Publications by authors named "Mohamed Tamer"

Cardiomyocytes (CMs) lost during ischemic cardiac injury cannot be replaced due to their limited proliferative capacity. Calcium is an important signal transducer that regulates key cellular processes, but its role in regulating CM proliferation is incompletely understood. Here we show a robust pathway for new calcium signaling-based cardiac regenerative strategies.

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Background And Aims: Rectal prolapse (RP) is a debilitating condition and can cause symptoms of fecal incontinence, obstructed defecation, incomplete evacuation of the rectum, and pain. In recent years, there has been increasing evidence that prolapse development is strongly associated with pelvic hiatus (GH) size (normal 4.5 +/- 0.

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Colorectal operations are amongst the most frequently performed surgical procedures worldwide. Success of colorectal surgery is significantly influenced by occurrence of postoperative complications; Efforts are directed in detecting risk factors for these complications and trials to avoid risk factors to reduce complications rate. This study was conducted to assess the impact of mechanical bowel preparation in preventing post-operative anastomotic leakage in adult patients undergoing elective restorative colorectal surgery.

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Article Synopsis
  • - Aplastic anemia (AA) and hypoplastic myelodysplastic syndrome (MDS) are similar bone marrow failure diseases, making diagnosis challenging; this study explored using flow cytometry for differentiation.
  • - Researchers analyzed bone marrow and blood samples from 44 participants: 17 with AA, 13 with hypoplastic MDS, and 14 healthy controls, focusing on CD34 levels and cell apoptosis.
  • - Findings revealed that hypoplastic MDS patients had more CD34+ cells with lower apoptosis, while AA patients had fewer CD34+ cells but higher apoptosis, suggesting distinct biological differences that could aid in accurate diagnosis.
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Cardiac cellular fate transition holds remarkable promise for the treatment of ischemic heart disease. We report that overexpressing two transcription factors, Sall4 and Gata4, which play distinct and overlapping roles in both pluripotent stem cell reprogramming and embryonic heart development, induces a fraction of stem-like cells in rodent cardiac fibroblasts that exhibit unlimited ex vivo expandability with clonogenicity. Transcriptomic and phenotypic analyses reveal that around 32 ± 6.

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This study investigates the feasibility of implementing a solar-assisted adsorption chiller in an industrial building at the Oriental Weavers International factory located in 10th of Ramadan City, Cairo, Egypt. The objective is to replace an inefficient split air conditioning system currently used to cool the Jacquard units during carpet manufacturing. The research begins by analyzing the performance of the existing cooling system to establish a baseline.

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  • Obesity leads to lipid accumulation in heart cells (cardiomyocytes), causing stress and heart damage, which can result in heart failure.
  • Researchers found that PAK3 levels are higher in the hearts of obese individuals and in mice that are stressed by diet, making them more prone to heart issues due to toxic lipid buildup.
  • Knocking down PAK3 can reduce fat-induced toxicity in heart cells, suggesting that targeting PAK3 might be a potential treatment for obesity-related heart problems.
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The adult mammalian heart has limited regenerative capacity following injury, leading to progressive heart failure and mortality. Recent studies have identified the spiny mouse ( ) as a unique model for mammalian cardiac isch3emic resilience, exhibiting enhanced recovery after myocardial infarction (MI) compared to commonly used laboratory mouse strains. However, the underlying cellular and molecular mechanisms behind this unique response remain poorly understood.

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Testing drugs in vivo and in vitro have been essential elements for the discovery of new therapeutics. Due to the recent advances in in vitro cell culture models, such as human-induced pluripotent stem cell-derived cardiomyocytes and 3D multicell type organoid culture methods, the detection of adverse cardiac events prior to human clinical trials has improved. However, there are still numerous therapeutics whose adverse cardiac effects are not detected until human trials due to the inability of these cell cultures to fully model the complex multicellular organization of an intact human myocardium.

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Chronic kidney disease (CKD) is a functional and/or structural kidney damage that lasts more than three months duration. This study aimed to analyze CD4+ T-lymphocytes levels in chronic CKD patients specifically, during the coronavirus disease 2019 (COVID-19) pandemic to assess the adaptive cell-mediated immunity. The study measured absolute CD4+ T-lymphocytes counts by flowcytometry among participating individuals.

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Article Synopsis
  • Gene therapies like TNNT2-4Fpolycistronic-NIL have shown promise in treating subacute ischaemic heart failure (IHF) by inducing cardiomyocyte (CM) cell cycle re-entry but need testing in chronic IHF settings for broader clinical relevance.
  • In the study, rats with induced chronic IHF were treated with TNNT2-4Fpolycistronic-NIL, which led to reduced scar size and improved left ventricular function over four months, though it didn't prevent LV dilation associated with chronic IHF.
  • The findings suggest that this gene therapy effectively promotes CM regeneration in chronic IHF, highlighting potential new treatment avenues for this widespread condition.
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Results: Incidence of local recurrence was slightly higher in Group A (8.7%) than in Group B (4.3%) but was not statistically significant.

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Cardiomyocytes (CMs) lost during ischemic cardiac injury cannot be replaced due to their limited proliferative capacity, which leads to progressive heart failure. Calcium (Ca) is an important signal transducer that regulates key cellular processes, but its role in regulating CM proliferation is incompletely understood. A drug screen targeting proteins involved in CM calcium cycling in human embryonic stem cell-derived cardiac organoids (hCOs) revealed that only the inhibition of L-Type Calcium Channel (LTCC), but not other Ca regulatory proteins (SERCA or RYR), induced the CM cell cycle.

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Recombinant adeno-associated viruses (rAAVs) have emerged as one of the most promising gene therapy vectors that have been successfully used in pre-clinical models of heart disease. However, this has not translated well to humans due to species differences in rAAV transduction efficiency. As a result, the search for human cardiotropic capsids is a major contemporary challenge.

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Background: Androgenetic alopecia (AGA) is the most common type of progressive hair loss in men and women. AGA is characterized by the miniaturization of the hair follicle, leading to the transformation of terminal hair to vellus hair.

Objective: To evaluate the efficacy and safety of injecting two different concentrations of botulinum toxin A (BTA) for the treatment of AGA in Egyptian patients.

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Background: Cardiac reprogramming is a technique to directly convert nonmyocytes into myocardial cells using genes or small molecules. This intervention provides functional benefit to the rodent heart when delivered at the time of myocardial infarction or activated transgenically up to 4 weeks after myocardial infarction. Yet, several hurdles have prevented the advancement of cardiac reprogramming for clinical use.

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Background And Purpose: Myocardial infarction (MI) is the leading cause of mortality globally due in part to the limited ability of cardiomyocytes (CMs) to regenerate. Recently, we demonstrated that overexpression of four-cell cycle factors, CDK1, CDK4, cyclin B1 and cyclin D1 (4F), induced cell division in ~20% of the post-mitotic CMs overexpressed 4F. The current study aims to identify a small molecule that augments 4F-induced CM cycle induction.

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Despite the development of clinical treatments, heart failure remains the leading cause of mortality. We observed that p21-activated kinase 3 (PAK3) was augmented in failing human and mouse hearts. Furthermore, mice with cardiac-specific PAK3 overexpression exhibited exacerbated pathological remodeling and deteriorated cardiac function.

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Diabetes is a metabolic disorder with an increased risk of developing heart failure. Inflammation and damaged vasculature are the cardinal features of diabetes-induced cardiac damage. Moreover, systemic metabolic stress triggers discordant intercellular communication, thus culminating in cardiac dysfunction.

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Heart failure with preserved ejection fraction is a growing public health concern, a disease with poor health outcomes, and is showing increased prevalence globally. This review paper explores the literature with a focus on the pathophysiology and microbiology of preserved ejection fraction heart failure while drawing connections between preserved and reduced ejection fraction states. The discussion teases out the cellular level changes that affect the overall dysfunction of the cardiac tissue, including the clinical manifestations, microbiological changes (endothelial cells, fibroblasts, cardiomyocytes, and excitation-contraction coupling), and the burden of structural diastolic dysfunction.

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The conventional drug delivery systems have several limitations, such as the high frequency of administration, several off-target effects, and the need for tissue specificity. Recently, smart drug shuttles have emerged, and the nano applications provided a new opportunity for advancing the drug delivery system to become tissue targeted and decrease the frequency of administration. The recent development of nanovectors as drug carriers has gone through several steps of evolution that ended with the development of logic-embedded nanovectors.

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Background: Muscle wasting is a common complication of chronic kidney disease (CKD) that is associated with higher mortality. Although the mechanisms of myofibre loss in CKD has been widely studied, the contribution of muscle precursor cell (MPC) senescence remains poorly understood. Senescent MPCs no longer proliferate and can produce proinflammatory factors or cytokines.

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The loss of cardiomyocytes after myocardial infarction (MI) leads to heart failure. Recently, we demonstrated that transient overexpression of 4 cell cycle factors (4F), using a polycistronic non-integrating lentivirus (TNNT2-4F-NIL) resulted in significant improvement in cardiac function in a rat model of MI. Yet, it is crucial to demonstrate the reversal of the heart failure-related pathophysiological manifestations, such as renin-angiotensin-aldosterone system activation (RAAS).

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There is need for a reliable in vitro system that can accurately replicate the cardiac physiological environment for drug testing. The limited availability of human heart tissue culture systems has led to inaccurate interpretations of cardiac-related drug effects. Here, we developed a cardiac tissue culture model (CTCM) that can electro-mechanically stimulate heart slices with physiological stretches in systole and diastole during the cardiac cycle.

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