Intestinal flora and linear growth in children.

The gut microbiota plays a critical role in human growth and development as well as the regulation of human pathophysiological processes. According to research, the gut microbiota controls the host's growth and development in areas such as nutrition, metabolism, endocrine hormones, and immune modulation. The human gut microbiota has an important role in child and adolescent growth, especially when nutritional conditions are poor. In this review, we focus on recent findings about the gut microbiota's influence on child growth, including the relationship between the gut microbiota and linear growth during pregnancy, infancy, childhood, and adolescence. Furthermore, we also review some mechanisms by which intestinal flora influence the host's linear growth. Although the data supports a link between intestinal flora and linear development in children, our review has limitations that prohibit us from fully verifying the causal relationship between gut flora and linear development in children. Improving the gut microbiota, in conjunction with renutrition techniques, has the potential to ameliorate the growth and development impairments currently associated with chronic illness and malnutrition in children.

The Biological Function of POLA2 in Hepatocellular Carcinoma.

INTRODUCTION: The role and prognostic value of POLA2 in liver cancer were comprehensively analyzed through TCGA, GEO, and ICGC databases, and the role of POLA2 in liver cancer cells and the regulatory mechanism involved were further verified through cell experiments. Hepatocellular carcinoma (HCC) is the most prevalent malignancy with high morbidity and mortality. Consequently, it is critical to identify robust and reliable predictive biomarkers and therapeutic targets for HCC patients. POLA2 is involved in the regulation of various tumors, but the specific role of POLA2 in HCC has not been reported. The regulatory role and prognostic value of POLA2 in HCC were determined by bioinformatics techniques and cell experiments. METHOD: The specific role and prognostic value of POLA2 in HCC were comprehensively analyzed by combining the expression data of POLA2 in TCGA, GEO, and ICGC databases and clinical data. In clinical samples, the expression of POLA2 in liver cancer was verified by QPCR. Further, the regulatory role of POLA2 in HCC was explored through cell experiments such as CCK-8, clonal formation experiment, EDU cell proliferation experiment, and flow cytometry. In terms of mechanism exploration, western blot was used to verify the specific regulatory mechanism that POLA2 participated in. Finally, the relationship between POLA2 and immune invasion of HCC was analyzed by using the TIMER database. RESULT: A POLA2 expression and prognosis analysis of HCC patients was conducted using the TCGA, GEO, and ICGC databases. We hypothesized that POLA2 might be one of the key factors contributing to the HCC progression. According to a combined analysis of TCGA, ICGC, and GEO databases, POLA2 was highly expressed in HCC. This was further confirmed in clinical samples using the qPCR. POLA2 knockdown was also performed in vitro on HCC cell lines to study the changes in their biological behavior. We confirmed that POLA2 was associated with HCC proliferation by CCK-8, Colony Formation, and EDU assay. We verified the POLA2's involvement in cell cycle regulation using flow techniques. The relationship between POLA2 and PI3K/AKT/mTOR pathway was explored using Western Blotting experiments regarding its mechanism. Further analysis revealed that the POLA2 expression was significantly associated with HCC immune infiltration. CONCLUSION: Our study demonstrated POLA2's importance in HCC development and progression and its potential role as a biomarker for disease progression on multiple levels. POLA2 has an important role in regulating the cell cycle and cell proliferation. By interfering with the cell cycle and proliferation, HCC cell growth is inhibited. Furthermore, POLA2 expression was significantly associated with immune infiltration. POLA2 may play a role in HCC immunotherapy based on its correlation with several immune cell types' genetic markers. The findings of this study are expected to lead to new anticancer strategies for HCC.

Establishment of an endoplasmic reticulum stress-associated lncRNAs model to predict prognosis and immunological characteristics in hepatocellular carcinoma.

BACKGROUND: The endoplasmic reticulum stress (ERS) and unfolded protein response (UPR) pathways play an essential role in the pathophysiology of hepatocellular carcinoma (HCC), and activation of the UPR pathway is strongly associated with tumor growth. However, the function of ERS-associated long non-coding RNAs (lncRNAs) in HCC is less recognized. METHODS: We have used TCGA (The Cancer Genome Atlas) to obtain clinical and transcriptome data for HCC patients and the GSEA (Gene Set Enrichment Analysis) molecular signature database to get the ERS gene. ERS-associated prognostic lncRNA was determined using univariate Cox regression study. Then, least absolute shrinkage and selection operator and multivariate Cox regression study were used to construct ERS-associated lncRNAs risk model. Next, we use Kaplan-Meier (KM) survival study, time-dependent receiver operating characteristic (ROC) curve, univariate and multivariate Cox regression study to validate and evaluate the risk model. GSEA reveals the underlying molecular mechanism of the risk model. In addition, differences in Immune cell Infiltration Study, half-maximal inhibitory concentration (IC50) and immune checkpoints blockade (ICB) treatment between high and low risk groups were analyzed. RESULTS: We constructed a risk model consisting of 6 ERS-associated lncRNAS (containingMKLN1-AS, LINC01224, AL590705.3, AC008622.2, AC145207.5, and AC026412.3). The KM survival study showed that the prognosis of HCC patients in low-risk group was better than that in high-risk group. ROC study, univariate and multivariate Cox regression study showed that the risk model had good predictive power for HCC patients. Our verification sample verified the aforesaid findings. GSEA suggests that several tumor- and metabolism-related signaling pathways are associated with risk groups. Simultaneously, we discovered that the risk models may help in the treatment of ICB and the selection of chemotherapeutic drugs. CONCLUSIONS: In this article, we created an ERS-associated lncRNAs risk model to help prognostic diagnosis and personalized therapy in HCC.

ASF1B, as an Independent Prognostic Biomarker, Correlates with Immune Infiltrates in Hepatocellular Carcinoma.

BACKGROUND: Hepatocellular Carcinoma (HCC) is one of the fastest-growing malignancies globally. The impact of surgical treatment is limited, and molecular targeted therapy has not yielded a consistent efficacy. This warrants for identification of novel molecular targets. The Anti- Silencing Function of 1B histone chaperone (ASF1B) was previously studied in numerous cancers. However, the understanding of its role in HCC is limited. METHODS: The TIMER database was used to analyze the ASF1B expression in pan-cancer and paracarcinoma tissues. ASF1B expression in HCC was confirmed using the HCCDB database, Quantitative real-time PCR (q-PCR), and Western Blot (WB) assays. The relationship between clinicopathological parameters and ASF1B expression was analyzed using UALCAN, whereas the prognostic value of ASF1B was evaluated using the GEPIA database. Linkedomics and cBioPortal databases were used to validate the ASF1B co-expression associated with immune infiltration by the TIMER database. Moreover, cell proliferation after ASF1B-knockdown was determined through CCK8 and clone formation assays. RESULTS: ASF1B was highly expressed in HCC tissues, and the expression levels were linked to tumor grade, race, and disease stage. Univariate and multivariate Cox models showed that ASF1B is an independent prognostic factor in HCC. CCK8 and clone formation assays demonstrated that ASF1B promotes cell proliferation. Gene co-expression analysis in Linkedomics demonstrated that HJURP, KIF2C, KIF4A, KIF18B, and KIFC1 expressions were closely associated with ASF1B and immune infiltrate cells. CONCLUSION: This study shows that ASF1B promotes the proliferation of HCC. Besides, ASF1B could be a potential prognostic biomarker for HCC patients.

Adjusting Local Molecular Environment for Giant Ambient Thermal Contraction.

A low-energy triggered switch that can generate mechanoresponse has great technological potential. A submolecular moiety, S-dibenzocyclooctadiene (DBCOD) that is composed of a flexible eight-membered ring connecting to a phenyl ring at each end, undergoes a conformational change from twist-boat to chair under a low-energy stimulus such as near infrared irradiation, resulting in thermal contraction of DBCOD-based polymer. Experimental evidence corroborated by theoretical calculations indicates that introducing molecular asymmetry can reduce crystallinity significantly and consequently facilitate the kinetics of the conformational change. It has been demonstrated that the negative thermal expansion (NTE) coefficient of a DBCOD-based polymer system can be adjusted in a range from -1140 to -2350 ppm K-1 . -2350 ppm K-1 is ≈10 times better than the value reported by the second best NTE system.

Large negative thermal expansion of a polymer driven by a submolecular conformational change.

Mechanoresponsive polymers hold great technological potential in drug delivery, 'smart' optical systems and microelectromechanical systems. However, hysteresis and fatigue (associated with large-scale polymer chain rearrangement) are often problematic. Here, we describe a polyarylamide film that contains s-dibenzocyclooctadiene (DBCOD), which can generate unconventional and completely reversible thermal contraction under low-energy stimulation. The films exhibit a giant negative thermal expansion coefficient of approximately -1,200 ppm K(-1) at ambient or near-ambient temperatures, much higher than any known negative-thermal-expansion materials under similar operating conditions. Mechanical characterization, calorimetry, spectroscopic analysis and density-functional theory calculations all point to the conformational change of the DBCOD moiety, from the thermodynamic global energy minimum (twist-boat) to a local minimum (chair), as the origin of this abnormal thermal shrinkage. This newly identified, low-energy-driven, thermally agile molecular subunit opens a new pathway to creating near-infrared-based macromolecular switches and motors, and for ambient thermal energy storage and conversion.