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Shebaita, A., M. M. Khairy, A. E. Salama, and M. Ashour, "A Viterbi decoder core with no trace-back unit", Microelectronics, 2003. ICM 2003. Proceedings of the 15th International Conference on: IEEE, pp. 374–377, 2003. Abstract
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Gramoun, A., M. F. Manolson, J. N. M. Heersche, D. P. Trebec, and S. Y. Mao, "Vitaxin (R), an alphav beta3 blocking antibody, inhibits osteoclastic resorption by decreasing the number of attached osteoclasts.", JOURNAL OF BONE AND MINERAL RESEARCH, vol. 19: AMER SOC BONE & MINERAL RES 2025 M ST, NW, STE 800, WASHINGTON, DC 20036-3309 USA, pp. S154–S154, 2004. Abstract
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El Din, U. S., A. Fayed, M. M. El Nokeety, D. O. Abdulazim, and M. M. Salem, "Vitamin-D deficiency is encountered in almost all egyptian stage 3-5 chronic kidney disease patients in spite of the sunny weather.", Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia, vol. 30, issue 6, pp. 1389-1397, 2019. Abstract

Currently, there is no available data about Vitamin D status among Egyptian chronic kidney disease (CKD) patients. This cross-sectional study is looking for the prevalence of Vitamin D deficiency among Stage 3a-5 CKD Egyptian patients and its possible associations. We studied 1624 Stage 3a-5 CKD adults (689 males and 935 females) together with 200 normal control persons. All the recruited candidates were tested for body mass index (BMI); serum levels of blood urea nitrogen, creatinine, calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25 hydroxy vitamin D (25(OH)D), albumin, and uric acid (UA); urine albumin/creatinine ratio (ACR), and estimated glomerular filtration rate. The optimal level of Vitamin D was encountered in only 1.4% of CKD patients versus 52% of the normal controls. A total of 1107 (68.2%) CKD patients versus 23 (11.5%) controls had serum 25(OH)D <20 ng/mL (mean ± standard deviation = 16.8 ± 5.8 versus 37.3±7.6 ng/mL for CKD versus control group, respectively, P <0.001). There was a highly statistically significant positive correlation between serum 25(OH)D and serum Ca (r = 0.299, P <0.001) and a highly statistically significant negative correlation between serum 25(OH)D on the one hand and serum P, serum PTH, serum UA, and urine ACR on the other hand (r = -0.46, -0.69, -0.73, and -0.8, respectively, P <0.001). Vitamin D deficiency is very common among Egyptian CKD patients. Serum P, UA, and urine ACR ratio are the most important variables which are found to be negatively associated with serum 25(OH)D.

A.M.Al-Sherbini, E. - S., A. H.ElNoury, M. N. E. Rouby, and T. Ibrahim, "Vitamin E(a-tocopherol) enhancesthePDTactionofhematoporphyrin derivatives oncervicalcancercells", Medical LaserApplication, vol. 24, issue 24, pp. 65–73, 2009. 38.pdf
ElFattah, A. A. A., H. M.Al-Yousef, A. A. - M. Bekairi, and H. A. Al-Sawaf, "Vitamin E protects the brain against oxidative injury stimulated by excessive aluminum intake.", Biochemistry and Molecular Biology international, (Australia) , vol. 46, issue 6, pp. 1175-1180, 1998.
Al-Hashem, F., M. Abd Ellatif, A. M. Shams Eldeen, S. S. Kamar, B. Al-Ani, and M. A. Haidara, "Vitamin E protects against the modulation of TNF-α-AMPK axis and inhibits pancreas injury in a rat model of L-arginine-induced acute necrotising pancreatitis.", Archives of physiology and biochemistry, pp. 1-9, 2020. Abstract

BACKGROUND: Acute pancreatitis (AP) associated with the modulation of TNF-α-AMPK axis in the presence and absence of vitamin E has not been investigated before.

MATERIAL AND METHODS: Rats were either injected with L-arginine (2.5 gm/kg) before being sacrificed after 48 h or were pre-treated with vitamin E (60 mg/kg) and continued receiving vitamin E until the end of the experiment.

RESULTS: AP was developed as demonstrated by infiltration of inflammatory cells and profound pancreas tissue damage, which were substantially protected by vitamin E. In addition, L-arginine injections significantly ( < .0001) increased the expression of TNF-α mRNA and protein, and decreased phospho-AMPK and IL-10 mRNA and protein that was significantly ( < .0001) protected by vitamin E. Furthermore, vitamin E inhibited L-arginine-induced blood levels of LDH, amylase, and myeloperoxidase.

CONCLUSIONS: L-arginine-induced acute pancreatitis modulates TNF-α-AMPK axis, IL-10 and other AP biomarkers, which is protected by vitamin E; thus, may offer therapeutic potential in humans.

Al-Hashem, F., M. Abd Ellatif, A. M. Shams Eldeen, S. S. Kamar, B. Al-Ani, and M. A. Haidara, "Vitamin E protects against the modulation of TNF-α-AMPK axis and inhibits pancreas injury in a rat model of L-arginine-induced acute necrotising pancreatitis", Archives of Physiology and Biochemistry, 2020.
Eid, R. A., M. Al-Shraim, M. S. Zaki, S. S. Kamar, N. S. Abdel Latif, S. Negm, B. Al-Ani, and M. A. Haidara, "Vitamin E protects against monosodium glutamate-induced acute liver injury and hepatocyte ultrastructural alterations in rats.", Ultrastructural pathology, vol. 43, issue 4-5, pp. 199-208, 2019. Abstract

Food additives such as nitrates and nitrites, and monosodium glutamate (MSG) used in the food industry increase the risk of certain cancers and inflict damage to vital organs. We sought to determine whether the antioxidant vitamin E can protect against liver injuries induced by a toxic dose of MSG in a rat model of MSG-induced acute liver injury. The model group of rats received a daily dose of MSG (4 gm/kg) for 7 days, whereas the protective groups were either received a 100 mg/kg vitamin E plus MSG or 300 mg/kg vitamin E plus MSG for 7 days. Rats were then sacrificed at day 8. Transmission and light microscopy images revealed substantial liver tissue damage induced by MSG in the model group as demonstrated by apoptotic hepatocytes with Pyknotic nuclei and irregular nuclear membrane, and cytoplasm displayed many vacuoles, swollen mitochondria, dilated endoplasmic reticulum, dilated blood sinusoids and bundles of collagen fibers in extracellular space. Treatment of the model group with vitamin E showed a substantial protection of liver tissue and hepatocellular architecture by 300 mg/kg vitamin E compared to a partial protection by 100 mg/kg vitamin E. In addition, MSG significantly ( < .05) modulated serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD), and glutathione peroxidase (GPx), which were significantly ( < .05) protected with vitamin E. Thus, vitamin E at 300 mg/kg effectively protects against MSG-induced acute liver injury in rats, possibly via the inhibition of inflammation, and up-regulation of endogenous antioxidants.

Eid, R. A., M. Al‑Shraim, M. S. Zaki, S. S. Kamar, N. A. S. Latif, S. Negm, B. Al-Ani, and M. A. Haidara, "Vitamin E protects against monosodium glutamate-induced acute liver injury and hepatocyte ultrastructural alterations in rats", Ultrastructural Pathology, vol. 43, issue 4, pp. 199-208, 2019.
Shoukry, H. S., R. A. D. W. A. T. HASSANIEN, R. A. Rasheed, M. O. A. T. A. Z. M. KAMEL, E. R. Ibrahim, and H. A. L. A. S. IBRAHIM, "Vitamin E Improves Doxorubicin Induced Nephrotoxicity; Possible Underlying Mechanisms", Medical journal of Cairo University , vol. Vol. 86,, 2018.
Mona K Galal, Abdel Azim A Khalaf, H. A. Ogaly, and Marwa A Ibrahim, "Vitamin E attenuates neurotoxicity induced bydeltamethrin in rats", BMC Complementary and Alternative Medicine, vol. 14, pp. 458-464, 2014. vit E_against_DM neurotoxicity.pdf
Mona K Galal, Abdel Azim A Khalaf, H. A. Ogaly, and Marwa A Ibrahim, "Vitamin E attenuates neurotoxicity induced by deltamethrin in rats.", BMC complementary and alternative medicine, vol. 14, pp. 458, 2014 Dec 02. Abstract

BACKGROUND: The safety of Deltamethrin (DM) has been raised as a point of concern. The current investigation was envisaged to explore the responsiveness of oxidative stress parameters, DNA fragmentation and expression levels of TP53, cycloxygenase 2 (COX2) and cytochrome p4502E1 (CYP2E1) as toxicological endpoint in rats treated with DM. as well as attention was provided to the neuroprotective effect of vitamin E (VE).

METHODS: Four different groups of rats were used in this study, group I served as control, group II received DM (0.6 mg/kg BW), group III received both DM plus VE and finally group IV received VE only (200 mg/kg BW). The treatment regimen was extending for one month for all groups and the brain tissues were collected for further analysis.

RESULTS: The obtained results showed a highly statistically significant increase in lipid peroxidation (LPO) content, nitric oxide concentration, and DNA fragmentation percentage and expression level of CYP2E1, TP53 and COX2 genes, in addition statistical significant reduction in total antioxidant capacity in DM treated group as compared to control were detected. Oral administration of VE attenuated the neurotoxic effects of DM through improvement of oxidative status, DNA fragmentation percentage and suppressing the expression level of CYP2E1, TP53 and COX2 genes.

CONCLUSION: From this study we concluded that VE supplementation has beneficial impacts on DM neurotoxicity in rats through its antioxidant and antiapoptotic properties.

Ibrahim, M., H. Ogaly, and A. A. Khalaf, "Vitamin E attenuates neurotoxicity induced by deltamethrin in rats", BMC complementary and alternative medicine , vol. 14, issue 1, pp. 458, 2014. my_paper_dm_ve.pdf
Mona, Kgalal, K. A. Abdel Azeim, A. O. Hanan, and I. A. Marwa, "Vitamin E attenuates neurotoxicity induced by deltamethrin in rat published in BMC complementary andAlternative Medicine ,14 ,458", BMC Complementary and Alternative Medicine, vol. 14, issue 1, pp. 458, 2014.
Mona, Kgalal, K. A. Abdel Azeim, A. O. Hanan, and I. A. Marwa, "Vitamin E attenuates neurotoxicity induced by deltamethrin in rat published in BMC complementary andAlternative Medicine ,14 ,458", BMC Complementary and Alternative Medicine, vol. 14, issue 1, pp. 458, 2014.
El-Ghany, W. A. A., "Vitamin E and its impact on poultry production: An Update", Journal of the Hellenic Veterinary Medical Society, vol. 73, issue 1, pp. 3571–3582, 2022. 10.12681_jhvms.25836_1.pdf
Hassan, W. N., I. Bin-Jaliah, M. A. Haidara, R. A. Eid, E. H. A. Heidar, M. Dallak, and B. Al-Ani, "Vitamin E ameliorates alterations to the articular cartilage of knee joints induced by monoiodoacetate and diabetes mellitus in rats.", Ultrastructural pathology, vol. 43, issue 2-3, pp. 126-134, 2019. Abstract

We recently reported an animal model of osteoarthritis (OA) induced by a combination of the chondrocyte glycolysis inhibitor, monoiodoacetate (MIA) and the agent that induces diabetes mellitus, streptozotocin (STZ). Here we investigated the potential protective effect of the antioxidant and anti-inflammatory agent, vitamin E against MIA+STZ-induced OA. Therefore, rats were either injected once with MIA (2 mg/50 μL) + 65 mg/kg STZ before being sacrificed after 8 weeks (model group) or were treated immediately after MIA+STZ injections with vitamin E (600 mg/kg; thrice a week) before being sacrificed after 8 weeks (treatment group). Using scanning and transmission electron microscopy examinations, we observed in the model group a substantial damage to the articular cartilage of the knee joint as demonstrated by the destruction of the chondrocytes, territorial matrix, disrupted lacunae, collagen fibers, and profound chondrocyte ultrastructural alterations such as degenerated chondrocyte, irregular cytoplasmic membrane, damaged mitochondria and rough endoplasmic reticulum, vacuolated cytoplasm, presence of lipid droplets and different sizes of lysosomes, which were substantially but not completely protected by vitamin E. H&E stained sections of knee joint articular cartilage showed that MIA+STZ induced damage to the chondrocyte and territorial matrix. Vitamin E also significantly ( < .05) inhibited MIA+STZ-induced blood levels of the inflammatory biomarkers, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) that are known to be modulated in OA and diabetes. We conclude that vitamin E protects against MIA+STZ-induced knee joints injuries in rats, which is associated with the inhibition of biomarkers of inflammation.

A.M.Al-Sherbini, E. - S., A. H.ElNoury, M. N. E. Rouby, and T. Ibrahim, "Vitamin E (a-tocopherol) enhances the PDT action of hematoporphyrin derivatives on cervical cancer cells", Medical Laser Application , vol. 24, pp. 65–73, 2009.
Alrefaie, Z., and A. 'em Alhayani, "Vitamin D₃ improves decline in cognitive function and cholinergic transmission in prefrontal cortex of streptozotocin-induced diabetic rats.", Behavioural brain research, vol. 287, pp. 156-62, 2015 Jul 1. Abstract

Complications of diabetes mellitus include cognitive impairments and functional changes in the brain. The present study aimed to investigate the possible beneficial effect of vitamin D3 on episodic memory and cholinergic transmission in the prefrontal cortex of streptozotocin-induced diabetic rats. Thirty male Wistar rats (150-200 g) were included into control, diabetic and diabetic supplemented with vitamin D3 groups. Diabetes was induced by single intraperitoneal injection of streptozotocin 45 mg/kg in citrate buffer. Vitamin D3 was administered orally in a dose of 500 IU/kg/day in corn oil for 10 weeks. Then rats were subjected to novel object recognition test to examine for episodic memory. Animals were sacrificed under diethyl ether anesthesia and prefrontal cortices were dissected to measure the activity of choline acetyl transferase (CAT) and acetyle choline esterase (ACE) enzymes to assess for cholinergic transmission. Diabetic rats spent significantly less time exploring the novel object compared to control animals. Vitamin D3 significantly attenuated the diabetes-induced impairment so that animals again spent significantly more time exploring the novel object. The CAT activity was significantly decreased in diabetic animals while the ACE activity was significantly increased compared to control non-diabetic animals. Diabetes-induced alterations in enzyme activity in the prefrontal cortex were mitigated by vitamin D3 supplementation. The present findings demonstrate the potential effect of vitamin D3 supplementation on cognitive function in diabetic animals. It is possible that this effect is mediated through enhancing the prefrontal cortex cholinergic transmission.

Alrefaie, Z., and I. Moustafa, "Vitamin D3 favorable outcome on recognition memory and prefrontal cortex expression of choline acetyltransferase and acetylcholinesterase in experimental model of chronic high-fat feeding.", The International journal of neuroscience, vol. 130, issue 3, pp. 262-269, 2020. Abstract

High-fat diet (HFD) consumption and insufficient vitamin D levels are globally increasing phenomena. The present study assessed the effect of chronic HFD feeding with and without vitamin D supplementation on recognition memory and prefrontal cortex expression of choline acetyltransferase (CAT) and acetylcholinesterase (Achase). Forty male Wistar rats were subjected to four dietary regimens ( = 10); control diet (10% fat), control + vitamin D3, high-fat diet (HFD 45% fat) and HFD + vitamin D3 for 6 months. Rats were tested for the novel object recognition test, and their prefrontal cortices were assessed for expression of CAT and Achase. Recognition memory was impaired in HFD-fed rats compared to control rats as evidenced by significantly decreased discrimination index in the novel object recognition test. Moreover, CAT expression was significantly decreased while Achase expression was significantly increased in the prefrontal cortex of HFD-fed rats. Vitamin D3 supplementation with HFD significantly increased the exploration of the novel object and the discrimination index and attenuated the alterations in the prefrontal cortex CAT and Achase expression. The present findings support the potential effect of vitamin D on recognition memory and cholinergic transmission in the prefrontal cortex and add to the pathophysiology of HFD consumption.

Al-Sultan, A. I., T. T. Amin, M. A. Abou-Seif, and M. R. Al Naboli, "Vitamin D, parathyroid hormone levels and insulin sensitivity among obese young adult Saudis", Eur Rev Med Pharmacol Sci, vol. 15, no. 2, pp. 135–147, 2011. Abstract
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Asmaa, M., M. Moustafa, N MORCOS GEORGE, F MARWA, and M. D. Abdallah, "Vitamin D Supports (3-Cell Remodeling Capacity and Could Reduce High Fat Diet-induced Insulinitis in Pups Born to Diabetic Mothers", The Medical Journal of Cairo University, vol. 86, 2018.
Abdel Aziz, A. T., and W. Fathy., "Vitamin D supplementation potentiate antiviral SOC therapy in chronic HCV patients.", The Arab Journal of Laboratory Medicine, vol. 44, issue 3, pp. 683-689, 2019. Abstractvitamin_d_supplementation_potentiate_antiviral_soc_therapy_in_chronic_hcv_patients..pdf

Background: HCV is major health problem worldwide, that can lead to hepatic fibrosis, decompensation, and hepatocellular carcinoma. The current standard of care therapy (SOC) for chronic HCV is pegylated interferon/ribavirin (Peg-IFN/ RBV). It has been reported that vitamin D has immune-modulatory effect and alleviates the inflammatory diseases in addition to its role in bone homeostasis. The aim of this study is to evaluate the effect of combined vitamin D supplementation and SOC therapy in chronic HCV patients.
Methods: One hundred chronic HCV patients were classified into two groups (Group 1): 50 patients received the SOC therapy (Group 2): 50 patients received the SOC therapy + vitamin D3. During the treatment course, Vitamin D, liver function were evaluated in 6, 12, 24 and 48 weeks.
Results: vitamin D deficiency was found in both groups at basal time of the study, which then elevated up on treatment. The patients received vitamin D turn HCV RNA negative after 12 weeks of treatment, while those in group1 became negative after 48 weeks. Vitamin D supplementation has positive impact on treatment outcome where sustained viral response (SVR) was achieved in nearly all patients in group 2.
Conclusion: vitamin D accelerate the antiviral treatment effect and has positive impact on sustained viral response.
Key words: vitamin D, HCV, Interferon therapy.