[Establishment of a topographic map assessment system for facial and cervical wounds and scars of burn patients based on the Delphi method].

Objective: To construct a targeted and accurate evaluation system for facial and cervical wounds and scars of burn patients. Methods: The method combining literature analysis and survey research was adopted, and the basic principles of item system construction were followed. From June to August 2020, based on the aesthetic standards of facial and cervical plastic surgery, the topographic map assessment system for facial and cervical wounds and scars of burn patients was preliminarily formed, focusing on the assessment of wounds and scars in the necks and faces of patients after burns. In September 2020, 38 experts in the relevant fields were consulted in advance and the questionnaire was revised according to the experts' opinions. From December 2020 to March 2021, the Delphi method was applied to conduct inquiry by correspondence with 35 experts in relevant fields from Guangzhou, Shenzhen, Shanghai, Beijing, and other cities, who met the inclusion criteria, and the items were screened and established. The effective recovery rate of inquiry questionnaire was calculated to determine the level of enthusiasm of experts, the average authority coefficient of all items was calculated to determine the level of expert authority, the average importance expert score, the average coefficient of variation, and the average full score rate of all the third-level items were calculated to determine the concentration of expert opinions, the average coefficients of variation and Kendall's harmony coefficients of the importance, sensitivity, and operability expert scores of all the third-level items were calculated to determine the degree of coordination of expert opinions. The Kendall's harmony coefficients for the importance, sensitivity, and operability expert scores of all the third-level items were statistically analyzed with chi-square test. Results: Among the 35 experts consulted by Delphi method, mainly were male, aged (48±10) years, with 8-38 years of working experience, mainly with associate senior titles and above, all with a bachelor's degree or above education background, and of whom 11 were burn experts, 7 were wound repair experts, 4 were plastic surgery experts, and 13 were rehabilitation medicine experts. Finally, a topographic map assessment system for facial and cervical wounds and scars of burn patients was formed, including 4 first-level items, 21 second-level items, 40 third-level items, and 1 mask. The effective recovery rate of inquiry questionnaire was 100% (35/35). The average authority coefficient of all items was 0.89. The average importance expert score was 4.67, the average coefficient of variation of importance expert score was 0.01, and the average full score rate of all the third-level items was 86.3%. The average coefficients of variation of the importance, sensitivity, and operability expert scores of all the third-level items were 0.01, 0.01, and 0.02, respectively. The Kendall's harmony coefficients for the importance, sensitivity, and operability expert scores of all the third-level items were statistically significant (with χ2 values of 1 201.53, 745.67, and 707.07, respectively, P<0.05). Conclusions: The established topographic map assessment system for facial and cervical wounds and scars of burn patients has high scientificity and reliability, which can be used for the evaluation of facial and neck wounds or scars in burn patients.

[Analysis of the clinical characteristics and therapeutic effect of refractory juvenile dermatomyositis to tofacitinib].

Objective: To elucidate the clinical features of patients with refractory juvenile dermatomyositis (JDM), and to explore the efficacy and safety of tofacitinib in the treatment of refractory JDM. Methods: A total of 75 JDM patients admitted to the Department of Rheumatology and Immunology in Shenzhen Children's Hospital from January 2012 to January 2021 were retrospectively analyzed, and to analyze the clinical manifestations, efficacy and safety of tofacitinib in the treatment of refractory JDM. Patients were divided into refractory group with using of glucocorticoids in combination with two or more anti-rheumatic drugs for treatment, and the presence of disease activity or steroid dependence after a one-year follow-up. The non-refractory group is defined as clinical symptoms disappeared, laboratory indicators were normal, and clinical remission was achieved after initial treatment, and the clinical manifestations and laboratory indexes of the two groups were compared. The Mann-Whitney U test, Fisher's precision probability test was used for intergroup comparison. Binary Logistic multivariate regression analysis was used to identify risk factors for refractory JDM. Results: Among the 75 children with JDM, 41 were males and 34 were females with a age of onset of 5.3 (2.3, 7.8) years. The refractory group consisted of 27 cases with a age of onset of 4.4 (1.5, 6.8) years, while the non-refractory group consisted of 48 cases with a age of onset of 5.9 (2.5, 8.0) years. Compared with 48 cases in the non-refractory group, the proportion of interstitial lesions and calcinosis in the refractory group was higher than that in the non-refractory group (6 cases (22%) vs. 2 cases (4%), 8 cases (30%) vs. 4 cases (8%), both P<0.05). Binary Logistic regression analysis showed that observation group were more likely to be associated with to interstitial lung disease (OR=6.57, 95%CI 1.22-35.31, P=0.028) and calcinosis (OR=4.63, 95%CI 1.24-17.25, P=0.022). Among the 27 patients in the refractory group, 22 cases were treated with tofacitinib, after treatment with tofacitinib, 15 of 19 cases (86%) children with rashes showed improvement, and 6 cases (27%) with myositis evaluation table score less than 48 score both were improved, 3 of 6 cases (27%) had calcinosis were relieved, and 2 cases (9%) had glucocorticoid-dependence children were successfully weaned off. During the tofacitinib treatment, there was no increase in recurrent infection, blood lipids, liver enzymes, and creatinine were all normal in the 22 cases. Conclusions: Children with JDM with calcinosis and interstitial lung disease are more likely to develop refractory JDM. Tofacitinib is safe and effective for refractory JDM.

Curative effects of vancomycin and cefotaxime combined with gamma globulin respectively in neonatal septicemia and their influences on PCT, CRP and hs-CRP.

OBJECTIVE: To explore the curative effects of vancomycin and cefotaxime combined with gamma globulin respectively in neonatal septicemia and their influences on PCT, CRP, and hs-CRP, so as to provide references for clinical treatment. PATIENTS AND METHODS: 181 patients with neonatal septicemia admitted to Huangshi Maternity and Child Health Hospital from April 2012 to August 2014 were selected as the study subjects. Patients treated with vancomycin combined with gamma globulin were selected as group A (96 cases) and those treated with cefotaxime combined with gamma globulin were selected as group B (85 cases). The improvement time of clinical symptoms (milk rejection, nervous system symptoms, body temperature), hospital stays, mortality, medicine curative effects, adverse reactions, complications, and levels of serum CRP, PCT, and hs-CRP of patients before and after treatment were compared between the two groups. RESULTS: The improvement time of clinical symptoms like body temperature, milk rejection, and neurological symptoms, as well as hospital stays in group A were lower than those in group B (p<0.05); the total effective rate of medicine curative effects in group B was better than that in group A (p<0.05); there was no significant difference in levels of serum CRP, PCT, and hs-CRP between the two groups before treatment (p>0.05); after treatment, levels of serum CRP, PCT, and hs-CRP in both groups decreased significantly, and levels of serum CRP, PCT, and hs-CRP in group B decreased more significantly than those in group A (p<0.05). CONCLUSIONS: Cefotaxime combined with gamma globulin in the treatment of patients with neonatal septicemia has short improvement time in clinical symptoms, high total effective rate of drugs, low mortality, fewer adverse reactions and complications, and can significantly reduce levels of serum CRP, PCT, and hs-CRP, which is worthy of further promotion and application in clinical practice.

Association of host genetics with intestinal microbial relevant to body weight in a chicken F2 resource population.

Host-microbiota interactions describe a co-evolution and mutualistic symbiosis. Gut microbial communities are important for diverse host functions. However, in birds, the relationship between the composition of the intestinal microbiota and the genetic variation of the host is not clearly understood. To dissect these interactions, a Chinese yellow broiler line (genetically selected for a high growth rate) and Huiyang Beard chickens (low growth rate) were crossed, generating an F2 population. The population structures of the gut microbes in the phenotypically high and low 91-d body weight individuals of both sexes in the F2 population were studied. Interestingly, a non-metric multidimensional scaling analysis revealed that the microbiota of the high-weight and low-weight females was clearly separated into 2 clusters. A ß-diversity analysis showed that the locus rs16775833 within the doublesex and mab-3-related transcription factor (DMRT) gene cluster accounted for approximately 21% of the variation in the population structure of the gut microbiota. Furthermore, the 2 genetic loci rs15142709 and rs15142674 were significantly associated with specific species of Methanobacterium. These loci are located in the pleiomorphic adenoma gene 1 (PLAG1) and lck/yes-related novel tyrosine kinase (LYN) genes, which are involved in cell differentiation and growth. This finding suggests evidence for the influence of the host genetics on the composition of the gut microbiota in birds and the importance and utility of the host-microbe status to better understand its effect on the potential growth of birds.

[Association between hematocrit and risk of incident hypertension: a cohort study].

Objective: To explore the association between hematocrit level and risk of incident hypertension. Method: Subjects who participated at least two times routine health check-up in Health Management Center of Shandong Province Hospital between January 2005 and January 2010 were eligible for inclusion. After excluding participants with known hypertension and other related diseases, a prospective cohort with 20 606 subjects (female: 8 218, male: 12 388) was established. Cox-proportional hazard model was used to assess the association between hematocrit and the development of hypertension for female and male respectively. Results: During the 51 352 person-years of follow-up, newly developed hypertension was confirmed in 3 695 cases. For female, the age-adjusted hazard ratios (95%CI) for incident hypertension were 1.00 (reference), 1.06(0.86-1.29), 1.37(1.14-1.65), 1.60(1.34-1.92), respectively (P for trend<0.000 1) through the 3 quartiles of hematocrit levels.After adjusting multiple factors (age, smoking, drinking habit, physical activity, body mass index(BMI), systolic blood pressure, fasting blood glucose, serum creatinine, high-density lipoprotein, gamma-glutamyl transferase, white blood count), the hazard ratios (95%CI) were 1.00(reference), 1.05(0.85-1.29), 1.25(1.03-1.51), and 1.22(1.00-1.48), respectively (P for trend=0.016 9). For male, the hazard ratio (the highest vs. the lowest hematocrit level) after adjusting age or age and life style factors (smoking, drinking habit, physical activity) was 1.23 (1.11-1.37), 1.21(1.09-1.35), respectively. Other analyses of relationship hematocrit with incident hypertension were not statistically significant in male. Conclusions: Higher hematocrit level is associated with higher risk of incident hypertension, especially in female.

Propofol suppresses invasion and induces apoptosis of osteosarcoma cell in vitro via downregulation of TGF-ß1 expression.

OBJECTIVE: Osteosarcoma (OS) is the most common malignant tumor of the bone, with a high mortality rate and poor prognosis. Propofol has been proposed to play a role of antitumor in various cancers. However, the functions and mechanisms of propofol in OS is still not clear. MATERIALS AND METHODS: The different concentrations of propofol were co-incubated with osteosarcoma MG-63 lines for 72 hrs. Cell proliferation, apoptosis, and invasion were detected by MTT assay, Flow cytometry analysis, and Matrigel invasion assay. Western blot was used to detect the TGF-ß1 protein levels. MG-63 cells were treated with human recombinant TGF-ß1 (rh TGF-ß1) to assess the role of TGF-ß1 in propofol-induced anti-tumor activity. RESULTS: Propofol significantly inhibited cell proliferation and invasion and promoted apoptosis of MG-63 lines cells. Propofol also efficiently reduced TGF-ß1 expression. Moreover, restoration of TGF-ß1 by rhTGF-ß1 treatment reversed the effects of propofol on the biological behavior of OS cells. CONCLUSIONS: Propofol can effectively inhibit proliferation and invasion and induce apoptosis of OS cells through, at least partly, downregulation of TGF-ß1 expression.

Propofol suppresses invasion, angiogenesis and survival of EC-1 cells in vitro by regulation of S100A4 expression.

OBJECTIVE: Propofol possess anticancer properties in several cancers. In the present study, we investigate the effect of propofol on the human esophageal squamous cell carcinomas (ESCC) EC-1 cells in vitro and its molecular mechanisms of action. MATERIALS AND METHODS: EC-1 cells were explored to 10-100 µmol/L propofol for 72 h or 100 µmol/L/mL propofol for 24-72 h. EC-1 cells were explored to 100 µmol/L propofol for 24 h, then was transiently transfected into PcDNA3.1-S100A4 cDNA or PcDNA3.1 plasmid for 48 hrs. MTT, TUNEL, ELISA, migration, tube formation and immunoblotting were analized. RESULTS: Propofol inhibits invasion, angiogenesis, proliferation and induces apoptosis in a dose and time-dependence manner, followed by deseased S100A4 expression by Western blot assay. Pre-transfection of PcDNA3.1-S100A4 cDNA inhibits propofol-induced apoptosis and promotes invasion and angiogenesis in EC-1 cells in vitro. CONCLUSIONS: Propofol inhibited invasion, angiogenesis and induces apoptosis of human EC-1 cells in vitro through regulation of S100A4 expression. It not only can be an anesthesia agent, but also plays a important role of inhibiting the migration and angiogenesis of ESCC cells in the therapy of ESCC patients.

Propofol suppresses proliferation, invasion and angiogenesis by down-regulating ERK-VEGF/MMP-9 signaling in Eca-109 esophageal squamous cell carcinoma cells.

BACKGROUND AND AIMS: Propofol (2,6-diisopropylphenol), one of the most commonly used intravenous anaesthetic agents during cancer resection surgery, has been reported to have the ability of influencing the invasion of human cancer cells. However, the mechanisms are not very clear. In this study, we investigated the effects of propofol on the proliferation, invasion and angiogenesis of human Eca-109 cells, and explored the mechanism. METHODS: The human Eca-109 cells was treated with propofol at the concentrations of 10-100 µmol/L for 72 hours or at the concentration of 100 µmol for 8-72 hours. Cell viability was determined by the MTT assay; the effect of propofol on apoptosis by 5'-triphosphate-biotin nick end labeling (TUNEL) staining. The effect of propofol on angiogenesis was determined by the chicken chorioallantoic membrane (CAM) angiogenesis assay. The effect of propofol on cell invasion using a modified Matrigel Boyden chamber assay. ERK1/2, MMP-9 and VEGF leves was detected by western blotting assay. RESULTS: In human Eca-109 cells, propofol significantly promoted cell apoptosis and inhibited proliferation in a dose and time-dependent manner. Furthermore, propofol inhibited dose and time-dependent invasion and angiogenesis. Propofol significantly dose and time-dependently down-regulated gene expression and protein production of ERK/pERK, VEGF and MMP-9. The functional effects and MMP-9/VEGF inhibition were shown to be dependent on the ERK/VEGF and ERK/MMP-9 signaling pathways. It was noteworthy that the ERK activator (phorbol 12-myristate 13-acetate [PMA]) treatment increased the MMP-9/VEGF levels after propofol treatment, and led to significant increase of proliferation, invasion and angiogenesis. CONCLUSIONS: These findings indicate that propofol inhibited proliferation, invasion and angiogenesis of human Eca-109 cells in vitro through modulation of ERK-VEGF /MMP-9 signaling. Propofol not only can be an anesthesia agent which reduces pain but plays an important role of inhibiting the migration and angiogenesis of ESCC cells in the therapy of ESCC patients.

Prognostic significance of PUMA in pancreatic ductal adenocarcinoma.

OBJECTIVES: To investigate retrospectively whether alterations of p53 upregulated mediator of apoptosis (PUMA) protein levels and somatic mutations of the PUMA gene are characteristic of pancreatic ductal adenocarcinoma (PDAC). METHODS: Immunohistochemical analyses of PUMA were performed in pancreatic tumour tissue samples, and paired normal pancreatic tissue samples, from patients with PDAC. Apoptosis was detected using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling assay. RESULTS: A total of 70 patients with PDAC had samples available; 49 cases (70.0%) had high PUMA protein levels. PUMA was not detected in paired normal tissue samples. Significantly higher levels of PUMA protein were detected in low-grade tumours (tumour -node-metastasis stages I and II), compared with higher grade (stage III) tumours. Of the PDAC cases, the mean apoptosis index value for PUMA-positive specimens was significantly higher than that for PUMA-negative specimens. Overall survival was significantly associated with PUMA immunoreactivity. CONCLUSIONS: High levels of PUMA in PDAC tumour cells suggest that PUMA expression may play a role in pancreatic tumourigenesis.

Inducible expression of AML1-ETO fusion protein endows leukemic cells with susceptibility to extrinsic and intrinsic apoptosis.

AML1-ETO, a leukemia-associated fusion protein generated by the frequently occurred chromosome translocation t(8;21) in acute myeloid leukemia, was shown to exert dichotomous functions in leukemic cells, that is, growth arrest versus differentiation block. By the analysis of oligonucleotide microarray, AML1-ETO was shown to modulate the expressions of an impressive array of pro- and anti-apoptotic genes. Here, we investigate potential effects of the ecdysone inducible AML1-ETO expression on apoptosis of leukemic U937 cell line. We show that AML1-ETO significantly stabilizes death receptor Fas protein and increases proapoptotic Bak in addition to reducing Bcl-2 expression. Accordingly, inducible AML1-ETO expression is followed by apoptosis to a lower degree. Especially, AML1-ETO endows leukemic cells with the susceptibility to anti-Fas agonist antibody, ultraviolet light and camptothecin analog NSC606985-induced apoptosis with increased activation of caspase-3/8. Considering that apoptosis-enhancing effect of AML1-ETO would not be favorable to the leukemogenesis harboring the t(8;21) translocation, it must be overcome to fulfill their leukemogenic potential. Complementary to this prediction is that two AML1-ETO-carrying leukemic cells, Kasumi-1 and SKNO-1, present similar sensitivity to apoptosis induction with AML1-ETO-negative leukemic cells. Therefore, genetic and/or epigenetic screenings of apoptosis-related genes modulated by AML1-ETO deserve to be explored for understanding the mechanisms of AML1-ETO-induced leukemogenesis.