Adolescent ; Child ; Humans ; Male ; Nephritis, Interstitial ; pathology ; Uveitis ; pathology

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Hypertension, Renal ; Infant ; Male ; Retrospective Studies

Child ; Drug Resistance, Bacterial ; Humans ; Pneumococcal Infections ; drug therapy ; prevention & control ; Pneumococcal Vaccines ; immunology

Globally, pneumonia is the leading cause of childhood mortality. Pneumonia is the second killer of children less than 5 years of age in China. The World Heath Organization and United Nations Children′s Fund launched the integrated Global Action Plan for the Prevention and Control of Pneumonia and Diarrhea (GAPPD) in 2013. The ambitious goal is to end preventable childhood deaths due to pneumonia by 2025. Countries or regions should achieve the following goals: (1) reduce mortality from pneumonia in children less than 5 years of age to fewer than 3 per 1 000 live births; (2) reduce the incidence of severe pneumonia by 75% in children less than 5 years of age compared to 2010 levels. If the implementation of key interventions is accelerated, the mortality rate of childhood pneumonia will drop substantially every year, which makes the goal achievable.
Child Mortality ; trends ; Child, Preschool ; China ; epidemiology ; Humans ; Infant ; Infant, Newborn ; Pneumonia ; mortality ; Time Factors

Objective To investigate the expressions of CYCLIND1 CDK4 in pancreatic cancer and their relationship with clinlicopathological parameters.Methods Immunohistochemical detector with new second generational tow steps method was used to detect the expressions of CYCLIND1 CDK4 and PCNA in 48 cases of pancreatic cancer and 14 cases of chronic pancreatitis.Results The expressions of CYCLIND1 CDK4 proteins in pancreatic cancer were 70.85%(34/48)and 62.50%(30/48) respectively.The CYCLIND1 and CDK4 proteins were increased(P

AIM: To investigate the molecular mechanism by which the SARS-CoV S protein induces chemokine IP-10 in airway epithelial cells.METHODS: cDNA microarrays were used to screen the gene expression profiles of human bronchial epithelial cells(16HBEs) stimulated by SARS-CoV S protein.In addition,RT-PCR,EMSA,and Western blotting were performed to analyze the phosphorylation of JAK/STAT signal pathway.The changes of IRF-1 and IP10 gene expression and the influence by the corresponding inhibitors were analyzed.RESULTS: IRF-1,a key transcription factor of the JAK/STAT signal pathway,was activated in human bronchial epithelial cells after stimulation by the S protein of SARS-CoV.The IP-10 gene expression was detected 2 h following the phosphorylation of STAT1 after 15 min,which was blocked by STAT1or JAK2 inhibitors.Electrophoretic mobility shift assay(EMSA) demonstrated that the nuclear proteins bound to ISRE and GAS but not NF-?B DNA motif.CONCLUSION: The SARS-CoV S protein induces IP-10 gene expression in human bronchial epithelial cells through activation of the JAK/STAT signal pathway,suggesting that the JAK/STAT signal pathway activated by virus plays key roles in virus infection related acute lung injury.

Objective p38 Mitogen-activated protein kinase (MAPK) is a crossing center of various pathways. In this study, protein transduction system based on human immunodeficiency virus (HIV)-1 transactivator of transcription (TAT), which is an efficient delivery peptide of the foreign proteins into cells, was employed to study p38 MAPK functions in eukaryotic cells. Methods p38 And its dominant negative form, p38AF, were constructed into pET-His-TAT vector correctly to verify that the recombinant plasmids were well-founded through restriction enzyme digestion and DNA sequencing. The two proteins, His-TAT-p38 and His-TAT-p38AF, were expressed and purified in Escherichia coli by SDS-PAGE. Then they were incubated with ECV304 cells respectively and readily transduced into cells in a time-dependent and dose-dependent manner. The cells were stimulated by sorbitol. Activating transcription factor (ATF) 2 phosphorylation level was checked using Western blot to assess the activity of endogenous p38. Results Compared with controls, it was found that His-TAT-p38 increased the level ofATF2 phosphorylation in sorbitol-stimulated ECV304 cells, while His-TAT-p38AF inhibited it, indicating p38 MAPK protein delivery system based on TAT was constructed successfully. TAT-p38 and its dominant negative form possessed high biological activity after transduction into ECV304 cells by TAT protein delivery system. The results showed that p38AF fused with TAT could inhibit the transduction of endogenous p38 signal pathway in part, and other pathway might regulate p38 phosphorylation. Conclusions Our study provides a novel pathway to inhibit p38 signal pathway and establish a new method to study p38 function.

Actinidia ; chemistry ; Animals ; Cell Line, Tumor ; Connexin 43 ; metabolism ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; administration & dosage ; isolation & purification ; pharmacology ; Humans ; Immunohistochemistry ; Lung Neoplasms ; metabolism ; pathology ; prevention & control ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Random Allocation ; Xenograft Model Antitumor Assays

Sepsis is an infection induced systemic inflammatory response syndrome and is a major cause of morbidity as well as mortality in intensive care units. A growing body of evidence suggests that the activation of a proinflammatory cascade is responsible for the development of immune dysfunction, susceptibility to severe sepsis and septic shock. The present theories of sepsis as a dysregulated inflammatory response and immune function, as manifested by excessive release of inflammatory mediators such as high mobility group box 1 protein (HMGB1), are supported by increasing studies employing animal models and clinical observations of sepsis. HMGB1, originally described as a DNA-binding protein and released passively by necrotic cells and actively by macrophages/monocytes, has been discovered to be one of essential cytokines that mediates the response to infection, injury and inflammation. A growing number of studies still focus on the inflammation-regulatory function and its contribution to infectious and inflammatory disorders, recent data suggest that HMGB1 formation can also markedly influence the host cell-mediated immunity, including T lymphocytes and macrophages. Here we review emerging evidence that support extracellular HMGB1 as a late mediator of septic complications, and discuss the therapeutic potential of several HMGB1-targeting agents in experimental sepsis. In addition, with the development of traditional Chinese medicine in recent years, it has been proven that traditional Chinese herbal materials and their extracts have remarkable effective in treating severe sepsis. In this review, we therefore provide some new concepts of HMGB1-targeted Chinese herbal therapies in sepsis.

Objective To improve the recognition of renal impairment with long- standing cyanotic congenital heart disease, to avoid occurrence of renal impairment before and after cardiac surgery. Methods The clinical, laboratory data and treatment course of renal impairment in one child with long - standing cyanotic congenital heart disease were investigated in this study, and the related literature were reviewed Results After 10 years of cyanotic congenital heart disease course, this child presented with nephritic syndrome, renal dysfunction, hyperuricaemia, secondary polycythaemia. After loosen the limitation on fluid intake,decrease the blood viscosity and urine protein,the child was transferred to other hospital for cardiac surgery. Conclusions Children with long- standing cyanotic congenital heart disease can lead to renal impairment, we must pay attention to renal impairment to decrease incidence of acute renal failure after cardiac surgery.