METHODS: An online cross-sectional survey that assessed PA avoidance, two types of weight stigma, and PA level was completed in late 2023 by 884 Taiwanese young adults aged between 20 and 40 years (63.9% females). Multinomial logistic regression and structural equation modeling (SEM) were used to assess the associations between variables and perform the mediation analysis.
RESULTS: Cognitive behavioral symptoms and negative consequences related to gaming disorder were more common among participants with lower PA than those with moderate to high PA. Individuals at risk of gaming disorder exhibited higher level of PA avoidance, internalized weight stigma, and perceived weight stigma. The SEM found a direct association between gaming disorder and PA, which was negatively mediated by PA avoidance. However, this direct effect was not present when the association was negatively mediated by serial mediations of weight stigma and PA avoidance.
DISCUSSION AND CONCLUSIONS: Higher gaming disorder was associated with higher levels of PA, but this association may not be present when taking into account the mediation effect of weight stigma and PA avoidance. The findings suggest complex relationships and further research is needed to examine individual differences and relationships among clinical groups.
METHOD: In this study, we investigated the effects of methanol neurotoxicity on memory function and pathological outcomes in the hippocampus of adolescent rats and examined the efficacy of Light- Emitting Diode (LED) therapy. Methanol induced neurotoxic rats showed a significant decrease in the latency period, in comparison to controls, which was significantly improved in LED treated rats at 7, 14 and 28 days, indicating recovery of memory function. In addition, methanol neurotoxicity in hippocampus caused a significant increase in cell death (caspase3+ cells) and cell edema at 7 and 28 days, which were significantly decreased by LED therapy. Furthermore, the number of glial fibrillary acid protein astrocytes was significantly lower in methanol rats, compared to controls, whereas LED treatment caused their significant increase. Finally, methanol neurotoxicity caused a significant decrease in the number of brain-derived neurotrophic factor (BDNF+) cells, but also circulating serum BDNF, at 7 and 28 days, compared to controls, which were significantly increased by LED therapy. Importantly, LED significantly increased the number of Ki-67+ cells and BDNF levels in the serum and hypothalamus in control-LED rats, compared to controls without LED therapy.
CONCLUSION: In conclusion, chronic methanol administration caused severe memory impairments and several pathological outcomes in the hippocampus of adolescent rats which were improved by LED therapy.
AIM OF THE STUDY: To assess the motor and cognitive effects of acute oral administration of CT root methanolic extract and hippocampal long-term plasticity in the CA1 region of the CCH rat model.
MATERIALS AND METHODS: Male Sprague Dawley rats (200-300 g) were subjected to permanent bilateral occlusion of common carotid arteries (PBOCCA) or sham operation. Then, these rats were given oral administration of CT root extract at doses of 100, 200 or 300 mg/kg on day 28 post-surgery and tested using behavioural tests (open-field test, passive avoidance task, and Morris water maze) and electrophysiological recordings (under urethane anaesthesia).
RESULTS: Treatment with CT root extract at the doses of 200 and 300 mg/kg resulted in a significant enhancement in memory performance in CCH rats induced by PBOCCA. Furthermore, CCH resulted in inhibition of long-term potentiation (LTP) formation in the hippocampus, and CT root extract rescued the LTP impairment. The CT root extract was confirmed to improve the glutamate-induced calcium increase via calcium imaging using primary cultured rat neurons. No significance difference was found in the CaMKII expression. These results demonstrated that CT root extract ameliorates synaptic function, which may contribute to its improving effect on cognitive behaviour.
CONCLUSIONS: Our findings demonstrated an improving effect of CT root extract on memory in the CCH rat model suggesting that CT root extract could be a potential therapeutic strategy to prevent the progression of cognitive deterioration in vascular dementia (VaD) and Alzheimer's disease (AD) patients.
METHODS: Male Swiss albino mice (18-22 g bw) were pretreated with methanolic extract of sesame seeds (MSSE) (100 and 200 mg/kg/day, p.o) for a period of 14 days. Scopolamine (0.3 mg/kg, i.p.) was injected on day 14, 45 ± 10 min after MSSE administration. Antiamnesic effect of MSSE was evaluated using step-down latency (SDL) on passive avoidance apparatus and transfer latency (TL) on an elevated plus maze. To unravel the mechanism of action, we examined the effects of MSSE on the genes such as acetyl cholinesterase (AChE), muscarinic receptor M1 subtype (mAChRM1 ), and brain derived neurotrophic factor (BDNF) expression within hippocampus of experimental mice. Further, its effects on bax and bcl-2 were also evaluated. Histopathological examination of hippocampal CA1 region was performed using cresyl violet staining.
RESULTS: MSSE treatment produced a significant and dose dependent increase in step down latency in passive avoidance test and decrease in transfer latency in elevated plus maze in scopolamine intoxicated injected mice. MSSE down-regulated AChE and mAChRM1 and up-regulated BDNF mRNA expression. Further, it significantly down-regulated the bax and caspase 3 and up-regulated bcl-2 expression in scopolamine intoxicated mice brains. Mice treated with MSSE showed increased neuronal counts in hippocampal CA1 region when compared with scopolamine-vehicle treated mice.
CONCLUSION: Sesame seeds have the ability to interact with cholinergic components involved in memory function/restoration and also an interesting candidate to be considered for future cognitive research. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1955-1963, 2016.
PURPOSE: To study the various surgical practices of different surgeons in the Asia-Pacific region.
OVERVIEW OF LITERATURE: Given the diversity among Asia-Pacific surgeons, there is no clear consensus on the preferred management strategies for cervical myelopathy. In particular, the role of prophylactic decompression for silent cervical spinal stenosis is under constant debate and should be addressed.
METHODS: Surgeons from the Asia-Pacific Spine Society participated in an online questionnaire comprising 50 questions. Data on clinical diagnosis, investigations and outcome measures, approach to asymptomatic and silent cervical spinal stenosis, guidelines for surgical approach, and postoperative immobilization were recorded. All parameters were analyzed by the Mantel-Haenszel test.
RESULTS: A total of 79 surgeons from 16 countries participated. Most surgeons used gait disturbance (60.5%) and dyskinetic hand movement (46.1%) for diagnosis. Up to 5.2% of surgeons would operate on asymptomatic spinal stenosis, and 18.2% would operate on silent spinal stenosis. Among those who would not operate, most (57.1%) advised patients on avoidance behavior and up to 9.5% prescribed neck collars. For ossification of the posterior longitudinal ligament (OPLL), anterior removal was most commonly performed for one-level disease (p<0.001), whereas laminoplasty was most commonly performed for two- to four-level disease (p=0.036). More surgeons considered laminectomy and fusion for multilevel OPLL. Most surgeons generally preferred to use a rigid neck collar for 6 weeks postoperatively (p<0.001).
CONCLUSIONS: The pooled recommendations include prophylactic or early decompression surgery for patients with silent cervical spinal stenosis, particularly OPLL. Anterior decompression is primarily suggested for one- or two-level disease, whereas laminoplasty is preferred for multilevel disease.
MATERIALS AND METHODS: In this study, DET (0.625. 1.25 and 2.5 mg/kg, i.p.) was administered in rats for 21 days and those animals were challenged with single injection of LPS (250 μg/kg, i.p.) for 7 days. Cognitive and behavioral assessment was carried out for 7 days followed by molecular assessment on brain hippocampus. Statistical significance was analyzed with one-way analysis of variance followed by Dunnett's test to compare the treatment groups with the control group.
KEY FINDINGS: DET ameliorated LPS-induced neuroinflammation by suppressing major pro-inflammatory mediators such as iNOS and COX-2. Furthermore, DET enhanced the anti-inflammatory cytokines and concomitantly suppressed the pro-inflammatory cytokines and chemokine production. DET treatment also reversed LPS-induced behavioral and memory deficits and attenuated LPS-induced elevation of the expression of AD markers. DET improved synaptic-functionality via enhancing the activity of pre- and post-synaptic markers, like PSD-95 and SYP. DET also prevented LPS-induced apoptotic neurodegeneration via inhibition of PARP-1, caspase-3 and cleaved caspase-3.
SIGNIFICANCE: Overall, our studies suggest DET can prevent neuroinflammation-associated memory impairment and neurodegeneration and it could be developed as a therapeutic agent for the treatment of neuroinflammation-mediated and neurodegenerative disorders, such as AD.