Blood purification plays an important role in the treatment of severe acute pancreatitis. Extracorporeal blood anticoagulation is an important strategy to achieve smooth circulation in blood purification circuits. We aimed to investigate the efficacy, safety, and impact on circulating cytokines of using heparin or nafamostat mesylate anticoagulation in patients with severe acute pancreatitis during continuous renal replacement therapy.

Background/Objectives: Sepsis and septic shock remain leading causes of morbidity and mortality in intensive care units (ICUs) worldwide. While activation of the hypothalamic-pituitary-adrenal (HPA) axis is a vital adaptive response, the dissociation between cortisol and adrenal androgens like dehydroepiandrosterone (DHEA) is hypothesized to correlate with poor outcomes. This study aimed to evaluate the prognostic value of serum cortisol, DHEA, and the Cortisol/DHEA ratio in patients with sepsis admitted to the ICU. Methods: Clinical and laboratory data from 106 adult sepsis patients in a tertiary care hospital were retrospectively analyzed. Disease severity was assessed using Sequential Organ Failure Assessment (SOFA), Acute Physiology and Chronic Health Evaluation II (APACHE II), and Glasgow Coma Scale (GCS) scores. Baseline cortisol and DHEA levels were measured at the time of diagnosis. Logistic regression and Cox proportional hazards models were employed to identify predictors of in-hospital mortality and time to death, respectively. Results: A total of 106 adult sepsis patients with a mean age of 73.63 ± 13.70 years (55 female, 51.9%) were included in the study population. In the final logistic regression model, higher SOFA score was associated with greater odds of in-hospital mortality Odds ratio (OR) = 1.39 per 1-point increase, 95% Confidence interval (CI): 1.15-1.69, p < 0.001). Higher platelet count (PLT) was associated with lower odds of mortality (OR = 0.958 per 10 × 10[9]/L increase, 95% CI: 0.919-0.998, p = 0.042), whereas higher urea was associated with greater odds of mortality (OR = 1.112 per 10 mg/dL increase, 95% CI: 1.020-1.212, p = 0.016). The model area under the curve (AUC) was 0.7956. In univariable Cox analysis, higher baseline DHEA was associated with a greater hazard of death (Hazard ratio (HR) = 1.03, 95% CI: 1.014-1.046, p = 0.0002). In the final multivariable Cox proportional hazards model, baseline cortisol remained independently associated with the hazard of death (HR = 1.014, 95% CI: 1.007-1.022, p < 0.001), whereas DHEA was not retained. Notably, the Cortisol/DHEA ratio did not demonstrate independent prognostic value in either modeling approach. Conclusions: Higher baseline DHEA levels were associated with an increased hazard of death in univariable Cox proportional hazards analysis but did not retain independent prognostic significance in the final multivariable Cox proportional hazards model. While SOFA score remains the central prognostic tool, integrating continuous markers such as platelets and urea enhances risk stratification. The Cortisol/DHEA ratio offers no incremental prognostic utility over established clinical parameters.

Background/Objectives: This study aimed to develop and internally validate the RIN-IM model, which integrates routinely measured biomarkers reflecting renal dysfunction, systemic immune-inflammatory activation, albumin-related alterations during acute illness, and metabolic stress, for prediction of 28-day mortality in critically ill adults. Methods: This retrospective cohort study included 1000 adults admitted to the intensive care unit (ICU) between January 2020 and June 2025. The first available demographic, clinical, and laboratory measurements obtained within 24 h of ICU admission were analyzed. The five prespecified RIN-IM predictors-serum creatinine, serum albumin, SII, PIV, and the TyG index-were initially evaluated as continuous variables; SII and PIV were natural-log-transformed, and potential nonlinear associations were examined using restricted cubic splines. Ridge-penalized logistic regression was used to address coefficient instability arising from correlation between SII and PIV. After evaluation of the primary continuous model, a simplified point-based score was derived by assigning 0-2 points to clinically ordered categories for each component, producing a total score of 0-10. Scores were categorized as low- (0-3), intermediate- (4-6), or high-risk (7-10). The primary outcome was 28-day all-cause mortality. Model performance was assessed using discrimination, calibration, Brier score, formal paired AUC comparisons, incremental-value testing, and decision-curve analysis. The complete development procedure was internally validated using 1000 bootstrap resamples. Results: Overall, 300 of 1000 patients (30.0%) died within 28 days. Mortality increased across the RIN-IM risk categories, from 7.6% (32/420) in the low-risk group to 27.2% (98/360) in the intermediate-risk group and 77.3% (170/220) in the high-risk group (p < 0.001). After adjustment for the clinical reference variables, each one-point increase in the simplified RIN-IM Score was associated with higher odds of 28-day mortality (adjusted OR, 1.68; 95% CI, 1.54-1.84; p < 0.001). The primary continuous model had an apparent AUC of 0.907 (95% CI, 0.885-0.929) and an optimism-corrected AUC of 0.898. The corresponding values for the simplified score were 0.890 (95% CI, 0.861-0.919) and 0.878, respectively. The apparent difference between the continuous and simplified models was 0.017 (95% CI, 0.007-0.028; p = 0.001). The simplified RIN-IM Score had higher discrimination than APACHE II (ΔAUC, 0.070; 95% CI, 0.038-0.102; p < 0.001) and SOFA (ΔAUC, 0.090; 95% CI, 0.057-0.123; p < 0.001). Adding RIN-IM to the clinical reference model increased the apparent AUC from 0.821 to 0.923 (ΔAUC, 0.102; 95% CI, 0.078-0.126; p < 0.001) and improved the Brier score from 0.160 to 0.112. Conclusions: In this single-center cohort, the RIN-IM model showed good discrimination and calibration for predicting 28-day mortality. The simplified score retained most of the predictive information of the continuous model and may complement established clinical severity scores using routinely available early laboratory measurements. External validation and clinical-impact studies are required before routine implementation.

Southwestern white pine (Pinus strobiformis) is native to the U.S. and Mexico and is susceptible to the pathogen Cronartium ribicola, which causes the disease white pine blister rust. A major gene, Cr3, confers resistance to the disease. While Cr3 has been observed at low frequency in the periphery of the species range, its presence in the core of the range, in Mexico, is unknown, as are the frequency and geographic pattern of this resistance. We conducted one of the first range-wide assessments of resistance to white pine blister rust in a five-needle pine, evaluating 20,533 seedlings from 475 families over ten years of monitoring. Patterns of Mendelian segregation within open pollinated families were used to infer major gene resistance (MGR) genotypes of maternal parent trees and to estimate its geographic frequency. We identified up to 34 of the 475 parent trees as heterozygous for MGR. Four of the heterozygous parents were located within the core of the species range in Mexico. Range-wide, the estimated Cr3 frequency was 3% in zygotes and 2 to 4% in gametes, depending on trial type. The probability of being stem symptom free was frequent in the northern and eastern portions of the range. These findings inform genetic conservation efforts and identify seed sources for further field testing and reforestation and restoration. Because much of the range lies in Mexico and has yet to be impacted by C. ribicola these results provide a unique opportunity for proactive management in the face of a spreading disease.

Background Acute respiratory distress syndrome (ARDS) is frequently complicated by acute kidney injury (AKI) and is associated with adverse outcomes. Continuous renal replacement therapy (CRRT) is commonly used in critically ill patients with hemodynamic instability; however, nationally representative data evaluating outcomes associated with CRRT use in ARDS complicated by AKI are limited. Materials and methods We conducted a retrospective cohort study using the Healthcare Cost and Utilization Project National Inpatient Sample (HCUP-NIS) from 2016 to 2021. Adult hospitalizations with ARDS and AKI were identified using ICD-10-CM codes. Patients with end-stage renal disease were excluded. Multivariable logistic regression analyses were performed to evaluate the association between CRRT use and in-hospital outcomes, adjusting for demographics, comorbidities, hospital characteristics, and primary payer. Discharge weights were applied to generate nationally representative estimates. Results Among an estimated 485,035 hospitalizations with ARDS and AKI, 26,995 (5.6%) patients received CRRT. Unadjusted in-hospital mortality was significantly higher among patients receiving CRRT compared with those not receiving CRRT (77.7% vs. 43.1%, p < 0.001). After multivariable adjustment, CRRT use remained associated with higher odds of in-hospital mortality (adjusted odds ratio [aOR] 3.30; 95% CI 3.06-3.55) and higher odds of mechanical ventilation, cardiac arrest, sepsis, vasopressor use, disseminated intravascular coagulation, extracorporeal membrane oxygenation use, and arrhythmia (all p < 0.001). Conclusions Because patients requiring CRRT likely represent those with greater illness severity and because physiologic severity measures (e.g., Sequential Organ Failure Assessment [SOFA] and Acute Physiology and Chronic Health Evaluation [APACHE] scores) are unavailable in the HCUP-NIS, these associations should be interpreted cautiously and likely reflect confounding by indication and residual confounding rather than a direct causal effect of CRRT. CRRT use was associated with substantially higher in-hospital mortality, complication burden, and healthcare resource utilization, identifying a subgroup of patients with severe multisystem organ failure and poor short-term prognosis.