The cultural context influences women’s antenatal care and postpartum knowledge. This study aims to determine the traditional practices related to maternal health in Morocco. We conducted in-depth qualitative interviews with 37 women from three different Moroccan regions on the first postpartum day. We used thematic content to analyze data, and an a priori coding framework was created utilizing the pertinent literature. Beliefs regarding pregnancy and postpartum positively affect maternal health, such as family support, prolonged rest for health recovery, and specific dietary precautions according to the mode of delivery of the new mother. However, some practices may negatively affect maternal health, such as cold postpartum treatment through traditional medicine and not seeking prenatal care after the first pregnancy experience. Such practices include painting newborns with henna, using kohl and oil to hasten the umbilical cord’s descent, and producing solutions based on chicken throat to cure respiratory ailments in newborns that might harm their health.

Barium chloride (BaCl₂), a known environmental pollutant, induces organ-specific oxidative stress through disruption of redox homeostasis. This study evaluated the protective effects and safety profile of sodium copper chlorophyllin (SCC) and ascorbic acid (ASC) against BaCl₂-induced oxidative damage in the liver and brain of mice using a two-phase experimental protocol. Animals received either SCC (40 mg/kg), ASC (160 mg/kg), or their combination for 14 days prior to BaCl₂ exposure (150 mg/L in drinking water for 7 days), allowing evaluation of both preventive and therapeutic effects. Toxicological and behavioral assessments confirmed the absence of systemic toxicity or neurobehavioral alterations following supplementation. Body weight, liver and kidney indices, and biochemical markers (Aspartate Aminotransferase (ASAT), Alanine Aminotransferase (ALAT), creatinine) remained within physiological ranges, and no anxiogenic or locomotor effects were observed. In the brain, BaCl₂ exposure significantly increased SOD (+49%), CAT (+66%), GPx (+24%), and GSH (+26%) compared to controls, reflecting a robust compensatory antioxidant response. Although lipid peroxidation (MDA) showed a non-significant increase, SCC, ASC, and their combination reduced MDA levels by 42%, 37%, and 55%, respectively. These treatments normalized antioxidant enzyme activities and GSH, indicating an effective neuroprotective effect. In contrast, the liver exhibited a different oxidative profile. BaCl₂ exposure increased MDA levels by 80% and GSH by 34%, with no activation of SOD, CAT, or GPx. Histological analysis revealed extensive hepatocellular necrosis, vacuolization, and inflammatory infiltration. SCC significantly reduced hepatic MDA by 39% and preserved tissue architecture, while ASC alone or combined with SCC exacerbated inflammation and depleted hepatic GSH by 71% and 78%, respectively, relative to BaCl₂-exposed controls. Collectively, these results highlight a differential, organ-specific response to BaCl₂-induced oxidative stress and the therapeutic potential of SCC and ASC. SCC emerged as a safer and more effective agent, particularly in hepatic protection, while both antioxidants demonstrated neuroprotective effects when used individually or in combination.

Chronic myeloid leukemia (CML) is driven by the constitutive tyrosine kinase activity of the BCR::ABL1 fusion protein and is effectively treated with tyrosine kinase inhibitors (TKIs). However, therapeutic resistance and the persistence of leukemic stem cells (LSCs) remain important clinical challenges. TKI resistance cannot be explained solely by BCR::ABL1-dependent mechanisms and involves a complex interplay between signaling, metabolic, redox, and autophagic adaptations. In this review, we integrate current knowledge on BCR::ABL1-dependent and BCR::ABL1-independent resistance mechanisms, with particular emphasis on metabolic reprogramming in CML LSCs and TKI-resistant leukemic cells. Available evidence indicates that primitive CML populations can exhibit enhanced mitochondrial oxidative metabolism, whereas TKI-resistant and persistent leukemic populations may engage glycolysis, the pentose phosphate pathway, fatty acid oxidation, and amino acid metabolism to different extents. Rather than representing mutually exclusive metabolic states, oxidative and glycolytic programs may coexist and vary according to cellular differentiation, microenvironmental conditions, and therapeutic pressure. These metabolic adaptations are interconnected with major signaling pathways, including PI3K/AKT/mTOR, JAK/STAT, Wnt/β-catenin, and Hedgehog signaling, as well as with redox regulation and autophagy. Preclinical studies suggest that combining TKIs with metabolism- or autophagy-directed interventions may help exploit vulnerabilities associated with leukemic persistence. However, the heterogeneity of metabolic phenotypes, potential toxicity to normal hematopoietic cells, and limited clinical validation of candidate metabolic biomarkers currently constrain their therapeutic translation. Further studies are therefore required to determine which metabolic dependencies are clinically actionable and whether biomarker-guided strategies can improve the targeting of persistent CML cells.

Chronic myeloid leukaemia (CML) is driven by the constitutively active BCR::ABL1 fusion tyrosine kinase. Although tyrosine kinase inhibitors (TKIs) have dramatically improved patient survival, therapeutic resistance and the persistence of leukemic stem cells (LSCs) remain major barriers to durable disease control and treatment-free remission. This review examines BCR::ABL1-dependent and independent mechanisms of TKI resistance, with particular emphasis on metabolic reprogramming as an adaptive component of CML persistence. Accumulating evidence indicates that resistant and primitive CML populations do not conform to a single metabolic phenotype. Instead, therapeutic pressure selects and reshapes heterogeneous cell states capable of dynamically redistributing energy production and substrate utilization among glycolysis, oxidative phosphorylation, fatty acid oxidation, glutamine metabolism, and other amino acid pathways. This metabolic plasticity is further influenced by mitochondrial fitness, redox regulation, the bone marrow microenvironment, epigenetic-metabolic interactions, and immunometabolic mechanisms. Single-cell and spatial approaches are beginning to resolve the cellular heterogeneity underlying these adaptive states and their association with treatment response. Metabolic vulnerabilities therefore provide a rationale for combining BCR::ABL1 inhibition, including asciminib, with strategies targeting mitochondrial metabolism, glycolysis, fatty acid oxidation, glutamine utilization, autophagy, or hypoxia-responsive pathways. However, most such combinations remain preclinical, highlighting the need for biomarker-guided patient stratification and prospective clinical validation.

Background/Objectives: Chronic myeloid leukemia (CML) is a hematopoietic stem cell malignancy initiated by the BCR::ABL1 oncoprotein. Although tyrosine kinase inhibitors (TKIs) have revolutionized CML therapy, resistance remains a major clinical challenge. Emerging evidence suggests that metabolic reprogramming contributes to TKI resistance, yet its relationship with oxidative stress and autophagy remains poorly characterized. Methods: Metabolic profiles, redox-related parameters, and autophagy markers were assessed in parental K562, imatinib-sensitive K562-S, and imatinib-resistant K562-R cells. Metabolic activity was first assessed via the MTT assay to determine the half-maximal inhibitory concentration (IC₅₀) for each line, which was subsequently used as the treatment dose. Glycolytic and mitochondrial functions were profiled via Seahorse extracellular flux analysis under basal conditions. Oxidative stress was assessed via reactive oxygen species (ROS) and nitric oxide (NO) levels, and the levels of autophagy markers (p62 and LC3-I/II) were measured via Western blotting. Results: Imatinib reduced metabolic activity in K562 and K562-S cells (IC₅₀ = 0.445 and 0.137 µM, respectively), whereas K562-R cells retained high metabolic activity across the tested range (0.1–1 µM), which was consistent with a resistant phenotype. Compared with parental K562 cells, both K562-S and K562-R cells presented reduced glycolytic activity. K562-S cells displayed greater basal respiration than K562-R cells, which presented reduced basal respiration and proton leakage but preserved spare respiratory capacity, indicating a distinct mitochondrial respiratory phenotype. Imatinib increased ROS in K562 and K562-S cells but not in K562-R cells, whereas NO increased in all three lines. Autophagy-related alterations occurred in K562 and K562-S cells, while K562-R cells presented minimal changes. Conclusions: Imatinib resistance involves distinct metabolic and autophagic adaptations across K562-derived cell lines. These pathways may represent potential therapeutic targets warranting further investigation to overcome TKI resistance in CML.

Les femmes jouent un rôle central dans la planification familiale, mais leur capacité à exercer un contrôle sur leur fertilité est souvent influencée par des facteurs sociaux et relationnels. Cette étude explore les connaissances, attitudes et pratiques des femmes à l’égard de la planification familiale et des méthodes contraceptives actuellement disponibles, parmi la population des femmes mariées en âge de procréer vivant dans les zones rurales au Maroc. Nous avons mené des entretiens approfondis en face à face avec 49 femmes marocaines mariées dans une maternité rurale pendant leur période post-partum. À l’aide de questions ouvertes, nous avons examiné leurs pratiques contraceptives, leur autonomie décisionnelle et les influences sociales qui déterminent leurs choix en matière de procréation. La plupart des participantes a déclaré utiliser des contraceptifs oraux, bien que nombre d’entre elles ait connu au moins une grossesse non désirée en raison d’une mauvaise utilisation des contraceptifs. Les femmes ont exprimé leur préférence pour des familles moins nombreuses afin d’assurer leur stabilité financière et une meilleure qualité de vie. Cependant, elles se heurtent souvent à la résistance de leur mari et de leur famille élargie lorsqu’elles tentent d’utiliser un moyen de contraception ou de limiter la taille de leur famille. Les idées fausses concernant les dispositifs intra-utérins (DIU) étaient très répandues, de nombreuses femmes exigeant le consentement de leur conjoint en raison de préoccupations liées à la santé sexuelle. Nos résultats soulignent le rôle important des facteurs sociaux et relationnels dans les choix des femmes en matière de procréation. Il est essentiel de s’attaquer aux idées fausses et d’améliorer l’accès à l’éducation en matière de santé génésique. L’implication des maris dans les séances de conseil peut renforcer les efforts de planification familiale et soutenir l’autonomie des femmes dans les décisions relatives à la fécondité.