Exploring the Impact of Combined Thai Yoga and Elastic Band Exercise on Physical Fitness and Exercise Capacity in Older Patients with Type 2 Diabetes

Study purpose. Although it is acknowledged that exercise can positively affect both physical and biochemical markers in older individuals with type 2 diabetes (T2DM), there are still uncertainties about the specific impacts of combining Thai yoga with an elastic band exercise in this population. The objective of the study was to assess the impact of a 12-week program involving Thai yoga combined with an elastic band exercise on the physical fitness and functional exercise capacity among older individuals with T2DM. Materials and methods. A total of 42 participants, consisting of 20 men and 22 women with T2DM and a mean age of 64.6±3.6 years, were randomly assigned to two groups: the control group and the exercise group. The exercise group engaged in a daily regimen of Thai yoga combined with an elastic band exercise for 40 minutes, 5 days a week, over a 12-week period. In contrast, the control group maintained their regular routines. Physical fitness and functional exercise capacity were assessed both before and after the 12-week intervention. Results. The exercise group showed significant reductions in body weight (58.7±11.9 vs. 58.0±12.0 kg), body mass index (24.2±3.0 vs. 23.9±3.0 kg/m2), waist circumference (33.6±3.6 vs. 33.1±3.6 in), and waist-hip ratio (0.90±0.06 vs. 0.89±0.06) (p < 0.001). Additionally, there were notable improvements in physical fitness parameters, including hand grips, back strength, leg strength (p < 0.01), and trunk flexibility (p < 0.001). Functional exercise capacity, indicated by the 6-minute walk test and estimated peak oxygen consumption (p < 0.01), also improved significantly. Conclusions. Thai yoga combined with an elastic band exercise enhances physical fitness and functional exercise capacity in older individuals with T2DM. This improvement has the potential to enhance their cardiopulmonary performance. Consequently, this exercise regimen is considered a health alternative for older individuals with T2DM

The Neuroprotective Effect of Zingiber cassumunar Roxb. Extract on LPS-Induced Neuronal Cell Loss and Astroglial Activation within the Hippocampus

The systemic administration of lipopolysaccharide (LPS) has been recognized to induce neuroinflammation which plays a significant role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In this study, we aimed to determine the protective effect of Zingiber cassumunar (Z. cassumunar) or Phlai (in Thai) against LPS-induced neuronal cell loss and the upregulation of glial fibrillary acidic protein (GFAP) of astrocytes in the hippocampus. Adult male Wistar rats were orally administered with Z. cassumunar extract at various doses (50, 100, and 200 mg/kg body weight) for 14 days before a single injection of LPS (250 μg/kg/i.p.). The results indicated that LPS-treated animals exhibited neuronal cell loss and the activation of astrocytes and also increased proinflammatory cytokine interleukin- (IL-) 1β in the hippocampus. Pretreatment with Z. cassumunar markedly reduced neuronal cell loss in the hippocampus. In addition, Z. cassumunar extract at a dose of 200 mg/kg BW significantly suppressed the inflammatory response by reducing the expression of GFAP and IL-1ß in the hippocampus. Therefore, the results suggested that Z. cassumunar extract might be valuable as a neuroprotective agent in neuroinflammation-induced brain damage. However, further investigations are essential to validate the possible active ingredients and mechanisms of its neuroprotective effect

Pinostrobin mitigates neurodegeneration through an up-regulation of antioxidants and GDNF in a rat model of Parkinson’s disease [version 2; peer review: 2 approved, 1 approved with reservations]

Background: One of the most common neurodegenerative diseases is Parkinson’s disease (PD); PD is characterized by a reduction of neurons containing dopamine in the substantia nigra (SN), which leads to a lack of dopamine (DA) in nigrostriatal pathways, resulting in motor function disorders. Oxidative stress is considered as one of the etiologies involved in dopaminergic neuronal loss. Thus, we aimed to investigate the neuroprotective effects of pinostrobin (PB), a bioflavonoid extracted from Boesenbergia rotunda with antioxidative activity in PD. Methods: Rats were treated with 40 mg/kg of PB for seven consecutive days before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. After completing the experiment, the brains including SN and striatum were used for histological studies and biochemical assays. Results: PB treatment demonstrated a reduction of free radicals in the SN as indicated by significantly decreased MDA levels, whereas the antioxidative enzymes (SOD and GSH) were significantly increased. Furthermore, PB treatment significantly increased glial cell line-derived neurotrophic factor (GDNF) immunolabelling which has neurotrophic and neuroprotective effects on the survival of dopaminergic neurons. Furthermore, PB treatment was shown to protect CA1 and CA3 neurons in the hippocampus and dopaminergic neurons in the SN. DA levels in the SN were increased after PB treatment, leading to the improvement of motor function of PD rats. Conclusions: These results imply that PB prevents MPTP-induced neurotoxicity via its antioxidant activities and increases GDNF levels, which may contribute to the therapeutic strategy for PD

Sepsis otopathy: experimental sepsis leads to significant hearing impairment due to apoptosis and glutamate excitotoxicity in murine cochlea

SUMMARY Hearing loss is frequent in intensive care patients and can be due to several causes. However, sepsis has not been examined as a possible cause. The aim of this study is to assess the influence of experimental sepsis on hearing thresholds and to evaluate pathological changes in the cochlea. The cecal ligation puncture technique was used to induce sepsis in 18 mice. Results were compared with those from 13 sham-operated and 13 untreated control mice. The hearing thresholds of the animals were evaluated with auditory evoked brainstem responses prior to the induction of sepsis and again at the peak of the disease. Immediately after the second measurement, the mice were sacrificed and the inner ears harvested and prepared for further evaluation. The cochleae were examined with light microscopy, electron microscopy and immunohistochemistry for Bax, cleaved caspase-3 and Bcl-2. The mice with sepsis showed a significant hearing loss but not the control groups. Induction of apoptosis could be shown in the supporting cells of the organ of Corti. Furthermore, excitotoxicity could be shown at the basal pole of the inner hair cells. In this murine model, sepsis leads to significant hearing impairment. The physiological alteration could be linked to apoptosis in the supporting cells of the organ of Corti and to a disturbance of the synapses of the inner hair cells