Notes

NO-Donor Dihydroartemisinin Derivatives while Multitarget Providers to treat Cerebral Malaria.
n as compared with Epinephrine plus Placebo.
To compare the efficacy of insulin infusion of 0.05 Unit/kg/hour versus 0.1 Unit/kg/hour in the management of pediatric diabetic ketoacidosis (DKA).

Randomized, double-blind controlled clinical trial.

Pediatric critical care division of a tertiary care hospital from October 2014 to July 2018.

Children aged 12 years or younger with a diagnosis of DKA. Children with septic shock and those who had received insulin before enrollment were excluded. Intervention Low-dose (0.05 Unit/kg/hour) vs. Standard-dose (0.1 Unit/kg/hour) insulin infusion.

Low-dose (0.05 Unit/kg/hour) vs. read more Standard-dose (0.1 Unit/kg/hour) insulin infusion.

The primary endpoint was time for resolution of DKA (pH ≥7.3, bicarbonate ≥15 mEq/L, beta-hydroxybutyrate <1 mmol/L). Secondary outcomes were the rate of fall in blood glucose until 250 mg/dL or less and the rate of complications (hypokalemia, hypoglycemia, and cerebral edema).

Sixty patients were analyzed on an intention-to-treat basis (Low-dose group n=30; Standard-dose groated complications in the low-dose group. Hence, low-dose insulin infusion can be a safer approach in the management of pediatric DKA.The purpose of this study was to investigate the differentiation trajectory of gastric cancer (GC) cells and its clinical relevance and generate a prognostic risk scoring (RS) signature based on GC differentiation-related genes (GDRGs) to predict overall survival (OS). Integrated single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data from GC samples were used for analysis. The cell differentiation trajectory analysis identified three subsets with distinct differentiation states, of which subsets I/II were involved in metabolic disorders, subset II were also associated with hypoxia tolerance, and subset III were related to immune-related pathways. GC samples were divided into three GDRG-based molecular subtypes, and it was found that molecular typing based on cell differentiation successfully predicted patient OS, clinicopathological features, immune infiltration status, and immune checkpoint gene expression. An eight-GDRG-based prognostic RS signature was generated, and the OS of the high-risk group was significantly worse than that of the low-risk group. By integrating the GDRG-based RS signature with prognostic clinicopathological characteristics, a clinicopathologic-genomic nomogram was constructed, and this nomogram yielded strong predictive performance and high accuracy. The study highlights the implication of GC cell differentiation for predicting patient clinical outcome and potential immunotherapy response and proposes a promising treatment direction for GC.Gastric cancer (GC) is a heterogeneous disease with different clinical manifestations and prognoses. Alternative splicing (AS) is a determinant of gene expression and contributes to protein diversity from a rather limited gene transcript in metazoans. AS events are associated with different aspects of cancer biology, including cell proliferation, apoptosis, invasion, etc. Here, we present a comprehensive analysis of the prognostic AS profile in GC. GC-specific AS (GCAS) events were analyzed, and overall survival-associated GCAS (OS-GCAS) events were verified among the genome-wide AS events identified in The Cancer Genome Atlas (TCGA) database. In total, 1,287 GCAS events of 837 genes and 173 OS-GCAS events of 130 genes were identified. The parental genes of OS-GCAS events were significantly enriched in the development of GC. Protein-protein interaction (PPI) and OS-GCAS-associated splicing factor (SF) interaction networks were constructed. Multivariate Cox regression analysis with least absolute shrinkage and selection operator (LASSO) penalty was performed to establish a prognostic risk formula, representing 23 OS-GCAS events. The low-risk group had better OS than the high-risk group and lower immune and stromal scores. Cox proportional hazard regression was applied to generate an AS-clinical integrated prognostic model with a considerable area under the curve (AUC) value in both the training and validation datasets. Our study provides a profile of OS-GCAS events and an AS-clinical nomogram to predict the prognosis of GC.
This study aimed to investigate the aberrant expression of hsa_circ_0002874 in non-small cell lung cancer (NSCLC) and elucidate associated molecular mechanisms that influence apoptosis and induce paclitaxel (PTX) resistance.

Inhibitors were used to downregulate circRNA or miRNA expression. pCDNA plasmid transfection and mimics were used to upregulate circRNA or miRNA expression. Dual-luciferase reporter assays were conducted to evaluate interactions between miR1273f and MDM2. Xenograft tumor models were used to assess the effect of hsa_circ_0002874 and miR1273f on tumor growth. NSCLC tissues and matched non-cancerous tissues were also collected for correlation analysis.

hsa_circ_0002874 acts as a sponge for miR1273f which targets MDM2/P53. The stability of the hsa_circ_0002874/miR1273f/MDM2/P53 pathway was verified by upregulating and downregulating the expression of hsa_circ_0002874 and miR1273f. hsa_circ_0002874 downregulation or miR1273f upregulation reversed the resistance of the A549/Taxol cells in xenograft models. The expression of hsa_circ_0002874 was high, and the level of MDM2 was low in NSCLC tissues. P53 was only weakly expressed in NSCLC tissues with high expression of MDM2.

hsa_circ_0002874 is strongly expressed in NSCLC tissues and maybe a potential marker for PTX resistance. hsa_circ_0002874 downregulation could regulate miR1273f/MDM2/P53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis
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hsa_circ_0002874 is strongly expressed in NSCLC tissues and maybe a potential marker for PTX resistance. hsa_circ_0002874 downregulation could regulate miR1273f/MDM2/P53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis in vitro and vivo.The interplay between microbiota and host metabolism plays an important role in health. Here, we examined the relationship between age, gut microbiome and host serum metabolites in male C57BL/6J mice. Fecal microbiome analysis of 3, 6, 18, and 28 months (M) old mice showed that the Firmicutes/Bacteroidetes ratio was highest in the 6M group; the decrease of Firmicutes in the older age groups suggests a reduced capacity of gut microflora to harvest energy from food. We found age-dependent increase in Proteobacteria, which may lead to altered mucus structure more susceptible to bacteria penetration and ultimately increased intestinal inflammation. Metabolomic profiling of polar serum metabolites at fed state in 3, 12, 18 and 28M mice revealed age-associated changes in metabolic cascades involved in tryptophan, purine, amino acids, and nicotinamide metabolism. Correlation analyses showed that nicotinamide decreased with age, while allantoin and guanosine, metabolites in purine metabolism, increased with age. Notably, tryptophan and its microbially derived compounds indole and indole-3-lactic acid significantly decreased with age, while kynurenine increased with age.
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