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PMID: 

Bioinformation. 2018 ;14(9):421-424. Epub 2018 Dec 21. PMID: 31223202

Abstract Title: 

Colony Collapse Disorder (CCD) in Honey BeesCaused by EMF Radiation.

Abstract: 

Honey bees are one of the treasures in the world. An increase of waveform communication leads to good information exchange of mankind. In the biological view, it causes a lot of side effects and lifestyle changes in other living organisms. The drastic changes are causing the natural imbalance in the ecosystem and become a global issue. There are significant reasons for bee colony collapse disorder (CCD) like pesticides, disease and climate change. Recent studies reveal that a cell phone tower and mobile phone handset are also causing side effects to honey bees due to radiation emission. Most of the researchers concentrated on biological and behavioral changes in a honey bee due to radiation effects. For that, the real-time radiation levels have experimented but the different technical perspectives such as radiation emission levels, handset radiation emission measures and multi-sources of radiation are needed to be considered during research. This study aimed to provide possible research extensions of colony collapse disordercaused by cell tower and mobile handsets.

PMID: 

Electromagn Biol Med. 2019 Jul 13:1-10. Epub 2019 Jul 13. PMID: 31304806

Abstract Title: 

The impact of exposure of diabetic rats to 900 MHz electromagnetic radiation emitted from mobile phone antenna on hepatic oxidative stress.

Abstract: 

The excessive exposure of patients with type 2 diabetes mellitus (T2DM) to electromagnetic radiation (EMR) from mobile phones or their base stations antenna may influence oxidative stress and development of diabetic complications. Here, we investigated the effects of exposing type 2 diabetic rats to EMR of 900 MHz emitted from GSM mobile phone antenna for 24 hours/day over a period of 28 days on hyperglycemia and hepatic oxidative stress. Male Sprague-Dawley rats were divided into 4 groups (12 rats/group): control rats, normal rats exposed to EMR, T2DM rats generated by nicotinamide/streptozotocin administration, and T2DM rats exposed to EMR. Our results showed that the exposure of T2DM rats to EMR nonsignificantly reduced the hyperglycemia and hyperinsulinemia compared to unexposed T2DM rats. The exposure of T2DM rats to EMR for 28 days increased the hepatic levels of MDA and Nrf-2 as well asthe activities of superoxide dismutase (SOD) and catalase but decreased phosphorylated Akt-2 (pAkt-2) as compared to unexposed T2DM rats. Therefore, the decrease in the hepatic pAkt-2 in T2DM rats after the exposure to EMR may result in elevated level of hepatic MDA, even though the level of Nrf-2 and the activities of SOD and catalase were increased.BGL: blood glucose level; EMR: electromagnetic radiation; GSM: global system for mobile communication; HO: hydrogen peroxide; LSD: least significance difference; MDA:malondialdehyde; Nrf-2: nuclear factor erythroid 2- related factor 2; PI3K: phosphoinositide-3-kinase; pAkt-2: phosphorylated Akt-2; Akt-2: protein kinase; ROS: reactive oxygen species; SEM: standard error of the mean; STZ: streptozotocin; SOD: superoxide dismutase ; O: superoxide radical; CT: threshold cycle; T2DM: type 2 diabetes mellitus.

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PMID: 

Arthritis Res Ther. 2019 Jun 24 ;21(1):153. Epub 2019 Jun 24. PMID: 31234900

Abstract Title: 

A novel function of artesunate on inhibiting migration and invasion of fibroblast-like synoviocytes from rheumatoid arthritis patients.

Abstract: 

INTRODUCTION: Anti-malarial drug artesunate can suppress inflammation and prevent cartilage and bone destruction in collagen-induced arthritis model in rats-suggesting it may be a potent drug for rheumatoid arthritis (RA) therapy. We aimed to investigate its effect on the invasive property of fibroblast-like synoviocytes (FLS) from patients with RA.METHODS: Synovial tissues were obtained by closed needle biopsy from active RA patients, and FLS were isolated and cultured in vitro. RA-FLS were treated with artesunate at various concentrations, while methotrexate or hydroxychloroquine was employed as comparator drugs. Cell viability, proliferation, cell cycle, apoptosis, migration, invasion, and pseudopodium formation of RA-FLS were assessed by CCK-8 assays, EdU staining, Annexin V-FITC/PI staining, transwell assays, or F-actin staining, respectively. Further, relative changes of expressed proteases were analyzed by Proteome profiler human protease array and verified by quantitative real-time PCR (qPCR), Western blot, and ELISA. The expression of signaling molecules of MAPK, NF-κB, AP-1, and PI3K/Akt pathways were measured by qPCR and Western blot. PDK-1 knockdown by specific inhibitor AR-12 or siRNA transfection was used to verify the pharmacological mechanism of artesunate on RA-FLS.RESULTS: Artesunate significantly inhibited the migration and invasion of RA-FLS in a dose-dependent manner with or without TNF-α stimulation. The effect was mediated through artesunate inhibition of MMP-2 and MMP-9 production, and pre-treatment with exogenous MMP-9 reversed the inhibitory effect of artesunate on RA-FLS invasion. Artesunate had a stronger inhibitory effect on migration and invasion of RA-FLS as well as greater anti-inflammatory effect than those of hydroxychloroquine. Similar inhibitory effect was detected between artesunate and methotrexate, and synergy was observed when combined. Mechanistically, artesunate significantly inhibited PDK-1 expression as well as Akt and RSK2 phosphorylation-in a similarmanner to PDK-1-specific inhibitor AR-12 or PDK-1 knockdown by siRNA transfection. This inhibition results in suppression of RA-FLS migration and invasion as well as decreased MMP-2 and MMP-9 expression.CONCLUSIONS: Our study demonstrates artesunate is capable of inhibiting migration and invasion of RA-FLS through suppression of PDK1-induced activation of Akt and RSK2 phosphorylation-suggesting that artesunate may be a potential disease-modifying anti-rheumatic drug for RA.

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Cooking with spices: Which ones are your favorites? https://weil.ws/2oOuHM5 

PMID: 

J Dent Sci. 2018 Dec ;13(4):334-341. Epub 2018 Jul 20. PMID: 30895142

Abstract Title: 

Acemannan increased bone surface, bone volume, and bone density in a calvarial defect model in skeletally-mature rats.

Abstract: 

Background/purpose: Acemannan, aβ-(1-4)-acetylated polymannose extracted fromgel, has been proposed as biomaterial for bone regeneration. The aim of this study was to investigate the effect of acemannan in calvarial defect healing.Materials and methods: Acemannan was processed to freeze-dried sponge form and disinfected by UV irradiation. Thirty-five female Sprague-Dawley rats were used in thestudy. Seven-mm diameter mid-calvarial defects were created and randomly allocated into blood clot control (C), acemannan 1 mg (A1), 2 mg (A2), 4 mg (A4), and 8 mg (A8) groups (n = 7). After four weeks, the calvarial specimens were subjected to microcomputed tomography (microCT) and histopathological analysis.Results: MicroCT revealed a significant increase in bone surface and bone volume in the A1 and A2 groups, and tissue mineral density in the A4 and A8 groups compared with the control group ( 

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PMID: 

J Cell Physiol. 2019 Aug ;234(10):18329-18343. Epub 2019 Mar 19. PMID: 30891764

Abstract Title: 

Hepatoprotective effect of Aloe vera against cartap- and malathion-induced toxicity in Wistar rats.

Abstract: 

Exposure to mixture of pesticides in agricultural practices pose a serious threat to the nontarget animals. In present work, we have evaluated the synergistic effect of cartap and malathion on rat liver followed by impact of Aloe vera leaves aqueous extract, which is not known. The animals in eight groups were used; each containing six rats: Group 1 acted as a control, Group 2-control with A. vera leaves aqueous extract, Group 3-with cartap, Group 4-with malathion, Group 5-with mixture of cartap and malathion, Group 6-cartap with the pretreatment of A. vera leaf extract, Group 7-malathion with the pretreatment of A. vera leaf extract, Group 8-mixture of cartap and malathion with the pretreatment of A. vera leaf extract . The animals treated for 15 days were killed after 24hr of last treatment. The biochemical studies in the rat liver demonstrated significant perturbations in the levels of nonenzymatic (glutathione and malondialdehyde) and enzymatic (superoxide dismutase, catalase, and glutathione- S-transferase) antioxidative indices. The histopathological examination of liver revealed serious congestion in central vein and the disorganization of hepatic cords due to pesticide treatment. The administration of A. vera leaves aqueous extract was able to markedly protect rat liver from the pesticides-induced toxicity. The data indicated that pesticides were able to significantly induce oxidative stress which was substantially reduced by the application of plant extract .

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PMID: 

J BUON. 2019 Mar-Apr;24(2):746-753. PMID: 31128032

Abstract Title: 

Aloe emodin exerts potent anticancer effects in MIAPaCa-2 and PANC-1 human pancreatic adenocarcinoma cell lines through activation of both apoptotic and autophagic pathways, sub-G1 cell cycle arrest and disruption of mitochondrial membrane potential.

Abstract: 

PURPOSE: To study the anticancer effects of aloe emodin against the MIAPaCa-2 and PANC-1 human pancreatic adenocarcinoma cancer cell lines by evaluating its effect on autophagic cell death, mitochondrial membrane potential (ΛΨm) loss and cell cycle arrest.METHODS: The MTT assay was employed to examine the anti-proliferative effect of aloe emodin on these cells, and inverted phase contrast and fluorescence microscopes were used to evaluate apoptotic induction. Flow cytometry was performed to examine the effects of aloe emodin onΛΨm and cell cycle phase distribution.RESULTS: The findings indicated that aloe emodin induced dose-dependent cytotoxicity in both pancreatic carcinoma cells with MIAPaCa-2 cells being more susceptible than PANC-1, along with inhibiting cancer cell colony formation. Aloe emodin-treated cells exhibited cell shrinkage along with distortion of the normal cell morphology. In addition, these cells showed chromatin condensation, membrane blebbing and predominantly emitted red fluorescence, which signified apoptosis. Following treatment with aloe emodin (10, 40 and 80µM) the early apoptotic cell percentage increased to 17.5, 39.6 and 58.8%, respectively, while late apoptotic cells percentage increased to 22.3, 27.6 and 37.2% respectively. There was also a marked increase in the loss of ΛΨm in the aloe emodin-treated cells, as well as dose-dependent sub-G1 cell cycle arrest. Furthermore, aloe emodin treatment led to a substantial enhancement of the conversion of light chain 3 (LC3)-l to LC3-ll and this increase was shown to follow aloe emodin dose-dependent pattern, thus indicating that aloe emodin may induce autophagy in addition to apoptosis.CONCLUSION: To sum up, aloe emodin inhibits cancer cell growth in human pancreatic carcinoma cells and it was shown that these anticancer effects are mediated via both apoptotic and autophagic pathways, cell cycle arrest and loss of mitochondrial membrane potential.

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PMID: 

Front Cell Infect Microbiol. 2019 ;9:157. Epub 2019 May 15. PMID: 31157174

Abstract Title: 

Aloe-emodin AttenuatesPathogenicity by Interfering With the Oligomerization ofα-Toxin.

Abstract: 

α-toxin, an essential virulence factor secreted by(), is a critical exotoxin in multiple infections. In this study, we found that aloe-emodin (AE), a natural compound lacking anti-activity, could inhibit the hemolytic activity ofα-toxin. Oligomerization assays, molecular dynamics simulations, and fluorescence-quenching analyses were used to determine the mechanism of this inhibition. The oligomerization of α-toxin was restricted by the engagement of AE with K110, T112, and M113 of the toxin, which eventually resulted in inhibition of the hemolytic activity. Lactate dehydrogenase and live/dead assays demonstrated that AE decreased the injury of human lung epithelial cells (A549) and mouse lung macrophages (MH-S) mediated by. Furthermore, treatment with AE showed robust protective effects in mice infected by. These findings suggest that AE effectively inhibited the pore-forming activity ofα-toxin and showed a protective effect againstvirulenceand, which may provide a new strategy and new antibacterial agent for clinical treatment ofinfections.

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PMID: 

Onco Targets Ther. 2019 ;12:3713-3721. Epub 2019 May 14. PMID: 31190872

Abstract Title: 

Anti-tumor effect of aloe-emodin on cervical cancer cells was associated with human papillomavirus E6/E7 and glucose metabolism.

Abstract: 

Aloe-emodin, an anthraquinone present in aloe latex, has been shown to have anti-proliferative properties in cervical cancer disease, all cases of which are almost caused by human papillomavirus (HPV), with the products of E6/E7. It is suggested that aloe-emodin may play an important role in HPV-induced cervical cancer cells.Hela and SiHa cells were treated with various concentrations of aloe-emodin. MTT assay and flow cytometry were used to identify the cell growth and apoptosis. The expressions of HPV E6, E7 and GLUT1 (glucose transporter-1) were detected by real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot (WB). The glucose uptake, lactate production and ATP production in HeLa and SiHa cells were also investigated.The results indicate that aloe-emodin promoted the apoptosis of HeLa and SiHa cells and decreased the expressions of HPV-related protein E6 and E7. Furthermore, aloe-emodin inhibited glucose metabolism by reducing GLUT1 expression. Overexpression of GLUT1 significantly weakened the apoptosis induced by aloe-emodin in HeLa cells.In this study, we found that aloe-emodin induce apoptosis of cervical cancer cells, which was associated with HPV E6 and E7 and glucose metabolism.

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PMID: 

Hum Exp Toxicol. 2019 Jun 30:960327119860174. Epub 2019 Jun 30. PMID: 31256688

Abstract Title: 

modulates X-ray induced hematological and splenic tissue damage in mice.

Abstract: 

The present study was premeditated to examine the radioprotective effects of aqueousgel extract against whole-body X-ray irradiation-induced hematological alterations and splenic tissue injury in mice. Healthy male balb/c mice were divided into four groups: group 1, control; group 2,(50 mg/kg body weight) administered per oral on alternate days for 30 days (15 times); group 3, X-ray exposure of 2 Gy (0.25 Gy twice a day for four consecutive days in the last week of the experimental protocol); and group 4,+ X-ray. X-ray exposure caused alterations in histoarchitecture of spleen along with enhanced clastogenic damage as assessed by micronucleus formation and apoptotic index. Irradiation caused an elevation in proinflammatory cytokines like tumor necrosis factor and interleukin-6, total leucocyte counts, neutrophil counts and decreased platelet counts along with unaltered red blood cell counts and hemoglobin. Irradiation also caused an elevation in reactive oxygen species (ROS), lipid peroxidation (LPO) levels, lactate dehydrogenase activity and alterations in enzymatic and nonenzymatic antioxidant defense mechanism in plasma and spleen. However, administration ofgel extract ameliorated X-ray irradiation-induced elevation in ROS/LPO levels, histopathological and clastogenic damage. It also modulated biochemical indices, inflammatory markers, and hematological parameters. These results collectively indicated that thegel extract offers protection against whole-body X-ray exposure by virtue of its antioxidant, anti-inflammatory and anti-apoptotic potential.

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