Use of vertebroplasty to prevent proximal junctional fractures in adult deformity surgery: a biomechanical cadaveric study

Background contextVertebral compression fractures at the proximal junction are common complications of long spinal fusion surgeries that can contribute to the development of proximal junctional kyphosis or proximal junctional failure. To our knowledge, no biomechanical studies have addressed the effect of vertebral augmentation at the proximal junction.PurposeTo evaluate the effectiveness of prophylactic vertebroplasty in reducing the incidence of vertebral compression fractures at the proximal junction after a long spinal fusion in a cadaveric spine model.Study designBiomechanical cadaveric study.MethodsWe divided 18 cadaveric spine specimens into three groups of six spines each: a control group, a group treated with one-level prophylactic vertebroplasty at the upper instrumented vertebra, and a group treated with two-level prophylactic vertebroplasty at the upper instrumented vertebra and the supra-adjacent vertebra. In all spines, the pedicles were instrumented from L5 to T10. Using eccentric axial loading, the specimens were then compressed until failure. Failure was defined as a precipitous decrease in load with increasing compression. The effect of augmentation on load-to-failure was checked using linear regression. The effect of augmentation on incidence of adjacent fractures was checked using logistic regression. Differences at the level of p<.05 were considered significant. KyphX cement introducer was donated by Kyphon, and the pedicle screws were donated by DePuy.ResultsFractures occurred in 12 of 18 specimens: five in the control group, six in the one-level group, and only one in the two-level group; these differences were statistically significant.ConclusionsProphylactic vertebroplasty at the upper instrumented level and its supra-adjacent vertebra reduced the incidence of junctional fractures after long posterior spinal instrumentation in this axially loaded cadaveric model. Additional studies are necessary to determine if these results are translatable to clinical practice.     

长链非编码RNA 在胰腺癌中的研究进展

长链非编码RNA(lncRNAs)是一类转录本长度超过200nt、不具备蛋白编码功能的RNA分子。LncRNAs能够在表观遗传、基因转录水平以及转录后水平等不同层面发挥作用。此外,新近发现的微小RNA、环状RNA等可与lnc RNAs交互作用,参与恶性肿瘤的发生与发展过程。近年来,研究发现大量的lncRNAs异常表达于胰腺癌组织和细胞中,在胰腺癌的发生发展中也起着重要作用。因此,笔者就多种异常表达的lncRNAs在胰腺癌中的作用及机制进行综述。     

Analysis of long noncoding RNA-associated competing endogenous RNA network in glucagon-like peptide-1 receptor agonist-mediated protection in β cells

BACKGROUND Long noncoding RNAs(lncRNAs) and mRNAs are widely involved in various physiological and pathological processes. The use of glucagon-like peptide-1 receptor agonists(GLP-1 RAs) is a novel therapeutic strategy that could promote insulin secretion and decrease the rate of β-cell apoptosis in type 2 diabetes mellitus(T2 DM) patients. However, the specific lncRNAs and mRNAs and their functions in these processes have not been fully identified and elucidated.AIM To identify the lncRNAs and mRNAs that are involved in the protective effect of GLP-1 RA in β cells, and their roles.METHODS Rat gene microarray was used to screen differentially expressed(DE) lncRNAs and mRNAs in β cells treated with geniposide, a GLP-1 RA. Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were performed to assess the underlying functions of DE mRNAs. Hub mRNAs were filtered using the STRING database and the Cytoscape plugin, CytoHubba. In order to reveal the regulatory relationship between lncRNAs and hub mRNAs, their co-expression network was constructed based on the Pearson coefficient of DE lncRNAs and mRNAs, and competing endogenous RNA(ceRNA) mechanism was explored through miRanda and TargetScan databases.RESULTS We identified 308 DE lncRNAs and 128 DE mRNAs with a fold change filter of ≥ 1.5 and P value 0.05. GO and KEGG pathway enrichment analyses indicated that the most enriched terms were G-protein coupled receptor signaling pathway, inflammatory response, calcium signaling pathway, positive regulation of cell proliferation, and ERK1 and ERK2 cascade. Pomc, Htr2 a, and Agtr1 a were screened as hub mRNAs using the STRING database and the Cytoscape plugin, CytoHubba. This result was further verified using SwissTargetPrediction tool. Through the co-expression network and competing endogenous(ceRNA) mechanism, we identified seven lncRNAs(NONRATT027738, NONRATT027888, NONRATT030038, etc.) co-expressed with the three hub mRNAs(Pomc, Htr2 a, and Agtr1 a) based on the Pearson coefficient of the expression levels. These lncRNAs regulated hub mRNA functions by competing with six miRNAs(rno-miR-5132-3 p, rno-miR-344 g, rno-miR-3075, etc.) via the ceRNA mechanism. Further analysis indicated that lncRNA NONRATT027738 interacts with all the three hub mRNAs, suggesting that it is at a core position within the ceRNA network.CONCLUSION We have identified key lncRNAs and mRNAs, and highlighted here how they interact through the ceRNA mechanism to mediate the protective effect of GLP-1 RA in β cells.     

Current understandings and perspectives on non-cancer health effects of benzene: A global concern

Objective

Benzene, as a volatile organic compound, is known as one of the main air pollutants in the environment. The aim of this review is to summarize all available evidences on non-cancerous health effects of benzene providing an overview of possible association of exposure to benzene with human chronic diseases, specially, in those regions of the world where benzene concentration is being poorly monitored.

Methodology

A bibliographic search of scientific databases including PubMed, Google Scholar, and Scirus was conducted with key words of “benzene toxic health effects”, “environmental volatile organic compounds”, “diabetes mellitus and environmental pollutants”, “breast cancer and environmental pollution”, “prevalence of lung cancer”, and “diabetes prevalence”. More than 300 peer reviewed papers were examined. Experimental and epidemiologic studies reporting health effects of benzene and volatile organic compounds were included in the study.

Results

Epidemiologic and experimental studies suggest that benzene exposure can lead to numerous non-cancerous health effects associated with functional aberration of vital systems in the body like reproductive, immune, nervous, endocrine, cardiovascular, and respiratory.

Conclusion

Chronic diseases have become a health burden of global dimension with special emphasis in regions with poor monitoring over contents of benzene in petrochemicals. Benzene is a well known carcinogen of blood and its components, but the concern of benzene exposure is more than carcinogenicity of blood components and should be evaluated in both epidemiologic and experimental studies. Aspect of interactions and mechanism of toxicity in relation to human general health problems especially endocrine disturbances with particular reference to diabetes, breast and lung cancers should be followed up.     

Genome sequencing in a genetically elusive multigenerational long QT syndrome pedigree identifies a novel LQT2-causative deeply intronic KCNH2 variant

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Reversal of ischemia-induced mitochondrial dysfunction after coronary reperfusion

This study was designed to clarify the mechanism of the reversal of ischemia-induced mitochondrial dysfunction after a reperfusion of the myocardium in dogs. The occlusion of the left anterior descending coronary artery for 30 min led to the significant increase of acyl-CoA level in ischemic mitochondria and the ischemic mitochondrial function was disturbed. Pre-infusion of 1 ml/kg of lipid before occlusion further increased the acyl-CoA accumulation in ischemic mitochondria, and concomitantly, the mitochondrial dysfunction was extended much more. On the other hand, 40 min of reperfusion following 30 min of occlusion diminished the accumulation of acyl-CoA in the reperfused mitochondria and restored the mitochondrial function. However, when lipid was pre-infused, acyl-CoA level in the reperfused mitochondria was still high and mitochondrial dysfunction was observed. Administration of carnitine prior to reperfusion not only suppressed the accumulation of acyl-CoA in the reperfused mitochondria but also preserved the mitochondrial function, despite the pre-infusion of lipid. There was a clear reciprocal correlation (r = ?0.97) between acyl-CoA level and mitochondrial function. These results suggest that acyl-CoA accumulation is one of the important factors in ischemia-induced mitochondrial dysfunction, and that reversal of the dysfunction after reperfusion is closely dependent upon the lowering of the acyl-CoA accumulation.