Kaasreece8200

Accuracy, sensitivity, specificity, F1 scores, and positive predictive values were used to assess performance.

Of 1,312 patients, 737 (56.2%) were abused. check details Model 1 had an accuracy of 86.3%, sensitivity of 87.2%, specificity of 85.1%, F1 score of 0.86, and positive predictive value (PPV) of 88.7% for the validation set with an area under the receiver Operating Curve (ROC AUC) of 0.86. NLP based Model 2 had an accuracy of 93.4%, sensitivity 92.5%, specificity of 94.6%, F1 score of 0.93, and PPV of 95.9% for the validation set, with a ROC AUC of 0.94. Most features had weak individual correlations with abuse (r<0.3).

Deep learning models accurately distinguished child physical abuse from non-abuse, and NLP further improved the accuracy of the models. Such models could be developed to run in real-time in the electronic medical record and alert clinicians when certain criteria are met, which would prompt them to pursue the diagnosis of abuse.

III STUDY TYPE Diagnostic.

III STUDY TYPE Diagnostic.

High-risk neuroblastoma is a deadly disease; poor prognosticators are MYCN-amplification and TERT-overexpression. We hypothesized that Gene Set Enrichment Analysis (GSEA) could identify pathways associated with MYCN-amplification and that inhibition of these pathways could decrease tumor growth.

We analyzed the Neuroblastoma-Kocak dataset (GSE45547, n=649) and identified pathways associated with MYCN-amplification. Inhibitors were selected from upregulated gene sets for in vitro cytotoxicity testing using ST16-patient-derived primary neuroblastoma cells and in vivo testing using orthotopic ST16-patient-derived xenografts (PDX) in mice. Tumor volume was measured with ultrasound and tumor sections examined after H&E staining.

GSEA identified significantly overexpressed gene sets in MYCN-amplified tumors including MYC targets, cell cycle mitotic genes, TERT associated genes, loss of RB1 gene sets, and E2Fs targets. Several genes were potential Bromodomain-containing protein 4 (Brd4) targets, making Brd4 inhibitors - JQ1, AZD5153 - and cyclin-dependent kinase (Brd4's binding partner) inhibitors - dinaciclib - potential therapeutic agents. JQ1 and dinaciclib were synergistic in inducing cytotoxicity in vitro. Dinaciclib-AZD5153 in vivo decreased tumor size compared to control, and increased tumor lymphocyte infiltration and necrosis on histology.

GSEA is a powerful approach to identify upregulated genes and potential therapeutic targets. Dinaciclib-AZD5153 combination therapy can be effective against MYCN-amplified and TERT-overexpressing neuroblastoma tumors.

GSEA is a powerful approach to identify upregulated genes and potential therapeutic targets. Dinaciclib-AZD5153 combination therapy can be effective against MYCN-amplified and TERT-overexpressing neuroblastoma tumors.

the aim of this clinical trial was to evaluate the safety and efficacy of early enteral feeding (EEN) following intestinal anastomosis in neonates with congenital gastrointestinal malformation.

a multicenter, prospective, randomized controlled trial (registered under chictr.org.cn Identifier no.ChiCTR-INR-17014179) was conducted between 2018 and 2019. Four centers in China analyzed 156 newborns of congenital gastrointestinal malformation undergoing intestinal anastomosis to EEN group (n=78) or control (C) group (n=78). The primary outcomes of this study were length of postoperative stay (LOPS) and time to full feeds. Secondary outcomes included morbidity of complications, parenteral nutrition (PN) duration, feeding intolerance, 30 day mortality rate and 30 day readmission rate.

the mean time to full feeds and LOPS in the EEN group were 15.0 (9.8-22.8) days and 17.6 (12.0-29.8) days, while that were 18.0 (12.0-24.0) days and 20.0 (15.0-30.3) days in C groups respectively. There was no significant difference between two groups(P>0.05). No significant intergroup difference was found with respect to postoperative morbidity, PN duration or feeding intolerance(P>0.05).

early enteral feeding following intestinal anastomosis in neonates with congenital gastrointestinal malformation is safe. Post-operative outcomes demonstrated a trend toward improvement.

Level Ⅰ.

Level Ⅰ.

To report the sequelae of and preventive strategies for selected lower urinary tract (LUT) complications, i.e., posterior urethral diverticulum (PUD), intraoperative LUT injuries, postoperative dysuria, and fistula recurrence in male imperforate anus (IA) with rectourethral/rectovesical (RU/RV) fistula after laparoscopy-assisted anorectoplasty (LAARP) or posterior sagittal anorectoplasty (PSARP).

153 boys with IA and RU/RV fistula treated 1986-2019 by LAARP (n=56) or PSARP (n=97) at two unrelated institutes were studied retrospectively.

After mean follow-up of 17.0 years (range 36.5 days-32.0 years), the overall incidences of LUT complications were LAARP (6/56; 10.7%); PSARP (7/97; 7.2%); p=0.55, comprising PUD LAARP (n=5), PSARP (n=0); p=0.006; injuries LAARP (n=0), PSARP (n=5); p=0.16; dysuria LAARP (n=1), PSARP (n=1); p>0.999; and recurrence LAARP (n=0), PSARP (n=1); p>0.999. Mean onset of PUD was 5.1 years (range 1.0-15.1 years).

PUD surgery (n=2/5), conservative (n=3/5); injuries intraoperative repair (n=5/5); dysuria conservative (n=2/2), and recurrence redo PSARP (n=1/1).

Strategies devised to improve dissection accuracy resolved the specific technical issues causing LUT complications (remnant RU fistula dissection in LAARP and blind posterior access in PSARP). Currently, the incidence of new cases of PUD and LUT injuries is zero.

Level III.

Level III.

Patients with neuroblastoma, a common childhood malignancy, often have poor prognosis. It is mandatory to develop an accurate and efficient diagnostic tool for neuroblastomas, so that the treatment can be started early. Graphene quantum dot (GQD), a nanomaterial, can be used to carry proteins, genetic materials, or drugs. GD2, a disialoganglioside, is a surface antigen expressed on neuroblastoma. This study investigated the in vivo targeting and imaging of neuroblastomas using GD2-targeting GQDs.

GQDs were synthesized and conjugated with anti-GD2 antibody (anti-GD2/GQDs). In vitro cytotoxicity of GQDs and anti-GD2/GQDs was studied in human neuroblastoma cells by 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide)-based colorimetric assay. The tumor tracking and imaging of anti-GD2/GQDs in mice were investigated by in vivo imaging system (IVIS).

Treatment with GQDs or anti-GD2/GQDs induced no or mild cytotoxicity in fibroblasts and neuroblastoma cells. After co-incubation, GQDs and anti-GD2/GQDs were located in the cytoplasm and nucleus of neuroblastoma cells, with GQDs showing a blue fluorescence and anti-GD2/GQDs an orange/red emission.