AIM:To establish a mouse model of pulmonary fibrosis induced by multiple intratracheal instilla-tions of bleomycin(BLM).METHODS:C57BL/6J mice were randomly divided into five groups:control group(n=5),multiple high-dose BLM(BLM-MH)group(n=10),multiple medium-dose BLM(BLM-MM)group(n=8),multiple low-dose BLM(BLM-ML)group(n=7),and single medium-dose BLM(BLM-SM)group(n=6).The pulmonary fibrosis mod-el was induced by single or multiple intratracheal instillations of BLM.Survival curves were plotted at day 56,and lung tis-sue was collected for lung coefficient calculation.Pathological changes in lung tissue were assessed using hematoxylin-eo-sin(H&E)staining and Masson staining.Indicators of lung fibrosis,such as hydroxyproline(HYP),were measured.Dif-ferentially expressed genes in patients with IPF were screened using the GEO database,and kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment analysis was performed to identify pathways associated with IPF.Western blot was used to detect changes in these pathways in the lung tissues of the model mice.RESULTS:The survival rates were 50%in the BLM-MH group and 87.5%in the BLM-MM group,with no deaths in other groups.Compared with the control group,the BLM-MH and BLM-MM groups showed significantly increased lung coefficients(P＜0.05),lung tissue dam-age,inflammation levels,degree of pulmonary fibrosis(P＜0.05 or P＜0.01),and HYP content.The BLM-MH and BLM-MM groups,compared with the BLM-SM group,showed significantly elevated levels of inflammation,fibrosis,and HYP content(P＜0.05 or P＜0.01).GEO database and KEGG enrichment analysis revealed that the extracellular matrix-recep-tor interaction pathway(ECM-RIP)may be involved in IPF development.The expression levels of ECM-RIP pathway-re-lated proteins,such as phosphorylated focal adhesion kinase(p-FAK)and phosphorylated Src protein(p-Src),were in-creased in the lung tissues of the model mice compared with the control group.Compared with the BLM-SM group,the BLM-MH group exhibited significant increases in the protein levels of p-FAK and p-Src in the lung tissue(P＜0.05).CONCLUSION:The murine model of pulmonary fibrosis established through repeated intratracheal instillations of BLM effectively mimics the pathological characteristics of the disease,providing a valuable experimental model for the investiga-tion of idiopathic pulmonary fibrosis pathogenesis and for the development of therapeutic agents.

AIM:To establish a mouse model of pulmonary fibrosis induced by multiple intratracheal instilla-tions of bleomycin(BLM).METHODS:C57BL/6J mice were randomly divided into five groups:control group(n=5),multiple high-dose BLM(BLM-MH)group(n=10),multiple medium-dose BLM(BLM-MM)group(n=8),multiple low-dose BLM(BLM-ML)group(n=7),and single medium-dose BLM(BLM-SM)group(n=6).The pulmonary fibrosis mod-el was induced by single or multiple intratracheal instillations of BLM.Survival curves were plotted at day 56,and lung tis-sue was collected for lung coefficient calculation.Pathological changes in lung tissue were assessed using hematoxylin-eo-sin(H&E)staining and Masson staining.Indicators of lung fibrosis,such as hydroxyproline(HYP),were measured.Dif-ferentially expressed genes in patients with IPF were screened using the GEO database,and kyoto encyclopedia of genes and genomes(KEGG)pathway enrichment analysis was performed to identify pathways associated with IPF.Western blot was used to detect changes in these pathways in the lung tissues of the model mice.RESULTS:The survival rates were 50%in the BLM-MH group and 87.5%in the BLM-MM group,with no deaths in other groups.Compared with the control group,the BLM-MH and BLM-MM groups showed significantly increased lung coefficients(P＜0.05),lung tissue dam-age,inflammation levels,degree of pulmonary fibrosis(P＜0.05 or P＜0.01),and HYP content.The BLM-MH and BLM-MM groups,compared with the BLM-SM group,showed significantly elevated levels of inflammation,fibrosis,and HYP content(P＜0.05 or P＜0.01).GEO database and KEGG enrichment analysis revealed that the extracellular matrix-recep-tor interaction pathway(ECM-RIP)may be involved in IPF development.The expression levels of ECM-RIP pathway-re-lated proteins,such as phosphorylated focal adhesion kinase(p-FAK)and phosphorylated Src protein(p-Src),were in-creased in the lung tissues of the model mice compared with the control group.Compared with the BLM-SM group,the BLM-MH group exhibited significant increases in the protein levels of p-FAK and p-Src in the lung tissue(P＜0.05).CONCLUSION:The murine model of pulmonary fibrosis established through repeated intratracheal instillations of BLM effectively mimics the pathological characteristics of the disease,providing a valuable experimental model for the investiga-tion of idiopathic pulmonary fibrosis pathogenesis and for the development of therapeutic agents.

Langerhans cell histiocytosis (LCH) is a rare disease characterized by the proliferation of Langerhans cells and the destruction of local tissue. LCH large occurs in children, whilst incidence of the elderly population is extremely low, and there are few related studies. LCH lesions can involve multiple organs and systems, including bone tissue, lymph nodes, skin, liver, and spleen. However, it is rare that multiple soft tissues are implicated for eldly patients with LCH and present with soft tissue mass as the main manifestation. Here is a report on the clinical features, treatment and prognosis of an elderly LCH with multiple soft tissue masses as the main manifestation, in order to provide clinical reference.

Myeloproliferative neoplasms (MPN) are a group of clonal disorders of hematopoietic stem cells, and JAK2 V617F gene mutation is the main basis for the diagnosis of MPN. Previous studies have shown that BCR-ABL fusion gene and JAK2 V617F gene mutation are mutually exclusive in MPN patients, but in recent years, patients with a double mutation of both genes are often reported. The article synthesizes the relevant domestic and foreign literature in recent years, and reviews the BCR-ABL fusion gene and JAK2 V617F mutation double-positive MPN.

We hereby reported a fetus with abnormal head shape, ventricular septal defect, gallbladder enlargement, low-set ears and local umbilical cord glial edema at 22 and 25 weeks of gestation ultrasound scan. A 15.318 Mb heterozygous microdeletion on chromosome 1p32.1p31.1, arr[GRCh37]1p32.1p31.1(61,279,239-76,597,189)×1, was indentified by chromosomal microarray analysis. The chromosome karyotype of the fetus was 46,XY,del(1)(p32.1p31.1). Therefore, this case was diagnosed as 1p32p31 microdeletion syndrome and proved to be a de novo variation based on routine G-banding analysis and chromosomal microarray analysis of the normal parents. This syndrome might present with abnormalities in the head shape, kidney, bladder and central nervous system. The couple decided to terminate the pregnancy after genetic counseling concerning the possible poor outcomes of the fetus.

Objective To investigate the association between the polymorphism of C-689T in the peroxisome proliferator-activated receptor-γ2 (PPARγ2) promoter and coronary heart disease (CHD). Methods This case-controlled study was conducted in nondiabetic Chinese Han people, which enrolled 455 patients with CHD (cases) and 693 subjects without CHD (controls). Data of clinical indexes were collected, including height, body weight, waist circumstance, systolic blood pressure (SBP), diastolic blood pressure (DBP), smoking, drinking, physical activity, as well as body mass index (BMI). Fasting blood glucose (FBG), plasma total cholesterol (TC) and triglyceride (TG) levels were measured. Polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine the PPARγ2 promoter C-689→T substitution. The genotype distribution of PPARγ2 promoter C-689T, allelic frequency, clinical indexes, and laboratorial measurements were compared between the two groups. The effect of genotype on the risk of CHD was assessed using univariate and multivariate regression model. Results The genotype frequencies of CC, CT and TT in PPARγ2 promoter C-689T were 89.7%, 9.9% and 0.4% in the case group, and 93.1%, 6.6% and 0.3% in the control group, respectively (CC vs. CT+TT, χ= 6.243, P=0.041). Carriers of -689T allele (n=95) had significantly higher TC level than non-carriers (n=1053) (5.12±1.26 vs. 4.76±1.22 mmol/L, P=0.001). Male carriers of -689T allele (n=51) were significantly higher in waist circumference, body weight, TC and TG than male non-carriers (n=656) (all P<0.05). In subjects whose BMI was over 25 kg/m, carriers of -689T allele (n=82) had significantly higher levels of waist circumference, BMI, SBP and TC than non-carriers (n=231) (all p<0.05). The -689T allele was an independent risk factor for CHD (OR=1.668, 95%CI: 1.031-2.705, P=0.037) after adjusting for age, gender, waist circumference, body weight, BMI, smoking, physical activities, SBP, DBP, FBG, TC and TG level. Conclusion These data support the hypothesis that the -689T allele is associated with an increased risk of CHD, in Chinese Han people and correlates significantly with the profiles of CHD-related risk factors.

Objective To investigate the clinic effect of Linezolid for community acquired methicillin resistant staphylococcus aureus (MRS A) pneumonia. Methods The clinic data of the patient- were collected from the First Affiliated Hospital of Sun Yat-Sen University, in addition, the body temperature and white blood cell counts were obtained as the index of treatment. Results It was proved that Linezolid was effective in treating community acquired MRSA pneumonia and showed well tolerance with few adverse events. Conclusion Linezolid demonstrated good clinical and antibacterial activity but very few adverse reactions in elderly patients with community acquired MRSA pneumonia.

Objective To establish a simple,easily-producible and practical cardiopulmonary cerebral resuscitation model in rabbits.Method Cardiac ventricular fibrillation was induced in 27 New Zealand rabbits by alternating electric current.The rabbits were randomly divided into three groups according to the duration of untreated cardiac arrest(CA):CA-8 min group(n = 9),CA-5 min group(n = 9)and CA-3 min group(n = 9).All animals received cardiopulmonary resuscitation(CPR)until return of spontaneous circulation(ROSC).The sample of vein blood was collected for the measurement troponin I level at 4 hours after ROSC.The animals were sacrificed at 72 hours after ROSC,hippocampus were removed and fixed in 3%formalin,and coronal sections were analyzed by TUNEL staining and N1SSLE staining.The other two animals without ventricular fibrillation or CPR served as sham-operated group.One-way ANOVA or Mann-Whitney rank was used to determine the statistical significance among the three groups.R×C test was used for ROSC,LSD test for multiple comparisons,and t test for comparisons of means between two independent samples.A two-tailed value of P＜0.05 was considered statistically significant.Results There were no differences in rate of ROSC among groups.No animals survived until 72 hours after ROSC in CA-8 min group and CA-5 min group,while three animals in CA-3 min group survived.In group CA-8 min,CA-5 min and CA-3 min,the survival time of animals after ROSC were(1.67 ± 2.55)h,(37.78 ± 30.27)h,(12.0 ± 14.97)h,respectively.There were significant differences in the survival time of animals after ROSC and troponin I level after ROSC 4 h between CA-3 min group and the other two groups(P＜0.05).Compared with animals in CA-3 min group,sham-operated animals(n = 2)did not have neuronal degeneration or TUNEL positive cells in the hippocampus CA1 area.Conclusions CPR initiated as soon as 3 min after CA can give longer survival tome to the rabbits.The rabbits have neuronal degeneration and apoptosis in the hippocampus CA1 area at 72 hours after ROSC.It may be an ideal animal model for investigation on CPCR.