency care of massive burns, resuscitation, anti-infection, prevention and treatment of internal organ injury, metabolic and nutritional support, repair of wound and rehabilitation, and special types of burns. The article also covers the researches in pathology, microbiology, immunology, cell biology, molecular biology, and tissue engineering pertaining to burn injury.

[Advancement in study of inhalation injury].

Inhalation injury is a major contributor to the morbidity and mortality associated with serious burns. The improvement in the understanding of smoke inhalation injury had been obtained in the last half century in China. The models of steam and smoke inhalation injury had been reproduced and a series of experimental studies had been performed. It was found that chemical bronchiotracheitis, pulmonary edema and alveolar collapse (atelectasis) were the primary pathologic findings after inhalation injury. The second inflammatory response would play an important role in the development of acute respiratory failure. The roles of some cytokines, inflammatory cells and pulmonary surfactants in the development of inhalation injury had been elucidated. The etiologic factors and the pathophysiologic changes in inhalation injury had been illustrated clearly. These basic science investigations had led to the advances in protective strategies for the complications of inhalation injury. Now the morbidity and mortality of inhalation injury have decreased markedly in China.

[Influence of HSP70 on function and energy metabolism of mitochondria in intestinal epithelial cells after hypoxia/reoxygenation].

OBJECTIVE: To investigate the effect of recombinant adenovirus-mediated heat shock protein 70 (HSP70) on energy metabolism of mitochondria in intestinal epithelial cells (IEC-6) after hypoxia/reoxygenation injury . METHODS: IEC-6 cells were transfected with HSP70 recombinant adenovirus vectors (Ad-HSP70) and empty adenovirus vectors. The expression of HSP70 protein was detected by Western blotting. Cultured IEC-6 cells were divided into: control group (without treatment), hypoxia/reoxygenation group (with challenge of hypoxia/reoxygenation) and Ad-HSP70 transfection group (with challenge of hypoxia/reoxygenation after Ad-HSP70 transfection). The activity of mitochondrial dehydrogenase was assessed by MTf method. The contents of cellular ATP, ADP , AMP and energy charge (EC)were determined by high-performance liquid chromatography (HPLC). RESULTS: The expression of HSP70 protein in IEC-6 cells was significantly upregulated after Ad-HSP70 transfection compared with empty adenovirus vector transfection. Compared with that in control group, the activity of mitochondrial dehydrogenase was significantly lowered in IEC-6 cells in hypoxia/reoxygenation group (P < 0.01). The activity of mitochondrial dehydrogenase in Ad-HSP70 transfection group was significantly greater than that in hypoxia/reoxygenation group (P < 0.01). Compared with those in control group,the content of cellular ATP was significantly decreased in hypoxia/reoxygenation group, the contents of cellular ADP and AMP were significantly increased. The above cell energy indices in Ad-HSP70 transfection group was similar to those in control group (P > 0.05), which were ameliorated compared with those in hypoxia/reoxygenation group (P < 0.050 or P < 0.01). The cellular EC in hypoxia/reoxygenation group (0.615 +/- 0.060) was significantly lower than that in control group (0.748 +/- 0.012, P < 0.01) and Ad-HSP70 transfection group (0.736 +/- 0.028, P < 0.01). CONCLUSION: Ad-HSP70 transfection in IEC-6 cells can upregulate the expression of HSP70, the content of cellular ATP and EC after hypoxia/reoxygenation, and protect mitochondrial function. Mitochondria may be one of main target organelles for HSP70 in protection of IEC against hypoxia/reoxygenation injury.

Apoptosis in cardiac myocytes during the early stage after severe burn.

BACKGROUND: Cardiac dysfunction after severe burn is associated with postburn myocardial injury. We hypothesize that myocyte apoptosis is triggered and presented as the pathologic basis of postburn myocardial injury during the early stage after severe burn, and that apoptosis may be related to inflammatory responses in the postburn myocardium. METHODS: Rats with 40% total body surface area full-thickness burn were used. The following functions were measured at several time points after the burn injury: myocyte apoptosis (TUNEL staining, DNA ladder, and caspase-3 activity assay); mRNA levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (reverse transcriptase-polymerase chain reaction [RT-PCR]); activities of myeloperoxidase and p38 mitogen activated protein (MAP) kinase (Western blots); and left cardiac function. RESULTS: TUNEL positive myocytes appeared as early as 6-hour and their numbers showed further increases at 12-hour and 24-hour postburn; DNA fragmentation was clearly observed, and caspase-3 activity was significantly increased in the myocardium after burn. Infiltration of neutrophils, evidenced by the levels of myeloperoxidase activity, expression of TNF-alpha, and p38 MAP kinase activity in the heart, were all significantly increased within 24-hour after burn. Cardiac function was decreased after burn, which approximately paralleled the increased amount of cardiac apoptosis. CONCLUSION: These results demonstrate that cardiomyocyte apoptosis progressively develops during the early stage after severe burn, which may in part contribute to burn-induced cardiac dysfunction. Myocardial inflammatory responses, evidenced by the increased infiltration of neutrophils, as well as production of TNF-alpha probably because of the activation of p38 MAP kinase, may be involved in burn-induced cardiomyocyte apoptosis.

Inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge.

This study was aimed to investigate the effects of SB203580, the specific p38 mitogen-activated protein (MAP) kinase inhibitor, on cardiac myocyte survival and secretion of cytokines in an in vitro model of hypoxia and burn serum challenge. Results demonstrated that hypoxia and burn serum induced a persistent activation of p38 MAP kinase in primary cultured neonatal rat cardiomyocytes during the 12h period of stimulation, concomitant with a time-dependent increased expression of tumor necrosis factor (TNF)-alpha and inducible nitric oxide (iNOS), a progressively developed oxidative stress reflected by malondialdehyde (MDA) production, and myocytes injury evidenced by the increased levels of released lactate dehydrogenase (LDH) and the decreased myocyte viability. Furthermore, hypoxia and burn serum resulted in a significant increase in myocyte apoptosis, which may account for the impairment of myocyte viability as observed. SB203580 abolished p38 MAP kinase activation, blunted the upregulation of TNF-alpha, iNOS and the subsequent nitric oxide (NO) production, reduced oxidative stress, and alleviated hypoxia and burn serum-induced myocytes injury or apoptosis. These results demonstrated for the first time that inhibition of p38 MAP kinase improves survival of cardiac myocytes with hypoxia and burn serum challenge possibly via reducing the production of cytokines, such as TNF-alpha and NO, and the subsequent oxidative stress, providing strong evidence that the excessive inflammatory cytokines produced by cardiomyocytes themselves may be sufficient to cause myocardial injury after burn.

Induction of heat shock protein 70 by sodium arsenite attenuates burn-induced intestinal injury in severe burned rats.

The present study was designed to assess the effects of induced heat shock protein 70 (HSP70) on intestinal injury after severe burn. Wistar rats were randomly divided into four groups: control group, burn group (B group), sodium arsenite pretreatment group (SA group), and sodium arsenite+quercetin pretreatment group (SA+Qu group). Plasma endotoxin and d-lactic acid content were determined at 3, 6, 12, 24, and 48h after severe burn. Samples of small intestine were obtained for histologic assessment of intestinal mucosal injury and the expression of HSP70 was assayed by Western blot. Apoptosis of the intestinal epithelial cells was examined by the TUNEL method. Results showed that SA pretreatment significantly increased expression of HSP70 in the small intestine. SA pretreatment attenuated the burn-induced increase in plasma endotoxin and d-lactic acid content, intestinal injury scores and the percentage of apoptotic intestinal epithelial cells. Co-administration of quercetin with SA abolished the SA-induced HSP70 over-expression and the beneficial effects of SA. Our findings suggest increasing expression of HSP70 induced by SA pretreatment attenuates burn-induced intestinal injury apparently by preventing apoptosis.

[Involvement of JNK signal pathway in hypoxia related upregulation of calcium/calmodulin-dependent serine protein kinase in endothelial cells].

OBJECTIVE: To investigate the expression of calcium/calmodulin-dependent serine protein kinase (CASK) induced by short-term hypoxia, and to explore the role of JNK pathway in this signal event. METHODS: EA. hy926 cells were cultured in normoxic condition for 0, 12, 24, 48, 72 h after being exposed to hypoxic condition for 3 h, then the cellular lysates were extracted. CASK promoter luciferase reporter recombinant was constructed and transfected into EA. hy926 cells for 48h. Cellular lysates were extracted 1, 3, 6, 12 h after hypoxia treatment and were used to detect firefly luciferase activity and rinella luciferase activity with luminometer. EA. hy926 cells were cultured under hypoxic condition for 1, 3, 6, 12 h or under normoxic condition, then the cell lysates were extracted and used to detect phospho-JNK with Western blot. EA. hy926 cells were pretreated with different concentrations of JNK specific inhibitor SP 600125 (0, 10, 100 nmol/L and 1,10 micromol/L) 1h before hypoxic treatment of various duration, and the cell lysates were extracted to detect CASK expression with Western blot. RESULTS: CASK expression was obviously elevated by hypoxia, and the high expression sustained for 72 h when the hypoxic cells were cultured in normal conditions, and it was significantly higher than that of normal controls. Dual luciferase reporter assay showed that CASK promoter activity was significantly increased after hypoxia (0.010 +/- 0.003, P < 0.01), and it reached the peak 12 hrs after hypoxia (0.192 +/- 0.023, P < 0.01). The phosphorylation of JNK was enhanced with the prolongation of hypoxic time. CASK protein expression was suppressed by JNK specific inhibitor SP600125 in a dose dependent manner, and it decreased to the lowest level with 10 micromol/L SP600125 pretreatment. CONCLUSION: JNK signal pathway is involved in short-term hypoxia related CASK upregulation.

[Effect of nuclear factor-kappaB activation on expression of proinflammatory cytokines in rat lung tissues in early stage of burn injury].

OBJECTIVE: To investigate the effect of nuclear factor-kappaB (NF-kappaB) activation on the expression of proinflammatory cytokines in the lung tissues of rats with early-stage burn injury. METHODS: Wistar rats were randomly divided into 3 groups, namely the normal control, burn, burn and PDTC treatment groups, and in the latter two groups, the rats were subjected to 35% TBSA full-thickness burns. Activation of pulmonary NF-kappaB at 1, 3, 6, 12, and 24 postburn hour (PBH) was tested by electrophoretic mobility shift assay , and the expressions of pulmonary tumor necrosis factor alpha (TNF alpha) and interleukin-8 (IL-8) mRNAs at 3, 6, 12, and 24 h were detected by RT-PCR. RESULTS: Compared to that of the control group, activity of pulmonary NF-kappaB in burned rats was markedly increased within 1 PBH and kept increasing till 24 h. Expressions of pulmonary TNF alpha and IL-8 mRNAs increased gradually, reaching the peak level at 6 PBH, and PDTC could effectively inhibit pulmonary NF-kappaB activation and expression of the pulmonary cytokines induced by the burn injury. CONCLUSION: Severe burn injury may activate pulmonary NF-kappaB, which ultimately leads to secretion of cytokines in the lung tissues.

[Influence of hypoxia on the proliferation and activity of human umbilical vein endothelial cells].

OBJECTIVE: To investigate the influence of hypoxia on the proliferation and activity of human umbilical vein vascular endothelial cells (EA. hy926). METHODS: EA. hy926 cells were cultured in vitro and divided into normal control and hypoxia groups. The cells in hypoxia group were placed into hypoxic jar and treated with mixed gases(94% N2 +5% CO2 + 1% O2) for 1,3,6 and 12 hours. Then the total proteins were extracted for the determination of the expression of vascular endothelial growth factor (VEGF) and proliferation cell nuclear antigen (PCNA). The cell cycle and growth curve were determined with flow cytometry and MTT method, respectively. RESULTS: The expression of PCNA protein began to increase at 3 post-hypoxia hour (PHH), peaked at 6 PHH, but without obvious difference compared with that at 12 PHH. The expression of VEGF began to increase at 1 PHH, peaked at 6 PHH, and decreased at 12 PHH, though it was still markedly higher than that of normoxia at 12 PHH. MTT results showed that the cell activity began to increase at 1 PHH, and it was still to increased at 3 PHH, then decreased at 6 PHH, and it was lower than that in control group at 12 PHH. The number of cells in G0/G1 phase was decreased, but the cells in S and G2/M phase was increased at 1, 3, 6 PHH when compared with those in normal controls. The proliferation index (PI) of cells in hypoxia group at 1PHH (43 +/- 9)%, 3PHH (39 +/- 11)%, 6 PHH (40 +/- 11))% were higher than that before hypoxia (32 +/- 9)% and 3 (39 +/- 11) % and 6 hours (40 +/- 11)% after hypoxia (P < 0.05). The PI was obviously lower at 12 PHH (27 +/- 4))% compared with that of cells under normoxic condition (P < 0.05). CONCLUSION: Short-term hypoxia is beneficial to promote the proliferation of the cells, but this effect will be inhibited with the prolongation of hypoxia.

[The effect of inhibiting EOLA1 expression in ECV304 cells].

OBJECTIVE: To study the effect of inhibiting the expression of endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1) on proliferation of human umbilical vein endothelial cell line ECV304. METHODS: After constructing and transfecting EGFP-EOLA1 fusion protein expressive vector into ECV304 cells, the transfected cells was cultured in M199 containing G418 for 5 weeks to screen the cell line stable expression EGFP-EOLA1 fusion protein. Oligonucleotides targeting EOLA1 at different sites were synthesized and inserted into pSinencer3.1/H1 vector. Then, the recombinant vector was transfected into the cultured ECV304 cells and the inhibiting effect to target gene EOLA1 was investigated by observing the green fluorescence in transfected cells under inverted fluorescent microscope and by Western blot assay. The proliferation of ECV304 cells was numbered when the expression of EOLA1 in ECV304 cells was inhibited by RNA interference. RESULTS: The ECV304 cell line stably expressing EGFP-EOLA1 fusion protein was constructed and the siEOLA1 interfere vectors can knock down EOLA1 gene expression specially. When blocking the expression of EOLA1 in ECV304 cells,the proliferation of cells slowed down. CONCLUSION: EOLA1 maybe has a role on the proliferation of cells.

Involvement of p38 MAP kinase in burn-induced degradation of membrane phospholipids and upregulation of cPLA2 in cardiac myocytes.

This study was aimed to evaluate the role of p38 mitogen-activated protein (MAP) kinase in the degradation of membrane phospholipids and the regulation of cytosolic phospholipase A2 (cPLA2) in cardiac myocytes after burn trauma. In an in vivo study, rats were randomized into four groups: (1) sham-burn group, (2) burn group (40% total body surface area full-thickness burn), (3) burn + SB203580 group, and (4) burn + vehicle group. The rats from each group were killed at varying times after burn to examine the p38 MAP kinase activation (by means of Western blot analysis and immunohistochemical assay), the expression of cPLA2 (by means of reverse transcriptase polymerase chain reaction), the level of cardiac membrane phospholipids, and the level of the remaining creatine kinase-MB (CK-MB) isoenzyme in the heart. These studies showed that burn resulted in a significant decrease in the level of cardiac membrane phospholipids from 3 to 24 h after burn, which was paralleled with a persistent activation of p38 MAP kinase and an increased expression of cPLA2 in the heart. SB203580, a selective inhibitor of p38 MAP kinase, inhibited the activation of cardiac p38 MAP kinase, suppressed the burn-induced upregulation of cPLA2 and the increased PLA2 activity, and prevented burn-induced decrease in the levels of the cardiac membrane phospholipids and the remaining creatine kinase-MB isoenzyme. In addition, the in vitro treatment of cardiac myocytes with SB203580 also abolished the upregulation of cPLA2 and the disturbance of phospholipid homeostasis elicited by hypoxia and burn serum challenge. Taken together, these results have demonstrated for the first time that p38 MAP kinase is involved in burn-induced membrane phospholipids degradation in cardiac myocytes, at least in part through the regulation of cPLA2.

[Some aspects worth concern in the management of burn injury].

Although the outcome of burn patients has been improved, many aspects of management of severe burn patients remain controversial. Here we focus on the management of hypermetabolism and the resuscitation of respiratory function. Currently, the fluid resuscitation method shifts from insufficient fluid regimen to excessive fluid loading. The benefit of colloid infusion and restrictive blood transfusion need to be authenticated by further clinical trial, and the best form of fluid resuscitation has yet to be identified. The respiratory management of burn patients had been improved. Early tracheostomy, ventilation with low tidal volume and bronchoalveolar toilet are recommended. Many potential beneficial treatment strategies have been identified by recent research in the metabolic response to burn injury. Although immunomodulation therapy is promising, most of them are not clinical viable,and further clinical research is warranted.

[The influence of terbutaline on VEGF gene expression in rat astrocytes after norepinephrine and burn serum induction].

OBJECTIVE: To investigate the influence of adrenoreceptor beta-agonists terbutaline on gene expression of vascular endothelial growth factor (VEGF) in rat astrocyte after induction by norepinephrine (NE) and burn serum. METHODS: The sera of normal and burn rats were separated for use. Primary astrocytes of brain tissue were isolated from neonatal 1-3 d rats and cultured and divided into following groups: (1) CONTROL GROUP: with 10% normal rat serum in the culture medium. (2) NEl, NE2, NE3 groups: with 10% burn rat serum and 10, 20, 50 micromol/L NE in the culture medium, respectively. (3) TBN1, TBN2, TBN3 groups: with 10% burn rat serum and 10, 20, 50 micromol/L NE and 10, 20, 50 micromol/L terbutaline in the culture medium, respectively. The mRNA and protein expression of VEGF in each group were determined with real-time PCR and Western blotting, respectively. RESULTS: There was a low protein expression of VEGF in control group, but it increased slightly in NE1 group, and then increase gradually in NE2, NE3 groups, and it was obviously increased in TBN1, TBN2, TBN3 groups. The mRNA expression of VEGF in NE1, NE2, NE3 groups were [(13.26 +/- 0.03), (10.37 +/- 0.04), (14.87 +/- 0.55) copies/g], respectively, which were significantly higher than that of control [(5.72 +/- 0.12) copies/g, P < 0.01]. In addition, the expression of VEGF mRNA in TBN1, TBN2, TBN3 groups was higher than that in control group, and expression of VEGF mRNA [(13.39 +/- 0.19), (15.77 +/- 0.11), (16.00 +/- 0.07) copies/g] was gradually increased, which showed obvious difference between TBN2 and NE2, and also between TBN3 and NE3 groups (P < 0.01). CONCLUSION: Terbutaline can increase gene expression of VEGF in rat astrocytes after induction by NE and burn serum.

[Investigation and analysis of the self-esteem level and social adaptation ability of hospitalized burn patients].

OBJECTIVE: To investigate the self-esteem level and social adaptation ability of hospitalized burn patients in our burn ward. METHODS: One hundred and twenty hospitalized burn patients in our burn ward were enrolled in the study and evaluated according to their sex, severity of burn injury and education level. Their self-esteem level and social adaptation ability were scored with the Felling of Inadequacy Scale and Abbreviated Burn Specific Health Scale. RESULTS: The general score of self-esteem of the patients with mild burns( 183+/-23) was obviously lower than that with moderate and severe burns (167+/-21 and 154 +/-24) , ( P <0.01). The self-esteem level of burn patients was different in different sex and education level. Among the self-esteem scores, male burn patients presented evidently higher scores of self evaluation, social ability, appearance, as well as the general score than those in the female ( P < 0.05). Moreover, the self evaluation score and study ability was higher in those with higher education level than those with lower education. Furthermore, the score of social adaptation ability was higher in the patients with mild burns than that in patients with moderate and severe burns ( P < 0. 01). The social adaptation ability and psychological function were much higher in male patients than those in female patients, but the former were weaker than the latter in regard to the body function. The psychological function, social relationship and general condition of the patients with lower education were better than those with higher education ( P <0. 05 ). CONCLUSION: There existed difference in the self-esteem and social adaptation ability in different burn patients during different periods.