Bioscience trends最新文献

Respiratory infectious diseases have long been a serious public health problem. This study explores the significance of respiratory infectious disease prevention and control systems worldwide, particularly during and after the COVID-19 pandemic. The epidemiology of many respiratory diseases such as influenza changed over the past two years, and the incidence of pathogens such as Mycoplasma pneumoniae and Bordetella pertussis has also increased. Based on influenza surveillance data in China, the influenza season in 2023 was notably delayed and extended, with A(H1N1) pdm09 being the predominant strain. This editorial also reviewed the gradual establishment of China's infectious disease prevention and control system following the 2003 SARS outbreak, highlighting the role of medical facilities in managing public health emergencies, conducting infectious disease pre-screening, and reporting cases to networks in real time. In the future, China will further develop an intelligent, multi-trigger infectious disease surveillance and early warning system to increase the early detection of unknown infectious diseases and optimize the allocation of medical resources. A robust infectious disease control system is crucial to addressing future pandemic threats.

In recent years, with the decline in HBV and HCV infections, there has been a corresponding reduction in both the morbidity and mortality of virus-associated HCC. Nevertheless, rising living standards, coupled with the increasing prevalence of metabolic disorders like diabetes and obesity, have led to a rapid surge in non-alcoholic fatty liver disease-associated hepatocellular carcinoma (NAFLD-HCC) incidence. The mechanisms underlying the progression from NAFLD to NAFLD-HCC are multifaceted and remain incompletely understood. Current research suggests that genetic predisposition, metabolic dysregulation, lipotoxicity, oxidative stress, and inflammation are key contributing factors. Given the complexity of these mechanisms and the frequent occurrence of metabolic comorbidities like type 2 diabetes mellitus (T2DM) and cardiovascular disease in NAFLD-HCC patients, there is a pressing need for tailored therapeutic strategies, along with novel prevention, monitoring, and treatment approaches that are personalized to the patient's pathophysiology. Due to the limited depth of research, incomplete understanding of pathogenesis, and insufficient clinical data on NAFLD-HCC treatment, current therapeutic approaches largely rely on tumor staging. In this review, we synthesize current research on the pathogenesis, surveillance, diagnosis, treatment, and prevention of NAFLD-HCC, and offer perspectives for future studies, particularly regarding its underlying mechanisms.

Alzheimer's disease (AD) is a severe neurodegenerative disorder, and the current treatment options are limited. Mesenchymal stem cell-derived exosomes (MSC-Exos) have garnered significant attention due to their unique biological properties, showcasing tremendous potential as an acellular alternative therapy for AD. MSC-Exos exhibit excellent biocompatibility and low immunogenicity, enabling them to effectively cross the blood-brain barrier (BBB) and deliver therapeutic molecules directly to target cells. They are highly efficacious in delivering nucleic acid-based drugs. Moreover, the production process of MSC-Exos benefits from a high proliferation capacity and multilineage differentiation potential, allowing for production while maintaining a stable composition. Despite the significant theoretical advantages of MSC-Exos, their clinical use still faces multiple challenges, including cross-contamination during isolation and purification processes, the complexity of their components, and the presence of potential adverse paracrine factors. Future research needs to focus on optimizing separation and purification techniques, enhancing delivery methods to improve therapeutic efficacy, and performing detailed analyses of the components of MSC-Exos. In summary, MSC-Exos hold promise as an effective option for the treatment of AD and other neurodegenerative diseases, driving their clinical research and use in related fields.

Japan, the world's most rapidly aging society, faces increasing financial strains related to personalized dementia care. The government has shifted its focus from prevention to coexistence with dementia, as outlined in the 2023 Basic Act on Dementia. Emphasis on financial inclusion aligns with the G20's 2019 "Fukuoka Policy Priorities on Aging and Financial Inclusion", which addresses financial exclusion due to cognitive decline and poor financial literacy. While economic activity among older adults is already hampered by legal challenges and risks associated with dementia, outcomes are expected to worsen as the assets of older adults with dementia are projected to reach 215 trillion JPY ($1.4 trillion USD) by 2030. Government measures and research in financial gerontology advocate for protecting older adults and promoting flexible financial practices. Enhanced efforts and shared research outcomes are crucial for Japan to be a leader as an advanced aging society.

Sorafenib is a recommended first-line therapy for advanced hepatocellular carcinoma (HCC). However, when used as monotherapy in patients in advanced stages, the prognosis remains suboptimal. This study aimed to evaluate the impact of transcatheter arterial chemoembolization (TACE) on survival outcomes in patients with advanced HCC treated with sorafenib, as well as to identify which subgroups may benefit most from the addition of TACE. This single-institution retrospective study included 92 patients diagnosed with Barcelona Clinic liver cancer (BCLC) stage C HCC who received sorafenib between August 2011 and December 2016. We assessed the influence of different treatment modalities on prognosis using multivariable regression analysis. Patients were categorized into three subgroups: those with vascular invasion, those with distant metastasis, and those with both risk factors. Baseline comparisons indicated no significant differences in clinical characteristics among the three groups. Survival analysis showed no statistically significant difference in overall survival (OS) between the subgroups. However, in the overall cohort of patients with BCLC stage C, multifactorial Cox regression analysis identified pre-treatment alpha-fetoprotein (AFP) levels (p = 0.020), alkaline phosphatase (ALP) levels (p = 0.034), and the absence of combination TACE therapy (p = 0.008) as independent risk factors affecting OS. Further subgroup Cox analyses revealed that the lack of combination TACE therapy was an independent risk factor for OS in both the vascular invasion group and the group with both risk factors. In conclusion, for patients with advanced HCC receiving sorafenib, the addition of TACE may enhance long-term survival, particularly in those with vascular invasion.

With the rapid growth of the elderly population, dementia has become a global challenge that governments must address. Given the incurable nature of dementia, rehabilitation interventions starting in the mild cognitive impairment (MCI) stage may offer a solution. For a rehabilitation intervention to be implemented as early as possible, existing problems of identification of MCI and development of MCI-specific forms of rehabilitation must be addressed. Use of computer technologies such as virtual reality and artificial intelligence might be helpful in overcoming these problems. Multi-disciplinary integrated approaches to rehabilitation should be the direction that dementia-related rehabilitation takes in the future. In addition to early rehabilitation, prevention of cognitive decline through the development of public community-based services for the elderly might be a more reasonable approach.

Diabetes-induced neuropathy represents a major etiology of dementia, highlighting an urgent need for the development of effective therapeutic interventions. In this study, we explored the role of fibronectin type III domain containing 5 (FNDC5)/Irisin in mitigating hyperglycemia-induced neurotoxicity in HT22 cells and investigated the underlying mechanisms. Our findings reveal that high glucose conditions are neurotoxic, leading to reduced viability of HT22 cells and increased apoptosis. Furthermore, the elevated expression of the intracellular ferroptosis marker Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), along with increased levels of ferrous ions and malondialdehyde (MDA), suggests that high glucose conditions may induce ferroptosis in HT22 cells. FNDC5/Irisin treatment effectively mitigates high glucose-induced neurotoxicity and ferroptosis in HT22 cells. Mechanistically, FNDC5/Irisin enhances cellular antioxidant capacity, regulates ACSL4 expression, and improves intracellular redox status, thereby inhibiting ferroptosis and increasing HT22 cell survival under high-glucose conditions. These results highlight the neuroprotective potential of FNDC5/Irisin in high glucose environments, offering a promising avenue for developing treatments for diabetes-related neurodegenerative diseases.

A better understanding of the causal relationship between spousal cognitive functioning and depression levels among middle-aged and older adults is vital for effective health policymaking under the globally severe aging challenge. However, the related evidence is often limited by potential omitted-variable bias and reverse causation. This study uses an instrumental variables approach, namely the two-stage least squares (2SLS) method, to examine the impact of spousal cognitive functioning on depression levels among middle-aged and older adults in China. The data were sourced from the China Health and Retirement Longitudinal Study (CHARLS) of 2020, including a total of 3,710 couples aged 45 years and above. Depression levels were measured using the Center for Epidemiologic Studies Depression Scale (CES-D-10), while cognitive functioning was assessed using the Mini-Mental State Examination (MMSE). Spousal social participation was employed as the instrumental variable to address omitted-variable bias and reverse causation. Additionally, an interaction effect test between gender and spousal cognitive functioning was conducted. The results show that for each one-point increase in the spouse's MMSE score, the CES-D-10 score of middle-aged and older adults decreased by 17.1% to 68.2%. The OLS results indicated that women, rural residents, and middle-aged individuals were more sensitive to these changes. The interaction effect test results confirmed that women were more affected by changes in spousal cognitive functioning. However, after a more reliable 2SLS analysis, the results for age groups shifted, showing that middle-aged individuals were more sensitive to these changes, with a decrease in depression levels reaching 70.0%, compared to 60.2% for the elderly group. Nonetheless, given the prevalence of depression among the elderly, the impact of spousal cognitive decline on depression in this group should not be overlooked. Our findings highlight the importance of spousal cognitive health in managing depression among both middle-aged and older adults, with particular attention to women and rural populations.

Coronary artery calcification (CAC) is an early marker for atherosclerosis and is mainly induced by the osteoblast-like phenotype conversion of vascular smooth muscle cells (VSMCs). Recent reports indicate that NOD-like receptor protein 3 (NLRP3)-mediated pyroptosis plays a significant role in the calcification of vascular smooth muscle cells (VSMCs), making it a promising target for treating calcific aortic valve disease (CAC). Ligustrazine, or tetramethylpyrazine (TMP), has been found effective in various cardiovascular and cerebrovascular diseases and is suggested to inhibit NLRP3-mediated pyroptosis. However, the function of TMP in CAC is unknown. Herein, influences of TMP on β-glycerophosphate (β-GP)-stimulated VSMCs and OPG^-/- mice were explored. Mouse Aortic Vascular Smooth Muscle (MOVAS-1) cells were stimulated by β-GP with si- caspase-3, si- Gasdermin E (GSDME) or TMP. Increased calcification, reactive oxygen species (ROS) level, Interleukin-1beta (IL-1β) and Interleukin-18 (IL-18) levels, lactate dehydrogenase (LDH) release, enhanced apoptosis, and activated cysteine-aspartic acid protease-3 (caspase-3)/GSDME signaling were observed in β-GP-stimulated MOVAS-1 cells, which was sharply alleviated by si-caspase-3, si-GSDME or TMP. Furthermore, the impact of TMP on the β-GP-induced calcification and injury in MOVAS-1 cells was abolished by raptinal, an activator of caspase-3. Subsequently, OPG^-/- mice were dosed with TMP or TMP combined with raptinal. Calcium deposition, increased nodules, elevated IL-1β and IL-18 levels, upregulated CASP3 and actin alpha 2, smooth muscle (ACTA2), and activated caspase-3/GSDME signaling in OPG^-/- mice were markedly alleviated by TMP, which were notably reversed by the co-administration of raptinal. Collectively, TMP mitigated CAC by inhibiting caspase-3/GSDME mediated pyroptosis.

Intrahepatic bile duct mucinous adenocarcinoma (IHBDMAC) is a rare pathological subtype of intrahepatic cholangiocarcinoma (IHCC), and its tumor biological features and survival outcomes have rarely been explored, especially when compared to the most common subtype, intrahepatic bile duct adenocarcinoma (IHBDAC). Therefore, the aim of this study was to explore the clinical features and survival outcomes of IHBDAC and IHBDMAC using the Surveillance, Epidemiology, and End Results (SEER) database from 2000 to 2021. A total of 1,126 patients were included, with 1,083 diagnosed with IHBDAC and 43 diagnosed with IHBDMAC. Patients with IHBDMAC presented with a more advanced T stage (55.8% vs. 36.9%, P = 0.012) and higher rate of lymph node metastasis (37.2% vs. 24.9%, P = 0.070). Cox regression identified advanced T stage, lymph node metastasis, and distant metastasis as poor survival predictors, while chemotherapy and surgery were protective factors. Survival analyses revealed significantly worse overall survival (OS) and cancer-specific survival (CSS) for IHBDMAC compared to IHBDAC (P < 0.05). Even after matching, patients with IHBDMAC still had a worse prognosis than those with IHBDAC. These findings highlight the aggressive nature of IHBDMAC and the need for tailored therapeutic strategies. Future research should focus on prospective studies and molecular insights to develop targeted treatments for IHBDMAC.