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The Secret of the Main College Water-Wells, Arba Minch College, Ethiopia.
To foster research integrity (RI), it is necessary to address the institutional and system-of-science factors that influence researchers' behavior. Consequently, research performing and research funding organizations (RPOs and RFOs) could develop comprehensive RI policies outlining the concrete steps they will take to foster RI. So far, there is no consensus on which topics are important to address in RI policies. Therefore, we conducted a three round Delphi survey study to explore which RI topics to address in institutional RI policies by seeking consensus from research policy experts and institutional leaders. A total of 68 RPO and 52 RFO experts, representing different disciplines, countries and genders, completed one, two or all rounds of the study. There was consensus among the experts on the importance of 12 RI topics for RPOs and 11 for RFOs. The topics that ranked highest for RPOs concerned education and training, supervision and mentoring, dealing with RI breaches, and supporting a responsible research process (e.g. through quality assurance). The highest ranked RFO topics concerned dealing with breaches of RI, conflicts of interest, and setting expectations on RPOs (e.g. about educating researchers about RI). Together with the research policy experts and institutional leaders, we developed a comprehensive overview of topics important for inclusion in the RI policies of RPOs and RFOs. The topics reflect preference for a preventative approach to RI, coupled with procedures for dealing with RI breaches. RPOs and RFOs should address each of these topics in order to support researchers in conducting responsible research.
Incidence of diabetes has increased significantly worldwide over recent decades. Our objective was to prepare and characterize a novel nano-carrier of hesperidin to achieve a sustained release of hesperidin and to explore the potency of the novel formula as an antidiabetic agent compared to metformin in type 2 diabetic rats.

Hesperidin was loaded on MgAl-layered double hydroxide (LDH). The formula was characterized using Fourier transform infrared spectroscopy (FTIR), X-ray powder diffraction (XRD), transmission electron microscopy, and dynamic light scattering. The release profile of hesperidin and MgAl-LDH-Hesperidin were studied in vitro. The parameters studied in vivowere blood glucose, glycated hemoglobin (HbA1c), insulin, lipid profile, and liver glycogen levels. We also investigated the levels of interleukin (IL)-17, tumor necrosis factor-Alfa (TNF-α), malondialdehyde (MDA), catalase, and the mRNA expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and nuclear factor erythroid 2-iabetic, antihyperlipidemic, antioxidant, and anti-inflammatory properties, and also is a promising agent for effective delivery of drugs to treat type 2 diabetes.
The constitutive activation of STAT3 through receptor tyrosine kinases triggered breast cancer cell growth and invasion-metastasis. Atiprimod impacts anti-proliferative, anti-carcinogenic effects in hepatocellular carcinoma, lymphoma, multiple myeloma via hindering the biological activity of STAT3. Dose-dependent atiprimod evokes first autophagy as a survival mechanism and then apoptosis due to prolonged ER stress in pituitary adenoma cells. The therapeutic efficiency and mechanistic action of atiprimod in breast cancer cells have not been investigated yet. BVD-523 manufacturer Thus, we aimed to modulate the pivotal role of ER stress in atiprimod-triggered apoptosis in MDA-MB-231 and MDA-MB-468 breast cancer cells.

Dose- and time-dependent atiprimod treatment inhibits cell viability and colony formation in MDA-MB-468 and MDA-MB-231 breast cancer cells. A moderate dose of atiprimod (2μM) inhibited STAT3 phosphorylation at Tyr705 residue and also suppressed the total expression level of p65. In addition, nuclear localization of STAT1, 3, and NF-κB was prevented by atiprimod exposure in MDA-MB-231 and MDA-MB-468 cells. Atiprimod evokes PERK, BiP, ATF-4, CHOP upregulation, and PERK (Thr980), eIF2α (Ser51) phosphorylation's. However, atiprimod suppressed IRE1α-mediated Atg-3, 5, 7, 12 protein expressions and no alteration was observed on Beclin-1, p62 expression levels. PERK/eIF2α/ATF4/CHOP axis pivotal role in atiprimod-mediated G1/S arrest and apoptosis via Bak, Bax, Bim, and PUMA upregulation in MDA-MB-468 cells. Moreover, atiprimod renders MDA-MB-231 more vulnerable to type I programmed cell death by plasmid-mediated increased STAT3 expression.

Atiprimod induced prolonged ER stress-mediated apoptosis via both activating PERK/eIF2α/ATF4/CHOP axis and suppressing STAT3/NF-κB transcription factors nuclear migration in TBNC cells.
Atiprimod induced prolonged ER stress-mediated apoptosis via both activating PERK/eIF2α/ATF4/CHOP axis and suppressing STAT3/NF-κB transcription factors nuclear migration in TBNC cells.
Industrial toxicants such as Carbon tetrachloride (CCl
) are known to disrupt the oxidative-antioxidative balance, which generates excessive amounts of free radicals leading to chronic or acute liver damage. Natural antioxidants, including Ajwa, play an important role in protecting against hepatotoxicity.

This study investigated the prophylactic impacts of ajwa seeds aqueous extract (ASE) against hepatic oxidative injury in rats induced by CCl
. Eighty male Wistar albino rats were equally assigned to eight groups one group receive no treatment, four groups were received CCl
-olive oil mixture [11(v/v)] (0.2ml/100g body weight (bw), intraperitoneally) two times/week for 4 weeks/rat alone or with 200mg Vit. C/kg bw or 5ml ASE/rat or both, and three groups received olive oil, Vit. C, or ASE. Vitamin C and ASE were orally administrated two weeks before CCl
injection and 4 weeks concomitant with CCl
. Lipid peroxidation, lipogenesis-related genes, hepatic histopathology, Bax immunostaining and DNA fragmentation were assessed. ASE protected hepatic damage by suppressing oxidative stress and elevating activities of antioxidant enzymes, including superoxide dismutase and catalase. ASE also regulated hepatic dyslipidemia, hepatic lipid accumulation and expression of SREBP-1 and FAS genes in CCl
-treated rats. ASE decreased apoptosis through inhibition of CCl
induced Bax activation in hepatocytes.

These observations provide evidence for the hepatoprotective potential of ASE via inhibiting hepatic lipogenesis and oxidative stress, suggesting being used as a natural product in attenuating CCl
induced oxidative damage, hepatotoxicity and associated dysfunction.
These observations provide evidence for the hepatoprotective potential of ASE via inhibiting hepatic lipogenesis and oxidative stress, suggesting being used as a natural product in attenuating CCl4 induced oxidative damage, hepatotoxicity and associated dysfunction.
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