ABSTRACT
The emergence of coronavirus disease 2019 (COVID-19) not only poses a serious threat to the health of people worldwide but also affects the global economy. The outbreak of COVID-19 began in December 2019, at the same time as the influenza season. However, as the treatments and prognoses of COVID-19 and influenza are different, it is important to accurately differentiate these two different respiratory tract infections on the basis of their respective early-stage characteristics. We reviewed official documents and news released by the National Health Commission of the People's Republic of China, the Chinese Center for Disease Control and Prevention (China CDC), the United States CDC, and the World Health Organization (WHO), and we also searched the PubMed, Web of Science, Excerpta Medica database (Embase), China National Knowledge Infrastructure (CNKI), Wanfang, preprinted bioRxiv and medRxiv databases for documents and guidelines from earliest available date up until October 3rd, 2020. We obtained the latest information about COVID-19 and influenza and summarized and compared their biological characteristics, epidemiology, clinical manifestations, pathological mechanisms, treatments, and prognostic factors. We show that although COVID-19 and influenza are different in many ways, there are numerous similarities; thus, in addition to using nucleic acid-based polymerase chain reaction (PCR) and antibody-based approaches, clinicians and epidemiologists should distinguish between the two using their respective characteristics in early stages. We should utilize experiences from other epidemics to provide additional guidance for the treatment and prevention of COVID-19.
Subject(s)
Female , Humans , Male , COVID-19/therapy , Diagnosis, Differential , Influenza, Human/therapy , Pandemics/prevention & control , Prognosis , SARS-CoV-2ABSTRACT
Objective@#To examine the prospective effect of cesarean section on pubertal development after controlling the polygenic susceptibility for early puberty in boys and girls,and to provide a reference for choosing a delivervary way beneficial to pubertal development.@*Methods@#Cluster sampling method was used to select 997 students of grade 1 to 3 from 2 priwary schools in Bengbu of Anhui in 2016 to establish the puberty development cohort. Delivery mode,birth weight,gestational age,early teeding way,family income and parental educational background were derived from parental questionnaire. Breast Tanner stage and testicular volume of 997 children were annually assessed. The polygenic risk score (PRS) was computed based on 17 SNPs derived from published genome-wide association studies for early pubertal timing. Kaplan-Meier analyses was used to examine associations between cesarean section with pubertal development in boys and girls.@*Results@#The average age of 997 children was 8.01±0.84 years old, and average BMI was (17.96±2.96) kg/m2. The prevalence of cesarean section for boys and girls was 43.30% and 32.47%, respectively. At baseline, the detection of thelarche in girls delivered by cesarean section (39.89%) was higher than that of girls delivered naturally (4.39%) (χ2=118.65, P<0.01). Similar result was observed during the last follow-up, the detection of thelarche in girls born by cesarean section (95.21%) was higher than girls born vaginally (68.48%), respectively (χ2=51.42, P<0.01). After adjusting for confounding factors (age, BMI, birthweight, infancy feeding, gestational age, household monthly income and parental education), girls delivered by cesarean section had maturation at significantly younger than girls who delivered naturally (Hazard Ratio, HR=1.98，95%CI=1.67-2.34，P<0.01).@*Conclusion@#Caesarean section might increase the risk of earlier age at pubertal onset in a sex-specific manner. Whether natural delivery could be one of the protective measures to prevent early pubertal timing in children warrants further investigation.
ABSTRACT
To examine the relationship between the levels of the serum vascular endothelial growth factor (VEGF) and the micrometastasis of peripheral blood in patients with non-small cell lung cancer (NSCLC), 108 NSCLC patients, including 40 patients with benign lung diseases and 30 healthy controls, were investigated. The serum VEGF levels were detected by ELISA and CK19 mRNA in peripheral blood by reverse transcriptase-polymerase chain reaction (RT-PCR). In NSCLC group, the serum VEGF levels and the positive rate of CK19 mRNA in peripheral blood were 479.8+/-268.5 pg/mL and 66.7%, which were significantly higher than those of the other two groups respectively (P0.05). Serum VEGF levels in the patients positive for CK19 mRNA was 561.7+/-325.6 pg/mL. It is significantly higher than that in the negative patients (P<0.01). There existed a significant correlation between serum VEGF levels and expression of CK19 mRNA in peripheral blood in NSCLC patients (P<0.001). The detection of serum VEGF levels and CK19 mRNA in peripheral blood is helpful in judging the condition and the prognosis of NSCLC patients, and serum VEGF levels and CK19 mRNA are independent of the pathological types of lung cancer. The micrometastasis in peripheral blood of NSCLC patients is significantly associated with serum VEGF levels.
ABSTRACT
Objective To test the reliability and validity of ICF Core Sets for Chinese COPD patients.Methods Fifty-two COPD patients were measured with ICF Core Sets for COPD patients and SF-36. For reliability test, the internal consistency was analyzed and expressed by Cronbach α coefficients and split-half reliability. For va-lidity test, the content validity and criterion validity were analyzed and expressed with Spearman rank correlation coef-ficients. Results For body function, body structure and activity and participation, there were good internal consis-tency (Cronbach α coefficients 0. 698～0.957). For environmental factors Crnnbach α coefficient and split-half reli-ability did not exist. Most items of body function, activity and participation and body structure possessed good content validity. There was concurrent validity for ICF components of body function, body structure and activity and participa-tion with SF-36, FEV1/FVC, COPD grade and health self-assessment. The environmental factors demonstrated poor reliability and validity. Conclusion The ICF Core Sets for COPD patients showed good reliability and validity. It is a good comprehensive functional measurement scale for COPD patients, but it is necessary to test the generality of this result, and some items need to be adjusted.
ABSTRACT
To compare the difference in tumor immunity and autoimmunity elicited by adenovirus (Ad) encoding human or murine tyrosinase-related protein 2 (AdhTRP2 or AdmTRP2), and to find the most effective way to induce immunity by AdhTRP2 or AdmTRP2, C57BL/6 mice were immunized with AdhTRP2 or AdmTRP2 intramuscularly at different doses of 10(5), 10(6), 10(7) and 10(8) separately (10 mice for each dose). Two weeks after the immunization, in vivo CTL assay and intracellular staining (ICS) of IFN-gamma were carried out to analyze the dose-effect relationship. Tumor growth and vitiligo (as an sign of autoimmunity) were observed until 3 months after challenge with 10(5) B16F10 tumor cells. The results showed that Ad encoding AdmTrp2 induced weak tumor immune response. Similar immunization with AdhTrp-2 elicited stronger protective immunity. CTL activity and IFN-gamma-produced CD8+T cells were directly proportional to dose of AdhTrp2 or AdmTrp2. Moreover, AdhTrp2 group showed tumor rejection in 100% of challenged mice till the end of 3rd month while 60% of mice immunized with AdmTrp2 were protected against tumor. In the whole process of this experiment, no vitiligo was observed in mice immunized either with AdhTrp2 or AdmTrp2. It is concluded that anti-melanoma responses induced by genetic vaccination expressing xenoantigens breaks immune tolerance effectively and is able to elicit strong antigen-specific cytotoxic T cell response without vitiligo.
Subject(s)
Adenoviridae/metabolism , Antineoplastic Agents/pharmacology , Cell Line, Tumor , Cytokines/metabolism , Immune System , Immune Tolerance , Interferon-gamma/metabolism , Intramolecular Oxidoreductases/biosynthesis , Intramolecular Oxidoreductases/genetics , Mice, Inbred C57BL , T-Lymphocytes, Cytotoxic/metabolism , Vitiligo/metabolismABSTRACT
In order to investigate the immunity of unloaded dendritic cells (DCs) derived from murine bone marrow to preexisting lung melanoma metastases of mice, MO5 were intravenously injected to induce lung metastases in syngeneic C57BL/6 mice. Unloaded GM-CSF DCs, PBS and DCs+SIINFEKEL were subcutaneously injected into the mice, which were divided as experimental group, negative control group and positive control group respectively. Monoclonal antibody was used to deplete NK or T cells separately. The immunity-inhibitory effects on the lung melanoma were observed and the corresponding effector cells were examined. It was found that in the experimental and positive groups, the regression was induced in metastatic nodules in the lungs of tumor-bearing mice,but abrogated by treatment with anti-asialo-GM1 but not anti-CD8. It was concluded that the unloaded DCs could suppress the lung melanoma metastases to some extent, which was mediated by NK cells, and could be used as a potent therapeutic agents for lung tumor.
ABSTRACT
The effects of exogenous p16ink4a gene on biological behaviors of human lung cancer cell line with homozygous deletion of p16ink4a gene were investigated. Exogenous p16ink4a gene was transfected by lipofectin into human lung cell line A549, in which p16ink4a gene was homozygously deleted. The expression of pl6ink4a mRNA and protein was detected by RT-PCR and immunocytochemistry, respectively. The changes in the behaviors of the transfected cell lines in vitro and in vivo were observed. In the transfected cell line A549, the exogenous p16ink4a gene could be stably expressed. The growth of A549 cells transfected with p16ink4a gene was obviously slowed down. Flow cytometry revealed that transfection of the exogenous p16ink4a gene resulted in A549 cell lines arrest in G1 phase of cell cycle. The tumorigenicity of these transfected cells in nude mice could be inhibited, and the tumor growth of nude mice was significantly suppressed. It was concluded that exogenous p16ink4a gene may be stably expressed in human lung cancer cell line A549. The expression of the introduced p16ink4a could block lung cancer cells to entry into S phase of cell cycle and inhibit tumor malignant growth both in vitro and in vivo.
ABSTRACT
The effects of exogenous p16(ink4a) gene on biological behaviors of human lung cancer cell line with homozygous deletion of p16(ink4a) gene were investigated. Exogenous p16(ink4a) gene was transfected by lipofectin into human lung cell line A549, in which p16(ink4a) gene was homozygously deleted. The expression of p16(ink4a) mRNA and protein was detected by RT-PCR and immunocyto-chemistry, respectively. The changes in the behaviors of the transfected cell lines in vitro and in vivo were observed. In the transfected cell line A549, the exogenous p16(ink4a) gene could be stably expressed. The growth of A549 cells transfected with p16(ink4a) gene was obviously slowed down. Flow cytometry revealed that transfection of the exogenous p16(ink4a) gene resulted in A549 cell lines arrest in G1 phase of cell cycle. The tumorigenicity of these transfected cells in nude mice could be inhibited, and the tumor growth of nude mice was significantly suppressed. It was concluded that exogenous p16(ink4a) gene may be stably expressed in human lung cancer cell line A549. The expression of the introduced p16(ink4a) could block lung cancer cells to entry into S phase of cell cycle and inhibit tumor malignant growth both in vitro and in vivo.
ABSTRACT
AIM: To investigate whether RNA interference (RNAi) induced by small interference RNA (siRNA) could suppress Polo- like kinase- 1 (Plk 1 ) expression and its effects in A549 cells. METHODS: A recombinant plasmid containing siRNA targeting Plk1 ( psiRNA - hH1 - Plk1 ) was transfected into A549 cells with Lipofectamine 2000.Expressions of Plk1, cyclin B1 and p53 protein were detected by Western blotting. Cell proliferation was evaluated by direct cell counting, while cell cycle and apoptosis were examined by flow cytometry, and expression of α - tubulin was detected by immunofluorescence. RESULTS: The results demonstrated that sequence specific siRNA targeting Plk1 was capable of suppressing Plk1 expression, and reflecting in lower kinase activity in A549 cells. The level of Plk1 protein was reduced by at least 70％ after 48 h of psiRNA - hH1 - Plk1 treatment relative to controls. Expressions of cyclin B1 and p53 were increased greatly after Plk1 depletion, and cells showed absence of microtubule polymerization and spindle abnormalities in staining for α -tubulin. Growth inhibition, G2/M arrest and apoptosis were observed in psiRNA -hH1 -Plk1 transfected group. CONCLUSION: All these data suggest that siRNA targeted against human Plk1 may be a valuable tool in cancer therapy.
ABSTRACT
The efficacy and safety of the recombinant mutant human tumor necrosis factor (rmhTNF) combined with chemotherapy vs chemotherapy alone in the treatment of patients with small cell lung cancer (SCLC) were evaluated in this study. The selected 37 patients with SCLC were divided into experimental group (n = 18) and control group (n = 19). Bothgroups were subjected to EP regimen. While in the experimental group, a regimen of 4 × 106 U/m2 rmhTNF intramuscular injection was given once a day from the 1st to 7th day and 11th to 17th day on the chemotherapy cycle.Twenty-one days were as a chemotherapy cycle and all patients received treatment with 2 cycles.The response rate was 83.3 % (15/18) in the experimental group and 63.2 % (12/19) in the control group respectively (P＜0.05). The KPS score after treatment was 78.4±9.6 in the experimental group and 71.2±9.7 in the control group with the difference being significant (P＜0.05).No severe adverse effects occurred in the two groups. It was concluded that the curative effectiveness of the rmhTNF combined with chemotherapy in the treatment of SCLC was more satisfactory than chemotherapy alone. The former could obviously improve the quality of life of the patients with SCLC.
ABSTRACT
In this study, the effect of prophylactic anti-inflammation on the development of smoke-induced emphysema was investigated. Young male guinea-pigs aged 1.5-2 months (weighing 198.3+/-26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, i.m., every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6+/-16.0 microm in Group A; 89.8+/-9.2 microm in Group B and 102.4+/-17.7 microm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80, P=0.0002) but comparable to that (94.8+/-13.2 microm) in group D (P>0.05). It is concluded that long-term prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.
Subject(s)
Animals , Male , Anti-Inflammatory Agents , Pharmacology , Guinea Pigs , Pentoxifylline , Pharmacology , Pulmonary Emphysema , Pathology , Random Allocation , Smoking , Triamcinolone Acetonide , PharmacologyABSTRACT
To study the expression of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) in lung cancer cells, and to testify if the PPAR-gamma agonists can inhibit human lung cancer cell growth through induction of apoptosis, PPAR-gamma was detected in two lung cancer cell lines by RT-PCR and immunohistochemistry, the inhibition of human lung cancer cell growth was investigated by MTT and cell counts, and the apoptosis was assessed by TUNEL. The results showed that: (1) PPAR-gamma expressed on two lung cancer cell lines; (2) PPAR-gamma activated by ligands could inhibit human lung cancer cell growth remarkably; (3) PPAR-gamma agonists could induce apoptosis to inhibit lung cancer cell growth. It was concluded that PPAR-gamma expressed in lung cancer cell can be activated by ligands and can inhibit lung cancer cell growth through induction of apoptosis.
Subject(s)
Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Carcinoma, Non-Small-Cell Lung , Pathology , Carcinoma, Small Cell , Pathology , Cell Division , Gene Expression Regulation, Neoplastic , Ligands , Lung Neoplasms , Pathology , Prostaglandin D2 , Pharmacology , Receptors, Cytoplasmic and Nuclear , Metabolism , Transcription Factors , Metabolism , Tumor Cells, CulturedABSTRACT
In this study, the effect of prophylactic anti-inflammation on the development of smoke-induced emphysema was investigated. Young male guinea-pigs aged 1.5-2 months (weighing 198.3+/-26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, i.m., every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6+/-16.0 microm in Group A; 89.8+/-9.2 microm in Group B and 102.4+/-17.7 microm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80, P=0.0002) but comparable to that (94.8+/-13.2 microm) in group D (P>0.05). It is concluded that long-term prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Pentoxifylline/pharmacology , Pulmonary Emphysema/etiology , Pulmonary Emphysema/pathology , Pulmonary Emphysema/prevention & control , Random Allocation , Smoking/adverse effects , Triamcinolone Acetonide/pharmacologyABSTRACT
AIM: To detect the changes of serum vascular endothelial growth factor(VEGF) level and the expression of peripheral blood cytokeratin 19(CK19) mRNA in patients with non-small cell lung cancer(NSCLC).METHODS: 96 patients with NSCLC,40 patients with benign lung diseases and 25 healthy controls were investigated.The VEGF level in serum was detected by ELISA and CK19 mRNA in peripheral blood was determined by using reverse transcriptase-polymerase chain reaction(RT-PCR).RESULTS: In NSCLC group,the serum VEGF level and the positive rate of CK19 mRNA in peripheral blood were(346.3?95.6) ng/L and 63.5%,which were significantly higher than those in other two groups respectively(P0.05).VEGF serum level in the patients who showed positive CK19 mRNA in peripheral blood was(407.4?121.2) ng/L.It is significantly higher than that in the negative patients(P
ABSTRACT
AIM: To localize the expression of forkhead/winged helix transcription factor(FOXP3) gene in different types of pathological lung tissues and explore its biological role in pathogenesis of human lung cancer.METHODS: By using RT-PCR and Western blotting,the expressions of FOXP3 mRNA and related protein in 153 samples including lung cancer(n=63),lung benign lesion(n=45) and normal lung tissues(n=45) were analyzed.RESULTS: The positive expressions of FOXP3 mRNA and its protein were observed in lung cancer and in benign lesion lung tissue samples with significant difference(P0.05).CONCLUSION: FOXP3 is a biomarker of CD4+CD25+ regulatory T cell.They are expressed both in lung cancer and benign lesion lung tissues,but not in normal lung tissue.The expression of FOXP3 is more intensive in cancer tissues than that in benign lesions.
ABSTRACT
AIM:To investigate the effect of Polo-like kinase-1(Plk1) depletion on cell cycle progression and cell growth in lung cancer cells.METHODS:A recombinant plasmid containing antisense RNA targeting Plk1(pcDNA3-Plk1) was transfected into A549 cells by lipofectine.RT-PCR and Western blotting were used to examine Plk1 gene expression.Cell proliferation was evaluated by cell counting and BrdU labeling.Cell cycle distribution and apoptosis were examined by flow cytometry.Inhibition rate(IR) of vinorebline(NVB) was determined by MTT assay.RESULTS:After transfected with pcDNA3-Plk1 into A549 cells,the expression levels of Plk1 mRNA and protein were greatly decreased.Abnormal morphological changes of cells and growth inhibition were observed in pcDNA3-Plk1 transfected cells.The BrdU labeling index was significantly lower than that in control group(P
ABSTRACT
The effects of tetramethylpyrazine ( TMPZ ) on the contraction of isolated guinea pig trachea induced by leukotrienes,histamine,prostagladin F2a , acetylcholine were observed. It was found that TMPZ exerts an inhibitory effect on the contraction induced by these asthmogenic mediators. It is non-competitive antagonist.