Abstract Background Despite increasing evidence that patients with heart failure (HF) are susceptible to sarcopenia, the reason for the association is not well understood. Objective The purpose of this study is to explore further the molecular mechanism of the occurrence of this complication. Methods Gene expression datasets for HF (GSE57345) and Sarcopenia (GSE1428) were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified using ‘edgeR’ and “limma” packages of R, and their functions were analyzed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Protein-protein interaction (PPI) networks were constructed and visualized using Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape. Hub genes were selected using the plugin cytoHubba and validation with GSE76701 for HF and GSE136344 for Sarcopenia. The related pathways and molecular mechanisms of the hub genes were performed by Gene set enrichment analysis (GSEA). The statistical analyses were performed using R software. P < 0.05 was considered statistically significant. Results A total of 114 common DEGs were found. Pathways related to growth factor, Insulin secretion and cGMP-PKG were enriched in both HF and Sarcopenia. CYP27A1, KCNJ8, PIK3R5, TIMP2, CXCL12, KIT, and VCAM1 were found to be significant hub genes after validation, with GSEA emphasizing the importance of the hub genes in the regulation of the inflammatory response. Conclusion Our study reveals that HF and Sarcopenia share common pathways and pathogenic mechanisms. These findings may suggest new directions for future research into the underlying pathogenesis. (HF sarcopenia understood complication GSE57345 GSE (GSE57345 GSE1428 (GSE1428 GEO (GEO database (DEGs ‘edgeR edgeR limma “limma GO (GO KEGG. KEGG . (KEGG) Proteinprotein Protein protein PPI (PPI STRING (STRING Cytoscape GSE7670 GSE13634 GSEA. (GSEA) software 005 0 05 0.0 11 factor cGMPPKG cGMP PKG CYP27A1 CYPA CYP KCNJ8 KCNJ PIK3R5 PIKR PIK TIMP2 TIMP CXCL12 CXCL KIT VCAM response pathogenesis GSE5734 (GSE5734 GSE142 (GSE142 (KEGG GSE767 GSE1363 (GSEA 00 0. 1 CYP27A PIK3R CXCL1 GSE573 (GSE573 GSE14 (GSE14 GSE76 GSE136 GSE57 (GSE57 GSE1 (GSE1 GSE7 GSE13 GSE5 (GSE5 (GSE

Resumo Fundamento Apesar das evidências crescentes de que pacientes com insuficiência cardíaca (IC) são suscetíveis à sarcopenia, o motivo da associação não é bem compreendido. Objetivo O objetivo deste estudo é explorar ainda mais o mecanismo molecular de ocorrência desta complicação. Métodos Conjuntos de dados de expressão gênica para HF (GSE57345) e Sarcopenia (GSE1428) foram obtidos do banco de dados Gene Expression Omnibus (GEO). Genes diferencialmente expressos (DEGs) foram identificados usando pacotes ‘edgeR’ e “limma” de R, e suas funções foram analisadas usando Gene Ontology (GO) e a Enciclopédia de Genes e Genomas de Kyoto (KEGG). Redes de interação proteína-proteína (PPI) foram construídas e visualizadas usando Search Tool for the Retrieval of Interacting Genes (STRING) e Cytoscape. Os genes hub foram selecionados usando o plugin cytoHubba e validados com GSE76701 para IC e GSE136344 para Sarcopenia. As vias relacionadas e os mecanismos moleculares dos genes hub foram realizados pela análise de enriquecimento de genes (GSEA). As análises estatísticas foram realizadas no software R. P < 0,05 foi considerado estatisticamente significativo. Resultados Foram encontrados 114 DEGs comuns. As vias relacionadas ao fator de crescimento, secreção de insulina e cGMP-PKG estavam enriquecidas tanto na IC quanto na sarcopenia. Descobriu-se que CYP27A1, KCNJ8, PIK3R5, TIMP2, CXCL12, KIT e VCAM1 são genes hub significativos após validação com GSEA enfatizando a importância dos genes hub na regulação da resposta inflamatória. Conclusão Nosso estudo revela que a IC e a Sarcopenia compartilham vias e mecanismos patogênicos comuns. Estes achados podem sugerir novas direções para pesquisas futuras sobre a patogênese subjacente. (IC sarcopenia compreendido complicação GSE57345 GSE (GSE57345 GSE1428 (GSE1428 GEO. GEO . (GEO) (DEGs ‘edgeR edgeR limma “limma R GO (GO KEGG. KEGG (KEGG) proteínaproteína proteína PPI (PPI STRING (STRING Cytoscape GSE7670 GSE13634 GSEA. (GSEA) 005 0 05 0,0 significativo 11 comuns crescimento cGMPPKG cGMP PKG Descobriuse Descobriu se CYP27A1 CYPA CYP A KCNJ8 KCNJ PIK3R5 PIKR PIK TIMP2 TIMP CXCL12 CXCL VCAM inflamatória subjacente GSE5734 (GSE5734 GSE142 (GSE142 (GEO (KEGG GSE767 GSE1363 (GSEA 00 0, 1 CYP27A PIK3R CXCL1 GSE573 (GSE573 GSE14 (GSE14 GSE76 GSE136 GSE57 (GSE57 GSE1 (GSE1 GSE7 GSE13 GSE5 (GSE5 (GSE

ABSTRACT Background: While sarcopenia is an important clinical finding in individuals diagnosed with chronic heart failure (CHF), efforts to identify a reliable biomarker capable of predicting the overall muscular and functional decline in CHF patients have been unsuccessful to date. Objectives: The objectives of this study were to study the diagnostic utility of MicroRNA (miRNA)-1-3p as a predictor of sarcopenia status in individuals diagnosed with CHF. Methods: In total, 80 individuals with heart failure exhibiting a left ventricular ejection fraction < 50% were enrolled in this study. All patients were analyzed to assess miR-1-3p expression levels, with body composition being evaluated through dual-energy X-ray absorptiometry and sarcopenia being defined based on the sum of appendicular lean muscle mass (ALM) divided by height in meters squared and handgrip strength (HGS). In addition, the activation of the Akt/mTOR signaling pathway was evaluated in these individuals. Results: In total, 40 of the enrolled patients (50%) exhibited sarcopenia. Sarcopenic patients presented with increased miR-1-3p expression levels as compared to non-sarcopenic individuals (1.69 ± 0.132 vs. 1.22 ± 0.106; p < 0.05). With respect to sarcopenic indices, appendicular skeletal mass index was most strongly correlated with miR-1-3p expression, which was also strongly correlated with HGS. High levels of Akt/mTOR signaling pathway components were expressed in sarcopenic individuals, highlighting a significant relationship between miR-1-3p activity and signaling through this pathway. Moreover, miR-1-3p was identified as a specific marker for sarcopenia in individuals with CHF. Conclusion: These results suggest that circulating miR-1-3p levels are related to Akt/mTOR pathway activation and can offer valuable insight into the overall physical capacity and muscular integrity of CHF patients as a predictor of sarcopenia.

RESUMO Objetivo: Determinar a discrepância na morfologia coroa-raiz de dentes anteriores, utilizando tomografia computadorizada de feixe cônico (TCFC), e fornecer parâmetros para a expressão apropriada do torque. Método: No total, 200 tomografias elegíveis foram importadas para o software Invivo 5.4 para obtenção das secções médias vestibulolinguais dos dentes anteriores. Osoftware AutoCAD 2007 foi usado para medir a angulação coroa-raiz (ângulo Collum) e o ângulo formado por uma tangente ao centro da superfície vestibular da coroa e o longo eixo da coroa (ângulo da superfície vestibular). O software SPSS 18.0 foi utilizado para as comparações estatísticas das duas medições, com nível de significância de p< 0,05, e a análise de correlação de Pearson foi aplicada para investigar a associação entre as duas medições. Resultados: O valor do ângulo Collum do incisivo central superior foi próximo a 0°. Foram detectados valores significativamente negativos para o ângulo Collum nos incisivos laterais e caninos superiores, mas valores positivos nos caninos inferiores (p< 0,001). O ângulo da superfície vestibular no canino foi significativamente maior do que nos incisivos intra-arcada (p< 0,001), e nenhuma diferença significativa foi detectada entre incisivos centrais e laterais (p> 0,05). Também foi observada uma correlação positiva significativa entre as duas medições. Conclusões: As angulações coroa-raiz foram muito diferentes entre os dentes anteriores. Os caninos superiores e inferiores apresentaram considerável curvatura na superfície vestibular, associada a uma evidente angulação coroa-raiz. Consequentemente, desvios durante a colagem de braquetes podem desencadear maior erro na expressão de torque e aumentar o risco de fenestração alveolar e deiscência, sendo necessária uma avaliação antes da colagem.

ABSTRACT Objective: To determine the discrepancy of crown-root morphology of anterior teeth, using cone-beam computed tomography (CBCT), and to provide a guidance for proper torque expression. Methods: A total of eligible 200 CBCT were imported into Invivo v. 5.4 software, to obtain the middle labio-lingual sections of anterior teeth. AutoCAD 2007 software was applied to measure the crown-root angulation (Collum angle) and the angle formed by a tangent to the center of the labial surface and the long axis of the crown (labial surface angle). SPSS 18.0 was used for statistical comparisons of the two measurements, at the level of p< 0.05, and the Pearson correlation analysis was applied to investigate the association between the two measurements. Results: The value of Collum angle in maxillary central incisor was close to 0°. Significantly negative Collum angle in lateral incisors and maxillary canine, and positive value in mandibular canine were detected (p < 0.001). The labial surface angle in canine was significantly greater than the intra-arch incisors (p< 0.001), and no significant difference was detected between the central and lateral incisors (p > 0.05). Notably, there was also a significant positive correlation between the two measurements. Conclusions: The crown-root angulations were greatly different among anterior teeth. Accompanying the obvious crown-root angulations, the canines both in maxillary and mandibular arches presented considerable labial surface curvatures. Hence, equivalent deviation during bracket bonding might cause greater torque expression error and increase the risk of alveolar fenestration and dehiscence.

Abstract Background Osteoporosis (OP) is common in patients with chronic obstructive pulmonary disease (COPD). The relationship between OP and COPD has been primarily studied in male patients, and few reports are available in postmenopausal women. Objective The purpose of this study was to investigate the association between bone mineral density (BMD) and COPD in postmenopausal women. Methods This cross-sectional study included 133 clinically stable female ex-smokers with confirmed COPD, and 31 age-matched “ex-smoker” female controls. We analyzed groups according to their airway obstruction category. BMD was measured on dual-energy X-ray absorptiometry images of the left femoral neck. Results Patients with COPD had lower T-scores and higher prevalence of osteopenia/OP than the control group. In the COPD group, the airway obstruction category was significantly associated with the T-score after adjustment for confounders. Multivariate logistic regression analysis showed COPD was an independent marker for increased risk of osteopenia/OP in postmenopausal women. Conclusions COPD and airway obstruction category were strongly related to BMD. Postmenopausal women with COPD, especially those with severe airway obstruction, had a higher prevalence rate and a higher risk of osteopenia and OP than female controls without COPD.

The reaction mechanism of AgIII complex ([Ag(HIO6)2]5–) with ruthenium(II) bipyridine (Ru(bpy)32+) in acid medium was investigated. A novel flow injection chemiluminescence (CL) analysis method was developed for the detection of norfloxacin (NFLX) and ofloxacin (OFLX) in commercial drug, milk and human urine samples based on AgIII-ruthenium(II) bipyridine in acidic solution. Under optimal conditions, CL intensities were proportional to drug concentrations in the range of 1.6 × 10-9 to 8 × 10-6 g mL-1 for NFLX and 1.0 × 10-9 to 4 × 10-6 g mL-1 for OFLX. The detection limit was 1.0 × 10-9 g mL-1 for NFLX and 0.8 × 10-9 g mL-1 for OFLX. On the basis of the CL, UV and fluorescence spectra, possible reaction mechanisms were proposed.

Aconitum flavum Hand.-Mazz., Ranunculaceae, has been used for the treatment of rheumatism, traumatic injury in folk and clinical medicine, but the alkaloids has high toxicity. This study was designed to investigate the acute toxicity, anti-inflammatory and antinociceptive activities of non-alkaloids fractions from A. flavum in rodents. The anti-inflammatory activity was evaluated by inflammatory models of dimethylbenzene-induced ear vasodilatation and acetic acid-induced capillary permeability enhancement test in mice and carrageenan-induced paw edema in rats whereas the antinociceptive activity was evaluated using acetic acid-induced writhes, hot plate test and formalin test in mice. The result showed that the LD50 value of BtOH and EtOAc fractions could not be determined as no lethality was observed up to 40 g/kg (p.o.) in mice. BtOH fraction significantly decreased the dimethylbenzene-induced ear vasodilatation, carrageenan-induced paw edema and acetic acid-induced capillary permeability. EtOAc fraction only significantly attenuated paw edema and capillary permeability at the dose of 500 mg/kg. In antinociceptive test, BtOH and EtOAc fractions significantly reduced the writhing number evoked by acetic acid injection and the licking time in both phases of the formalin test. Meanwhile BtOH and EtOAc fractions had significant effect on hot plate test after 90 min. Our data indicate that the BtOH and EtOAc fractions of NAF are no toxicity. BtOH and EtOAc fractions not only inhibit inflammatory and peripheral inflammatory pain but also have central antinociceptive effect.

We investigated the effect of propofol (Prop) administration (10 mg kg-1 h-1, intravenously) on lipopolysaccharide (LPS)-induced acute lung injury and its effect on cluster of differentiation (CD) 14 and Toll-like receptor (TLR) 4 expression in lung tissue of anesthetized, ventilated rats. Twenty-four male Wistar rats were randomly divided into three groups of 8 rats each: control, LPS, and LPS+Prop. Lung injury was assayed via blood gas analysis and lung histology, and tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels were determined in bronchoalveolar lavage fluid using ELISA. Real-time polymerase chain reaction was used to detect CD14 and TLR4 mRNA levels, and CD14 and TLR4 protein expression was determined by Western blot. The pathological scores were 1.2 ± 0.9, 3.3 ± 1.1, and 1.9 ± 1.0 for the control, LPS, and LPS+Prop groups, respectively, with statistically significant differences between control and LPS groups (P < 0.05) and between LPS and LPS+Prop groups (P < 0.05). The administration of LPS resulted in a significant increase in TNF-α and IL-1β levels, 7- and 3.5-fold, respectively (P < 0.05), while treatment with propofol partially blunted the secretion of both cytokines (P < 0.05). CD14 and TLR4 mRNA levels were increased in the LPS group (1.48 ± 0.05 and 1.26 ± 0.03, respectively) compared to the control group (1.00 ± 0.20 and 1.00 ± 0.02, respectively; P < 0.05), while propofol treatment blunted this effect (1.16 ± 0.05 and 1.12 ± 0.05, respectively; P < 0.05). Both CD14 and TLR4 protein levels were elevated in the LPS group compared to the control group (P < 0.05), while propofol treatment partially decreased the expression of CD14 and TLR4 protein versus LPS alone (P < 0.05). Our study indicates that propofol prevents lung injury, most likely by inhibition of CD14 and TLR4 expression.