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Social capital theory suggests that network structure influences human behavior. Based on this premise, this study investigates how two distinct network structures—brokerage and closure—affect support provision in Online Support Groups (OSGs). Twelve years of data were collected from an online cancer community based in South Korea. Using computational methods, we measured support behaviors, network structures, and social capital. The findings reveal that brokers, through exposure to non-redundant information, provide social support in larger volumes, with higher quality, and in a more timely manner. While closure has limited explanatory power for overall support behaviors, it specifically facilitates provision of improved quality of emotional support through one’s enhanced trust. Additionally, the results highlight the importance of recognizing the dynamic developmental stages of OSGs to fully understand the social mechanisms driving support provision. These findings offer significant insights into the mobilization of social support through network structures in the OSG context.

Over the last two decades, the incidence and mortality rates of gynecologic cancers have increased at a constant rate in China. Gynecologic cancers have become one of the most serious threats to women's health in China. With the widespread use of social media, an increasing number of individuals have employed social media to produce, seek, and share cancer-related information. However, health information on social media is not always accurate. Health, and especially cancer-related, misinformation has been widely spread on social media, which can affect individuals' attitudinal and behavioral responses to cancer. The aim of this study was to examine the nature and diffusion of gynecologic cancer-related misinformation on Weibo, the Chinese equivalent of Twitter. A total of 2691 tweets related to 2 gynecologic cancers-breast cancer and cervical cancer-posted on Weibo from June 2015 to June 2016 were extracted using the Python Web Crawler. Two medical school graduate students with expertise in gynecologic diseases were recruited to code the tweets to differentiate between true information and misinformation as well as to identify the types of falsehoods. The diffusion characteristics of gynecologic cancer-related misinformation were compared with those of the true information. While most of the gynecologic cancer-related tweets provided medically accurate information, approximately 30% of them were found to contain misinformation. Furthermore, it was found that tweets about cancer treatment contained a higher percentage of misinformation than prevention-related tweets. Nevertheless, the prevention-related misinformation diffused significantly more broadly and deeply than true information on social media. The findings of this study suggest the need for controlling and reducing the cancer-related misinformation on social media with the efforts from both service providers and medical professionals. More specifically, it is important to correct falsehoods related to the prevention of gynecologic cancers on social media and increase individuals' capacity to assess the veracity of Web-based information to curb the spread and thus minimize the consequences of cancer-related misinformation.

Apolipoprotein A5 (apoA5) has been identified to play an important role in lipid metabolism, specifically in triglyceride (TG) and TG-rich lipoproteins (TRLs) metabolism. Numerous evidence has demonstrated for an association between apoA5 and the increased risk of obesity and metabolic syndrome, but the mechanism remains to be fully elucidated. Recently, several studies verified that apoA5 could significantly reduce plasma TG level by stimulating lipoprotein lipase (LPL) activity, and the intracellular role of apoA5 has also been proved since apoA5 is associated with cytoplasmic lipid droplets (LDs) and affects intrahepatic TG accumulation. Furthermore, since adipocytes provide the largest storage depot for TG and play a crucial role in the development of obesity, we could infer that apoA5 also acts as a novel regulator to modulate TG storage in adipocytes. In this review, we focus on the association of gene and protein of apoA5 with obesity and metabolic syndrome, and provide new insights into the physiological role of apoA5 in humans, giving a potential therapeutic target for obesity and associated disorders.

Drug delivery systems with high content of drug can minimize excipients administration, reduce side effects, improve therapeutic efficacy and/or promote patient compliance. However, engineering such systems is extremely challenging, as their loading capacity is inherently limited by the compatibility between drug molecules and carrier materials. To mitigate the drug-carrier compatibility limitation towards therapeutics encapsulation, we developed a sequential solidification strategy. In this strategy, the precisely controlled diffusion of solvents from droplets ensures the fast in-droplet precipitation of drug molecules prior to the solidification of polymer materials. After polymer solidification, a mass of drug nanoparticles is embedded in the polymer matrix, forming a nano-in-micro structured microsphere. All the obtained microspheres exhibit long-term storage stability, controlled release of drug molecules, and most importantly, high mass fraction of therapeutics (21.8–63.1 wt%). Benefiting from their high drug loading degree, the nano-in-micro structured acetalated dextran microspheres deliver a high dose of methylprednisolone (400 μg) within the limited administration volume (10 μL) by one single intrathecal injection. The amount of acetalated dextran used was 1/433 of that of low drug-loaded microspheres. Moreover, the controlled release of methylprednisolone from high drug-loaded microspheres contributes to improved therapeutic efficacy and reduced side effects than low drug-loaded microspheres and free drug in spinal cord injury therapy. High drug loading improves therapeutic efficacy and reduces side effects in drug delivery. Here, the authors use controlled diffusion of solvents to precipitate drug nanoparticles in polymer particles while the polymer is solidifying and demonstrate the particles for drug delivery in a spinal cord injury model.

Achieving high selectivity of Li + and Mg 2+ is of paramount importance for effective lithium extraction from brines, and nanofiltration (NF) membrane plays a critical role in this process. The key to achieving high selectivity lies in the on-demand design of NF membrane pores in accordance with the size difference between Li + and Mg 2+ ions, but this poses a huge challenge for traditional NF membranes and difficult to be realized. In this work, we report the fabrication of polyamide (PA) NF membranes with ultra-high Li + /Mg 2+ selectivity by modifying the interfacial polymerization (IP) process between piperazine (PIP) and trimesoyl chloride (TMC) with an oil-soluble surfactant that forms a monolayer at oil/water interface, referred to as OSARIP. The OSARIP benefits to regulate the membrane pores so that all of them are smaller than Mg 2+ ions. Under the solely size sieving effect, an exceptional Mg 2+ rejection rate of over 99.9% is achieved. This results in an exceptionally high Li + /Mg 2+ selectivity, which is one to two orders of magnitude higher than all the currently reported pressure-driven membranes, and even higher than the microporous framework materials, including COFs, MOFs, and POPs. The large enhancement of ion separation performance of NF membranes may innovate the current lithium extraction process and greatly improve the lithium extraction efficiency. Achieving high selectivity of Li+ and Mg2+ is of paramount importance for effective lithium extraction from brines, and nanofiltration (NF) membrane plays a critical role in this process. Here the authors report the fabrication of polyamide NF membranes with ultra-high Li + /Mg2+ selectivity by modifying the interfacial polymerization process with an oil-soluble surfactant.

The inverse seesaw mechanism provides a concise scenario to produce tiny neutrino masses. Here we investigate the Majoron dark matter arising from the U ( 1 ) L symmetry spontaneous breaking and matter–antimatter asymmetry in the framework of a high scale inverse seesaw mechanism. Due to the existence of a lepton-number-violating mass term, the Majoron gets its mass from radiative corrections. On the other hand, the Noether’s theorem indicates that the Majoron can obtain a non-zero initial velocity in the early universe, and then generates the relic abundance via kinetic misalignment mechanism. With the same initial Majoron velocity, the observed baryon asymmetry can also be explained through the so-called spontanous bayogenensis mechanism.

The COVID-19 pandemic resulted in public anger due to its disruptive and harmful nature. However, anger remains an understudied concept despite its potential to persuade the public and spark action. The current study investigates the role of anger in driving COVID-19 vaccination intentions. In Study 1, through a rolling-cross sectional survey of U.S. adults during the early stages of the COVID-19 epidemic ( N = 6,141), it was found that anger towards COVID-19 was associated with increased use of social and traditional media news, which was then related to improved vaccination intentions. In Study 2, utilizing computational analysis of a Twitter (now X) dataset using an AI classifier, 15 targets of anger were identified from real-world anger expressions in social media discourse about COVID-19. Building on these insights, Study 3 involved a representative survey of U.S. adults during the post-emergency declaration stage of COVID-19 ( N = 1,005). This survey aimed to replicate the findings of Study 1 while incorporating the anger targets identified in Study 2. The results revealed that different targets of anger were associated with vaccination intentions through the consumption of traditional news media. Although social media was a prominent channel for news about vaccination at the beginning of the pandemic, our findings suggest that traditional media news use may be an important link in understanding the relationship between anger and vaccination intentions. Theoretical, practical, and methodological implications are discussed.

Observational studies have shown that low serum levels of vitamin D have been associated with an atherogenic lipid profile. However, the intervention studies gave divergent results. We conducted a meta-analysis of randomized controlled trials that evaluated the effects of vitamin D supplementation on blood lipids. A systematic literature search was conducted via MEDLINE, Cochrane library, and EMBASE for randomized controlled clinical trials assessing the effects of vitamin D supplementation on lipids. The mean change in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) from baseline was treated as a continuous variable. In all, 12 clinical trials consisting of 1346 participants were included in the analysis. The pooled estimate of effect for vitamin D supplementation on LDL-C was 3.23 mg/dl (95% confidence interval, 0.55 to 5.90 mg/dl). No statistically significant effects for vitamin D supplementation were observed for TC, HDL-C and TG (differences in means were 1.52 mg/dl (-1.42 to 4.46 mg/dl), -0.14 mg/dl (-0.99 to 0.71 mg/dl) and -1.92 mg/dl (-7.72 to 3.88 mg/dl) respectively). The lipid modulating effects of vitamin D supplementation should be further investigated though large-scale, randomized trials with adequate doses which can effectively elevated the active form of vitamin D in plasma and with proper population which has hyperlipemia as an inclusion criterion.

Background Vascular calcification is a closely linked to cardiovascular diseases, such as atherosclerosis, chronic kidney disease, diabetes, hypertension and aging. The extent of vascular calcification is closely correlate with adverse clinical events and cardiovascular all-cause mortality. The role of autophagy in vascular calcification is complex with many mechanistic unknowns. Methods In this review, we analyze the current known mechanisms of autophagy in vascular calcification and discuss the theoretical advantages of targeting autophagy as an intervention against vascular calcification. Results Here we summarize the functional link between vascular calcification and autophagy in both animal models of and human cardiovascular disease. Firstly, autophagy can reduce calcification by inhibiting the osteogenic differentiation of VSMCs related to ANCR, ERα, β-catenin, HIF-1a/PDK4, p62, miR-30b, BECN1, mTOR, SOX9, GHSR/ERK, and AMPK signaling. Conversely, autophagy can induce osteoblast differentiation and calcification as mediated by CREB, degradation of elastin, and lncRNA H19 and DUSP5 mediated ERK signaling. Secondly, autophagy also links apoptosis and vascular calcification through AMPK/mTOR/ULK1, Wnt/β-catenin and GAS6/AXL synthesis, as apoptotic cells become the nidus for calcium-phosphate crystal deposition. The failure of mitophagy can activate Drp1, BNIP3, and NR4A1/DNA‑PKcs/p53 mediated intrinsic apoptotic pathways, which have been closely linked to the formation of vascular calcification. Additionally, autophagy also plays a role in osteogenesis by regulating vascular calcification, which in turn regulates expression of proteins related to bone development, such as osteocalcin, osteonectin, etc. and regulated by mTOR, EphrinB2 and RhoA. Furthermore, autophagy also promotes vitamin K2-induced MC3T3 E1 osteoblast differentiation and FGFR4/FGF18- and JNK/complex VPS34–beclin-1-related bone mineralization via vascular calcification. Conclusion The interaction between autophagy and vascular calcification are complicated, with their interaction affected by the disease process, anatomical location, and the surrounding microenvironment. Autophagy activation in existent cellular damage is considered protective, while defective autophagy in normal cells result in apoptotic activation. Identifying and maintaining cells at the delicate line between these two states may hold the key to reducing vascular calcification, in which autophagy associated clinical strategy could be developed.