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Certain fish and amphibians retain a robust capacity for cardiac regeneration throughout life, but the same is not true of the adult mammalian heart. Whether the capacity for cardiac regeneration is absent in mammals or whether it exists and is switched off early after birth has been unclear. We found that the hearts of 1-day-old neonatal mice can regenerate after partial surgical resection, but this capacity is lost by 7 days of age. This regenerative response in 1-day-old mice was characterized by cardiomyocyte proliferation with minimal hypertrophy or fibrosis, thereby distinguishing it from repair processes. Genetic fate mapping indicated that the majority of cardiomyocytes within the regenerated tissue originated from preexisting cardiomyocytes. Echocardiography performed 2 months after surgery revealed that the regenerated ventricular apex had normal systolic function. Thus, for a brief period after birth, the mammalian heart appears to have the capacity to regenerate.

We recently identified a brief time period during postnatal development when the mammalian heart retains significant regenerative potential after amputation of the ventricular apex. However, one major unresolved question is whether the neonatal mouse heart can also regenerate in response to myocardial ischemia, the most common antecedent of heart failure in humans. Here, we induced ischemic myocardial infarction (MI) in 1-d-old mice and found that this results in extensive myocardial necrosis and systolic dysfunction. Remarkably, the neonatal heart mounted a robust regenerative response, through proliferation of preexisting cardiomyocytes, resulting in full functional recovery within 21 d. Moreover, we show that the miR-15 family of microRNAs modulates neonatal heart regeneration through inhibition of postnatal cardiomyocyte proliferation. Finally, we demonstrate that inhibition of the miR-15 family from an early postnatal age until adulthood increases myocyte proliferation in the adult heart and improves left ventricular systolic function after adult MI. We conclude that the neonatal mammalian heart can regenerate after myocardial infarction through proliferation of preexisting cardiomyocytes and that the miR-15 family contributes to postnatal loss of cardiac regenerative capacity.

The adult mammalian heart has limited potential for regeneration. Thus, after injury, cardiomyocytes are permanently lost, and contractility is diminished. In contrast, the neonatal heart can regenerate owing to sustained cardiomyocyte proliferation. Identification of critical regulators of cardiomyocyte proliferation and quiescence represents an important step toward potential regenerative therapies. Yes-associated protein (Yap), a transcriptional cofactor in the Hippo signaling pathway, promotes proliferation of embryonic cardiomyocytes by activating the insulin-like growth factor and Wnt signaling pathways. Here we report that mice bearing mutant alleles of Yap and its paralog WW domain containing transcription regulator 1 (Taz) exhibit gene dosage-dependent cardiac phenotypes, suggesting redundant roles of these Hippo pathway effectors in establishing proper myocyte number and maintaining cardiac function. Cardiac-specific deletion of Yap impedes neonatal heart regeneration, resulting in a default fibrotic response. Conversely, forced expression of a constitutively active form of Yap in the adult heart stimulates cardiac regeneration and improves contractility after myocardial infarction. The regenerative activity of Yap is correlated with its activation of embryonic and proliferative gene programs in cardiomyocytes. These findings identify Yap as an important regulator of cardiac regeneration and provide an experimental entry point to enhance this process.

Baltim Eastern and Northern gas fields in the offshore Nile Delta have very high gas condensate accumulations. Therefore, the present research evaluates Abu Madi and Qawasim Formations and defines the petrophysical parameters for them using various data from five wells composed of wireline logs (gamma-ray, density, neutron, sonic, resistivity), core data, pressure data, and cross-plots. In the current study, the formations of the main reservoirs were evaluated qualitatively and quantitatively based on the petrophysical analysis to assess the production potential. Based on the lithological identification, the two main reservoirs (Abu Madi and Qawasim Formations) are composed of sandstone, calcareous shale, and siltstone. The main petrophysical parameters (Shale volume, effective porosity, net thickness, and fluid saturations) were mapped to track the areal petrophysical variations in the field. The results of the petrophysical analysis reveal that the main reservoirs are promising for the hydrocarbon potential with effective porosity of 18%, low shale content with an average value of about 21%, higher gas saturation of average value of nearly 58%, net reservoir thickness ranges from 25.5 to 131.5 m, net pay thickness (effective thickness) ranges from 6 to 61 m. Also, the conventional core analysis affirms that the main reservoirs are of good effective porosity with high horizontal and vertical permeability values. There is a good match between the well-log results and the pressure data with the production data (DST “perforation tests”). Baltim East (BE3) well has the most desired petrophysical characteristics in the Baltim East gas field, while, the Baltim North-1 (BN1) well showed the most favorable petrophysical parameters in the Baltim North gas field. Different fluid contacts (gas water contact GWC) were detected by integrating all reservoir pressures. The integration of different data in our present work (well logs, core measurements, and pressure data) could reduce the drilling risks and help to determine the best locations for future exploration and development, which is considered a big challenge in the petroleum industry.

The PTAH oil field in Egypt’s northern Western Desert offers considerable potential for hydrocarbon production. This research centers on the Shiffah formation and evaluates its petrophysical properties using data from four wells. The analysis involves wireline logs (including gamma-ray, density, neutron, sonic, and resistivity), core samples, pressure readings, and cross-plots. A combination of qualitative and quantitative techniques was employed to assess the formation’s hydrocarbon-bearing capacity. The Shiffah formation primarily comprises sandstone, calcareous shale, and siltstone. Key petrophysical parameters such as shale volume, effective porosity, net thickness, and fluid saturations were mapped to evaluate variations across the field. Findings indicate that the reservoirs have an average shale content of 2.5%, an effective porosity of 11%, and an oil saturation averaging 47.84%. The net reservoir thickness ranges from 97.5 to 655 feet, with the net pay zones between 6.5 and 137 feet. These results underscore the potential for hydrocarbons within the field. Core analysis supports these findings, highlighting favorable horizontal and vertical permeability values. The correlation between well-log data and pressure information also aligns with production outcomes from Drill Stem Tests (DST). Among the wells, Ptah-1X exhibited the most promising petrophysical properties, whereas Ptah-4X was determined to be a dry well, with water saturation as high as 98%. Reservoir pressure analysis helped to pinpoint key fluid contacts, such as the oil–water contact (OWC). Pickett’s plot was used to calculate formation water resistivity, yielding values between 0.0170 and 0.0176 across the four wells. This comprehensive evaluation of the Shiffah formation offers valuable insights into its hydrocarbon potential and guides future exploration and drilling.

Early reperfusion of ischemic cardiac tissue remains the most effective intervention for improving clinical outcome following myocardial infarction. However, abnormal increases in intracellular Ca²⁺ during myocardial reperfusion can cause cardiomyocyte death and consequent loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Therapeutic modulation of Ca²⁺ handling provides some cardioprotection against the paradoxical effects of restoring blood flow to the heart, highlighting the significance of Ca²⁺ overload to IR injury. Cardiac IR is also accompanied by dynamic changes in the expression of microRNAs (miRNAs); for example, miR-214 is upregulated during ischemic injury and heart failure, but its potential role in these processes is unknown. Here, we show that genetic deletion of miR-214 in mice causes loss of cardiac contractility, increased apoptosis, and excessive fibrosis in response to IR injury. The cardioprotective roles of miR-214 during IR injury were attributed to repression of the mRNA encoding sodium/calcium exchanger 1 (Ncx1), a key regulator of Ca²⁺ influx; and to repression of several downstream effectors of Ca²⁺ signaling that mediate cell death. These findings reveal a pivotal role for miR-214 as a regulator of cardiomyocyte Ca²⁺ homeostasis and survival during cardiac injury.

The aim of this study is to investigate friction stir welding (FSW) to join A304 austenitic stainless steel and low carbon steel A283 Gr. C in-lap configuration to clad the carbon steel with highly corrosion-resistant stainless steel. Thus, a wide range of FSW parameters were investigated such as FSW tool rotation rate from 200 to 400 rpm, tool traverse speed from 25 to 75 mm/min, and vertical forces of 20 to 32 KN. The FSW parameters combination of high welding rotation rate (400 rpm) and high vertical forces (32 KN) results in rejected joints in terms of surface appearance and clear surface defects. On the other hand, rotation rates of 200 and 300 rpm with different welding speeds and vertical forces resulted in some sound joints that were further investigated for microstructure and mechanical properties. The sound lap joints were examined via optical microstructure, SEM, and EDS investigations. For the mechanical properties, both tensile shear testing and hardness testing were used. The transverse macrographs showed intermixing between the two dissimilar materials with an almost irregular interface. The hardness profile in both materials showed a significant increase across the different regions from the Base Material (BM) to the nugget zone, with a maximum value of 260 Hv in the stainless steel and 245 Hv in the carbon steel. This increase is mainly attributed to the grain refining in the weld region due to the dynamic recrystallization and transformations upon the thermomechanical cycle. The tensile shear load of the joints varied from 20 to 27 KN for the FSWed joints, with the highest joint tensile shear load of 27 KN for that produced at 300 rpm tool rotation and 25 mm/min welding speed.

The in vivo microenvironment of tissues provides myriad unique signals to cells. Thus, following isolation, many cell types change in culture, often preserving some but not all of their in vivo characteristics in culture. At least some of the in vivo microenvironment may be mimicked by providing specific cues to cultured cells. Here, we show that after isolation and during maintenance in culture, adherent rat islets reduce expression of key β-cell transcription factors necessary for β-cell function and that soluble pancreatic decellularized matrix (DCM) can enhance β-cell gene expression. Following chromatographic fractionation of pancreatic DCM, we performed proteomics to identify soluble factors that can maintain β-cell stability and function. We identified Apolipoprotein E (ApoE) as an extracellular protein that significantly increased the expression of key β-cell genes. The ApoE effect on beta cells was mediated at least in part through the JAK/STAT signaling pathway. Together, these results reveal a role for ApoE as an extracellular factor that can maintain the mature β-cell gene expression profile.

Ischemic heart disease is the leading cause of death worldwide. The blockade of coronary arteries limits oxygen-rich blood to the heart and consequently there is cardiomyocyte (CM) cell death, inflammation, fibrotic scarring, and myocardial remodeling. Unfortunately, current therapeutics fail to effectively replace the lost cardiomyocytes or prevent fibrotic scarring, which results in reduced cardiac function and the development of heart failure (HF) in the adult mammalian heart. In contrast, neonatal mice are capable of regenerating their hearts following injury. However, this regenerative response is restricted to the first week of post-natal development. Recently, we identified that cholinergic nerve signaling is necessary for the neonatal mouse cardiac regenerative response. This demonstrates that cholinergic nerve stimulation holds significant potential as a bioelectronic therapeutic tool for heart disease. However, the mechanisms of nerve directed regeneration in the heart remain undetermined. In this review, we will describe the historical evidence of nerve function during regeneration across species. Specifically, we will focus on the emerging role of cholinergic innervation in modulating cardiomyocyte proliferation and inflammation during heart regeneration. Understanding the role of nerves in mammalian heart regeneration and adult cardiac remodeling can provide us with innovative bioelectronic-based therapeutic approaches for treatment of human heart disease.

Myocardial infarction (MI) leads to cardiomyocyte death, which triggers an immune response that clears debris and restores tissue integrity. In the adult heart, the immune system facilitates scar formation, which repairs the damaged myocardium but compromises cardiac function. In neonatal mice, the heart can regenerate fully without scarring following MI; however, this regenerative capacity is lost by P7. The signals that govern neonatal heart regeneration are unknown. By comparing the immune response to MI in mice at P1 and P14, we identified differences in the magnitude and kinetics of monocyte and macrophage responses to injury. Using a cell-depletion model, we determined that heart regeneration and neoangiogenesis following MI depends on neonatal macrophages. Neonates depleted of macrophages were unable to regenerate myocardia and formed fibrotic scars, resulting in reduced cardiac function and angiogenesis. Immunophenotyping and gene expression profiling of cardiac macrophages from regenerating and nonregenerating hearts indicated that regenerative macrophages have a unique polarization phenotype and secrete numerous soluble factors that may facilitate the formation of new myocardium. Our findings suggest that macrophages provide necessary signals to drive angiogenesis and regeneration of the neonatal mouse heart. Modulating inflammation may provide a key therapeutic strategy to support heart regeneration.