The predictive value of confusion assessment method-intensive care unit and intensive care delirium screening checklist for delirium in critically ill patients in the intensive care unit: A systematic review and meta-analysis.

BACKGROUND: Approximately 16%-89% of patients developed delirium during hospitalization in the intensive care unit (ICU). Studies on the accuracy and clinical application of ICU delirium screening tools exist, but the results are inconsistent. Moreover, the accuracy of different screening tools varied greatly. AIM: To compare the diagnostic accuracy of Confusion Assessment Method-Intensive Care Unit (CAM-ICU) and Intensive Care Delirium Screening Checklist (ICDSC) for delirium screening in critically ill patients in the ICU. STUDY DESIGN: We searched PubMed, Embase, Cochrane Central Register of Controlled Trials, Medline, and SciELO databases for relevant studies by combining relevant medical subject headings (MeSH) and keywords. Each database was searched from its creation to 30 January 2024. The included literature was screened by title, abstract, and full text. The diagnostic studies were summarized using Stata 14.0 software. SEN, SPE, PLR, NLR, DOR, and 95% confidence interval (CI) of the diagnostic studies were combined, the SROC analysis was performed, and the area under curve was estimated. RESULTS: Thirty-two articles from the database met the inclusion criteria. The number of studies on CAM-ICU and ICDSC was 28 and 14, respectively. For CAM-ICU, the pooled sensitivity and specificity were 0.81 (95% CI: 0.81-0.81) and 0.94 (95% CI: 0.94-0.94), and the hierarchical SROC curve was 0.96 (95% CI: 0.93-0.97). Regarding the ICDSC, The pooled sensitivity and specificity were 0.79 (95% CI: 0.68-0.86) and 0.90 (95% CI: 0.84-0.93), and the hierarchical SROC curve was 0.92 (95% CI: 0.89-0.94). Regarding the likelihood ratio, the CAM-ICU has a high PLR of 14.24 (95% CI: 14.24-14.24) and a low NLR of 0.20 (95% CI: 0.20-0.20). The ICDSC has a low PLR of 7.64 (95% CI: 5.37-10.87) and a high NLR of 0.24 (95% CI: 0.16-0.35). CONCLUSIONS: CAM-ICU showed good performance in terms of screening and diagnostic efficacies for delirium in critically ill patients. In view of the diagnostic accuracy of these two tools in delirium assessment, the strategies on how to increase their implementation in delirium screening among ICU patients are the focus of future research. RELEVANCE FOR CLINICAL PRACTICE: CAM-ICU is recommended as the first choice to evaluate delirium in clinical practice, followed by ICDSC. Future studies can explore the predictive value of CAM-ICU and ICDSC in different special populations and different types of delirium.

IgA nephropathy with podocytic infolding glomerulopathy.

(A) Immunofluorescence staining showed moderate immunoglobulin A depositions in the mesangial areas (++) of glomeruli (Bars = 100 µm). (B) Segmentally mild mesangial proliferation and mesangial matrix expansion (arrowhead) with mild thickening of glomerular capillary walls (PAS, ×400).

Identification of two novel SALL1 mutations in chinese families with townes-brocks syndrome and literature review.

BACKGROUND: Townes-Brocks syndrome is a rare autosomal dominant genetic syndrome caused by mutations in SALL1. The clinical features of Townes-Brocks syndrome are highly heterogonous. Identification of new SALL1 mutations and study of the relation between SALL1 mutations and clinical features can facilitate diagnosis of Townes-Brocks syndrome. METHODS: We collected clinical data and blood samples of the two patients and their family members for whole-exome sequencing and Sanger sequencing. Prediction analysis of the SALL1variation protein structure was achieved using Alphafold. The clinical materials and gene sequencing results were analyzed. The clinical materials and gene sequencing results were analyzed. The related literature of Townes-Brocks syndrome were searched and the genotype-renal phenotype analysis was performed combined with this two cases. RESULTS: Based on the clinical features and gene sequencing results, the two patients were diagnosed as Townes-Brocks syndrome. Two novel SALL1 mutations (c.878-887del and c.1240G > T) were identified, both of which were pathogenic mutations. The correlation between genotypes and renal phenotypes in Townes-Brocks syndrome patients caused by SALL1 mutation were summarized. CONCLUSION: This study identified two novel mutations and provided new insights into the correlation of genotypes and renal phenotypes of Townes-Brocks syndrome.

Egress Regulatory Factors: How Toxoplasma Exits from Infected Cells?

Toxoplasma gondii is an obligatory intracellular protozoan in the family Apicomplexa. It infects almost one-third of the world's population and causes toxoplasmosis, a prevalent disease. The parasite's egress from infected cells is a key step in the pathology caused by T. gondii. Moreover, T. gondii's continuous infection relies heavily on its capacity to migrate from one cell to another. Many pathways are involved in T. gondii egress. Individual routes may be modified to respond to various environmental stimuli, and many paths can converge. Regardless of the stimuli, the relevance of Ca2+ as a second messenger in transducing these signals, and the convergence of various signaling pathways in the control of motility and, ultimately, egress, is well recognized. This review attempts to outline intra- and extra-parasitic regulators that mediate T. gondii egress, and provides insight into potential clinical interventions and research.

Depletion of CUL4B in macrophages ameliorates diabetic kidney disease via miR-194-5p/ITGA9 axis.

Diabetic kidney disease (DKD) is the most prevalent chronic kidney disease. Macrophage infiltration in the kidney is critical for the progression of DKD. However, the underlying mechanism is far from clear. Cullin 4B (CUL4B) is the scaffold protein in CUL4B-RING E3 ligase complexes. Previous studies have shown that depletion of CUL4B in macrophages aggravates lipopolysaccharide-induced peritonitis and septic shock. In this study, using two mouse models for DKD, we demonstrate that myeloid deficiency of CUL4B alleviates diabetes-induced renal injury and fibrosis. In vivo and in vitro analyses reveal that loss of CUL4B suppresses migration, adhesion, and renal infiltration of macrophages. Mechanistically, we show that high glucose upregulates CUL4B in macrophages. CUL4B represses expression of miR-194-5p, which leads to elevated integrin α9 (ITGA9), promoting migration and adhesion. Our study suggests the CUL4B/miR-194-5p/ITGA9 axis as an important regulator for macrophage infiltration in diabetic kidneys.

Preliminary characterization and expression of Vasa-like gene in Schistosoma japonicum.

The Vasa gene is a vital germline marker to study the origin and development of germ cells and gonads in many organisms. Until now, little information was available about the characteristics of the Vasa gene in Schistosoma japonicum (S. japonicum). In this study, we cloned the open reading frame (ORF) of the S. japonicum Vasa-like gene (Sj-Vasa). The expression pattern and tissue localization of Sj-Vasa were also analyzed. Our results showed that Sj-Vasa shared the general feature of DEAD-box family member proteins. Sj-Vasa was transcribed and expressed throughout the S. japonicum life cycle with transcription exhibiting high levels at day 24 in both male and female worms, and the expression level in the female was always higher than that in the male. Sj-Vasa protein was localized in a variety of tissues of adult schistosomes, including the gonads (ovary, vitellarium, and testes), the subtegument, and some cells of the parenchyma. To our knowledge, this is the first report of preliminary characterization and expression of the Vasa-like gene that may play an important role in the development of the worm, especially in reproductive organs of S. japonicum.