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Our aim was to explore the patterns of intrinsic capacity (IC) impairments among community-dwelling older adults and the associations of these different patterns with excessive polypharmacy, potentially inappropriate medications, and adverse drug reactions in a nationwide population-based study. A cross-sectional study included older adults from the Taiwan Integrated Care for Older People (ICOPE) program in 2020. The study subjects comprised 38,308 adults aged 65 years and older who participated in the ICOPE Step 1 screening and assessed six domains of IC following the World Health Organization (WHO) ICOPE approach. Latent class analysis was adopted to identify distinct subgroups with different IC impairments patterns. The associations between different IC impairments patterns and unfavorable medication utilization, including excess polypharmacy (EPP), potentially inappropriate medications (PIMs), and adverse drug reactions (ADRs), were assessed by multivariate logistic regression models. Latent class analysis identified five distinct subgroups with different IC impairment patterns: robust (latent class prevalence: 59.4%), visual impairment (17.7%), physio-cognitive decline (PCD) with sensory impairment (12.3%), depression with cognitive impairment (7.7%), and impairments in all domains (2.9%). Compared to the robust group, all other groups were at higher odds for unfavorable medication utilization. The “depression with cognitive impairment” group (EPP: aOR=4.35, 95% CI 3.52–5.39, p<0.01; PIMs: aOR=2.73, 95% CI 2.46–3.02, p<0.01) and the “impairment in all domains” group (EPP: aOR=9.02, 95% CI 7.16–11.37, p<0.01; PIMs: aOR=3.75, 95% CI 3.24–4.34, p<0.01) remained at higher odds for EPP and PIMs after adjustment. We identified five distinct impairment patterns of IC, and each impairment pattern, particularly the “depression with cognitive impairment” and “impairment in all domains”, was associated with higher odds of EPP and PIMs. Further longitudinal and intervention studies are needed to explore long-term outcomes of different impairment pattern and their reversibility.

Intrinsic capacity (IC), defined by the World Health Organization's Integrated Care for Older People (ICOPE) framework, is crucial for promoting healthy aging. Understanding the associations between IC impairments and age-related biomarkers can provide insights into the underlying pathophysiological mechanisms and potential interventions. To investigate the associations between IC impairments (ICOPE step 1 and step 2, respectively) and aging-related biomarkers, including inflammatory and cardiometabolic markers, in community-dwelling middle-aged and older adults. Cross-sectional analysis of data from 755 participants (aged 50–64 years, n=212; 65–74 years, n=357; ≥75 years, n=186) enrolled in the Gan-Dau Healthy Longevity Plan, a community-based survey in Taipei City, Taiwan, from 2022. IC impairments assessed by ICOPE Step 1 (screening) and Step 2 (in-depth assessment) across six domains: locomotion, vitality, vision, hearing, cognition, and psychological well-being. Levels of inflammatory biomarkers (albumin, white blood cell count, neutrophils, lymphocytes, monocytes, neutrophil-to-lymphocyte ratio [NLR], lymphocyte-to-monocyte ratio [LMR], platelet-to-lymphocyte ratio [PLR]) and cardiometabolic biomarkers (low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], total cholesterol, fasting glucose, triglycerides, triglyceride-glucose [TyG] index). Of the 755 participants, the mean age was 68.5 years, and 68.2% were women. The proportion of participants with any IC impairment increased with age: 63.2% for those aged 50–64, 65.8% for those aged 65–74, and 74.7% for those aged ≥75 years based on ICOPE Step 1. For ICOPE Step 2, the proportions were 59.9%, 56.9%, and 64.0%, respectively. Impairments in locomotion and cognition were significantly higher in the oldest age group (≥75 years). Adjusted for covariates, IC impairment (ICOPE Step 2) was associated with higher levels of neutrophil count (β = 3.17, p = 0.015) and NLR (β = 0.34, p = 0.021) in those aged 50–64 years, and higher levels of monocyte count in those aged 65–74 years (β = 0.65, p = 0.001) and ≥75 years (β = 0.68, p = 0.037). In conclusion, IC impairments were associated with alterations in specific inflammatory biomarkers, suggesting potential interactions between IC, age, and inflammatory processes. Longitudinal studies are warranted to establish causal relationships and elucidate the underlying mechanisms linking IC impairments, immune dysregulation, and the aging process.

Human papillomaviruses (HPVs) are associated with a number of benign and malignant neoplasms. To substantiate the relationship between HPV DNA and colorectal carcinomas, 70 carcinomas and 37 adenomas were analysed in this study. Specific types of HPV DNA in colorectal tumours were detected by polymerase chain reaction (PCR) and Southern blot hybridisation. HPV DNA was detected in 11 of 37 (29.7%) adenomas and in 52.9% 37 of 70 (52.9%) of carcinomas. The expression of HPV DNA in adenomas and carcinomas, especially that of HPV 16 in HPV positive cases (4 of 11 v 26 of 37), was significantly different (p < 0.05). There was no correlation, however, between HPV and the location, differentiation, stage, or survival of malignant neoplasms. These data suggest that HPV DNA, especially type 16, is associated with colorectal carcinogenesis.

About 10% of gastric carcinomas including lymphoepithelioma-like carcinoma and adenocarcinoma are associated with Epstein-Barr virus (EBV) infection. In EBV-associated gastric carcinomas, the tumor cells express Epstein-Barr nuclear antigen 1 (EBNA-1) but not EBNA-2, -3A, -3B, or -3C, leader protein, or latent membrane proteins (LMPs) because of gene methylation. Only a few exceptional cases have LMP1 expression in tumor cells as demonstrated by immunohistochemical studies. To elucidate the biological effects of LMP1 and the significance of its restricted expression in EBV-associated gastric carcinomas, the LMP1 gene was transferred into EBV-negative gastric carcinoma cell lines (SCM1 and TMC1) and into EBV-negative nasopharyngeal carcinoma (NPC) cells (HONE-1) as a control. The biological effects of LMP1 in gastric carcinoma cells were monitored in vitro and in vivo. These results showed that the consequence of LMP1 expression is a growth enhancement in NPC cells, but it is a growth suppression in gastric carcinoma cells. The LMP1-expressing gastric carcinoma cells had a reduced growth rate, colony-forming efficiency, mean colony size, and tumorigenicity and a lower malignant cytological grade. The reduced growth rate, colony-forming efficiency, and mean colony size were partially reversible in vitro with treatment with LMP1 antisense oligonucleotide. In addition, enhanced apoptosis was found in the LMP1-expressing gastric carcinoma cells. This suggests that LMP1 may negatively modulate the malignant potential of gastric carcinoma cells via an enhancement of apoptosis. We concluded that the restriction of LMP1 expression in EBV-associated gastric carcinomas may lead to a growth advantage for tumor cells by avoiding LMP1 apoptotic effects and immunologically mediated elimination.

Epstein-Barr virus (EBV) has been known to be associated with many malignant tumors, including nasopharyngeal carcinoma (NPC). Previous studies have indicated that an EBV-encoded oncoprotein, latent membrane protein 1 (LMP1), is expressed in many NPC tissues. LMP1 has been shown to stimulate HIV LTR through the two NF-kappa B binding sites within this promoter. In this study, we examined the feasibility of using this property of LMP1 as a therapeutic strategy for the treatment of NPC. This therapy consists of the preferential killing of the LMP1-expressing cells by gene transfer using the NF-kappa B-mediated herpes simplex virus thymidine kinase (HSVtk)/ganciclovir (GCV) system. The 800-bp HIV-LTR, which contains two NF-kappa B binding sites, was used to drive the HSVtk gene. Stable C33A cell clones expressing the LMP1 and the HSVtk genes were subjected to the GCV sensitivity test. Results showed that cells expressing both the LMP1 and the HSVtk genes were highly sensitive to GCV treatment. These cells were introduced into nude mice subcutaneously and tumors became palpable within 2 weeks. GCV was then introduced intraperitoneally to these mice and the sizes of the tumors were measured daily. Results showed that the tumors regressed in the group of mice carrying cells that stably expressed both the LMP1 and the HSVtk genes, but not in mice carrying cells containing LMP1 or HSVtk alone. Our data indicate that the HSVtk gene expressed from a NF-kappa B-binding motif-containing promoter that is regulated by LMP1 may be used as an in vivo gene therapy strategy of EBV LMP1-expressing cancers such as NPC.

This paper presents a scheme for fast identification of parameters in systems that yield large-order measurement vectors. The method can be applied to real-time identification and control. In the paper, the scheme is applied to identification and control of an optical model of a space antenna. Both the mathematical models and numerical results are presented.

Studies have already shown that intracellular calcium plays an important role in signalling cell cleavage in cytokinesis. However, the exact mechanics of calcium's participation in cytokinesis have yet to be fully understood. To better understand the temporal and spatial resolution of calcium, a calcium indicator probe was injected to zebrafish embryos and traced through confocal microscopy. Results support the hypothesis that calcium signalling is involved in cytokinesis and that proper concentrations of free calcium ions need to occur in the right place and the right time for the process to be complete.

Mechanistic target of rapamycin （mTOR） complex 1 （mTORC1） integrates signals from growth factors, cel- lular energy levels, stress and amino acids to control cell growth and proliferation through regulating trans- lation, autophagy and metabolism. Here we determined the cryo-electron microscopy structure of human mTORC1 at 4.4 A resolution. The mTORCI comprises a dimer of heterotrimer （mTOR-Raptor-mLST8） mediated by the mTOR protein. The complex adopts a hollow rhomboid shape with 2-fold symmetry. Notably, mTORC1 shows intrinsic conformational dynamics. Within the complex, the conserved N-terminal caspase- like domain of Raptor faces toward the catalytic cavity of the kinase domain of mTOR. Raptor shows no caspase activity and therefore may bind to TOS motif for sub- strate recognition. Structural analysis indicates that FKBP12-Rapamycin may generate steric hindrance forsubstrate entry to the catalytic cavity of mTORCI. The structure provides a basis to understand the assembly of mTORC1 and a framework to characterize the regu- latory mechanism of mTORC1 pathway.

This paper proposes a novel square 9-coil (3×3) matrix system for induction cooking applications in order to improve the heating performance. By means of finite element method (FEM) analysis, three different exciting modes for the proposed system are thoroughly investigated. The magnetic field and eddy currents distribution are studied for each case. Furthermore, thermal field computation is conducted to analyze and compare the heating performance for the proposed system with different exciting modes. The thermal field computation results indicate that the proposed square 9-coil system can effectively and significantly enhance the heating performance in terms of better uniformity and heating efficiency over conventional single coil systems. (5 pages)

Human papillomavirus (HPV) 16 DNA is closely associated with human cancers. It has been identified as an aetiological agent in cervical cancers and, recently, in colonic neoplasms. To further understand the role of HPV 16 DNA in colorectal carcinogenesis, NIH3T3 cells were transformed with high molecular weight DNA from colonic cancer cells and the expression of HPV 16 DNA detected. Both human Alu and HPV 16 DNA sequences were found in the type II foci of CC-M2T cells by Southern blot hybridisation. Additionally, 100% tumorigenicity in nude mice was seen. This study shows the transfection of HPV DNA from colonic cancers into NIH3T3 mouse cells and suggests that HPV type 16 might be associated with the malignant transformation of colonic cells.