Association between Albumin-Corrected Anion Gap and Mortality in Patients with Cardiogenic Shock.

Background: Cardiogenic shock (CS) is a critical illness with a high mortality rate in clinical practice. Although some biomarkers have been found to be associated with mortality in patients suffering from CS in previous studies. The albumin-corrected anion gap (ACAG) has not been studied in depth. Our study aimed to explore the relationship between ACAG and mortality in patients with CS. Methods: All baseline data was extracted from Medical Information Mart for Intensive Care-IV version: 2.0 (MIMIC-IV). According to the prognosis at 30 days of follow-up, they were divided into survivors and non-survivors groups. The survival curves between the two groups were drawn using the Kaplan-Meier method and the log-rank test. Valid factors were selected using the least absolute shrinkage and selection operator (LASSO) logistic analysis model. Analysis was performed to investigate the relationship between mortality and all enrolled patients using restricted cubic spline (RCS) and Cox proportional hazards models. Receiver operating characteristic (ROC) curves were used to assess the predictive ability of ACAG. Evaluation of final result stability using sensitivity analysis. Results: 839 cases were selected to meet the inclusion criteria and categorized into survivors and non-survivors groups in the final analysis. The ACAG value measured for the first time at the time of admission was selected as the research object. Kaplan-Meier (K-M) survival curves showed that cumulative 30- and 90-day survival decreased progressively with elevated ACAG (p < 0.001), and multifactorial Cox regression analyses showed ACAG to be an independent risk factor for increased 30- and 90-day mortality in patients suffering from CS (p < 0.05). RCS curves revealed that all-cause mortality in this group of patients increased with increasing ACAG ( χ 2 = 5.830, p = 0.120). The ROC curve showed that the best cutoff value for ACAG for predicting 30-day mortality in patients with CS was 22.625, with a sensitivity of 44.0% and a specificity of 74.7%. The relationship between ACAG and CS short-term mortality remained stable in all sensitivity analyses (All p < 0.05). Conclusions: The ACAG is an independent risk factor for 30- and 90-day mortality in CS patients and predicts poor clinical outcomes in CS patients. According to our study, elevated ACAG at admission, especially when ACAG > 20 mmol/L, was an independent predictor of all-cause mortality in CS.

The correlation between albumin-corrected anion gap and prognosis in patients with acute myocardial infarction.

AIMS: Acute myocardial infarction (AMI) is a cardiovascular disease with high morbidity and mortality. We collected patients with AMI from the Medical Information Mart for Intensive Care IV (v2.0) database and explored the association between serum albumin-corrected anion gap (ACAG) level and mortality in patients with AMI. METHODS AND RESULTS: Data of adult patients with AMI were collected. According to the 360 day prognosis, patients were divided into survival and non-survival groups. Based on the ACAG level, patients were then divided into normal and high ACAG groups. Cox hazard proportional models and restricted cubic splines (RCSs) were used to investigate the correlation between ACAG and mortality. Kaplan-Meier curves were created to compare the cumulative survival rates between the high and normal ACAG groups. The receiver operating characteristic (ROC) curve was used to analyse the predictive value of ACAG for the prognosis of patients with AMI. Sensitivity and subgroup analyses were conducted to revalidate the results. Finally, 1783 patients were included. Elevated ACAG (>20 mmol/L) was significantly associated with 30 and 360 day mortality (P < 0.001). Adjusted for multiple confounding factors, the Cox proportional hazard analysis showed that elevated ACAG (>20 mmol/L) was an independent risk factor of increased all-cause mortality in patients with AMI (hazard ratio 1.423, 95% confidence interval 1.206-1.678, P < 0.001). RCS analysis further showed that there was a non-linear trend relationship between ACAG and the risk of all-cause mortality at 30 and 360 days (χ2 = 10.750, P = 0.013; χ2 = 13.960, P = 0.003). Kaplan-Meier survival curves showed that the 30 and 360 day cumulative survival rates of patients with AMI were significantly lower (log-rank test, χ2 = 98.880, P < 0.001; χ2 = 105.440, P < 0.001) in the high ACAG group. ROC curve analysis showed that the area under the curve (AUC) of ACAG was 0.651, while the AUC of anion gap (AG) was 0.609, indicating that ACAG had a higher predictive value for 360 day mortality than AG. When combined with Sequential Organ Failure Assessment score, the predictive performance of ACAG for 360 day mortality was better, with an AUC of 0.699. Sensitivity and subgroup analyses were conducted suggesting the stability of our results. CONCLUSIONS: Elevated serum ACAG (≥20 mmol/L) is an independent risk factor for short-term and long-term mortality in critically ill patients with AMI, and it may assist clinicians and nurses identifying high-risk patients.

The Effect of Hyperbaric Oxygen on Bone Healing Efficiency After Maxillary Sinus Lateral Augmentation Using Xenograft: An In Vivo Pilot Study on Histomorphometric Analysis.

It was hypothesized that hyperbaric oxygen (HBO) could increase bone healing efficiency according to a protocol with a special window of healing time when maxillary sinus lateral augmentation is performed with only xenograft. The histomorphometric efficiency of HBO on the maxillary sinus lateral augmentation was examined by designing five different in vivo healing periods. Five patients receiving maxillary sinus lateral augmentation with xenograft each received a different treatment healing protocol: 6 weeks natural healing (control [Ctl]), 5 weeks with HBO (T1), 6 weeks with HBO (T2), 9 weeks with HBO (T3), and 13 months natural healing (TM). Biopsy samples were harvested, and quantitative histomorphometric analysis was performed regarding key factors BMP-2 and RUNX2. Analysis of variance and Tukey test were used for pairwise comparisons. Time-dependent relationships of the factors' expression densities were conducted using quadratic regression fitting. There were statistically significant differences among the groups, except for T2/T3 and T2/TM for BMP-2 and for T2/T3 and TM/Ctl for RUNX2. Both BMP-2 and RUNX2 showed quadratic trends, presenting an initial upward trend and eventually a downward trend depending on T1, T2, and T3 groups. Early stimulation, achieved by keeping HBO until 6 to 9 weeks after maxillary sinus lateral augmentation with xenograft, seemed to be the time window that benefitted bone healing efficiency the most.

[In vitro co-cultivation of Toxoplasma gondii tachyzoites with rat brain astrocytes].

Purified astrocytes were cultured in plates. When astrocytes grew over 80% of the plate, tachyzoites of Toxoplasma gondii RH strain were added for co-culture. In the period of 0-72 h, change of the astrocytes and tachyzoites was observed after Giemsa staining. In 0-48 h, monodansylcadaverine (MDC) was used to study the action of autophagy in the process of tachyzoites invading astrocytes. At 1 h co-culture, tachyzoites had entered in astrocytes and the autophagosomes appeared. At 4 h, the autophagosomes increased pronouncedly. However, after 12 h, number of autophagosomes considerably decreased and damage of the cells occurred. 48 h later, autophagosomes disappeared and more astrocytes were destroyed. At 72 h most cells destroyed and tachyzoites were released. The result showed that autophagy is inhibited when the astrocytes were in vitro infected by tachyzoites.