[Clinical epidemiological survey of primary liver cancer in Yunnan province from 2005 to 2014].

Objective: To investigate the clinical characteristics and changing trends of primary liver cancer in Yunnan province from 2005 to 2014, in order to provide theoretical basis for the prevention and treatment of liver cancer in this region. Methods: A retrospective survey was used to select inpatient cases of liver cancer who were initially diagnosed and treated in our hospital from 2005 to 2014 with simple random sampling. Patients socio-demographic and clinicopathological characteristics were extracted by a unified and standardized questionnaire, and the data were statistically analyzed. Results: A total of 1000 cases with liver cancer were included, aged (53.2±11.2) years, with a male-to-female ratio of 5.99/1.00. There was no significant change in the gender and age composition ratio of patients in the past 10 years. The proportion of patients with lower education level (primary or junior high school) were increased from 21.8% to 23.4%, and the proportion of patients with relatively higher education level were decreased from 58% to 38.2% (P<0.001). Smokers and non-smokers patients were decreased and increased from 58.8% to 44.4%, and 41.2% to 55.6% (P<0.001). The proportion of drinker patients were decreased from 46.4% to 35.2%. The proportion of patients with advanced liver cancer (stage C and D) were increased, while the proportion of patients with stage A and B showed a downward trend (P<0.001). The proportion of HBsAg-positive patients showed an upward trend, that is, rising from 69% in 2005 to 82% in 2014 (P=0.043). The proportion of HBeAg-positive patients showed a steady trend (P=0.008). The use rate of ultrasound examination in patients with liver cancer were decreased from 91.0% to 58.0% (P=0.001), while the use rate of computed tomography (CT), MRI, and PET/CT examinations were increased from 81.0% to 84.0% (P=0.05), 0 to 22% (P<0.001), and 0 to 3% (P=0.026) between 2005 to 2014. The proportion of surgical patients were increased (P=0.005), but the proportion of interventional patients did not change significantly (P=0.590). Surgery and interventional therapy were the most common treatment methods, and the proportion of patients treated with surgery over the past 10 years showed an upward trend (P=0.005), while the proportion of interventional therapy remained at a high level with no significant change (P=0.590). Conclusion: In Yunnan province, the incidence of liver cancer increases with age, and the proportion of male with liver cancer is almost six times that of women. Moreover, the low positive rate of alpha-fetoprotein levels and advanced clinical stage in this region are presently the main challenges against the liver cancer prevention and treatment. The application scope of CT, magnetic resonance imaging, PET-CT and other examination methods has gradually expanded, but the treatment methods are still mainly surgery and interventional therapy.

[IL-1ß inhibitor sensitizes to olaparib in homologous recombination deficiency proficient ovarian cancer cells].

Objective: To investigate the inhibitory effect of combined strategy of poly adenosine diphosphate ribose polymerase (PARP) inhibitor and interleukin-1ß (IL-1ß) inhibitor on homologous recombination deficiency (HRD)-proficient ovarian cancer cells. Methods: (1) HRD-proficient ovarian cancer cell lines OVCAR3 and CAOV3 were treated with PARP inhibitor olaparib. Screening by RNA sequencing analysis, the expression level of IL-1ß was validated by enzyme-linked immunosorbent assay (ELISA) and western blot. (2) The dose-response curves of IL-1ß inhibitor diacerein were evaluated by cell counting kit-8 (CCK-8) assays in OVCAR3 and CAOV3 cells. CCK-8 assays were further applied to determine the viabilities of OVCAR3 and CAOV3 cells. (3) To evaluate the synergistic effects of olaparib and IL-1ß inhibitor in vivo, the transplanted ovarian cancer model was constructed. BALB/c-nude mice (n=16) were injected intraperitoneally with 1×107 OVACR3 cells labelled with luciferase (OVCAR3-Luc). Immunohistochemistry (IHC) assay was performed to determine nuclear antigen associated with cell proliferation (Ki-67) expression. (4) Blood routine tests, kidney and liver function tests were performed to analyze the toxic reaction of different drug treatments. The potential drug-induced injuries of vital organs including heart, liver, spleen, lungs and kidneys of nude mice were determined by hematoxylin-eosin (HE) staining. Results: (1) The RNA sequencing results showed that the mRNA level of IL-1ß was the most significantly increased among the 25 differentially expressed genes in OVCAR3 cells treated with olaparib, compared to the negative control group. Olaparib treatment significantly promoted the secretion and expression of IL-1ß protein in both OVACR3 and CAOV3 cells by ELISA [(36.2±3.5) and (49.5±3.5) pg/ml, respectively; all P<0.001] and western bolt (2.87±0.37 and 2.05±0.08, respectively; all P<0.01). (2) The half maximal inhibitory concentration (IC50) value of IL-1ß inhibitor was determined as follows: 75 µmol/L for OVACR3 cells and 100 µmol/L for CAOV3 cells. The treatments were divided into four groups including control group, olaparib monotherapy group, IL-1ß inhibitor monotherapy group and the combination therapy group. The cell viabilities of each group in OVCAR3 and CAOV3 were determined by CCK-8 assay. The data in each group were showed as follows for OVCAR3 and CAOV3 cells: (100.0±0.4)% and (100.0±3.5)% in control group; (63.1±6.2)% and (63.3±3.8)% in olaparib monotherapy group; (61.6±4.7)% and (63.8±3.5)% in IL-1ß inhibitor monotherapy group; and (32.9±5.2)% and (30.0±1.3)% in the combination therapy group. The viability assay showed that the combined strategy exhibited a significant inhibition effect on OVACR3 and CAOV3 cells, compared to the monotherapy group and the control group (all P<0.01). (3) All mice with transplanted tumors of HRD-proficient ovarian cancer cells were randomly divided into four groups, and treated with four different treatments as mentioned above, respectively. After 4 weeks (on day 29), the vivo fluorescence imaging were determined. The results showed that the amount of fluorescence of transplanted tumors was mostly decreased in the combination therapy group [(0.5±0.4)×1010 p/s], compared to the control group [(4.2±1.0)×1010 p/s] or the groups treated with any single drug [(3.1±0.9)×1010, (2.2±0.9)×1010 p/s; all P<0.05]. Mice were then sacrificed under anesthesia, and all transplanted tumors detached and weighed for further investigation. The weight of transplanted tumors was significantly decreased in the combination therapy group [(0.09±0.03) g], compared to that in control group [(0.25±0.05) g] or groups treated with any single drug [(0.17±0.03), (0.19±0.04) g; all P<0.05]. The measurement of the expression of Ki-67 showed that it was significantly decreased in the combination therapy group (0.33±0.10), compared to that in the control group (1.00±0.20) or monotherapy groups (0.76±0.07, 0.77±0.12; all P<0.05). (4) There were no significant differences of body weights, blood routine test, renal and liver function tests among mice with different treatments (all P>0.05). Moreover, no significant injuries were observed in the vital organs among the four groups. Conclusions: The combination of olaparib and IL-1ß inhibitor synergistically exhibits significant cytotoxicity in HRD-proficient ovarian cancer cells. Moreover, the blood routine and blood biochemistry results confirmed the biosafety of the combination of olaparib and IL-1ß inhibitor.

[Research advances on exosomes derived from adipose-derived mesenchymal stem cells in promoting diabetic wound healing].

Impaired healing of diabetic wounds is mainly attributed to its pathological mechanism, and refractory diabetic wounds bring heavy burdens to patients and society. Exosomes derived from stem cells possess the similar ability as stem cells in promoting tissue regeneration and more clinical advantages and are gradually playing important roles in wound healing. In recent years, researches have shown that exosomes derived from adipose-derived mesenchymal stem cells (ADSC-EXOs) can promote the healing of diabetic wounds by participating in various processes of wound healing. This article reviews the pathological mechanism leading to impaired healing of diabetic wounds, the related mechanism and the application prospect of ADSC-EXOs in promoting diabetic wound healing.

Histopathology-Based Diagnosis of Oral Squamous Cell Carcinoma Using Deep Learning.

Oral squamous cell carcinoma (OSCC) is prevalent around the world and is associated with poor prognosis. OSCC is typically diagnosed from tissue biopsy sections by pathologists who rely on their empirical experience. Deep learning models may improve the accuracy and speed of image classification, thus reducing human error and workload. Here we developed a custom-made deep learning model to assist pathologists in detecting OSCC from histopathology images. We collected and analyzed a total of 2,025 images, among which 1,925 images were included in the training set and 100 images were included in the testing set. Our model was able to automatically evaluate these images and arrive at a diagnosis with a sensitivity of 0.98, specificity of 0.92, positive predictive value of 0.924, negative predictive value of 0.978, and F1 score of 0.951. Using a subset of 100 images, we examined whether our model could improve the diagnostic performance of junior and senior pathologists. We found that junior pathologists were able to delineate OSCC in these images 6.26 min faster when assisted by the model than when working alone. When the clinicians were assisted by the model, their average F1 score improved from 0.9221 to 0.9566 in the case of junior pathologists and from 0.9361 to 0.9463 in the case of senior pathologists. Our findings indicate that deep learning can improve the accuracy and speed of OSCC diagnosis from histopathology images.

[Role of NF-κB p65 and related cytokines in rats with liver function injury induced by dibutyl phthalate and benzo (a) pyrene].

Objective: To explore the role of nuclear factor-κB (NF-κB) p65 and related cytokines in rats with liver function injury induced by dibutyl phthalate (DBP) and benzo (a) pyrene (BaP) , in order to provide support for enriching the mechanism of liver injury induced by DBP and BaP. Methods: In September to December of 2019, a total number of 160 specific pathogen free Sprague Dawley rats were numbered in order of sex and body weight, then using the statistical table of random numbers, they were randomly divided into eight groups and each group consists of twenty animals (10 male and 10 female rats) , including blank control group, vehicle control group (given corn oil) , DBP 50 mg/kg (DBP(50)) group, DBP 250 mg/kg (DBP(250)) group, BaP 1 mg/kg (BaP(1)) group, BaP 5 mg/kg (BaP(5)) group, DBP 50 mg/kg plus BaP 1 mg/kg (DBP(50)+BaP(1)) group and DBP 250 mg/kg plus BaP 5 mg/kg (DBP(250)+BaP(5)) group, then DBP and BaP were administered to rats as a homogenous mixture in corn oil by gavage. After exposure for 90 days, liver was separated to test the mRNA and protein expression levels of NF-κB p65 by Real-time fluorescence quantitative polymerase chain reaction and Western blotting. Then serum of rats was collected to detect the levels of CXCL-13, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) by Enzyme-Linked Immunosorbent Assay, and the levels of alanine aminotransferase (ALT) , aspartate aminotransferase (AST) , albumin (ALB) and total protein (TP) were detected by Reitman-Frankel assay. Results: The protein expression of NF-κB p65 in BaP(1) group was not statistically significant, but the mRNA and protein expression levels of NF-κB p65 in the liver tissues of rats in other exposure group were higher than those in the blank control group (P<0.05) , and the expression levels of NF-κB p65 increased more obvious in the DBP and BaP co-exposed groups than those in the low and high dose groups that single-exposed to DBP and BaP (P<0.05) . The serum levels of CXCL-13 and IL-6 of rats in other group were obviously higher than those of the blank control group except for the BaP(1) group, and the increase was more obvious in the high-dose group that co-exposed to DBP and BaP (P<0.05) . While the level of TNF-α in each exposure group was higher than those in the blank control group and the levels of TNF-α in the DBP and BaP co-exposed groups were strongly augmented compared to those in the low and high dose groups that single-exposed to DBP and BaP (P<0.05) . What's more, compared with the blank control group, the level of ALT in each exposure group was increased significantly. Except for the BaP(1) group, the levels of AST in other exposed groups were increased (P<0.05) , and the levels of ALT and AST in the DBP and BaP co-exposed groups were significantly elevated in comparison to the low and high dose groups that single-exposed to DBP and BaP (P<0.05) . On the contrary, the level of ALB in each exposure group was significantly lower than that in the blank control group, especially decreased significantly in the DBP and BaP co-exposed group (P<0.05) . The level of TP decreased only in the high-dose group that single and co-exposed to DBP and BaP, and the decrease was more significant in the DBP and BaP co-exposed group (P<0.05) . When DBP exposed alone, Pearson correlation analysis showed that NF-κB p65 protein expression level was positively correlated with IL-6, TNF-α and ALT (r=0.762, 0.951, and 0.924, P<0.05) . After BaP exposed alone, the NF-κB p65 protein expression level was positively correlated with TNF-α and ALT (r=0.911 and 0.910, P<0.05) . When DBP and BaP exposed together, NF-κB p65 protein expression level was positively correlated with CXCL-13, IL-6, TNF-α, ALT and AST (r=0.711, 0.764, 0.955, 0.903 and 0.827, P<0.05) . In addition, Pearson correlation analysis showed a positive correlation between TNF-α and ALT (r=0.833 and 0.894, P<0.05) when DBP or BaP exposed alone. Furthermore, when DBP and BaP exposed together, CXCL-13, IL-6 and TNF-α were positively correlated with ALT (r= 0.871, 0.925 and 0.942, P<0.05) , and also positively correlated with AST (r=0.910, 0.892 and 0.890, P<0.05) . Conclusion: Single and co-exposed to DBP and BaP may regulate the abnormal secretion of related cytokines by upregulating the expression level of NF-κB p65 in rat liver tissue, thus leading to hepatocyte injury in rats, and the damage effect may be enhanced when DBP and BaP are exposed together.

Arsenite induces dysfunction of regulatory T cells through acetylation control of the Foxp3 promoter.

Arsenic is known to cause damage to the body's immune system by inducing epigenetic changes. However, the molecular mechanism of this damage remains elusive. Here, we report that arsenic disrupts the morphology of lymphocytes, decreases cell viability, and results in abnormal proportions of T lymphocyte subsets. Moreover, our results revealed that arsenic can reduce global acetylation of histone H4 at K16 (H4K16 ac) in lymphocytes via decreasing the level of males absent on the first but upregulates mRNA and protein levels of the forkhead/winged-helix box P3 (Foxp3) gene by increasing the acetylation of histone H4 at K16 (H4K16) at the promoter of Foxp3. Finally, arsenic-induced dysfunction of regulatory T cells (Tregs) could be ameliorated by trichostatin A. Our research indicates that arsenic-induced immunosuppressive effect in human lymphocytes may be related to the acetylation of H4K16 at the promoter of Foxp3 and that histone deacetylase inhibitors may play a role in the prevention and treatment of immune injury caused by arsenic.

Effect of appetite-conditioned reflex stimulation on early enteral nutrition tolerance after surgery.

OBJECTIVE: This study aimed to discuss the effects of appetite-conditioned reflex stimulation on the early enteral nutrition (EEN) tolerance, complications, and postoperative hospital stay in patients who underwent surgery. METHODS: Seventy patients who underwent laparoscopic radical resection of colorectal cancer surgery in our hospital between February and December 2017 were randomly divided into a stimulated appetite group (experimental group, including visual stimulation, nasal stimulation, taste stimulation and hearing stimulation) and a control group (n = 35). Both groups received EEN. EEN tolerance, complications, and postoperative hospital stay were then compared between the groups. RESULTS: Sixty-six patients, including 34 in the experimental group and 32 in the control group, completed the relevant experiment. The experimental group had significantly lower incidence rates of nausea, vomiting, bloating, use of prokinetic drugs, and gastric tube replacement (P < 0.05), and shorter tolerable regular eating time (5.0 ± 1.0 d vs 6.4 ± 1.9 d, P < 0.05) and postoperative hospital stay (7.0 ± 2.0 d vs 8.0 ± 1.8 d, P < 0.05) than the control group. No significant difference in complication rate was detected (P > 0.05). CONCLUSION: Appetite-conditioned reflex stimulation can improve EEN tolerance, decrease the risk of complications, and shorten ordinary diet recovery time and hospital stay.

CDCA2 promotes proliferation and migration of melanoma by upregulating CCAD1.

OBJECTIVE: This study aims at investigating the functional role of CDCA2 (cell division cycle associated 2) in enhancing proliferative and migratory abilities in melanoma by upregulating CCAD1, thus aggravating the progression of melanoma. PATIENTS AND METHODS: CDCA2 levels in melanoma tissues and cell lines were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. Regulatory effects of CDCA2 on proliferative and migratory abilities in melanoma cells were assessed by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU), and wound healing assay, respectively. At last, rescue experiments were conducted to explore the involvement of CCAD1 in CDCA2-regulated progression of melanoma. RESULTS: CDCA2 was upregulated in melanoma tissues, especially in those with metastasis. Identically, in vitro level of CDCA2 was upregulated in melanoma cell lines. The knockdown of CDCA2 in A375 and sk-mel-110 cells inhibited the proliferative and migratory abilities. The overexpression of CCAD1 could partially abolish the inhibitory effects of silenced CDCA2 on proliferative and migratory abilities in melanoma. CONCLUSIONS: CDCA2 stimulates proliferative and migratory abilities in melanoma cells by upregulating CCAD1, thus aggravating the malignant progression of melanoma.

Risk factors for disease progression in patients with mild to moderate coronavirus disease 2019-a multi-centre observational study.

OBJECTIVES: Since December 2019, the novel coronavirus disease 2019 (COVID-19) that emerged in Wuhan city has spread rapidly around the world. The risk for poor outcome dramatically increases once a patient progresses to the severe or critical stage. The present study aims to investigate the risk factors for disease progression in individuals with mild to moderate COVID-19. METHODS: We conducted a cohort study that included 1007 individuals with mild to moderate COVID-19 from three hospitals in Wuhan. Clinical characteristics and baseline laboratory findings were collected. Patients were followed up for 28 days for observation of disease progression. The end point was the progression to a more severe disease stage. RESULTS: During a follow up of 28 days, 720 patients (71.50%) had recovered or were symptomatically stable, 222 patients (22.05%) had progressed to severe disease, 22 patients (2.18%) had progressed to the critically ill stage and 43 patients (4.27%) had died. Multivariate Cox proportional hazards models identified that increased age (hazard ratio (HR) 2.56, 95% CI 1.97-3.33), male sex (HR 1.79, 95% CI 1.41-2.28), presence of hypertension (HR 1.44, 95% CI 1.11-1.88), diabetes (HR 1.82, 95% CI 1.35-2.44), chronic obstructive pulmonary disease (HR 2.01, 95% CI 1.38-2.93) and coronary artery disease (HR 1.83, 95% CI 1.26-2.66) were risk factors for disease progression. History of smoking was protective against disease progression (HR 0.56, 95% CI 0.34-0.91). Elevated procalcitonin (HR 1.72, 95% CI 1.02-2.90), urea nitrogen (HR 1.72, 95% CI 1.21-2.43), α-hydroxybutyrate dehydrogenase (HR 3.02, 95% CI 1.26-7.21) and D-dimer (HR 2.01, 95% CI 1.12-3.58) at baseline were also associated with risk for disease progression. CONCLUSIONS: This study identified a panel of risk factors for disease progression in individuals with mild to moderate COVID-19.

The role of quinazoline in ameliorating intervertebral disc degeneration by inhibiting oxidative stress and anti-inflammation via NF-κB/MAPKs signaling pathway.

OBJECTIVE: Previous studies have shown that Quinazoline (QNZ) plays extremely important roles in the cellular physiological activity, but it has been rarely examined on cell behavior following intervertebral disc degeneration (IVDD). The aim of this study was to investigate whether QNZ mediates oxidative stress and inflammation contributed to IL-1ß-induced nucleus pulposus (NP) cells degeneration in vitro. PATIENTS AND METHODS: NP were isolated cells from human disc samples collected from patients and the IL-1ß-induced NP cells degenerated model was constructed. The cells were randomly divided into 3 groups, namely, Control group, IL-1ß group (10 µM), QNZ + IL-1ß group (containing 10 nM QNZ and 10 µM IL-1ß). Then, the cell viability was determined by CCK-8 assay, and the levels of collagen I, collagen II, aggrecan, p16, p53, ß-galactosidase (ß-gal), antioxidant enzymes, 8-hydroxy-2-deoxyguanosine (8-OHdG), NF-κB/MAPKs signaling-related proteins and inflammatory factors were examined using Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in NP cells. Finally, the expressions of IL-1ß, IL-6, and TNF-α in the cell supernatants were also determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: This study showed that IL-1ß promoted the progress of IDD, with markedly increased expressions of collagen I, p16, p53, and ß-gal, as well as decreased expressions of collagen II and aggrecan. However, QNZ treatment could reverse the effects of IL-1ß. It was found that cell proliferation was increased, ROS level was decreased, antioxidant enzymes were upregulated, and inflammatory factors were reduced after QNZ stimulation. Moreover, NF-κB/MAPKs signaling proteins IKKß, IκBα, p65, ERK, JNK, and p38 were significantly dephosphorylated by QNZ. CONCLUSIONS: These results indicated that QNZ prevented NP degradation via restraining oxidative stress and inflammation through inhibition of the NF-κB/MAPKs signaling pathway. QNZ may become a novel insight into the therapy of IVDD in the future.

[New research advances and clinical treatment of scar].

Scar formation is the abnormal healing process of skin after being damaged. The mechanism of scar formation is not clear, and many studies have shown that it is affected by many factors. Based on the over deposition of collagen in scars, many researchers have carried out studies on the mechanism, pathological manifestation, and treatment method of scars. In the treatment aspect of scar, the combination of traditional and new treatment methods has been well accepted and achieved good results. To understand the new advances of scar research and combine it with clinical treatment transformation could lead to the development of more effective prophylactic and therapeutic strategies for scar treatment in the future.

[Advances in the research of autologous fat grafting in the prevention and treatment of scar].

Scars formed by various injuries can affect the appearance and psychology of patients. Therefore, more and more people pay attention to the prevention and treatment of scar. With the development of the autologous fat grafting, it has been gradually applied to the prevention and treatment of scar. At present, it has been confirmed by scholars that the autologous fat grafting could be an effective method to prevent and treat scar from basic research and clinical practice. At the same time, the deficiency of autologous fat grafting in the prevention and treatment of scar was also pointed out. This paper reviews the application, mechanism, and deficiency of autologous fat grafting in scar prevention and treatment.

[Effect of RKIP on proliferation and migration of malignant melanoma cells and potential mechanism].

Objective: To explore the effect and mechanism of Rafkinase inhibitor protein (RKIP) on proliferation and migration of malignant melanoma cells in vitro. Methods: The RKIP overexpression and down-regulated stable transfected strains of mouse malignant melanoma cell line B16 were constructed by recombinant lentiviral transfection technique and established as RKIP overexpression group and RKIP down-regulation group, the mouse malignant melanoma B16 cells without any treatment were used as a blank control group, and the proliferation activity and migration ability of each group were detected by cell counting kit-8 (CCK-8) and cell scratch test. The relative expression levels of CyclinD1, Calcium-dependent cell adhesin, Ki-67, Matrix metalloproteinase (MMP)-9, MMP-13, MMP-2 and Phosphatidylethanolamine binding protein (PEBP-1) were detected by quantitative real-time polymerase chain reaction (qPCR). Western blot was used to detect the difference of RKIP expression and the protein expression level of nuclear factor-kappa B (NF-κB) signaling pathway in each group. Results: Comparison of RKIP overexpression group and blank control group shown cell proliferation and migration were significantly inhibited in RKIP overexpression group (0.794±0.038 vs 1.200±0.081) (P<0.001). However, there was no significant difference in cell proliferation between RKIP down-regulation group and blank control group (1.077±0.084 vs 1.200±0.081) (P>0.05), and the cell migration ability of RKIP down-regulation group was significantly higher than that of the blank control group (P<0.001). In addition, there was no significant difference between the RKIP down-regulation group and the blank control group in PEBP-1 expression (P>0.05), while the expression levels of the remaining genes in the RKIP overexpression group were significantly lower than those in the blank control group, and the expression levels in the RKIP down-regulation group were significantly higher than those in the blank control group (P<0.001). Furthermore, the protein level of phosphorylated P65 (p-P65) in RKIP overexpression group was significantly lower than that in blank control group (0.080±0.000 vs 0.236±0.000), and RKIP down-regulation group was significantly higher than that in blank control group (1.139±0.001 vs 0.236±0.000) (both P<0.001). Conclusion: RKIP overexpression can inhibit the proliferation and migration of malignant melanoma cells, which may be related to the regulation of NF-κB signaling pathway-related protein p-P65.

[Review of 60 years' development of Department of Burns and Plastic Surgery in West China Hospital of Sichuan University].

Burn medicine of China started in 1958. Over the past 60 years, through the efforts of numerous burn discipline scholars, China's burn clinical and scientific research have reached the world's advanced level. Department of Burns and Plastics Surgery of West China Hospital of Sichuan University was founded in 1963. Department of Burns of our hospital was established earlier in China. In the past 60 years, professor Yu Baoliang, Ren Linsen, and Cen Ying had been working hard for the development of our department. Department of Burns and Plastic Surgery in West China Hospital of Sichuan University has developed from a pure therapeutic specialty group into one of the burn centers with strong technical force, first-class medical level, advanced instruments and equipment, rich scientific research achievements, and integrated medicine, teaching, and research in southwestern China, which enjoys high prestige at home and abroad.

[Advances in the research of effects of heat-shock factor 1 and heat-shock proteins on wound healing and the mechanism].

Heat-shock proteins (HSPs) are the protective proteins expressed by cells under stress. Heat-shock factors (HSFs) are the key factors to regulate HSPs. Researches about the effects of HSF1 and HSPs in cells after stress and the mechanism have become the important entry point to explore the cell response in wound healing after trauma. This article reviews the effects of HSPs and HSF1 which regulate the proteins on wound healing and the mechanism, so as to deliver message for studying effects of intervening HSF1 on expression of HSPs and wound healing and the mechanism.

[Integrated diagnosis and treatment of scar].

Scar is the common disease in the field of burn and plastic surgery, and its diagnosis and treatment should be involved in overwhelming majority hospitals. There are many substandard methods and medical hidden dangers in diagnosis and treatment of scar, due to the unevenness of doctors' clinical experience. According to the classification of integral scar and diabrotic scar, the problems related to diagnosis and treatment of scar are systemically summarized and normalized in this article for decrease in the incidence of adverse events and medical hidden dangers.

[Study of the correlation between the expression of angiotensin â ¡ and its receptors and collagen deposition in human keloid].

Objective: To study the correlation between the expression of angiotensin Ⅱ, angiotensin Ⅱ type 1 receptor (AT1R), angiotensin Ⅱ type 2 receptor (AT2R) and collagen deposition in human keloid. Methods: The keloid from 19 keloid patients and normal skin from 13 patients performed with free skin transplantation hospitalized in our unit from May 2014 to January 2015 were obtained. The expressions of angiotensin Ⅱ, AT1R, and AT2R were detected by immunohistochemical staining, and the results were semi-quantitatively analyzed by immunohistochemical scoring. The expression of collagen in keloid was detected by picrosirius-red staining, and the percentage of total collagen was calculated. Data were processed with t test. The expressions of angiotensin Ⅱ, AT1R, AT2R and the total content of collagen of 13 keloid patients were analyzed by Pearson correlation analysis. Results: (1) There was negative or probably positive expression of angiotensin Ⅱ in normal skin tissue, mainly distributed in the epidermal basal layer. The expression of angiotensin Ⅱ was strong in keloid, most distributed in spinous layer and basal layer of epidermis and most region of dermis, and was strongly positive in most cells, and most cells were fibroblasts. The expressions of AT1R and AT2R were similar to angiotensin Ⅱ in two types of tissue. The expressions of angiotensin Ⅱ, AT1R, and AT2R in keloid scored (305±34), (281±32), and (285±25) points, respectively, which were significantly higher than those in normal tissue [respectively (54±17), (89±47), and (97±32) points, with t values from 12.03 to 23.21, P values below 0.01]. (2) The total content of collagen in keloid was (88±4)%. There was a lot of thick and dense type Ⅰcollagen in keloid, with massive structure and distributed like bamboo segment and arranged in disorder. The expression of type Ⅲ collagen was increased, which was distributed scatteredly around type Ⅰcollagen. (3) There were positive correlations between the expressions of angiotensin Ⅱ, AT1R, AT2R and the total content of collagen in keloid (with r values from 0.452 to 0.720, P values below 0.05). Conclusions: The expressions of angiotensin Ⅱ, AT1R, and AT2R were abnormally increased in human keloid, which may play an important role in the collagen deposition of keloid.

[Investigation on events of bus on fire in 6 years in the mainland of China].

Objective: To retrospectively analyze the characteristics of events of bus on fire in 6 years in the mainland of China. Methods: Events of bus on fire happened between January 2009 and December 2014 were retrieved through Baidu search engine, Chinese Journals Full-text Database, and PubMed database in the search strategy with " bus" and " fire" or " arson" as keywords combined with the name of provinces, autonomous regions, and municipalities of the mainland of China. The occurrence time, region, cause of fire, casualties of each event were recorded, and the correlative analysis was conducted. Data were processed with Microsoft Excel software. Results: Totally 287 events of bus on fire were retrieved, among which 49 events happened in 2009, 36 events happened in 2010, 35 events happened in 2011, 37 events happened in 2012, and respectively 65 events happened in 2013 and 2014. The events of bus on fire most frequently happened in June and July, respectively 49 and 39 events. Among the distribution of occurrence regions of events of bus on fire, there were 78 events (27.18%) in east China, 52 events (18.12%) in northeast China, 41 events (14.29%) both in north China and south China. Among the causes of events of bus on fire, spontaneous combustion of bus ranked in the first (267 events, accounting for 93.03%), followed by arson (13 events, accounting for 4.53%). Among the 13 events of bus on fire caused by arson, 7 events happened between 16: 00 and 20: 00, and 3 events happened between 8: 00 and 10: 00. Totally 27 events of bus on fire (9.41%) were with casualties, among which 13 events (48.15%) were caused by spontaneous combustion of bus, 10 events (37.04%) were caused by arson, and 4 events (14.81%) were caused by traffic accidents. Arson caused the most severe casualties (at least 88 deaths and 287 injuries), followed by spontaneous combustion of bus (at least 35 deaths and 140 injuries) and traffic accidents (at least 9 deaths and 20 injuries). Conclusions: Events of bus on fire happened more frequently in recent years in the mainland of China, and the frequencies were much higher especially in June and July. Most events were caused by spontaneous combustion of bus, followed by arson. Most of the events of bus on fire caused by arson happened in the morning and evening rush hours of urban traffic, and althouth the occurrence rate was not high, the casualties were most severe.

Agonistic 4-1BB antibody fails to reduce disease burden during acute respiratory syncytial virus (RSV) infection.

Respiratory Syncytial Virus (RSV) remains a leading cause of infant morbidity and mortality worldwide. Despite this, there are limited therapeutic options. CD8 T cells have an integral role in controlling viral infections; strategies to enhance these responses may be clinically relevant. The T cell costimulatory receptor, 4-1BB, is known to play a role in expansion of antiviral CD8 T cells. In this study, we examined the effect of agonistic 4-1BB antibody at the time of RSV infection in mice. We show that this antibody did not improve outcomes in the setting of RSV infection but rather, led to increased weight loss and a reduction in RSV specific CD8 T cells in the lung. This work suggests caution in the use of agonistic 4-1BB antibody in the setting of viral infections.

Whole-Genome Sequence of "Candidatus Profftella armatura" from Diaphorina citri in Guangdong, China.

The genome of "Candidatus Profftella armatura" strain YCPA from Diaphorina citri in Guangdong, China, was sequenced. The strain has a chromosome of 457,565 bp, 24.3% G+C content, 364 predicted open reading frames (ORFs), and 38 RNAs, and a plasmid, pYCPA54, of 5,458 bp with 23.9% G+C content and 5 ORFs.