Objective:To investigate the effect of blue light combined with albumin treatment on heart, liver and nerve damage in neonatal jaundice.Methods:A total of 120 cases with neonatal jaundice in the Department of Pediatrics of Women's and Children's Hospital of Zhoushan from April 2017 to April 2018 were selected and divided into control group and observation group accorded to the random number method, with 60 cases in each group.The control group received blue light therapy.The observation group was given albumin treatment on the basis of the control group.The serum total bilirubin, bile acid, aspartate aminotransferase(AST), alanine aminotransferase(ALT), glutamyl transpeptidase(GGT), troponin(cTnT), creatine kinase isozyme(CK-MB), -hydroxybutyrate dehydrogenase(HBDH), myoglobin(MYO), S100B, neuron-specific enolase(NSE) and glial fibrillary acidic protein(GFAP) levels were determined.Results:Before treatment, there were no statistically significant differences in serum total bilirubin, bile acid, AST, ALT, GGT, cTnT, CK-MB, HBDH, MYO, S100B, NSE and GFAP levels between the two groups(all P>0.05). After treatment, the serum levels of total bilirubin[(142.67±13.02)μmol/L, (118.62±11.68)μmol/L], bile acid[(15.34±2.42)μmol/L, (7.83±2.07)μmol/L], AST[(32.17±6.34)U/L, (21.04±5.58)U/L], ALT[(25.83±4.16)U/L, (18.37±4.05)U/L], GGT[(55.24±6.37)U/L, (36.17±5.86)U/L], cTnT[(0.16±0.03)×10 -6μg/L, (0.09±0.02)×10 -6μg/L], CK-MB[(4.32±0.85)×10 -6U/L, (2.01±0.72)×10 -6U/L], HBDH[(213.04±43.61)U/L, (137.26±41.61)U/L], MYO[(22.15±3.64)×10 -6μg/L, (14.26±3.27)×10 -6μg/L], S100B[(1.41±0.28)×10 -9μg/L, (0.87±0.22)×10 -9μg/L], NSE[(15.29±2.12)×10 -9μg/L, (15.29±2.12)×10 -9μg/L] and GFAP[(19.34±0.96)×10 -9μg/L, (14.36±0.92)×10 -9μg/L] in the two groups were lower than those before treatment( t=5.214, 8.261; 7.216, 11.524; 4.027, 6.843; 3.248, 5.764; 7.129, 13.654; 6.524, 9.751; 6.854, 9.031; 4.026, 6.204; 4.521, 7.026; 4.276, 5.846; 4.812, 7.023; 7.062, 13.524, all P<0.05). The levels of serum total bilirubin, bile acid, AST, ALT, GGT, cTnT, CK-MB, HBDH, MYO, S100B, NSE and GFAP in the observation group were lower than those in the control group( t=10.651, 18.267, 10.208, 9.953, 17.066, 15.038, 16.063, 9.738, 12.490, 11.747, 17.157, 29.011, all P<0.05). Conclusion:Blue light combined with albumin treatment can alleviate heart, liver and nerve damage in neonatal jaundice.

BACKGROUND: Anlotinib is a newly developed small molecule multiple receptor tyrosine kinase (RTK) inhibitor that was approved for the treatment of patients with lung cancer in China. We aim to report 3 cases of rare complication of anlotinib-bronchial fistula (BF) during the treatment of lung cancer patients and summarize the possible causes. METHODS: We collected three patients who developed BF due to anlotinib treatment, and conducted a search of Medline and PubMed for medical literature published between 2018 and 2020 using the following search terms: "anlotinib," "lung cancer," and "fistula." RESULTS: Our literature search produced two case reports (three patients) which, in addition to our three patients. We collated the patients' clinical characteristics including demographic information, cancer type, imaging features, treatment received, risk factors for anlotinib related BF, and treatment-related outcomes. The six patients shared some common characteristics: advanced age, male, concurrent infection symptoms, diabetes mellitus (DM), advanced squamous cell and small cell lung cancers, centrally located tumors, tumor measuring ≥5 cm in longest diameter, and newly formed tumor cavitation after multi-line treatment especially after receiving radiotherapy. Fistula types included broncho-pericardial fistula, broncho-pleural fistula, and esophago-tracheobronchial fistula. Six patients all died within 6 months. CONCLUSIONS Although anlotinib is relatively safe, it is still necessary to pay attention to the occurrence of BF, a rare treatment side effect that threatens the quality of life and overall survival of patients. Anlotinib, therefore, requires selective use and close observation of high-risk patients.

PURPOSE: Details of patients hospitalized for asthma exacerbation in mainland China are lacking. To improve disease control and reduce economic burden, a large sample survey among this patient population is indispensable. This study aimed to investigate the clinical characteristics and outcomes of such patients.METHODS: A retrospective study was conducted on patients hospitalized for asthma exacerbation in 29 hospitals of 29 regions in mainland China during the period 2013 to 2014. Demographic features, pre-admission conditions, exacerbation details, and outcomes were summarized. Risk factors for exacerbation severity were analyzed.RESULTS: There were 3,240 asthmatic patients included in this study (57.7% females, 42.3% males). Only 28.0% used daily controller medications; 1,287 (39.7%) patients were not currently on inhaled corticosteroids. Acute upper airway infection was the most common trigger of exacerbation (42.3%). Patients with severe to life-threatening exacerbation tended to have a longer disease course, a smoking history, and had comorbidities such as hypertension, chronic obstructive pulmonary disease (COPD), and food allergy. The multivariate analysis showed that smoking history, comorbidities of hypertension, COPD, and food allergy were independent risk factors for more severe exacerbation. The number of patients hospitalized for asthma exacerbation varied with seasons, peaking in March and September. Eight patients died during the study period (mortality 0.25%).CONCLUSIONS: Despite enhanced education on asthma self-management in China during recent years, few patients were using daily controller medications before the onset of their exacerbation, indicating that more educational efforts and considerations are needed. The findings of this study may improve our understanding of hospital admission for asthma exacerbation in mainland China and provide evidence for decision-making.
Adrenal Cortex Hormones ; Asthma ; China ; Comorbidity ; Disease Progression ; Education ; Female ; Food Hypersensitivity ; Hospitalization ; Humans ; Hypertension ; Inpatients ; Medication Adherence ; Mortality ; Multivariate Analysis ; Pulmonary Disease, Chronic Obstructive ; Retrospective Studies ; Risk Factors ; Seasons ; Self Care ; Smoke ; Smoking

Objective: To investigate the characteristics and drug resistance of pathogenic bacteria of refractory mycoplasma pneumonia in children and the changes of serum interleukin-18 (IL-18) and interleukin-33 (IL-33) levels. Methods: From January 2016 to December 2017, 103 children with refractory mycoplasma infection admitted to the Maternal and Child Health Hospital of Zhoushan were selected in the study.Another 60 healthy subjects in our Hospital from January 2016 to December 2017 were selected as control group.The oropharyngeal secretions were collected in all children with refractory mycoplasma pneumonia, isolated and cultured pathogenic bacteria.Disk diffusion (K-B method) was used to detect the drug resistance of the main pathogens.Enzyme-linked immunosorbent assay was used to determine serum IL-18 and IL-33 levels. Results: The 117 strains of pathogenic bacteria were isolated from 103 children with refractory mycoplasma infection, of which 68 strains (58.12%) were Gram-negative bacilli, 39 strains (33.33%) were Gram-positive cocci, and 10 strains (8.55%) were fungi.Klebsiella pneumoniae was more resistant to cefuroxime than Acinetobacter baumannii to cefuroxime and ceftriaxone.Staphylococcus aureus and Staphylococcus epidermidis were more resistant to erythromycin and penicillin G than other Gram-positive cocci.The levels of serum IL-18 and IL-33 in the study group were higher than those in the control group (all P<0.05). Conclusion Gram-negative bacilli are the main pathogens of refractory mycoplasma pneumonia in children.The resistant rate of main Gram-negative bacilli to cephalosporins is higher.The resistant rate of main Gram-positive cocci to penicillin G and erythromycin is higher.The levels of serum IL-18 and IL-33 are significantly higher in patients with refractory mycoplasma pneumonia.

Objective To investigate the role and mechanism of miR-155 in invasion and metastasis of lung adenocarcinoma A549 cells.Methods Real-time PCR and fluorescence in situ hybridization were used to detect the miR-155 expression in patients′lung adenocarcinoma and adjacent tissue and lymph nodes.Scratch test and Transwell migration assay were used to assess the effect of miR-155 on the A549 cell migration and invasion capability.Bioinformatics software was used to predict the target genes of miR-155, and using luciferase to assay the target gene.Western blot and real-time PCR were performed to confirm the role of miR-155 expression in the regulation of target gene PTEN.Results The real-time quantitative PCR showed that the miR-155 expression levels in adjacent normal tissue, lung adenocarcinoma and metastatic lymph nodes were 4.1±0.5, 9.6±3.1 and 7.8±2.2, respectively.The in situ hybridization showed that the expression rates of miR-155 in the adjacent normal tissue, lung adenocarcinoma and metastatic lymph nodes were (23.2±15.3)%, (75.4±20.2 )% and (60.4±25.1)%,respectively.The Scratch assay showed that the wound healing rates in the miR-155 mimics group, miR-155 mimics NC group, miR-155 inhibitor group and miR-155 inhibitor NC group at 24 h were (43.2±2.2)%, (21.3±4.2)%, (24.3±5.3)%, and (35.2± 5.1)%, and that at 48 h were (75.2±4.5)%, (52.6±5.2)%, (39.4±4.2)%, and( 51.5±4.3)%, respectively.Dual luciferase reporter gene assay showed that the value of the luciferase in the miR -155 mimics group co-transfected with PTEN 3′UTR-containing wild-type and mutant plasmids were 4.7±0.5 and 7.3±0.7, and the miR-155 mimics luciferase values of the control group co-transfected with PTEN 3′UTR-containing wild-type and mutant plasmids were 7.8±0.9 and 7.5±0.8, respectively.The real-time quantitative fluorescence PCR showed that the relative expression of PTEN protein in the miR-155 mimics group, miR-155 mimics control group, miR-155 mimics inhibitor group, and miR-155 inhibitor control group were 0.5± 0.3, 1.0±0.1, 2.2±0.2 and 1.2 ±0.1, respectively.The Western blot assay detected that the relative expression of PTEN protein levels in the miR-155 mimics group, miR-155 mimics control group, miR-155 inhibitor group and miR-155 inhibitor control group were 0.4±0.1, 1.0±0.3, 2.8±0.2 and 1.4 ±0.1, respectively.The differences in PTEN mRNA and protein expressions of the four groups were statistically significant (P<0.05 for all).Conclusions miR-155 may promote the invasion and metastasis of lung adenocarcinoma through reducing the target PTEN gene expression.

Objective To investigate the role and mechanism of miR-155 in invasion and metastasis of lung adenocarcinoma A549 cells.Methods Real-time PCR and fluorescence in situ hybridization were used to detect the miR-155 expression in patients′lung adenocarcinoma and adjacent tissue and lymph nodes.Scratch test and Transwell migration assay were used to assess the effect of miR-155 on the A549 cell migration and invasion capability.Bioinformatics software was used to predict the target genes of miR-155, and using luciferase to assay the target gene.Western blot and real-time PCR were performed to confirm the role of miR-155 expression in the regulation of target gene PTEN.Results The real-time quantitative PCR showed that the miR-155 expression levels in adjacent normal tissue, lung adenocarcinoma and metastatic lymph nodes were 4.1±0.5, 9.6±3.1 and 7.8±2.2, respectively.The in situ hybridization showed that the expression rates of miR-155 in the adjacent normal tissue, lung adenocarcinoma and metastatic lymph nodes were (23.2±15.3)%, (75.4±20.2 )% and (60.4±25.1)%,respectively.The Scratch assay showed that the wound healing rates in the miR-155 mimics group, miR-155 mimics NC group, miR-155 inhibitor group and miR-155 inhibitor NC group at 24 h were (43.2±2.2)%, (21.3±4.2)%, (24.3±5.3)%, and (35.2± 5.1)%, and that at 48 h were (75.2±4.5)%, (52.6±5.2)%, (39.4±4.2)%, and( 51.5±4.3)%, respectively.Dual luciferase reporter gene assay showed that the value of the luciferase in the miR -155 mimics group co-transfected with PTEN 3′UTR-containing wild-type and mutant plasmids were 4.7±0.5 and 7.3±0.7, and the miR-155 mimics luciferase values of the control group co-transfected with PTEN 3′UTR-containing wild-type and mutant plasmids were 7.8±0.9 and 7.5±0.8, respectively.The real-time quantitative fluorescence PCR showed that the relative expression of PTEN protein in the miR-155 mimics group, miR-155 mimics control group, miR-155 mimics inhibitor group, and miR-155 inhibitor control group were 0.5± 0.3, 1.0±0.1, 2.2±0.2 and 1.2 ±0.1, respectively.The Western blot assay detected that the relative expression of PTEN protein levels in the miR-155 mimics group, miR-155 mimics control group, miR-155 inhibitor group and miR-155 inhibitor control group were 0.4±0.1, 1.0±0.3, 2.8±0.2 and 1.4 ±0.1, respectively.The differences in PTEN mRNA and protein expressions of the four groups were statistically significant (P<0.05 for all).Conclusions miR-155 may promote the invasion and metastasis of lung adenocarcinoma through reducing the target PTEN gene expression.

Objective To investigate effects of antioxidant stress protein hem e oxygenase-1 (HO-1) on lipopolysaccharide (LPS)-induced endoplasm ic reticulum stress (ERS) of rat hepatocytes. Methods The BRL cells (rat hepatocyte cell line) were cultured. The hepatocytes were treated with LPS, LPS+HO-1 si RNA , HO-1 siRNA and PB S solution, respectively. The cell viability was m easured by trypan blue ex-clusion test. The apoptosis cells were detected by the fluorescent dye Hoechst 33258. E xpressions of GR P78, C HO P, caspase-12 and HO-1 were detected by Western blotting. Results LPS caused an in-crease of HO-1 protein expression of rat hepatocytes in a dose-dependent and tim e-dependent m anner, a up-regulation of GRP78, CHO P and caspase-12, a decrease in cellviability,and an increase in apopto-sis rate of hepatocytes. Pretreatm ent of HO-1 siRNA inhibited the up-regulation of LPS-induced HO-1, however, aggravated ERS and cellular injury. Conclusion HO-1 inhibites ERS-m ediated cellular injury of rat hepatocytes induced by LPS.

Objective:Preparation and immune characteristic analysis of polyclonal antibody against hypervariable region protein of Taura syndrome virus major capsid protein VP 1 as a reference for studies on immunological diagnosis reagent.Methods:The recombinant vector pET-VP1 was transformed into E.coli BL21 for protein expression.Immunizing a New Zealand rabbit with purified VP1 protein,the titer of anti-VP1 serum was determined by Agar diffusion test and ELISA.Monoclonal phage specific binding to the purified VP1 protein was used for competitive inhibition test.Results: The VP1 protein was soluble and high expression in E.coli BL21.The biological activity titer of anti-VP1 serum reached 1∶26 ,1∶217 determined by Agar diffusion test and ELISA respectively.A litter binding activity of antiserum and VP 1 protein could be blocked by monoclonal phage , but would not affect the final positive result.Conclusion:High titer antibody Preparation of the VP 1 hypervariable region protein.The binding activity of the polyclonal antibody with VP1 protein was not affected by the mutations of VP 1 protein in minority areas ,so the antiserum could be used as immu-nological detection diagnosis agent.

Background and objective Pulmonary sarcomatoid carcinoma is a rare histologic subtype of non-small cell lung cancer. hTe effective treatment for this disease has not well deifned due to its extremely low morbidity. hTis study explores the clinicopathological characteristics and prognosis of 38 patients with PSC, so as to provide some clues for its diagnosis and treatment. Methods hTe study enrolled 38 patients with PSC that were diagnosed with histology or cytology in our hospital between January 2000 and December 2013. We retrospectively analyzed general clinical characteristics, smoking history, tumor size, TNM staging, pathology, immunohistochemistry, diagnostic method, treatment and prognosis. We used SPSS 19.0 statistical sotfware and Kaplan-Meier method to analyze our data. Results Patients in this study were aged from 26 to 76 years old (the median age was 57.5 years old). Among all of them, the male to female ratio was 4:1, and 81.6%of patients had smoking history. Cough and hemoptysis were the most common primary symptoms. hTe median survival was 21 months, while one-year survival rate, three-year survival rate and five-year survival rate were 68.4%, 31.6%and 18.4%respectively. Tumor size, TNM staging, distant metastasis and surgery therapy were associated with the prognosis of patients. Conclusion Patients with PSC present with no special symptoms generally. According to our study, factors that affect patients’ prognosis include tumor size, TNM staging, distant metastasis and surgery. Complete resection is the key treatment for PSC patients, but comprehensive chemoradiotherapy needs further exploration in evidence-based medicine. Biological target therapy may give new insight into treatment for PSC.

BACKGROUNDTumor cells can reduce the number of dendritic cells (DCs) in the tumor environment and cause DC dysfunction through autocrine or paracrine pathways. We sought to measure cyclooxygenase-2 (COX-2) expression in bombesin-inhibited DCs treated with theanine in vitro and to explore the protection and activation effects of theanine on DCs.

METHODSEnzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting were used to analyze the effects of theanine on COX-2 expression and interleukin (IL)-12/IL-10 secretion of bombesin-treated DCs.

RESULTSDCs acquired an impaired phenotype as a result of bombesin treatment. Theanine increased the expression of mature DC surface molecules. The number of cell apoptosis with the treatment of bombesin and theanine significantly decreased, accounting for 15.9%, compared with 26.1% of cell apoptosis with bombesin. COX-2 expression in bombesin-treated DCs was inhibited by theanine in a dose-dependent manner. Theanine promoted DC secretion of IL-12. IL-12 levels reached (137.4 ± 4.9) pg/ml with theanine at 200 µmol/L. However, theanine inhibited the secretion of IL-10 in a dose-dependent manner. IL-10 levels were only (58.4 ± 6.9) pg/ml with theanine at 200 µmol/L.

CONCLUSIONTheanine inhibits the transcription and translation of COX-2 and regulates the balance of IL-10/IL-12 secretion in bombesin-inhibited DCs, leading to the recovery of a state of activation in DCs.

Bombesin ; pharmacology ; Cells, Cultured ; Cyclooxygenase 2 ; metabolism ; Dendritic Cells ; drug effects ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Glutamates ; pharmacology ; Humans ; Interleukin-10 ; metabolism ; Interleukin-12 ; metabolism