Bonnerbarr2982

Neural regeneration devices interface with the nervous system and can provide flexibility in material choice, implantation without the need for additional surgeries, and the ability to serve as guides augmented with physical, biological (e.g., cellular), and biochemical functionalities. Given the complexity and challenges associated with neural regeneration, a 3D printing approach to the design and manufacturing of neural devices could provide next-generation opportunities for advanced neural regeneration via the production of anatomically accurate geometries, spatial distributions of cellular components, and incorporation of therapeutic biomolecules. A 3D printing-based approach offers compatibility with 3D scanning, computer modeling, choice of input material, and increasing control over hierarchical integration. Therefore, a 3D printed implantable platform could ultimately be used to prepare novel biomimetic scaffolds and model complex tissue architectures for clinical implants in order to treat neurological diseases and injuries. Further, the flexibility and specificity offered by 3D printed in vitro platforms have the potential to be a significant foundational breakthrough with broad research implications in cell signaling and drug screening for personalized healthcare. This progress report examines recent advances in 3D printing strategies for neural regeneration as well as insight into how these approaches can be improved in future studies.Hepatocellular carcinoma or Liver cancer (LC) is the sixth most common cancer and the fourth cause of death worldwide in 2018. There has not been a comprehensive study on the survival rate of patients with LC in Asia yet. Therefore, the present study was conducted to evaluate the survival rate of patients with LC in Asian countries. The methodology of the present study is based on the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analysis) statement. The researchers searched five international databases including Medline/PubMed, Scopus, Embase, Web of Knowledge and ProQuest until July 1, 2018. We also searched Google Scholar for detecting grey literature. The Newcastle-Ottawa Quality Assessment Form was used to evaluate the quality of selected papers. A total of 1425 titles were retrieved. 63 studies met the inclusion criteria. Based on the random-effect model one-year, three-year and five-year survival rate of LC were 34.8 % (95 % CI; 30.3-39.3), 19 % (95 % CI ; 18.2-21.8) and 18.1 % (95 % CI ;16.1-20.1) respectively. According to the results of our study, the LC survival rate in Asian countries is relatively lower than in Europe and North America. Copyright © 2020 Hassanipour et al.Osteoporosis affects about 200 million people worldwide and is a silent disease until a fracture occurs. Management of osteoporosis is still a challenge that warrants further studies for establishing new prevention strategies and more effective treatment modalities. For this purpose, animal models of osteoporosis are appropriate tools, of which the ovariectomized rat model is the most commonly used. The aim of this study is to provide a 4-step guideline for inducing a rat model of osteoporosis by ovariectomy (OVX) (1) selection of the rat strain, (2) choosing the appropriate age of rats at the time of OVX, (3) selection of an appropriate surgical method and verification of OVX, and (4) evaluation of OVX-induced osteoporosis. This review of literature shows that (i) Sprague-Dawley and Wistar rats are the most common strains used, both responding similarly to OVX; (ii) six months of age appears to be the best time for inducing OVX; (iii) dorsolateral skin incision is an appropriate choice for initiating OVX; and (iv) the success of OVX can be verified 1-3 weeks after surgery, following cessation of the regular estrus cycles, decreased estradiol, progesterone, and uterine weight as well as increased LH and FSH levels. Current data shows that the responses of trabecular bones of proximal tibia, lumbar vertebrae and femur to OVX are similar to those in humans; however, for short-term studies, proximal tibia is recommended. Osteoporosis in rats is verified by lower bone mineral density and lower trabecular number and thickness as well as higher trabecular separation, changes that are observed at 14, 30, and 60 days post-OVX in proximal tibia, lumbar vertebrae and femur, respectively. Copyright © 2020 Yousefzadeh et al.The quest for chemical entities able to curb the action of the phosphoinositide 3-kinase, (PI3K)/protein kinase B (AKT) signaling pathways is evolving as a potential therapeutic strategy for the treatment and/or prevention of neurodegenerative disorders including Alzheimer's disease (AD). In this study, the effects of a PI3K inhibitor, AS605240 on cognitive dysfunction and antioxidative defense parameters against intra-cerebroventricular-streptozotocin (ICV-STZ)-induced rat model of sporadic AD was evaluated. ICV administration of a single dose of STZ (3 mg/kg) was performed to induce behavioral and biochemical changes in rats using the stereotaxic technique. Animals were administered with varying doses of AS605240 (5, 10 and 15 mg/kg) orally, 1 h before ICV-STZ on day 1 and continued once daily for four weeks. The behavioral parameters (passive avoidance and Morris water maze), antioxidative defense parameters, amyloid-beta (Aβ) protein expression by Western blotting and immunostaining technique were estimated in brain tissue. AS605240 dose-dependently and significantly (p less then 0.05 and p less then 0.01 and p less then 0.001) improved ICV-STZ-induced cognitive impairment and attenuated the altered antioxidative related parameters including superoxide dismutase, lipid peroxidation, glutathione and nitrite levels. Further, the increased Aβ protein expression levels in brain tissue were markedly restored with AS605240 treatment. In conclusion, our study demonstrated that AS605240 exhibited immense potential in attenuating STZ-induced sporadic AD features in rats and may be developed as a therapeutic agent in the treatment and management of sporadic AD. Copyright © 2020 Alluri et al.In the present work we modified the procedure for isolation of naphthoquinones α-methylbutyrylshikon ( 1 ), acetylshikonin ( 2 ) and β-hydroxyisovalerylshikonin ( 3 ) from Onosma visianii Clem. We also investigated possible mechanisms of 1 , 2 and 3 as antitumor agents. Accordingly, we estimated concentrations of superoxide anion radical (O2 .-), nitrite (NO2 -) and glutathione in HCT-116 and MDA-MB-231 cell lines. Compounds 1 and 3 expressed significant prooxidative activity, while all tested compounds exhibited significant increase in nitrite levels. Also, all examined compounds significantly increased the concentration of oxidized glutathione (GSSG), suggesting significant prooxidative disbalance. The levels of reduced glutathione (GSH) were also elevated as a part of antioxidative cell response. The data indicate that induced oxidative imbalance could be one of the triggers for previously recorded decreased viability of HCT-116 and MDA-MB-231 cells exposed to tested naphthoquinone derivatives. Moreover, we examined interactions mode of compounds 1 , 2 and 3 with CT-DNA as one of the crucial targets of many molecules that express cytotoxic activity. The results obtained by UV-visible, fluorescence and molecular docking study revealed that 1 , 2 and 3 bound to CT-DNA through minor groove binding. Furthermore, the interactions between HSA and 1 , 2 and 3 were examined employing the same methods as for the CT-DNA interaction study. Based on the obtained results, it can be concluded that naphthoquinones 1 , 2 and 3 could be effectively transported by human serum albumin. As a conclusion, this study provides further insight of antitumor activity of selected naphthoquinones. Copyright © 2020 Vukic et al.Diabetes mellitus is a complex metabolic disorder that leads to various micro-vascular complications. The present study elucidated the effect of chloroform extract of leaves of Ficus glomerata (CHFG) in streptozotocin-induced early diabetic renal and neural complications. Wistar rats were injected with STZ (55 mg/kg, i.p.) to produce experimental diabetes. learn more Two weeks after the stabilization of diabetes, CHFG extract at the dose of 200 and 400 mg/kg (CHFG 200 and CHFG 400) and metformin at the dose of 250 mg/kg (Met 250) was administered to the diabetic rats for further two weeks. Diabetic rats showed an increase in blood glucose, plasma urea, uric acid, creatinine, triglyceride, and total cholesterol level. The change in behavioral parameters such as thermal hyperalgesia and cold allodynia with compromised sciatic nerve and kidney antioxidant status were seen in diabetic rats. Diabetic rats treated with CHFG 200, CHFG 400, and Met 250 showed a decrease in blood glucose, plasma urea, uric acid, creatinine, triglyceride, and total cholesterol level. Also, it improved altered behavioral parameters such as thermal hyperalgesia and cold allodynia. It also restored the sciatic nerve and kidney antioxidant status. The results of kidney and sciatic nerves histopathological study were in line with the results of biochemical parameters that confirmed the favorable role of CHFG. Characterization of CHFG by LC-MS revealed the presence of diverse phytoconstituents, which might be responsible for its protective effect. Copyright © 2020 Shaikh et al.Long-term exposure to high glucocorticoid levels induces memory impairment and neurodegeneration in Alzheimer's disease (AD) by increasing the expression of amyloid β and tau hyperphosphorylation (pTau). Previous studies showed beneficial effects of flavonoids in neurodegenerative models. 5,6,7,4'-tetramethoxyflavanone (TMF) is one of the active ingredients in Chromolaena odorata (L.), which R. M. King and H. Rob discovered in Thailand. This study focused on the effects of TMF on dexamethasone (DEX)-induced neurodegeneration, amyloidogenesis, pTau expression, neuron synaptic function, and cognitive impairment and the potential mechanisms involved. Mice were intraperitoneally administered DEX for 28 days before being treated with TMF for 30 days. The mice were randomly divided into six groups (twelve mice per group) control; TMF administration (40 mg/kg); pioglitazone administration (20 mg/kg); DEX administration (60 mg/kg); DEX administration plus TMF; and DEX administration plus pioglitazone. Behavioral tests showed that TMF significantly attenuated the memory impairment triggered by DEX. Consistently, TMF reduced DEX-induced amyloid beta production by reducing the expression of beta-site APP cleaving enzyme 1 (BACE1) and presenilin 1 (PS1), whereas it increased the gene expression of a disintegrin and metalloprotease 10 (ADAM10). TMF treatment also decreased pTau expression, inhibited phosphonuclear factor-kappa B (pNF-kB) and inhibited glycogen synthase kinase 3 (GSK-3) activity by increasing GSK3 phosphorylation (pGSK3). In addition, TMF also improved synaptic function by increasing the expression of synaptophysin (Syn) and postsynaptic density protein 95 (PSD95) while decreasing acetylcholine esterase activity. Conclusively, TMF provided neuroprotection against DEX-induced neurodegeneration. These findings suggest that TMF might have potential as a therapeutic drug for AD. Copyright © 2020 Pakdeepak et al.