Evaluation of the safety and potential lipid-lowering effects of oral hydrogen-rich coral calcium (HRCC) capsules in patients with metabolic syndrome: a prospective case series study.

Background: Metabolic syndrome is characterized by a cluster-like occurrence of conditions such as hypertension, hyperglycaemia, elevated low-density lipoprotein (LDL) cholesterol or triglycerides (TG) and high visceral fat. Metabolic syndrome is linked to the build-up of plaque within the artery, which leads to disorders of the circulatory, nervous and immune systems. A variety of treatments target the regulation of these conditions; nevertheless, they remain dominant risk factors for the development of type 2 diabetes (T2DM) and cardiovascular disease (CVD), which affect 26.9% of the US population. Management and intervention strategies for improving cholesterol and/or TG are worthwhile, and recent studies on hydrogen treatment are promising, particularly as molecular hydrogen is easily ingested. This study aimed to investigate the lipid-lowering effects and quality of life (QOL) improvement of hydrogen-rich coral calcium (HRCC) in patients with metabolic syndrome. Methods: The patients, all Taiwanese, were randomly assigned to 3 different doses (low, medium, and high) of HRCC capsules. The primary outcome was the adverse effects/symptoms during this 4-week use of HRCC capsules. The secondary outcome was lipid profile changes. Complete blood count, inflammatory biomarkers, and QOL were also measured before and after the course of HRCC. Results: Sixteen patients with metabolic syndrome completed this study (7 males, 9 females; mean age: 62 years; range: 32-80). No obvious adverse effects were recorded. Only changes in blood TG reached significance. The baseline TG value was 193.19 µL (SD = 107.44), which decreased to 151.75 µL (SD = 45.27) after 4 weeks of HRCC (p = 0.04). QOL showed no significant changes. Conclusion: This study is the first human clinical trial evaluating HRCC capsules in patients with metabolic syndrome. Based on the safety and potential TG-lowering effects of short-term HRCC, further long-term investigations of HRCC are warranted. Clinical trial registration: [ClinicalTrials.gov], identifier [NCT05196295].

Repetitive mild traumatic brain injury alters diurnal locomotor activity and response to the light change in mice.

Mild traumatic brain injury (mTBI) is a common cause of brain damage with a high incidence of multiple mTBIs found among athletes and soldiers. The purpose of this study is to examine the diurnal behavioral changes after multiple mTBIs. Adult mice were anesthetized; mTBI was conducted by dropping a 30-g weight to the right temporal skull once (mTBI1) or three times (mTBI3) over 3-week. Open-field motor behavior was recorded for 3 days after the last mTBI. In the first 4-hour exploratory phase, mTBI1 or mTBI3 equally reduced locomotor activity. A significant reduction of locomotor activity was found in the dark cycle between 4-72 hour in mTBI1 or mTBI3 mice; higher motor activity was seen after mTBI3 compared to mTBI1. In the light cycle, mTBI3 mice demonstrated an earlier immobilization followed by hyperactivity. The response to light change significantly correlated with the number of impacts. The IBA1 and BAX protein levels were equally increased in the lesioned cortex after mTBI1 and mTBI3. mTBI3 selectively upregulated the expression of circadian clock gene Per1 in hypothalamus and hippocampus as well as iNOS expression in the lesioned side cortex. Our data suggest multiple mTBIs alter diurnal locomotor activity and response to the change of light, which may involve Per1 expression in the lesioned brain.

Establishment of a repeated social defeat stress model in female mice.

Numerous studies have employed repeated social defeat stress (RSDS) to study the neurobiological mechanisms of depression in rodents. An important limitation of RSDS studies to date is that they have been conducted exclusively in male mice due to the difficulty of initiating attack behavior directed toward female mice. Here, we establish a female mouse model of RSDS by inducing male aggression toward females through chemogenetic activation of the ventrolateral subdivision of the ventromedial hypothalamus (VMHvl). We demonstrate that females susceptible to RSDS display social avoidance, anxiety-like behavior, reduction of body weight, and elevated levels of circulating interleukin 6. In contrast, a subset of mice we term resilient only display anxiety-like behaviors after RSDS. This model allows for investigation of sex differences in the neurobiological mechanisms of defeat‒induced depression‒like behaviors. A robust female social defeat model is a critical first step in the identification and development of novel therapeutic compounds to treat depression and anxiety disorders in women.