Development of an artificial intelligence-based multimodal model for assisting in the diagnosis of necrotizing enterocolitis in newborns: a retrospective study.

Objective: The purpose of this study is to develop a multimodal model based on artificial intelligence to assist clinical doctors in the early diagnosis of necrotizing enterocolitis in newborns. Methods: This study is a retrospective study that collected the initial laboratory test results and abdominal x-ray image data of newborns (non-NEC, NEC) admitted to our hospital from January 2022 to January 2024.A multimodal model was developed to differentiate multimodal data, trained on the training dataset, and evaluated on the validation dataset. The interpretability was enhanced by incorporating the Gradient-weighted Class Activation Mapping (GradCAM) analysis to analyze the attention mechanism of the multimodal model, and finally compared and evaluated with clinical doctors on external datasets. Results: The dataset constructed in this study included 11,016 laboratory examination data from 408 children and 408 image data. When applied to the validation dataset, the area under the curve was 0.91, and the accuracy was 0.94. The GradCAM analysis shows that the model's attention is focused on the fixed dilatation of the intestinal folds, intestinal wall edema, interintestinal gas, and portal venous gas. External validation demonstrated that the multimodal model had comparable accuracy to pediatric doctors with ten years of clinical experience in identification. Conclusion: The multimodal model we developed can assist doctors in early and accurate diagnosis of NEC, providing a new approach for assisting diagnosis in underdeveloped medical areas.

Crl activates transcription by stabilizing active conformation of the master stress transcription initiation factor.

σS is a master transcription initiation factor that protects bacterial cells from various harmful environmental stresses including antibiotic pressure. Although its mechanism remains unclear, it is known that full activation of σS-mediated transcription requires a σS-specific activator, Crl. In this study, we determined a 3.80 Å cryo-EM structure of an Escherichia coli transcription activation complex (E. coli Crl-TAC) comprising E. coli σS-RNA polymerase (σS-RNAP) holoenzyme, Crl, and a nucleic-acid scaffold. The structure reveals that Crl interacts with domain 2 of σS (σS2) and the RNAP core enzyme, but does not contact promoter DNA. Results from subsequent hydrogen-deuterium exchange mass spectrometry (HDX-MS) indicate that Crl stabilizes key structural motifs within σS2 to promote the assembly of the σS-RNAP holoenzyme and also to facilitate formation of an RNA polymerase-promoter DNA open complex (RPo). Our study demonstrates a unique DNA contact-independent mechanism of transcription activation, thereby defining a previously unrecognized mode of transcription activation in cells.

Bax inhibiting peptide reduces apoptosis in neonatal rat hypoxic-ischemic brain damage.

Neonatal hypoxic ischemic encephalopathy (HIE) has been reported to induce apoptosis in neonates. We, therefore, analyzed the ability of Bax-inhibiting peptide (BIP) to provide neuroprotective effects during hypoxic-ischemic brain damage (HIBD). Seven-day-old wistar rat pups (n = 198) were randomly divided into a sham-operated group (Group S, n = 18), saline group (Group C, n = 90) and BIP group (Group B, n = 90). Pathological changes in the cerebral tissues of rat pups were analyzed using hematoxylin and eosin stain, TUNEL and Western blot. The expression of cytochrome c and caspase-3 was determined using western blot technique. Rat pups demonstrated neurobehavioral alteration in Groups C and B. TUNEL-positive cells in the left hippocampus were significantly increased in Group C and Group B after HIBD (P < 0.01) when compared with Group S. There was a marked reduction in TUNEL positive cells in subgroups B1 through B4 when compared with the respective subgroups C1 through C5. Compared with Group S, the expression of caspase-3 and cytochrome c was significantly increased in Groups C and B (P < 0.01). The difference in expression of caspase-3 and cytochrome c between subgroups B1 through B4 and C1 through C4 was significant (P < 0.01). In conclusions, the neuro-protective effect of BIP was due to a reduction of nerve cell apoptosis in our neonatal HIE rat model. We propose that BIP has potential as a neuro-protective drug in neonatal HIE cases.