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Diabetic Parkinson's disease (DP) is a progressive neurodegenerative disease with metabolic syndrome that is increasing worldwide. Emerging research suggests that cannabidiol (CBD) is a neuropharmacological compound that acts against this disease, especially CBD in nano-formulation. The safety of cannabidiol lipid nanoparticles (CBD-LNP) was evaluated by assessing in vitro cytotoxicity in neurons and therapeutic outcomes in a DP animal model, including metabolic parameters and histopathology. CBD-LNPs were fabricated by using a microfluidization technique and showed significantly lower cytotoxicity than the natural form of CBD. The DP rats were induced by streptozotocin followed by a 4-week injection of MPTP with a high-fat diet. Rats were treated orally with a vehicle, CBD, CBD-LNP, or levodopa for 4 weeks daily. As a result, vehicle-treated rats exhibited metabolic abnormalities, decreased striatal dopamine levels, and motor and memory deficits. CBD-LNP demonstrated reduced lipid profiles, enhanced insulin secretion, and restored dopamine levels compared to CBD in the natural form. CBD-LNP also had comparable efficacy to levodopa in ameliorating motor deficits and memory impairment in behavior tests. Interestingly, CBD-LNP presented migration of damaged neuronal cells in the hippocampus more than levodopa. These findings suggest that CBD-LNP holds promise as an intervention addressing both metabolic and neurodegenerative aspects of DP, offering a potential therapeutic strategy. [ABSTRACT FROM AUTHOR]

Introduction: Stress disturbs the gut-brain axis and contributes to the development of mood disorders and memory impairment. Recent findings on the anti-stress effects of monoamine modulators have shown that the serotonin and norepinephrine reuptake inhibitor (SNRI) venlafaxine (Vlx) is more effective in stressed rodents. However, the effects of Vlx on microbiota and memory impairment- and stress-related behaviors are still unknown. Synbiotics (Syn), a mixture of probiotics and prebiotics, can modify the gut microbiome; however, the effects of anti-anxiety and anti-memory deficits are still not well understood. Therefore, this study proposed to compare the effectiveness of Vlx and Syn in the reduction of learned fearand memory impairment-like behaviors in an animal model of stress. Methods: Forty male adult Wistar rats were subjected to stress by immobilization in a restrainer for 2h per day and were administered 10mg/kg Vlx and/or 2g of Syn containing 1.0x1010 CFU probiotic strains and prebiotic oligosaccharides daily for 14 days. Learned fear, recognition memory and locomotor activity were evaluated by the elevated-T maze, novel objective recognition and open field tests. Blood samples and adrenal glands were collected to measure the circulating corticosterone levels and relative adrenal weights, which were used as markers of stress responses. Results: The immobilized-stressed rats showed hyperactivity in stress responses, as demonstrated by increased relative adrenal weights and serum corticosterone levels. Both Vlx and Syn reduced the increase in serum corticosterone levels in stressed rats. Furthermore, Vlx- and/or Syn-treated stressed rats had fewer learned fear-like behaviors and a higher discrimination index without any locomotor activity changes than vehicle-treated stressed rats. Conclusion: Syn supplementation had comparable effects to SNRIs in alleviating the risk of developing anxiety disorders and memory impairment in stressed individuals or psychiatric patients. [ABSTRACT FROM AUTHOR]

Introduction: Upper body muscular imbalance is a potential risk factor in various shoulder problems and respiratory functions. Exercises aimed at the pectoralis minor and scapular stabilizer muscles could alleviate muscular imbalances in forward shoulder posture (FSP). However, the efficacy of these exercises on respiratory function, including chest mobility, lung capacity, and respiratory muscle strength in FSP remains unclear. Material and methods: In this randomized clinical trial, 28 female participants with FSP, aged 18-23 years, were divided into the control and exercise groups. The exercise programs were conducted five days/week for eight weeks. The distance from the acromion process to the wall was measured to determine FSP. Pectoralis minor length (PL) were measured from coracoid process to the fourth costosternal joint, thoracic kyphosis (TK) was measured along the thoracic spines, chest expansion was measured from the amplitude of thoracic wall circumference during full expiration and inspiration, maximal respiratory muscle strength generated during respiration (MIP), and maximum respiratory muscle strength during expiration (MEP); all were assessed pre- and post-exercise intervention. Results: After the eight-week training program, an improvement in FSP was observed, manifested as decreased mean difference (p < 0.05) and TK (p < 0.003). The PL (p < 0.05) and lower part of chest expansion (p < 0.010) were restored compared to the control group. The strength generated in respiration (MIP) also improved in the exercise group (p < 0.013). Conclusions: An eight-week pectoral muscle stretching and scapular stabilizer strengthening programme could reduce FSP, improving chest mobility and respiratory muscle strength. [ABSTRACT FROM AUTHOR]

Previously, β-thalassemia, an inherited anemic disorder with iron overload caused by loss-of-function mutation of β-globin gene, has been reported to induce osteopenia and impaired whole body calcium metabolism, but the pathogenesis of aberrant calcium homeostasis remains elusive. Herein, we investigated how β-thalassemia impaired intestinal calcium absorption and whether it could be restored by administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or hepcidin, the latter of which was the liver-derived antagonist of intestinal iron absorption. The results showed that, in hemizygous β-globin knockout (BKO) mice, the duodenal calcium transport was lower than that in wild-type littermates, and severity was especially pronounced in female mice. Both active and passive duodenal calcium fluxes in BKO mice were found to be less than those in normal mice. This impaired calcium transport could be restored by 7-day 1,25(OH)2D3 treatment. The 1,25(OH)2D3-induced calcium transport was diminished by inhibitors of calcium transporters, e.g., L-type calcium channel, NCX1, and PMCA1b, as well as vesicular transport inhibitors. Interestingly, the duodenal calcium transport exhibited an inverse correlation with transepithelial iron transport, which was markedly enhanced in thalassemic mice. Thus, 3-day subcutaneous hepcidin injection and acute direct hepcidin exposure in the Ussing chamber were capable of restoring the thalassemia-associated impairment of calcium transport; however, the positive effect of hepcidin on calcium transport was completely blocked by proteasome inhibitors MG132 and bortezomib. In conclusion, both 1,25(OH)2D3 and hepcidin could be used to alleviate the β-thalassemia-associated impairment of calcium absorption. Therefore, our study has shed light on the development of a treatment strategy to rescue calcium dysregulation in β-thalassemia. [ABSTRACT FROM AUTHOR]

Background The postural abnormality, forward shoulder posture (FSP), is the most common cause of respiratory impairment in older individuals with chronic obstructive pulmonary disease (COPD). A recent study found that performing pectoral stretching and scapular strengthening exercises for eight weeks could reduce FSP in healthy participants. We aimed to determine the effects of pectoral stretching and scapular stabilizer strengthening exercises on FSP, chest wall mobility, respiratory muscle strength, and pulmonary function in male patients with COPD. Methods This study was randomized clinical trial. Forty male COPD patients with FSP aged 60-90 years were included and randomly allocated to control (n=20) and exercise (n=20) groups. Following completion of the scapulothoracic exercises (three days/week, for eight weeks), respiratory functions were assessed by measuring the magnitude of FSP, chest mobility, respiratory muscle strength, and pulmonary functions. Results FSP and thoracic kyphosis angle significantly decreased compared to controls (p<0.001, p<0.001). Middle and lower chest mobility markedly increased (p<0.001, p<0.001) and the pectoralis minor index significantly improved (p<0.001). The strength of the lower trapezius and serratus anterior muscles significantly increased at week eight of the exercise training (p<0.003, p<0.001). There was a marked increase in maximum inspiratory pressure and maximum expiratory pressure (p<0.001, p<0.001). Conclusions The eight-week combined pectoral muscles self-stretching and serratus anterior and lower trapezius strengthening exercises could be an effective treatment and/or prevention strategy for FSP reduction, leading to improved respiratory function in male COPD patients., Competing Interests: No competing interests were disclosed., (Copyright: © 2024 Thongchote K et al.)

A shear-thinning and self-healing hydrogel based on a gelatin biopolymer is synthesized using vanillin and Fe 3+ as dual crosslinking agents. Rheological studies indicate the formation of a strong gel found to be injectable and exhibit rapid self-healing (within 10 min). The hydrogels also exhibited a high degree of swelling, suggesting potential as wound dressings since the absorption of large amounts of wound exudate, and optimum moisture levels, lead to accelerated wound healing. Andrographolide, an anti-inflammatory natural product is used to fabricate silver nanoparticles, which are characterized and composited with the fabricated hydrogels to imbue them with anti-microbial activity. The nanoparticle/hydrogel composites exhibit activity against Escherichia coli, Staphylococcus aureus, and Burkholderia pseudomallei, the pathogen that causes melioidosis, a serious but neglected disease affecting southeast Asia and northern Australia. Finally, the nanoparticle/hydrogel composites are shown to enhance wound closure in animal models compared to the hydrogel alone, confirming that these hydrogel composites hold great potential in the biomedical field., (© 2023 Wiley-VCH GmbH.)

Purpose: The purpose of this in vivo study was to determine the effects of stress-induced depression and antidepressants on depressive-like behavior, microstructure, and histomorphology of the temporomandibular joint (TMJ) using rats., Methods: Experimentally induced depression in rats was created before being treated with two antidepressants; escitalopram (selective-serotonin-reuptake inhibitors) and atomoxetine (norepinephrine-reuptake inhibitors). Micro-computed tomography (Micro-CT) was performed to measure the change in bone volume and bone porosity of the condyle. Further histological evaluation of the condylar cartilage was performed., Results: Micro-CT scanning revealed a decrease in bone volume in the depression group. The bone porosity percentage significantly increased in both the escitalopram and atomoxetine groups compared with the control group and the depression group. Histopathological analysis showed increased thickness of cartilage layers in the depression group. In the atomoxetine group, there was a significant increase in the pre-hypertrophic and hypertrophic layer thickness and cell count, but a significant decrease in proteoglycans., Conclusion: The present study findings indicated the change in TMJ characteristics, especially on the superficial part of the condylar head in the depression group. Concerning the applicability of the different antidepressants, depression with the treatment of atomoxetine has the most disadvantages due to bone porosity and cartilaginous condyle changes.

Previously, β-thalassemia, an inherited anemic disorder with iron overload caused by loss-of-function mutation of β-globin gene, has been reported to induce osteopenia and impaired whole body calcium metabolism, but the pathogenesis of aberrant calcium homeostasis remains elusive. Herein, we investigated how β-thalassemia impaired intestinal calcium absorption and whether it could be restored by administration of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or hepcidin, the latter of which was the liver-derived antagonist of intestinal iron absorption. The results showed that, in hemizygous β-globin knockout (BKO) mice, the duodenal calcium transport was lower than that in wild-type littermates, and severity was especially pronounced in female mice. Both active and passive duodenal calcium fluxes in BKO mice were found to be less than those in normal mice. This impaired calcium transport could be restored by 7-day 1,25(OH)2D3 treatment. The 1,25(OH)2D3-induced calcium transport was diminished by inhibitors of calcium transporters, e.g., L-type calcium channel, NCX1, and PMCA1b, as well as vesicular transport inhibitors. Interestingly, the duodenal calcium transport exhibited an inverse correlation with transepithelial iron transport, which was markedly enhanced in thalassemic mice. Thus, 3-day subcutaneous hepcidin injection and acute direct hepcidin exposure in the Ussing chamber were capable of restoring the thalassemia-associated impairment of calcium transport; however, the positive effect of hepcidin on calcium transport was completely blocked by proteasome inhibitors MG132 and bortezomib. In conclusion, both 1,25(OH)2D3 and hepcidin could be used to alleviate the β-thalassemia-associated impairment of calcium absorption. Therefore, our study has shed light on the development of a treatment strategy to rescue calcium dysregulation in β-thalassemia., (Copyright © 2016 the American Physiological Society.)