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Background: It is unclear whether serum calcium on admission is associated with clinical outcomes in dilated cardiomyopathy (DCM). In this study, we conducted a retrospective study spanning a decade to investigate the prognostic value of baseline calcium in elderly patients with DCM. Methods: A total of 1,089 consecutive elderly patients (age ≥60 years) diagnosed with DCM were retrospectively enrolled from January 2010 to December 2019. Univariate and multivariate analyses were performed to investigate the association of serum calcium with their clinical outcomes. Results: In this study, the average age of the subjects was 68.36 ± 6.31 years. Receiver operating characteristic (ROC) curve analysis showed that serum calcium level had a great sensitivity and specificity for predicting in-hospital death, with an AUC of 0.732. Kaplan-Meier survival analysis showed that patients with a serum calcium >8.62 mg/dL had a better prognosis than those with a serum calcium ≤8.62 mg/dL (log-rank χ2 40.84, p < 0.001). After adjusting for several common risk factors, a serum calcium ≤8.62 mg/dL was related to a higher risk of long-term mortality (HR: 1.449; 95% CI: 1.115~1.882; p = 0.005). Conclusions: Serum calcium level could be served as a simple and affordable tool to evaluate patients' prognosis in DCM.
Subject(s)
Calcium , Cardiomyopathy, Dilated , Aged , Humans , Middle Aged , Prognosis , Retrospective Studies , Cardiomyopathy, Dilated/diagnosis , Hospital MortalityABSTRACT
Introduction: There is growing evidence of research indicating that the gut microbiota is involved in the development of sarcopenia. Nevertheless, there exists a notable deficiency in comprehension concerning the connection between irregularities in the intestinal microbiome and metabolic processes in older individuals suffering from sarcopenia. Methods: To analyze fecal samples obtained from a cohort of 30 older patients diagnosed with sarcopenia as well as 30 older patients without sarcopenia, this study employed 16S rDNA sequencing and liquid chromatography-mass spectrometry (LC-MS)-based non-targeted metabolomics profiling techniques. Results: As a result, we found that 29 genera and 172 metabolites were significantly altered in the sarcopenic patients. Among them, Blautia, Lachnospiraceae_unclassified, and Subdoligranulum were the bacteria with a potential diagnostic value for sarcopenia diagnosis. Correlation analysis between clinical indices and these gut bacteria suggested that the IL-6 level was negatively correlated with Blautia. Function prediction analysis demonstrated that 17 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways differ significantly between sarcopenic and non-sarcopenic patients. The primary classes of metabolites identified in the study included lipids and lipid-like molecules, organic acids and derivatives, and organoheterocyclic compounds. KEGG enrichment analysis showed that purine metabolism, arginine and proline metabolism, alanine, aspartate, and glutamate metabolism, butanoate metabolism, and histidine metabolism may contribute to the development of sarcopenia. The correlation study on gut microbiota and metabolites found that Lachnospiraceae_unclassified was positively associated with seven metabolites that were more abundant in the non-sarcopenia group and negatively correlated with three metabolites that were more abundant in the sarcopenia group. In addition, Subdoligranulum was positively correlated with seven metabolites that were lacking in sarcopenia and negatively correlated with two metabolites that were enriching in sarcopenia. Moreover, Blautia was positively associated with xanthosine. Discussion: We conducted a study on the intestinal microbiota and metabolic profile of elderly individuals with sarcopenia, offering a comprehensive analysis of the overall ecosystem. Through this investigation, we were able to validate existing research on the gut-muscle axis and further investigate potential pathogenic processes and treatment options for sarcopenia.
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Charge-transfer reactions are ubiquitous and play important roles in various gaseous environments, but, despite a long history of extensive research, our understanding of their dynamics at the quantum state-to-state level is still lacking. Here we report quantum-state-resolved experiments for the paradigmatic charge-transfer reaction Ar+ + N2 â Ar + N2+ using a three-dimensional velocity-map imaging crossed-beam apparatus with the Ar+ beam prepared exclusively in the spin-orbit state 2P3/2. High-resolution scattering images show strong dependence of rotational and angular distributions on the vibrational quantum number of the N2+ product. Trajectory surface-hopping calculations, which semi-quantitatively reproduce the experimental observations, support the existence of two distinct charge-transfer mechanisms. One of these, in the dominant N2+(v' = 1) channel, is the well-known long-distance harpooning mechanism. However, the highly rotationally excited products in the forward direction are attributed to a hard-collision glory scattering mechanism, which occurs on account of the strong attraction between the collisional partners counterbalanced by the short-range repulsive interaction.
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Here, we report the design and test of a pulsed low-energy ion beam source for crossed ion-molecule scattering studies. The ions are produced by laser photoionization based methods and thus can be prepared in well-defined quantum states. By using the combination of a double Einzel lenses setup and a specially designed shielding tube, a well spatially confined ion bunch with tunable kinetic energies in the range of 1.0-5.0 eV and typical spreads of â¼150 meV (full width at half maximum) can be formed in the center of a velocity-map imaging (VMI) stack. By combining it with a recently constructed three-dimensional VMI system, the present apparatus is readily available for quantum state-to-state crossed ion-molecule scattering studies.
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PURPOSE: Gastric cancer is a common tumor type associated with nutritional and immune status. The aim of the current study was to investigate the prognostic value of a preoperative prognostic nutritional index (PNI), composed of nutritional factors and immune factors in elderly patients undergoing gastric cancer surgery. PATIENTS AND METHODS: A total of 454 patients undergoing gastric cancer surgery were divided into two groups based on preoperative PNI scores: ≤45.1 (n = 307) and >45.1 (n = 147). Survival analysis was performed using the Kaplan-Meier method and Log rank tests. Univariate and multivariate analyses were conducted to identify independent prognostic factors using a Cox proportional hazards model. RESULTS: According to the X-tile program, the optimal cutoff value for predicting overall survival (OS) with the PNI was 45.1. The receiver operating characteristic analysis revealed that PNI exhibited 70.6% sensitivity and 56.5% speciï¬city for predicting death during long-term follow-up. The cumulative incidence of postoperative 4-year mortality indicated that the risk of death increased significantly for PNI ≤45.1. In multivariate analysis, preoperative PNI was a significant independent predictor of mortality. In the age-stratified subgroup analysis, preoperative PNI was more sensitive for the old elderly subgroup than for the young elderly subgroup. CONCLUSION: Preoperative PNI is a sensitive and specific prognostic predictor among elderly patients undergoing gastric cancer surgery.
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The C+ ion photofragment spectra and photodissociation branching ratios into the two energetically available channels, C(1D) + O(3P) and C(3P) + O(3P), have been obtained for the three CO isotopologues, 12C16O, 13C16O, and 12C18O, in the vacuum ultraviolet range 100500-102320 cm-1. The two vibronic states of 1Σ+ symmetry, F(3dσ) 1Σ+(υ' = 1) and J(4sσ) 1Σ+(υ' = 0), predominantly dissociate into the lowest channel C(3P) + O(3P) through interactions with the repulsive D'1Σ+ state. All three vibronic states of 1Π symmetry, E'1Π(υ' = 1, 2) and G(3dπ) 1Π(υ' = 0), dissociate into both of the channels above. The photodissociation branching ratios into the channel C(1D) + O(3P) for E'1Π(υ' = 1, 2) are found to be independent of both the rotational quantum number and e/f parity, while those for G(3dπ) 1Π(υ' = 0) strongly depend on the rotational quantum number, indicating very different predissociation pathways between the valence states E'1Π(υ' = 1, 2) and the Rydberg state G(3dπ) 1Π(υ' = 0). The potential energy curves of CO in the aforementioned energy range and below have recently been well constructed due to a series of interplays between high-resolution spectroscopic studies and theoretical calculations; the photodissociation branching ratios measured in this study can provide further benchmarks for future theoretical investigations which aim to understand the detailed predissociation dynamics of CO.
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A recent high resolution photoabsorption study revealed that the Rydberg W1Π(ν = 1) level of carbon monoxide (CO) is perturbed by the valence Eâ³1Π(ν = 0) level, and the predissociation linewidth shows drastic variation at the crossing point due to the interference effect [Heays et al., J. Chem. Phys. 141(14), 144311 (2014)]. Here, we reinvestigate the Rydberg W1Π(ν = 1) level for the three CO isotopologues, 12C16O, 13C16O, and 12C18O, by measuring the rotationally dependent photodissociation branching ratios. The C+ ion photofragment spectra obtained here reproduce the recent high resolution photoabsorption spectra very well, including the presence of the valence Eâ³1Π(ν = 0) level. The photodissociation branching ratios into the spin-forbidden channel C(1D) + O(3P) show sudden increases at the crossing point between the W1Π(ν = 1) and Eâ³1Π(ν = 0) levels, which is in perfect accordance with the drastic variation of the linewidth observed in the recent spectroscopic study. Further analysis reveals that the partial predissociation rate into the lowest channel C(3P) + O(3P) shows a much more prominent decrease at the crossing point, which is caused by the interference effect between the W1Π(ν = 1) and Eâ³1Π(ν = 0) levels, than that into the spin-forbidden channel C(1D) + O(3P), and this is the reason of the sudden increase as observed in the photodissociation branching ratio measurements. We hope that the current experimental investigation will stimulate further theoretical studies, which could thoroughly address all the experimental observations in a quantitative way.
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Liraglutide, a glucagon-like peptide-1 (GLP-1) analogue, has been demonstrated to reduce hepatic steatosis. However, the mechanism of the lipid-lowering effect of liraglutide in the liver remains unclear. The aim of the present study was to investigate the beneficial effect of liraglutide on diet-induced non-alcoholic fatty liver disease (NAFLD) and the underlying mechanism in rats. NAFLD was induced in Sprague-Dawley rats by feeding a high fat and high cholesterol (HFHC) diet. Liraglutide (0.6 mg/kg body weight/d) was injected intraperitoneally to the rats subjected to HFHC diet four weeks before sacrificing the animals. Body and liver weight, fasting blood glucose (FBG), fasting insulin, serum aminotransferase (ALT) and lipid accumulation in the liver were determined. Markers of oxidative stress, such as malondialdehyde (MDA), free fatty acid (FFAs), superoxide dismutase (SOD), and pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) were detected by colorimetric detection or enzyme-linked immunosorbent assay (ELISA). Serum and hepatic adiponectin were measured by ELISA. The expression of c-Jun N-terminal kinase-1 (JNK-1) and phosphorylated JNK-1 were examined by Western blotting. Liraglutide improved insulin resistance, decreased hepatic steatosis and reversed liver dysfunction. The hepatic levels of MDA, FFAs, and TNF-α were significantly decreased versus controls. Meanwhile, administration of liraglutide significantly increased SOD and adiponectin levels in the liver and inhibited the expression of JNK-1 and phosphorylated JNK-1 versus control rats. Liraglutide exerted anti-oxidative and anti-inflammatory effects in the liver and consequently reversed hepatic steatosis and insulin resistance. Such effects might be mediated by the elevation of adiponectin levels and the inactivation of JNK-1.