Vitiligo pathogenesis is related to the macrophage migration inhibitory factor (MIF) protein. This study aimed to assess the lesional MIF levels and gene polymorphisms (rs755622G>C) in patients with vitiligo. To assess the consequences of combining narrow‐band ultraviolet B with oral minipulse prednisolone as opposed to a combination with oral methotrexate on MIF levels in vitiligo patients, 50 unstable vitiligo patients and 50 controls were randomly chosen for comparison. MIF levels in skin homogenates and MIF (rs755622G>C) single nucleotide polymorphisms were assessed using the ELISA and the polymerase chain reaction restriction fragment length polymorphism (RFLP‐PCR) techniques. We found significantly higher lesional MIF levels, a higher frequency of both (GC) and (CC) genotypes, and a significantly more frequent mutant allele (C) in patients than in controls. In addition, there was a significantly lower frequency of the allele (C) among patients who exhibited moderate to marked therapeutic improvement than among those who showed minimal to mild improvement. In conclusion, tissue MIF and gene polymorphisms were associated with vitiligo. In addition, oral corticosteroids, narrow‐band ultraviolet B, methotrexate‐targeted tissue MIF, and gene polymorphisms can improve unstable vitiligo.

Vitiligo

10.1155/2023/9937187

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NLRP3 inflammasome pathway involved in the pathogenesis of metabolic associated fatty liver disease

Scientific Reports (2024)

Heba Ahmed Osman Sawsan Abuhamdah Mohammed H. Hassan Abdelkader Ahmed Hashim Abdelazeem E. Ahmed

Abstract The prevalence of Metabolic-associated fatty liver disease (MAFLD) has been steadily increasing worldwide, paralleling the global epidemic of obesity and diabetes. It is estimated that approximately one-quarter of the global population is affected by MAFLD. Despite its high prevalence, MAFLD often goes undiagnosed due to the lack of specific symptoms in its early stages. However, as the disease progresses, it can lead to more severe liver-related complications such as fibrosis, cirrhosis, and hepatocellular carcinoma. Therefore, we aimed to investigate the expression levels of the nucleotide-binding oligomerization domain, leucine-rich repeat (LRR)—containing proteins (NLR) family pyrin domain-containing protein 3 [NLRP3] inflammasome pathway components, NLRP3 and interleukin 1β (IL-1β) genes in patients with MAFLD with various degrees of steatosis and fibrosis. Participants were classified into two equal groups; MAFLD group: consisted of 120 patients with different degrees of hepatic fibrosis and steatosis based on fibro scan results. The non-MAFLD group was comprised of 107 participants. Molecular analysis of pyrin domain-containing protein 3 and IL-1β relative gene expressions was performed in the blood of all participants, using Real-time quantitative polymerase chain reaction (RT-qPCR). Patients with post-MAFLD hepatic fibrosis had significantly higher relative gene expression levels of IL-1β and NLRP3; with IL-1β > 1.1 had AUC of 0.919, sensitivity of 88.33, specificity of 96.26, PPV of 96.4, and NPV of 88 and 92.3 accuracy ( p value < 0.001). NLRP3 > 1.33 had a sensitivity of 97.5, specificity of 99.07, PPV of 99.2, NPV of 97.2, and 98.3 accuracy with an AUC of 0.991 ( p value < 0.001) as predictors of post-MAFLD hepatic fibrosis.. A significant increase in the mean relative gene expression levels of both IL-1β and NLRP3 found in patients with early fibrosis (F0-F1-2); 31.97 ± 11.8 and 6.76 ± 2.18, respectively; compared with patients with advanced hepatic fibrosis stages (F2-F3); 2.62 ± 3.71 and 4.27 ± 2.99 ( p < 0.001 each). The present study provides novel evidence for the possible involvement of IL-1β and NLRP3 inflammasome in metabolic-associated fatty liver disease pathogenesis and could be valid markers for the early detection of post-MAFLD hepatic fibrosis.

Pyrin domain

Steatosis

Pathogenesis

Liver disease

10.1038/s41598-024-69764-y

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Comparative study of the efficacy of pulsed electromagnetic field and low level laser therapy on mitogen-activated protein kinases

Biochemistry and Biophysics Reports (2017)

Ayman M. El-Makakey Radwa Mahmoud Elsharaby Mohammed H. Hassan Alaa Eldin Balbaa

Mitogen-Activated Protein Kinases (MAPKs) consist of three major signaling members: extracellular signal-regulated kinase (ERK), p38 and C-JUN N-terminal kinase (JNK). We investigated physiological effects of Pulsed Electromagnetic Field Therapy (PEMFT) and Low Level Laser Therapy (LLLT) on human body, adopting the expression level of mitogen-activated protein kinases as an indicator via assessment of the activation levels of three major families of MAPKS, ERK, p38 and JNK in the peripheral lymphocytes of patients before and after the therapies. Assessment for the expression levels of MAPKs families' were done, in the peripheral lymphocytes of patients recently have appendectomy, using flow cytometric analysis of multiple signaling pathways, pre and post LLLT and PEMFT application (twice daily for 6 successive days) on the appendectomy wound. There were non-significant differences in the expression levels of MAPKs families' pre- therapies application. But there were significant increase in the ERK expression levels post application of LLLT compared to its pre application (p<0.01). Also, there was significant increase in the ERK, p38 and C-Jun N terminal expression level values post application of PEMFT compared to its pre application expression levels (p<0.01 for each). The present study demonstrates that PEMFT has a powerful healing effect more than LLLT as it increase the activation of ERK, P38 and C-Jun-N Terminal while LLLT only increase the activation of ERK. LLLT has more potent pain decreasing effect than PEMFT as it does not activate P38 pathway like PEMFT.

10.1016/j.bbrep.2017.01.008

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Genetic Profile of ACE (I/D) (rs4646994) Single Nucleotide polymorphism Among Sample of Egyptian patients with Alzheimer Disease in Upper Egypt

SVU-International Journal of Medical Sciences (2023)

Mahmoud Ahmed Bekiet Khaled Elbeh Mohammed Abdullah Abbas Mohammed H. Hassan Shimaa Fathy Sakr

Background: Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by impaired memory and progressive cognitive and behavioral decline.Angiotensin converting enzyme (ACE) was suggested to have a role in inhibition of Aβ peptides accumulation with formation of plaque in vitro.The role of ACE (I/D) genotypes regarding AD development and severity is questionable.Objectives: to assess the role of ACE (I/D) single nucleotide polymorphism (SNP) as a possible genetic risk factor for AD occurrence and for prediction of the disease severity.Patients and Methods: This case-control study was carried out in the Neuropsychiatry Department, Qena University Hospital during the period between March 1 st 2019 and February 28 th 2020.The study included 50 AD patients and 50 healthy age, sex and education matched controls.All cases underwent clinical assessment using Mini Mental State Examination (MMSE), Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI) of the brain.Genetic analysis for ACE (I/D) (rs4646994) was done using conventional PCR with primers without restriction enzyme.Results: Mean age of the included patients was 70.1 ± 9.35 years with female predominance (60%).About 46% of patients had mild disease, 42% had moderate disease and 12% had severe disease based on MMSE assessment tool.Diabetes had higher frequency among AD group (30%).ACE homozygous DD genotype had higher frequency (OD=35.9;95%CI= [2.8-440.2])and D allele was significantly commoner among AD group than control group (OD=2.13;95% CI= [1.05-3.2]),(P ˂ 0.05 for all).However, no statistically significant differences in relation to degree of dementia and ACE (I/D) genotypes were recorded.Although homozygous DD genotype and D alleles had higher frequency among severe AD group (P˃0.05).Conclusion: an evidence of significant association between homozygous ACE (DD) and D allele among sample of AD patients in Upper Egypt.However, there is lack of significance association of ACE (I/D) SNP in prediction of disease severity.

Sample (material)

10.21608/svuijm.2023.230123.1654

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Assessments of Therapeutic Effects of Platelet-rich Plasma in Knee Osteoarthritis: Possible Role of Inflammatory Cytokines

Research Square (Research Square) (2020)

Mohammed H. Hassan Tahia H. Saleem Sawsan Abuhamdah Hamdy Tammam Nehal Ashraf Zaki

Abstract Background: Osteoarthritis (OA) is a multifactorial disease that commonly affects the knee. Tumor necrosis factor-α (TNF-α) is able to regulate inflammation in OA. Macrophage migration inhibitory factor (MIF) may be involved in the pathophysiology of arthritis . Platelet-rich plasma (PRP) may reduce pain associated with OA . The current study aimed to assess the possible therapeutic effects of PRP in patients with knee OA of various severities. Methods: A prospective study was performed on 90 patients were included and categorized into mild (30 cases, moderate (30 cases) and severe (30 cases) knee OA. Three intra-articular (I.A) injections of PRP, 2 weeks a part, were received. Pain score and MRI Osteoarthritis Knee Score (MOAKS) were assessed. Serial synovial fluid cytokines assays in the form of Tumor necrosis factor-α (TNF-α) and Macrophage migration inhibitory factor (MIF), were performed using commercially available ELISA assay kits. The assays were performed pre-injection (S1), two weeks from the 1 st I.A injection and two weeks from the 2 nd I.A injection (S3) for all included patients. Results: The mean values of pain score and synovial TNF-α and MIF levels were significantly higher levels (S1, pre-injection) among severe OA when compared with both mild and moderate cases, p˂0.05 for all. There were significantly lower pain score and synovial TNF-α and MIF levels at S3 in mild, moderate and severe knee OA when compared with S1 values, p˂0.05 for all. There was significant improvement in synovitis in both mild and moderate cases (p˂0.05 for both). Conclusion : I.A injection of PRP significantly reduces the synovial fluid TNF-α and MIF levels with great therapeutic effects on both synovitis via reducing inflammatory cytokines, and bone marrow lesions mainly for mild knee OA and to a lesser extent for moderate cases.

Proinflammatory cytokine

Pathophysiology

Knee pain

10.21203/rs.3.rs-63573/v1

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Men with idiopathic oligoasthenoteratozoospermia exhibit lower serum and seminal plasma melatonin levels: Comparative effect of night‑light exposure with fertile males

Experimental and Therapeutic Medicine (2020)

Mohammed H. Hassan Moustafa A. El Taieb Nahed Fares Hanan Mahmoud Fayed Rana Toghan

Melatonin is a darkness hormone secreted by the pineal gland, which serves a role in idiopathic oligoasthenoteratozoospermia (iOAT). The present study aimed to evaluate the seminal plasma and serum melatonin levels of 50 patients with iOAT and 50 normal fertile controls and the effects of exposure to light at night on semen parameters. Semen analyses were performed according to the World Health Organization 2010 guidelines. Measurements of serum and seminal plasma melatonin, serum TSH, FT3, FT4, free testosterone, prolactin, FSH and LH were performed using ELISA. The overall results revealed that the serum and seminal plasma levels of melatonin were lower in patients with iOAT compared with the control subjects (P=0.0004 and 0.01, respectively). Patients with iOAT who were exposed to light at night exhibited lower serum and seminal plasma melatonin levels compared with those who were not exposed to light at night (P<0.0001 and 0.02, respectively). Additionally, similar significant differences were identified in control subjects exposed to light at night when compared to non‑exposed controls. There was a significantly positive correlation between serum melatonin levels and sperm motility in the entire iOAT patient cohort (r=0.614; P<0.0001) and a significantly positive correlation between the serum and seminal plasma melatonin levels in the non‑exposed iOAT patient subgroup (r=0.753; P<0.001). Thus, darkness and sleep at night may improve the semen parameters of patients with iOAT, as evidenced by the effects of light exposure at night on the serum and seminal plasma levels of melatonin and, consequently, on semen parameters.

Darkness

10.3892/etm.2020.8678

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''Neurodegeneration and Oxidative Stress in Brain Tissues Induced by Tramadol with the Protective Effects of Royal Jelly in Rats''.

SVU- International Journal of Veterinary Sciences (2023)

Atef Khalil Amany Sayed Mowas Mohammed H. Hassan Hassan Ahmed Obeid Shanab

Tramadol hydrochloride (TH) is an opioid centrally acting analgesic used to treat moderate to severe acute and chronic pains.Therefore, it became the most prescribed opioid worldwide.In this study, we investigated the neurodegenerative disorders of tramadol in brain tissues and the protective role of royal jelly.Twenty male albino rats allocated into four groups: Group 1,served as a control group, and Group 2, administrated with tramadol at a dose of 20 mg/kg/b.W for 60 days.Group 3: rats administrated with tramadol at a dose of 20 mg/kg/b.W for 60 days and treated with royal jelly (RJ) in a 100 mg/kg dose.b.w.Group 4: Rats inoculated with royal jelly (RJ) at a dose of 100 mg/kg.b.w.Blood samples were collected for hematological and biochemical analysis.Brain tissues were harvested for neurodegeneration biomarkers detection and histopathological examinations.Administration of tramadol revealed a significant decrease in Hb concentration, RBCs count, PCV %, Lymphocytes %, and platelets number, while WBCS count, Neutrophiles, and monocytes % increased.Also, Tramadol induced a decrease in glucose-6phosphate dehydrogenase (G6PD) while creatine kinase -BB (CK-BB) and neuron-specific enolase enzymes (NSE) were decreased.Tramadol increased the lipid peroxidation MDA, while total antioxidants capacity (TAC) and glutathione reductase (GSH) concentrations were decreased.Histopathologically, tramadol-induced neurodegenerative changes in brain neurons manifested by acute necrosed neurons with gliosis and vascular congestions.The administration of royal jelly improved the previous deleterious effects by decreasing brain tissue oxidative stress.Tramadol misuse caused neurodegenerative effects and was relieved by RJ administration.

Royal Jelly

10.21608/svu.2023.215343.1276

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CRT-600.09 Validity of B-Type Natriuretic Peptide, Growth Differentiation Factor 15, and High-Sensitivity Troponin I Levels in Ischemic Heart Failure

КАРДИОЛОГИЯ УЗБЕКИСТАНА (2022)

Hossameldin M. Ismail Mohammed H. Hassan

Troponin T

10.1016/j.jcin.2022.01.212

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Clinical and genetic assessment of pediatric patients with Gaucher’s disease in Upper Egypt

Egyptian Journal of Medical Human Genetics (2016)

Tahia H. Saleem Mohammed H. Hassan Ahmed El‐Abd Ahmed Ayat A. Sayed Nahed Mohamed

Gaucher's disease (GD) is an autosomal recessive genetic disorder that results from pathogenic mutations of GBA gene encoding the enzyme glucocerebrosidase (acid β-glucosidase). Of the approximately 300 mutations associated with GD, 4 accounts for the majority of mutations seen in GD patients: N370S, L444P, 84 GG and IVS2+1. Establishing and providing, clinical and molecular backgrounds of pediatric patients with GD in Upper Egypt. The present study is a cross sectional study, carried out on 26 pediatric patients with GD. They were recruited from the pediatric outpatient clinics and inpatients Pediatric departments of Assiut and Qena University hospitals, Upper Egypt. Clinical evaluation and mutation analysis using commercially available strip assay kit after PCR amplification of the target gene were done for all included GD patients. Consanguinity between patients' parents was present in 73.1% of the included patients. 76.9% of included patients were of type 1 GD, while 23.1% were of type 3 GD and none of our patients was classified as type 2 GD. The main frequent clinical presentations of GD in this study were hepatosplenomegaly (88.5%); pallor (76.9%); abdominal distension (61.5%) and musculoskeletal involvement (37.1%). Neurological abnormalities of type 3 GD included in this study were squint, seizures and delayed mental development. Five different genotypes were detected, homozygous for the mutation L444P, homozygous for the mutation N370S, heterozygous for the mutations N370S and rec Ncil, heterozygous for IVS2 +1 and rec NciI, heterozygous for L444P and IVS2 +1. Non-neuropathic type 1 and type 3 GD were the only clinical types found in the present study. The most common mutant alleles found in this study were L444P and N370S.

Hepatosplenomegaly

Pallor

Outpatient clinic

Compound heterozygosity

Abdominal distension

10.1016/j.ejmhg.2016.08.005

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Citations (9)