Comparison between P-POSSUM and NELA risk score for patients undergoing emergency laparotomy in Egyptian patients.

BACKGROUND AND AIMS: The Portsmouth-Physiological and Operative Severity Score for the enumeration of Mortality and Morbidity (P-POSSUM) is one of the scores that is used most frequently for determining the likelihood of mortality in patients undergoing emergency laparotomy. National Emergency Laparotomy Audit (NELA) presents a novel and validated score. Therefore, we aimed to compare the performance of the NELA and P-POSSUM mortality risk scores in predicting 30-day and 90-day mortality in patients undergoing emergency laparotomy. METHODS: Between August 2020 and October 2022, this cohort study was undertaken at Menoufia University Hospital. We compared the P-POSSUM, preoperative NELA, and postoperative NELA scores in patients undergoing emergency laparotomy. All variables needed to calculate the used scores were collected. The outcomes included the death rates at 30 and 90 days. By calculating the area under the curve (AUC) for every mortality instrument, the discrimination of the various methods was evaluated and compared. RESULTS: Data from 670 patients were included. The observed risk of 30-day and 90-day mortality was 10.3% (69/670) and 13.13% (88/670), respectively. Concerning 30-day mortality, the AUC was 0.774 for the preoperative NELA score, 0.763 for the preoperative P-POSSUM score, and 0.780 for the postoperative NELA score. Regarding 90-day mortality, the AUCs for the preoperative NELA score, preoperative P-POSSUM score, and postoperative NELA score were 0.649 (0.581-0.717), 0.782 (0.737-0.828), and 0.663 (0.608-0.718), respectively. There was noticeable difference in the three models' capacity for discrimination, according to pairwise comparisons. CONCLUSIONS: The probability of 30-day and 90-day death across the entire population was underestimated by the NELA and P-POSSUM scores. There was discernible difference in predictive performance between the two scores.

Evaluation of antigen specific interleukin-1ß as a biomarker to detect cattle infected with Mycobacterium bovis.

Bovine tuberculosis (bTB) is a major world-wide health problem that has been difficult to control, due to the lack of an effective vaccine and limited ability of the tuberculin skin test (TST) and the ancillary whole blood interferon-gamma (IFN-γ) release assay (IGRA) to detect all infected animals. A 6 h cytokine flow cytometric IFN-γ (CFC) assay was developed in effort to overcome these limitations and expand methods for studying the mechanisms of bTB immunopathogenesis. The present study was conducted to evaluate IL-1ß as a biomarker to use in conjunction with the IFN-γ CFC assay to improve the diagnostic accuracy for bTB. Three animal groups with predefined Mbv infection status were used for analysis of IL-1ß in plasma from whole blood cultures stimulated with ESAT-6/CFP-10 for 20-24 h. Parallel stimulations were performed for enumeration of IFN-γ producing T cells. Data analysis showed that Mbv infected animals have a higher frequency of IFN-γ producing CD4+ T cells and plasma IL-1ß than animals exposed to non-tuberculous mycobacteria (NTM) or uninfected control animals, with a significant correlation between the two readouts, thus allowing differentiation between the three animal groups. IL-1ß has the potential to serve as an additional biomarker for detecting cattle infected with Mbv.

Protein kinase C-alpha mediates TNF release process in RBL-2H3 mast cells.

1 To clarify the mechanism of mast cell TNF secretion, especially its release process after being produced, we utilized an antiallergic drug, azelastine (4-(p-chlorobenzyl)-2-(hexahydro-1-methyl-1H-azepin-4-yl)-1-(2H)- phthalazinone), which has been reported to inhibit TNF release without affecting its production in ionomycin-stimulated RBL-2H3 cells. 2 Such inhibition was associated with the suppression of an ionomycin-induced increase in membrane-associated PKC activity rather than the suppression of Ca2+ influx, suggesting that PKC might be involved in TNF release process. 3 To see whether conventional PKC family (cPKCs) are involved, we investigated the effects of a selective cPKC inhibitor (Gö6976) and an activator (thymeleatoxin) on TNF release by adding them 1 h after cell stimulation. By this time, TNF mRNA expression had reached its maximum. Gö6976 markedly inhibited TNF release, whereas thymeleatoxin enhanced it, showing a key role of cPKC in TNF post-transcriptional process, possibly its releasing step. 4 To determine which subtype of cPKCs could be affected by azelastine, Western blotting and live imaging by confocal microscopy were conducted to detect the translocation of endogenous cPKC (alpha, betaI and betaII) and transfected GFP-tagged cPKC, respectively. Both methods clearly demonstrated that 1 microM azelastine selectively inhibits ionomycin-triggered translocation of (alpha)PKC without acting on betaI or betaIIPKC. 5 In antigen-stimulated cells, such a low concentration of azelastine did not affect either (alpha)PKC translocation or TNF release, suggesting a functional link between (alpha)PKC and the TNF-releasing step. 6 These results suggest that (alpha)PKC mediates the TNF release process and azelastine inhibits TNF release by selectively interfering with the recruitment of (alpha)PKC in the pathway activated by ionomycin in RBL-2H3 cells.