The relationship between serum anion gap levels and short-, medium-, and long-term all-cause mortality in ICU patients with congestive heart failure: a retrospective cohort study.

BACKGROUND: There hasn't been research done on the connection between serum anion gap (AG) levels and long-, medium-, and short-term all-cause mortality in congestive heart failure (CHF) patients. This study aims to investigate the association between serum anion gap levels and all-cause mortality in CHF patients after adjusting for other covariates. METHODS: For each patient, we gather demographic information, comorbidities, laboratory results, vital signs, and scoring data using the ICU (Intensive Care Unit) Admission Scoring System from the MIMIC-III database. The connection between baseline AG and long-, medium-, and short-term all-cause mortality in critically ill congestive heart failure patients was investigated using Kaplan-Meier survival curves, subgroup analysis, restricted cubic spline, and Cox proportional risk analysis. RESULTS: 4840 patients with congestive heart failure in total were included in this study. With a mean age of 72.5 years, these patients had a gender split of 2567 males and 2273 females. After adjusting for other covariates, a multiple regression analysis revealed that, in critically ill patients with congestive heart failure, all-cause mortality increased significantly with rising AG levels. In the fully adjusted model, we discovered that AG levels were strongly correlated with 4-year, 365-day, 90-day, and 30-day all-cause mortality in congestive heart failure patients with HRs (95% CI) of 1.06 (1.04, 1.08); 1.08 (1.05, 1.10); and 1.08 (1.05, 1.11) (p-value < 0.05). Our subgroup analysis's findings demonstrated a high level of consistency and reliability. K-M survival curves demonstrate that high serum AG levels are associated with a lower survival probability. CONCLUSION: Our research showed the association between CHF patients' all-cause mortality and anion gap levels was non-linear. Elevated anion gap levels are associated with an increased risk of long-, medium-, and short-term all-cause death in patients with congestive heart failure. Continuous monitoring of changes in AG levels may have a clinical predictive role.

The Effect of Government-Uninsured Optometric Services on the Use of Primary Care Providers.

INTRODUCTION: Eye care in many countries is provided by optometrists, ophthalmologists, primary care providers (PCPs, including family physicians and pediatricians) and emergency department (ED) physicians. In the province of Prince Edward Island (PEI), Canada, optometric services are not government-insured, while services provided by other eye care providers are government-insured. Clinics of optometrists, PCPs and ED physicians are widely distributed across the island. Clinics of ophthalmologists however are concentrated in the capital city Charlottetown. PURPOSE: To investigate if more patients visited government-insured PCPs and EDs for eye care when local optometric services are government-uninsured and government-insured ophthalmologists are potentially distant. METHODS: From PEI physician billing database, we identified all patients with an ocular diagnosis from 2010-2012 using International Classification of Diseases, 9th Revision (ICD-9) codes. The utilization of government-insured PCPs and EDs in five geographical regions was assessed utilizing patients' residential postal code. Of the five regions, Prince was the region farthest from the capital Charlottetown. RESULTS: Compared to utilization of government-insured PCPs for ocular diagnoses in Charlottetown (13.5% in 2010, 95% confidence interval [CI] 12.9-14.0%), the utilization in Prince (22.4% in 2010, 95% CI 21.7-23.1%) was nearly double (p<0.05). The utilization of ED physicians for ocular diagnoses was similarly double in Prince (8.8%, 95% CI 8.3-9.3%) versus Charlottetown (4.1%, 95% CI 3.8-4.5%). The utilization of ophthalmologists however was significantly lower in Prince (43%, 95% CI 41.4-42.9%) versus Charlottetown (56.3%, 95% CI 55.6-57.1%). Similar trends remained throughout 2010-2012. CONCLUSION: When optometric services are government-uninsured and government-insured ophthalmologist services are geographically distant, ocular patients utilized PCPs and ED physicians more frequently. Due to different levels of training and available equipment for eye examinations among PCPs, ED physicians and optometrists, the quality of eye care and cost-effectiveness of increased use of PCPs and ED physicians for ocular management warrant further investigation. TRIAL REGISTRATION: Not applicable.

Neurochemical and behavioral effects of the intrahippocampal co-injection of beta-amyloid protein1-40 and ibotenic acid in rats.

The present study was designed to investigate the effects of the intrahippocampal co-injection of beta-amyloid protein1-40 (Abeta(1-40)) with ibotenic acid (Ibo) on learning and memory in normal and aging model rats, and to explore the mechanism underlying the effects of the co-injection. The normal and aging rats were bilaterally injected Abeta(1-40) (4 microg for each side) with Ibo (2 microg for each side) into the hippocampus. Two weeks after the intrahippocampal injection, the exploratory behavior and learning-memory ability of the rats were tested by using open field, Y-maze and passive avoidance task. And the changes of membrane fluidity in hippocampal mitochondria, the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in hippocampus were also examined. The co-injection of Abeta(1-40) with Ibo induced tested rats a remarkable decrease in the explorative behaviors and a significant decline in learning-memory ability (P < 0.01). The neurochemical changes induced by the co-injection included a significant decrease in membrane fluidity of hippocampal mitochondria (P < 0.01), a significant decrease in the activity of SOD (P < 0.01), as well as a remarkable increase in the content of MDA (P < 0.01). The results suggest that co-injection of Abeta(1-40) with Ibo may induce an increase of hippocampal damage by peroxidation and a serious deficit in the learning and memory of the rats. The results also suggest that the co-injection of Abeta(1-40) with Ibo may provide a useful animal model for the Alzheimer's disease (AD) research.

Behavioral and neurochemical effects of the intrahippocampal co-injection of beta-amyloid protein 1-40 and ibotenic acid in rats.

The authors investigated the effects of bilateral intrahippocampal co-injection of Abeta1-40 (4 microg for each side) with ibotenic acid (Ibo, 2 microg for each side) on rats' performance in the open field behavior, Y-maze, and passive avoidance task, and also examined some neurochemical changes in hippocampus two weeks after the co-injection. The results showed that the co-injection of Abeta1-40 with Ibo induced a decrease in exploratory activity and a significant decline in learning-memory ability of the tested rats (p < .01). The neurochemistry changes induced by the co-injection included a significant decreased in membrane fluidity of hippocampal mitochondria (p < .01), a significant decrease in the activity of SOD (p < .01), and a remarkable increase in the content of MDA (p < .01). These results suggest that the co-injection of Abeta1-40 with Ibo may induce an increase of hippocampal damage by peroxidation, and a serious learning and memory impairment of the rats. The results also suggest that the co-injection of Abeta1-40 with Ibo may provide a useful animal model for Alzheimer's disease (AD) research.

Alzheimer amyloid beta-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus.

The perforant path projecting from the entorhinal cortex to the hippocampal dentate gyrus is a particularly vulnerable target to the early deposition of amyloid beta (Abeta) peptides in Alzheimer's brain. The authors previously showed that brief applications of Abeta at subneurotoxic concentrations suppressed the early-phase long-term potentiation (E-LTP) in rat dentate gyrus. The current study further examines the effect of Abeta on the late-phase LTP (L-LTP) in this area. Using multiple high-frequency stimulus trains, a stable L-LTP lasting for at least 3 h was induced in the medial perforant path of rat hippocampal slices. Bath application of Abeta(1-42) (0.2-1.0 microM) during the induction trains attenuated both the initial and late stages of L-LTP. On the other hand, Abeta(1-42) perfusion within the first hour following the induction primarily impaired the late stage of L-LTP, which resembled the action of the protein synthesis inhibitor emetine. Blockade of calcineurin activity with FK506 or cyclosporin A completely prevented Abeta-induced L-LTP deficits. These results suggest that Abeta(1-42) impaired both the induction and maintenance phase of dentate L-LTP through calcineurin-dependent mechanisms. In the concentration range effective for inhibiting L-LTP, Abeta(1-42) also reduced the amplitude of NMDA receptor-mediated synaptic currents in dentate granule cells via a postsynaptic mechanism. In addition, concurrent applications of Abeta(1-42) with the protein synthesis inhibitor caused no additive reduction of L-LTP, indicating a common mechanism underlying the action of both. Thus, inhibition of NMDA receptor channels and disruption of protein synthesis were two possible mechanisms contributing to Abeta-induced L-LTP impairment.