In this study, we considered heterogeneous and homogeneous chemical reactions in Eyring‐Powell ferrofluid past a stretchable surface. In addition, thermal radiation and magnetic dipole impacts are also considered. The direct numerical solution of the governing model is complex. For this, we simplified the model into coupled ordinary differential equations (ODEs) with the dimensionless variables. Then, we determined the computational solution of the resulting transformed ODE system via the Runge‐Kutta (RK) method. The impacts of interesting engineering parameters on temperature, velocity, and concatenation behaviors are presented through graphs. We concluded that the velocity field is reduced for higher values of ferromagnetic parameter β and fluid material parameters ß and H and arises the temperature field for higher values of thermal radiation R while the temperature field is reduced for Prandtl number Pr and dissipation parameter λ 1 . The obtained results of the current work are compared with published work, and we found that between them a good agreement can be seen in the table. The characteristics of skin fraction and Nusselt number are presented.

Ode

Ferrofluid

Dimensionless quantity

10.1155/2022/2501263

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Citations (13)

Sodium loss, extracellular volume overload and hypertension in peritoneal dialysis patients treated by automated peritoneal dialysis cyclers

The International Journal of Artificial Organs (2019)

Ahmed F. Mohamed Andrew Davenport

Achieving sodium balance is important for peritoneal dialysis patients, as sodium excess may lead to hypertension and extracellular water expansion. We wished to determine whether greater sodium removal had adverse consequences.We calculated 24-h urinary and peritoneal sodium losses in peritoneal dialysis patients treated by automated cyclers, when attending for peritoneal membrane and bioimpedance assessments.We reviewed 439 peritoneal dialysis patients, 56.7% male, average age 54.6 years, median sodium loss 110 (68-155) mmol/day. Sodium loss was strongly associated with urine volume, r = 0.37, protein nitrogen appearance rate, r = 0.29, and body cell mass, r = 0.21, all p < 0.001. We found no association with blood pressure or anti-hypertensive medication prescription, or extracellular water. On multivariable logistic regression analysis, sodium loss was associated with greater urine output, odds ratio 1.001, 95% confidence interval 1.00-1.001, p < 0.001, and protein nitrogen appearance (odds ratio 1.023, confidence interval 1.006-1.04), p = 0.008. Adjusting for body weight, sodium loss was associated with urine output (odds ratio 1.001, confidence interval 1.001-1.002, p < 0.001), and negatively with body fat index (odds ratio 0.96, confidence interval 0.93-0.99, p = 0.008) and co-morbidity grade (odds ratio 0.58, confidence interval 0.36-0.39, p = 0.023).Heavier peritoneal dialysis patients with greater estimated dietary protein intake (protein nitrogen appearance), those with greater residual renal function and peritoneal clearances, along with lower co-morbidity, had greater daily sodium losses. Adjusting for body weight, then sodium losses were greater with higher daily urine output, and lower in patients with proportionately more body fat and co-morbidity. Sodium losses would appear to primarily determined by body size and not associated with hypertension or extracellular water expansion.

Urine sodium

10.1177/0391398819864368

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Melatonin mitigates vincristine-induced peripheral neuropathy by inhibiting TNF-α/astrocytes/microglial cells activation in the spinal cord of rats, while preserving vincristine's chemotherapeutic efficacy in lymphoma cells

Toxicology and Applied Pharmacology (2024)

Engie S. El-Sawaf Nabila N. El Maraghy Hanan S. El‐Abhar Hala F. Zaki Beshay N. Zordoky

10.1016/j.taap.2024.117134

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The Predictive Value of Arteriogenic Erectile Dysfunction for Coronary Artery Disease in Men

The Journal of Sexual Medicine (2018)

Sherif Azab Hossam El Din Hosni Taha A. El Far Nashaat Nabil Ismail Yasser K. El Bakdady

Lipid Profile

10.1016/j.jsxm.2018.04.639

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Exacerbation of Mirror Movement Disorder: A Complex Case of Childhood-onset Mirror Movements Aggravated by Essential Tremors, and Parkinson's Disease

The Open Neurology Journal (2024)

Sara Zarei Farnoush Nasouri Setareh Kamali Shivani Patel Rahma Jamil

Background Mirror movement (MM), also known as bimanual synkinesis, is characterized by simultaneous involuntary movements of homologous muscles accompanying voluntary movements of contralateral body regions. MM can be observed in various neurological conditions, including cerebral palsy, corticobasal syndrome, Parkinson's disease, certain types of symptomatic epilepsies, Creutzfeldt-Jakob's disease, Huntington's disease, and others. Case Description A 52-year-old female with a history of epileptic seizures, essential tremors and mild MM was presented to a neurology clinic for seizure management. She had a long-standing history of seizures since childhood. Initial neurological examination revealed mild MM disorder. During the follow up visits, patient’s mirror movements were exacerbated months before she was diagnosed with Parkinson’s disease. Multiple antiepileptic drug regiments along with Carbidopa-levodopa were used and dose adjustments were done during follow up visits to help stabilize the patient’s symptoms. Conclusion In conclusion, this case highlights the progressive nature of mirror movement disorder (MMD) and its association with other neurological conditions, such as epilepsy, essential tremors, and Parkinson's disease. The primary aim of this study was to showcase that individuals with early childhood onset of MMD may experience a deterioration of their condition as they acquire additional neurological disorders, such as essential tremors or Parkinson's disease. Moreover, this study seeks to elucidate how the exacerbation of mirror movement symptoms in such cases can serve as an early indicator of the onset of Parkinson's disease. Medication adjustments played a crucial role in managing the patient's symptoms, emphasizing the importance of individualized treatment plans and close monitoring.

Movement Disorders

10.2174/011874205x281071231227063030

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Development and validation of an LC‒MS/MS method for the determination of cyclocreatine phosphate and its related endogenous biomolecules in rat heart tissues

BMC Chemistry (2024)

Ibrahim F. Abo-Elmagd Amr M. Mahmoud Medhat A. Al‐Ghobashy Marianne Nebsen Mostafa A. Rabie

The cardioprotective drug cyclocreatine phosphate has been awarded Food and Drug Administration-orphan drug designation for the prevention of ischemic injury to enhance cardiac graft recovery and survival in heart transplantation. Cyclocreatine phosphate is the water-soluble derivative of cyclocreatine. Estimating the levels of Cyclocreatine phosphate, Adenosine triphosphate, Creatine Phosphate, Creatine and Cyclocreatine helps us in understanding the energy state as well as evaluating the heart cells' function. The quantification of endogenous compounds imposes a challenging task for analysts because of the absence of a true blank matrix, whose use is required according to international guidelines. Recently, the International Council for Harmonization issued a new guideline that contains guidance on the validation of methods used to quantify endogenous components, such as the background subtraction approach that was employed in our current study. Specifically, we developed and validated a sensitive, reliable and accurate liquid chromatography-tandem mass spectrometry assay to determine simultaneously the levels of mentioned endogenous compounds in rat heart tissue. Tissue samples were prepared by protein precipitation extraction using water: methanol (1:1). Using Ultra Performance Liquid Chromatography, Chromatographic separation was achieved with ZORBAX Eclipse Plus C18 4.6 × 100 mm,3.5 μm column and conditions as following: ammonium acetate (pH 8.5): acetonitrile, 70:30 mobile phase, 0.7 mL/min flow rate and 25 °C temperature. Electrospray ionization mass detector with Multiple reaction monitoring mode was then employed, using both positive and negative modes, Analysis was carried out using 5.00–2000.00 ng/mL linear concentration range within 2 min for each analyte. According to Food and Drug Administration guidelines for bioanalytical methods, validation was carried out. We investigated the matrix effect, recovery efficiency and process efficiency for the analyte in neat solvent, postextraction matrix and tissue. The results stated mean percentage recoveries higher than 99%, accuracy 93.32–111.99%, and Relative Standard Deviation (RSD) below 15% within the concentration range of our study which indicated that target analytes' stability in their real matrix is sufficient under the employed experimental conditions. Development of a validated LC‒MS/MS method to quantify levels of CCrP, ATP, CrP, Crt, and CCr, simultaneously. LC‒MS/MS method is sensitive, simple and suitable for preclinical trials for CCrP quantitation in different biological fluids. Validated method with good selectivity, linearity, and stability for CCrP in the rat heart. Efficient CCrP quantitation to improve outcomes for heart transplant patients.

Biomolecule

10.1186/s13065-024-01304-1

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Pazopanib ameliorates rotenone-induced Parkinsonism in rats by suppressing multiple regulated cell death mechanisms

Food and Chemical Toxicology (2023)

Heba M. Mansour Ahmed F. Mohamed Mahmoud M. Khattab Aiman S. El‐Khatib

Pazopanib

Rotenone

RIPK1

Astrogliosis

10.1016/j.fct.2023.114069

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Neuroprotective effect of liraglutide in an experimental mouse model of multiple sclerosis: role of AMPK/SIRT1 signaling and NLRP3 inflammasome

Inflammopharmacology (2022)

Reham A. Ammar Ahmed F. Mohamed Mohamed M. Kamal Marwa M. Safar Noha F. Abdelkader

The heterogeneous nature of multiple sclerosis (MS) and the unavailability of treatments addressing its intricate network and reversing the disease state is yet an area that needs to be elucidated. Liraglutide, a glucagon-like peptide-1 analogue, recently exhibited intriguing potential neuroprotective effects. The currents study investigated its potential effect against mouse model of MS and the possible underlying mechanisms. Demyelination was induced in C57Bl/6 mice by cuprizone (400 mg/kg/day p.o.) for 5 weeks. Animals received either liraglutide (25 nmol/kg/day i.p.) or dorsomorphin, an AMPK inhibitor, (2.5 mg/Kg i.p.) 30 min before the liraglutide dose, for 4 weeks (starting from the second week). Liraglutide improved the behavioral profile in cuprizone-treated mice. Furthermore, it induced the re-myelination process through stimulating oligodendrocyte progenitor cells differentiation via Olig2 transcription activation, reflected by increased myelin basic protein and myelinated nerve fiber percentage. Liraglutide elevated the protein content of p-AMPK and SIRT1, in addition to the autophagy proteins Beclin-1 and LC3B. Liraglutide halted cellular damage as manifested by reduced HMGB1 protein and consequently TLR-4 downregulation, coupled with a decrease in NF-κB. Liraglutide also suppressed NLRP3 transcription. Dorsomorphin pre-administration indicated a possible interplay between AMPK/SIRT1 and NLRP3 inflammasome activation as it partially reversed liraglutide's effects. Immunohistochemical examination of Iba+ microglia emphasized these findings. In conclusion, liraglutide exerts neuroprotection against cuprizone-induced demyelination via anti-inflammatory, autophagic flux activation, NLRP3 inflammasome suppression, and anti-apoptotic mechanisms, possibly mediated, at least in part, via AMPK/SIRT1, autophagy, TLR-4/ NF-κB/NLRP3 signaling. The potential mechanistic insight of Lira in alleviating Cup-induced neurotoxicity via: (1) AMPK/SIRT1 pathways activation resulting in the stimulation of brain autophagy flux (confirmed by lowering Beclin-1 and LC3-B protein expression). (2) Inhibition of NLRP3 inflammasome activation, as evidenced by reduced HMGB1, TLR-4, NF-κB and NLRP3 protein expression, alongside diminishing the activation of its downstream cascade as reflected by reduced levels of caspase-1 and IL-1β protein expression. (3) A possible modulating interplay between the previously mentioned two pathways.

10.1007/s10787-022-00956-6

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Citations (45)