Early intramedullary nailing for femoral fractures in patients with severe thoracic trauma: A systemic review and meta-analysis.

PURPOSE: Early intramedullary nailing (IMN) within the first 24 h for multiply injured patients with femoral fracture and concomitant thoracic trauma is controversial. Previously published studies have been limited in size and their outcomes have been inconclusive. A meta-analysis was conducted to evaluate the available data in order to guide care and help improve the outcomes for these patients. METHODS: We searched the literature up to December 2011 in the main medical search engines and identified 6 retrospective cohort studies that explored the safety of early IMN in patients with both femoral fracture and chest injury. Our primary outcome was the rates of pulmonary complication (pneumonia, adult respiratory distress syndrome, fat embolism syndrome), multiple organ failure (MOF) and mortality. RESULTS: We found no statistically significant difference in the rate of pulmonary complications, MOF or mortality in the patients treated with early IMN. CONCLUSION: Early IMN for femoral fractures does not increase the mortality and morbidity in chest- injured patients in the studies analyzed.

Hsa_circ_0041103 induces proliferation, migration and invasion in bladder cancer via the miR-107/FOXK1 axis.

OBJECTIVE: CircRNAs have been proven to be vital during the process of malignant tumors. Their functions in bladder cancer (BCa) process remain largely unclear. This study aims to elucidate the role of circ0041103 in affecting the malignant phenotypes of BCa, and the possible molecular mechanism. PATIENTS AND METHODS: Circ0041103 expression levels in BCa tissues and cell lines were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The clinical significance of circ0041103 in influencing tumor size, tumor staging and lymphatic metastasis of BCa was analyzed. Regulatory effects of circ0041103 on proliferative and metastatic capacities of T24 and UM-UC-3 cells were examined through functional experiments. The binding target of circ0041103 and its downstream protein were predicted by online bioinformatic tools, which were further confirmed by Dual-Luciferase reporter assay and Pearson correlation test. The role of circ0041103/miR-107/ FOXK1 axis in regulating BCa process was explored by rescue experiments. RESULTS: Circ0041103 was abnormally upregulated in BCa tissues and cell lines. Its level was higher in BCa tissues with a larger tumor size, or worse tumor staging, or BCa cases with lymphatic metastasis. Knockdown of circ0041103 inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells. MiR-107 was the binding target of circ0041103, and FOXK1 was the downstream gene of miR-107. Overexpression of circ0041103 could reverse the inhibited proliferative and metastatic capacities of T24 and UM-UC-3 cells overexpressing miR-107. CONCLUSIONS: Circ0041103 is upregulated in BCa and predicts a poor prognosis in BCa. It stimulates BCa cells to proliferate and migrate via the miR-107/FOXK1 axis.

[A multicenter study of the condition of children's rheumatic disease associated medical resources in Fujian province].

Objective: To investigate general condition of children's rheumatic disease associated medical resources in Fujian Province. Methods: This questionnaire-based survey was conducted in 19 hospitals in Fujian province from December 2, 2018 to May 1, 2019. The questionnaire was designed to survey the general condition of the medical resources and the hospitalization of patients with rheumatic diseases from January 1, 2014 to December 1, 2018. Results: In the 19 hospitals, there were 15 general hospitals and 4 children's hospitals, and only 5 hospitals had children's rheumatic specialist clinic. There were only 53-62 beds for rheumatic disease patients in the 19 hospitals, accounting for 1.7%-2.0% of the total inpatient beds (3 137). There are 29 pediatric rheumatologists in total, accounting for 2.6% (29/1 120) of the total pediatricians. In the past five years, 613 patients with rheumatic diseases, accounting for 0.1% (613/625 214) of total hospitalized patients, were treated in these hospitals. Among them, 201 had juvenile idiopathic arthritis, 295 had systemic lupus erythematosus, 39 had dermatomyositis, 7 had scleroderma, and 57 had inflammatory bowel disease, 9 had Sjogren's syndrome, 5 had Behcet's disease, and none had overlap syndrome or mixed connective tissue disease. Conclusion: The medical resources of children rheumatic diseases in Fujian province are insufficient which need to be developed.

[Analysis of variants in complement genes in Han Chinese children with atypical hemolytic uremic syndrome].

Objective: To investigate the prevalence and characteristics of pathogenic variants in complement genes in Han Chinese children with atypical hemolytic uremic syndrome (aHUS). Method: Eleven Han Chinese children with aHUS, including 9 boys and 2 girls aged between 1 year and 4 months and 13 years, were investigated in Department of Pediatrics, Fuzhou General Hospital, from November 1998 to February 2014. Analysis of variants of all the exons of 10 complement genes (CFH, MCP, CFI, C3, CFB, CFHR1, CFHR2, CFHR3, CFHR4 and CFHR5), including 25 bases from 3' end and 25 bases from 5' end, was performed in the 11 cases by targeted sequence capture and next generation sequencing. Significant variants detected by next generation sequencing were confirmed by Sanger sequencing. To understand pathogenicity of variants found in the captured genes, we investigated genetic conservation by multiple protein sequence alignment among different species, and analyzed whether the variants were located in protein domains or not, and investigated functional significance by functional computational prediction methods. Result: Twenty-seven percent of Han Chinese children with aHUS carried pathogenic variants in the 10 complement genes. Pathogenic variant CFB 221G>A (R74H) was detected in Patient 3 and Patient 9, which was not found in parents of Patient 3' , and was found in healthy father of patient 9. Pathogenic variant CFHR5 242C>T (P81L) was found in Patient 2, and was found in healthy father of patient 2. However, no pathogenic variants in genes CFH, MCP, CFI, C3, CFHR1, CFHR2, CFHR3 and CFHR4 were identified. Conclusion: Pathogenic variants in the 10 complement genes were identified in 3/11 of Han Chinese children with aHUS in our study and CFB was the most frequently mutated gene.

Traumatic carotid cavernous fistula concomitant with pseudoaneurysm in the sphenoid sinus.

SUMMARY: This study was designed to elucidate the generating mechanism, diagnosis and treatment of traumatic carotid cavernous fistula (tCCF) concomitant with pseudoaneurysm in the sphenoid sinus. Six cases of tCCF concomitant with pseudoaneurysm in the sphenoid sinus were analyzed in this study. Clinical history, neurological examination, CT and MRI scans, pre- and postembolization cerebral angiograms and follow-up data were included. All patients presented with massive epistaxis and symptoms of tCCF. The pseudoaneurysms and fistulas were occluded with detachable balloons, and preservation of the parent artery in two cases. One patient also had indirect carotid cavernous fistula (CCF) on the contralateral side embolized by transfacial vein approach with microcoils. Complete symptom resolution was achieved in all cases, without procedure related complications. During the follow-up period all patients returned to work. Falling from a high speed motorcycle without wearing a helmet may be one of the main causes of this disease. The site of impact during the accident mostly localizes in the frontal and lateral of the orbit. Intracavernous sinus hypertension of tCCF combining with fracture of the lateral wall of the sphenoid may lead to the formation of a pseudoaneurysm in the sphenoid sinus. MRI scan is very helpful in the diagnosis of this disease before the patient receives angiography. Detachable balloon occlusion of the pseudoaneurysm and fistula is a safe and efficient treatment.

Late memory-related genes in the hippocampus revealed by RNA fingerprinting.

Although long-term memory is thought to require a cellular program of gene expression and increased protein synthesis, the identity of proteins critical for associative memory is largely unknown. We used RNA fingerprinting to identify candidate memory-related genes (MRGs), which were up-regulated in the hippocampus of water maze-trained rats, a brain area that is critically involved in spatial learning. Two of the original 10 candidate genes implicated by RNA fingerprinting, the rat homolog of the ryanodine receptor type-2 and glutamate dehydrogenase (EC 1.4.1.3), were further investigated by Northern blot analysis, reverse transcription-PCR, and in situ hybridization and confirmed as MRGs with distinct temporal and regional expression. Successive RNA screening as illustrated here may help to reveal a spectrum of MRGs as they appear in distinct domains of memory storage.

Calexcitin: a signaling protein that binds calcium and GTP, inhibits potassium channels, and enhances membrane excitability.

A previously uncharacterized 22-kDa Ca(2+)-binding protein that also binds guanosine nucleotides was characterized, cloned, and analyzed by electrophysiological techniques. The cloned protein, calexcitin, contains two EF-hands and also has homology with GTP-binding proteins in the ADP ribosylation factor family. In addition to binding two molecules of Ca2+, calexcitin bound GTP and possessed GTPase activity. Calexictin is also a high affinity substrate for protein kinase C. Application of calexcitin to the inner surface of inside-out patches of human fibroblast membranes, in the presence of Ca2+ and the absence of endogenous Ca2+/calmodulin kinase type II or protein kinase C activity, reduced the mean open time and mean open probability of 115 +/- 6 pS K+ channels. Calexcitin thus appears to directly regulate K+ channels. When microinjected into molluscan neurons or rabbit cerebellar Purkinje cell dendrites, calexcitin was highly effective in enhancing membrane excitability. Because calexcitin translocates to the cell membrane after phosphorylation, calexcitin could serve as a Ca(2+)-activated signaling molecule that increases cellular excitability, which would in turn increase Ca2+ influx through the membrane. This is also the first known instance of a GTP-binding protein that binds Ca2+.