Abstract Studies have shown that manual and electrical acupuncture have significant effects on brain functions. However, these treatments often evoke pain and fear. Non-invasive acupuncture therapies, such as mechanical (acupressure) and thermal (moxibustion), have been developed and shown to effectively relieve pain and treat various conditions. However, little is known about their influence on brain network function. The current study explored the effects of mechanical, thermal, and combined thermal and mechanical stimulations on acupoint Large Intestine 4 (LI4, Hegu) on EEG in fifty-two healthy participants. A 30-minute combined thermal and mechanical stimulation on LI4 enhanced the powers of the β and γ bands and reduced the ratio of θ/β in both the parietal and temporal lobes when compared with the same stimulation on the control point. In contrast, neither the mechanical nor thermal stimulation alone had such effects. The distinct impact of combined thermal and mechanical stimulation, as opposed to either method alone, underscores the importance of joint activation of thermosensory, touch, and pain-sensory fibers for effective acupoint stimulation. Furthermore, our findings provide insights into the use of combined thermal plus mechanical stimulation as an effective non-invasive alternative therapy.
Hypoxic-ischemic encephalopathy (HIE) is a complex condition which is associated with high mortality and morbidity. However, few promising treatments for HIE exist. In the present study, the central objective was to identify the therapeutic effect of pilose antler polypeptides (PAP) on HIE in rats. Sprague-Dawley (SD) rats (14 days old) were used and divided into three groups, including control group, hypoxic-ischemia (HI) group and PAP group. After 21 days of treatment, locomotor activity was improved in PAP-treated rats, brain atrophy was decreased and cerebral edema was mitigated to some extent. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis indicated that PAP administration decreased the expressions of inflammatory cytokines and apoptosis genes in hippocampus compared with HI group. Furthermore, the mRNA expressions of genes related to neurotrophic factors were significantly increased in the hippocampus. In addition, the expressions of oxidative stress markers were all down-regulated after PAP administration. Moreover, PAP up-regulated both the mRNA and protein levels of SDF1 and CXCR4, which may activate the SDF1/CXCR4 axis to moderate brain injury. These results suggest that PAP may be potentially used in the treatment of HIE.
The formation of an O–O bond during electrocatalytic water oxidation is significant. The combination of a surfactant and catalyst prevents the production of hydrogen peroxide to provide a new pathway for oxygen evolution in copper porphyrin.
Sleep is highly conserved across animal species. Both wake- and sleep-promoting neurons are implicated in the regulation of wake–sleep transition at dusk in Drosophila . However, little is known about how they cooperate and whether they act via different mechanisms. Here, we demonstrated that in female Drosophila , sleep onset was specifically delayed by blocking the Shaker cognate L channels [Shal; also known as voltage-gated K + channel 4 (K v 4)] in wake-promoting cells, including large ventral lateral neurons (l-LNvs) and pars intercerebralis (PI), but not in sleep-promoting dorsal neurons (DN1s). Delayed sleep onset was also observed in males by blocking K v 4 activity in wake-promoting neurons. Electrophysiological recordings show that K v 4 channels contribute A-type currents in LNvs and PI cells, but are much less conspicuous in DN1s. Interestingly, blocking K v 4 in wake-promoting neurons preferentially increased firing rates at dusk ∼ZT13, when the resting membrane potentials and firing rates were at lower levels. Furthermore, pigment-dispersing factor (PDF) is essential for the regulation of sleep onset by K v 4 in l-LNvs, and downregulation of PDF receptor (PDFR) in PI neurons advanced sleep onset, indicating K v 4 controls sleep onset via regulating PDF/PDFR signaling in wake-promoting neurons. We propose that K v 4 acts as a sleep onset controller by suppressing membrane excitability in a clock-dependent manner to balance the wake–sleep transition at dusk. Our results have important implications for the understanding and treatment of sleep disorders such as insomnia. SIGNIFICANCE STATEMENT The mechanisms by which our brains reversibly switch from waking to sleep state remain an unanswered and intriguing question in biological research. In this study, we identified that Shal/K v 4, a well known voltage-gated K + channel, acts as a controller of wake–sleep transition at dusk in Drosophila circadian neurons. We find that interference of K v 4 function with a dominant-negative form (DNK v 4) in subsets of circadian neurons specifically disrupts sleep onset at dusk, although K v 4 itself does not exhibit circadian oscillation. K v 4 preferentially downregulates neuronal firings at ZT9–ZT17, supporting that it plays an essential role in wake–sleep transition at dusk. Our findings may help understand and eventually treat sleep disorders such as insomnia.
Glucocorticoids (GCs) are a group of steroid hormones secreted by the adrenal glands in circadian cycles, and the dysregulation of GC signaling has been suggested to cause metabolic syndrome. Even though prolonged GC exposure is associated with serious side effects such as metabolic syndrome and central nervous system disorders, the use of GCs in anti-inflammatory and immunosuppressive therapies has been continuously rising. Meanwhile, the exact mechanisms by which GCs can influence the lipid metabolism as well as behavior and how they are affected by time remain unknown. In this study, the effects of two different long-term GC dosing regimens on lipid metabolism and behavior were investigated. Male Wistar rats received daily administrations of the GC dexamethasone sodium phosphate (DEX, 0.5 mg/kg body weight) at either ZT0 (Dex0) or ZT12 (Dex12). After 6 weeks of treatment, DEX-treated rats, especially those treated at ZT0, had higher hepatic lipid accumulation and serum triglyceride levels and less locomotor activity than did control rats. In addition, serum levels of corticosterone, 5-hydroxy tryptamine and norepinephrine were decreased in the Dex0 group but not in the Dex12 group compared to the control group. Furthermore, quantitative real-time polymerase chain reaction analysis indicated that the chronic administration of GCs at ZT0 upregulated genes related to glycolysis and lipid synthesis and downregulated genes related to fatty acid β-oxidation in the liver more remarkably than administration at ZT12. Both DEX-treated groups displayed severely altered expression patterns of the core clock genes Bmal1 and Per2 in the liver and in fat. In addition, the expression of glutamate aspartate transporter, glial fibrillary acidic protein and glutamate transporter-1, astrocyte-related genes important for maintaining nervous system functions, was drastically decreased in the hippocampus of DEX-treated rats, especially when DEX was given at ZT0. In conclusion, our findings confirm that the severity of side effects, indicated by altered lipid metabolism and behavioral activity, depends on the timing of GC administration and is associated with the degree of glucocorticoid receptor dysfunction after dosing at disparate time points.
Oxidative stress caused free radical and mitochondrial damage plays a critical role in the progression of aging and age-related damage at the cellular and tissue levels. Antioxidant supplementation has received growing attention and the effects of antioxidant on aging are increasingly assessed in both animal and human studies. However, additional and more promising treatments that contribute to the expansion of anti-aging therapies are needed. Astaxanthin, a super antioxidant carotenoid and free radical scavenger, inhibits lipid peroxidation more potently than vitamin E. In the present study, we investigated the preventative effects of astaxanthin on aging using an accelerated aging model: mice chronically treated with a combination of D-galactose and jet lag. After 6 weeks of treatment, astaxanthin administration tended to protect the liver weight loss in aged mice. It is probably by upregulating the mRNA expression of galactose-1-phosphate uridyltransferase, which contribute to the enhancement of D-galactose metabolism. Astaxanthin supplementation also improved muscle endurance of aged mice in a swimming test. These results were associated with reduced oxidative stress in serum and increased anti-oxidative enzymes activities and mRNA expression in vivo. Moreover, astaxanthin reversed the dysregulation of aging-related gene expression caused by the combination of D-galactose and jet lag in the liver and kidney of mice. In conclusion, astaxanthin prevents liver weight loss, ameliorates locomotive muscular function, exerts significant anti-aging effects by reducing oxidative stress and improving the expression of age-related genes in D-galactose and jet lag-induced aging model.
Graphical Abstract The Front Cover shows the design of Co-porphyrin-engineered phenolic resins with intramolecular phenolic hydroxyl groups to facilitate proton and electron transfers for efficient oxygen electrocatalysis, which is bioinspired by cytochrome c oxidases, and shows the excellent performance of Zn-air batteries assembled with the hybrid material. More information can be found in the Research Article by Wonwoo Nam, Rui Cao and co-workers.
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