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Weight regain within one year after weight loss is frequently observed and is referred to as yo-yo dieting or weight cycling. In this study, we explore the effects of yo-yo dieting on the liver, adipose tissue, and muscle characteristics of male zebrafish. Four-month-old AB wild-type male zebrafish were randomly assigned to three groups: high-calorie intake (H, seven meals per day), low-calorie intake (L, two meals per day), and yo-yo diet (the low- and high-calorie alternation switched every two weeks) groups. Feeding the fish the H diet for over 8 weeks led to steatosis and damage to the liver. The yo-yo diet reduced liver lipid accumulation at week eight but caused a similar degree of lipid accumulation as the H diet thereafter. It was found that twenty weeks of yo-yo dieting actually exacerbated hepatic damage. Compared to the L diet, feeding the fish on the yo-yo and H diets for a period of 20 weeks significantly increased the size of muscle fibers, resulting in higher speed during burst swimming and a significant increase in the size and number of adipocytes in the abdominal tissue. To summarize, short-term yo-yo dieting was found to attenuate hepatosteatosis and maintain fast-twitch muscle function. Long-term yo-yo dieting preserved fast-twitch muscle function and muscle fiber size; however, it exacerbated the pathological changes in the liver.

Dietary restriction (DR) is a potential intervention for ameliorating ageing-related damages. Mitochondrial quality control is the key mechanism for regulating cellular functions in skeletal muscle. This study aimed to explore the effect of age and DR on the homeostasis of mitochondrial quality control in skeletal muscle. To study the effect of age on mitochondrial homeostasis, young (3 months old) male C57BL/6J mice were fed ad libitum (AL) until 7 (Young), 14 (Middle), and 19 months (Aged) of age. For the DR intervention, 60% of AL intake was given to the mice at 3 months of age until they reached 19 months of age (16 months). The quadriceps femoris muscle was collected for further analysis. Significant changes in the skeletal muscle were noticed during the transition between middle age and the elderly stages. An accumulation of collagen was observed in the muscle after middle age. Compared with the Middle muscle, Aged muscle displayed a greater expression of VDAC, and lower expressions of mitochondrial dynamic proteins and OXPHOS proteins. The DR intervention attenuated collagen content and elongated the sarcomere length in the skeletal muscle during ageing. In addition, DR adjusted the abnormalities in mitochondrial morphology in the Aged muscle. DR downregulated VDAC expression, but upregulated OPA1 and DRP1 expressions. Taken together, greater pathological changes were noticed in the skeletal muscle during ageing, especially in the transition between middle age and the elderly, whereas early-onset DR attenuated the muscular ageing via normalising partial functions of mitochondria.

The synergic effects of activated carbon and transition metals on the hydrogenation characteristics of commercial ZK60 magnesium alloy were investigated. Severe plastic deformation was performed using equal-channel angular pressing with an internal die angle of 120° and preheating at 300 °C. The ZK60 alloy samples were processed for 12 passes using route BA. The deformed ZK60 alloy powder was blended with activated carbon and different concentrations of transition metals (Ag, Pd, Co, Ti, V, Ti) using high-energy ball milling for 20 h at a speed of 1725 rpm. The amount of hydrogen absorbed and its kinetics were calculated using Sievert’s apparatus at the higher number of cycles at a 300 °C ab/desorption temperature. The microstructure of the powder was analyzed using an X-ray diffractometer and scanning electron microscope. The results indicated that 5 wt% activated carbon presented the maximum hydrogen absorption capacity of 6.2 wt%. The optimal hydrogen absorption capacities were 7.1 wt%, 6.8 wt%, 6.7 wt%, 6.64 wt%, 6.65 wt%, and 7.06 wt% for 0.5 Ag, 0.3 Co, 0.1 Al, 0.5 Pd, 2 Ti, and 0.5 V, respectively. The hydrogen absorption capacities were reduced by 35.21%, 26.47%, 41.79%, 21.68%, 26.31%, and 26.34% after 100 cycles for 5C0.5Ag, 5C0.3Co, 5C0.1Al, 5C0.5Pd, 2Ti, and 5C0.5V, respectively. Hydrogen absorption kinetics were significantly improved so that more than 90% of hydrogen was absorbed within five minutes.

The demand for high-power, high-density VCSEL light sources in applications such as space, artificial intelligence, silicon photonics, and autonomous vehicles is steadily increasing. VCSEL chips are epitaxially grown on GaAs substrates and then packaged by attaching them to a mounting bracket using high-temperature-resistant adhesives. This issue limits the VCSEL’s output power, and restricts its application range. We propose first removing the VCSEL epitaxial layer from the GaAs substrate and transferring it to a CuW substrate. The VCSEL chip is then mounted on an AlN substrate using a metal eutectic bonding technique. The results indicate that bonding 36 VCSELs with a wavelength of 840 nm to CuW chips and mounting them onto an AlN substrate to form an array achieved voltage of 8.59 V and a driving current of 18 A. The output optical power reached 57.68 W, with a reduced packaging thermal resistance of 0.232 K/W.

The lack of structural information impeded the access of efficient luminescence for the exciplex type thermally activated delayed fluorescence (TADF). We report here the pump-probe Step-Scan Fourier transform infrared spectra of exciplex composed of a carbazole-based electron donor (CN-Cz2) and 1,3,5-triazine-based electron acceptor (PO-T2T) codeposited as the solid film that gives intermolecular charge transfer (CT), TADF, and record-high exciplex type cyan organic light emitting diodes (external quantum efficiency: 16%). The transient infrared spectral assignment to the CT state is unambiguous due to its distinction from the local excited state of either the donor or the acceptor chromophore. Importantly, a broad absorption band centered at ~2060 cm −1 was observed and assigned to a polaron-pair absorption. Time-resolved kinetics lead us to conclude that CT excited states relax to a ground-state intermediate with a time constant of ~3 µs, followed by a structural relaxation to the original CN-Cz2:PO-T2T configuration within ~14 µs. The development of exciplex-type hosts for thermally activated delayed fluorescence organic light-emitting diodes is hindered by a lack of structural information for these donor:acceptor blends. Here, the authors report the pump-probe Step-Scan Fourier transform IR spectra for a D:A exciplex host.

IntroductionDescribe real-world treatment of osteoporosis and romosozumab treatment patterns in Japan.Materials and methodsData for patients initiating romosozumab or other antiosteoporotic medications between March 01, 2018, and May 31, 2022, were extracted from the Medical Data Vision (MDV) and Japan Medical Data Center (JMDC) databases. Patients were categorized into four cohorts: those who newly initiated romosozumab within the first (MDV: n = 4782; JMDC: n = 2578) or second (MDV: n = 3888; JMDC: n = 2446) year after launch and those who initiated teriparatide (TPTD; MDV: n = 14,576; JMDC: n = 8259) or non-TPTD antiosteoporotic medications within the first year of romosozumab launch (MDV: n = 352,142; JMDC: n = 185,785).ResultsMean age, sex, baseline cardiovascular history, comorbidities, and concomitant medications were similar across cohorts. In the MDV database, fracture history was higher in the romosozumab year-1 (59.3%), year-2 (64.1%), and TPTD (65.5%) cohorts versus the non-TPTD cohort (24.4%). Similar rates were identified in the JMDC database: romosozumab year-1 (64.7%), year-2 (66.6%), TPTD (67.5%), and non-TPTD (27.8%). Vertebral fractures were most common in all cohorts. 12-month romosozumab discontinuation varied between the year-1 and year-2 cohorts in MDV (62.4% and 58.8%) and JMDC (57.1% and 52.7%), whereas mean number of injections remained consistent (MDV: 9.7 and 9.8; JMDC: 7.3 and 7.8). Romosozumab persistence was lower in year-1 versus year-2 (MDV: 37.6% and 42.9%; JMDC: 41.2% and 47.3%).ConclusionPatients initiating romosozumab and TPTD had a high fracture history. Given the dual effects of promoting bone formation and suppressing resorption, improving romosozumab adherence and persistence over time may be important for antiosteoporotic therapy.

Electron ptychography has emerged as a popular technology for high-resolution imaging by combining the high coherence of electron sources with the ultra-fast scanning electron coil. However, the limitations of conventional pixelated detectors, including poor dynamic range and slow data readout speeds, have posed restrictions in the past on conducting electron ptychography experiments. We used the Gatan STELA pixelated detector to capture sequential diffraction data of monolayer two-dimensional (2D) materials for ptychographic reconstruction. By using the pixelated detector and electron ptychography, we demonstrate the observation of the radiation damage at atomic resolution in Transition Metal Dichalcogenides (TMDs).

Background Long-term consumption of an excessive fat and sucrose diet (Western diet, WD) has been considered a risk factor for metabolic syndrome (MS) and cardiovascular disease. Caveolae and caveolin-1 (CAV-1) proteins are involved in lipid transport and metabolism. However, studies investigating CAV-1 expression, cardiac remodeling, and dysfunction caused by MS, are limited. This study aimed to investigate the correlation between the expression of CAV-1 and abnormal lipid accumulation in the endothelium and myocardium in WD-induced MS, and the occurrence of myocardial microvascular endothelial cell dysfunction, myocardial mitochondrial remodeling, and damage effects on cardiac remodeling and cardiac function. Methods We employed a long-term (7 months) WD feeding mouse model to measure the effect of MS on caveolae/vesiculo-vacuolar organelle (VVO) formation, lipid deposition, and endothelial cell dysfunction in cardiac microvascular using a transmission electron microscopy (TEM) assay. CAV-1 and endothelial nitric oxide synthase (eNOS) expression and interaction were evaluated using real-time polymerase chain reaction, Western blot, and immunostaining. Cardiac mitochondrial shape transition and damage, mitochondria-associated endoplasmic reticulum membrane (MAM) disruption, cardiac function change, caspase-mediated apoptosis pathway activation, and cardiac remodeling were examined using TEM, echocardiography, immunohistochemistry, and Western blot assay. Results Our study demonstrated that long-term WD feeding caused obesity and MS in mice. In mice, MS increased caveolae and VVO formation in the microvascular system and enhanced CAV-1 and lipid droplet binding affinity. In addition, MS caused a significant decrease in eNOS expression, vascular endothelial cadherin, and β-catenin interactions in cardiac microvascular endothelial cells, accompanied by impaired vascular integrity. MS-induced endothelial dysfunction caused massive lipid accumulation in the cardiomyocytes, leading to MAM disruption, mitochondrial shape transition, and damage. MS promoted brain natriuretic peptide expression and activated the caspase-dependent apoptosis pathway, leading to cardiac dysfunction in mice. Conclusion MS resulted in cardiac dysfunction, remodeling by regulating caveolae and CAV-1 expression, and endothelial dysfunction. Lipid accumulation and lipotoxicity caused MAM disruption and mitochondrial remodeling in cardiomyocytes, leading to cardiomyocyte apoptosis and cardiac dysfunction and remodeling.

Millions of patients worldwide are implanted with permanent pacemakers for the treatment of cardiac arrhythmias and conduction disorders. The increased use of these devices has established a growing clinical need to mitigate associated complications. Pacemaker leads, in particular, present the primary risks in most implants. While wireless power transfer holds great promise in eliminating implantable device leads, anatomical constraints limit efficient wireless transmission over the necessary operational range. We thereby developed a transmitter-centered control system for wireless power transfer with sufficient power for continuous cardiac pacing. Device safety was validated using a computational model of the system within an MRI-based anatomical model. The pacer was then fabricated to meet the acute constraints of the anterior cardiac vein (ACV) to enable intravascular deployment while maintaining power efficiency. Our computational model revealed the wireless system to operate at > 50 times below the tissue energy absorption safety criteria. We further demonstrated the capacity for ex vivo pacing of pig hearts at 60 beats per minute (BPM) and in vivo pacing at 120 BPM following pacer deployment in the ACV. This work thus established the capacity for wireless intravascular pacing with the potential to eliminate complications associated with current lead-based deep tissue implants.

Pulmonary artery hypertension (PAH) pathology involves extracellular matrix (ECM) remodeling in cardiac tissues, thus promoting cardiac fibrosis progression. miR-29a-3p reportedly inhibits lung progression and liver fibrosis by regulating ECM protein expression; however, its role in PAH-induced fibrosis remains unclear. In this study, we aimed to investigate the role of miR-29a-3p in cardiac fibrosis progression in PAH and its influence on ECM protein thrombospondin-2 (THBS2) expression. The diagnostic and prognostic values of miR-29a-3p and THBS2 in PAH were evaluated. The expressions and effects of miR-29a-3p and THBS2 were assessed in cell culture, monocrotaline-induced PAH mouse model, and patients with PAH. The levels of circulating miR-29a-3p and THBS2 in patients and mice with PAH decreased and increased, respectively. miR-29a-3p directly targets THBS2 and regulates THBS2 expression via a direct anti-fibrotic effect on PAH-induced cardiac fibrosis. The circulating levels of miR-29a-3p and THBS2 were correlated with PAH diagnostic parameters, suggesting their independent prognostic value. miR-29a-3p targeted THBS2 expression via a direct anti-fibrotic effect on PAH-induced cardiac fibrosis, indicating miR-29a-3p acts as a messenger with promising therapeutic effects.