REVIEW AND STUDY OF METAL COMPLEXES WITH ANTIFUNGAL POTENTIAL AGAINST Candida albicans STRAINS
Background: Candidiasis, caused mainly by Candida albicans yeast, is a pathology that affects a significant amount of people in the world, mainly women, thus being a public health issue. In addition, clinical practice has found it difficult to treat candidiasis for two reasons: the multidrug resistance associated with the exacerbated use of available drugs and the high number of side effects caused by current antifungal drugs. In this scenario, this work is a literature review on the antifungal activity of metal complexes against C. albicans since they are extensively studied for their varied applications in health sciences, as an object of study in the area of inorganic chemistry, in the subareas of bioinorganic chemistry and pharmaceutical chemistry. Aim: The present work consists of a literature review in electronic databases on the potential antifungal action against Candida albicans presented by metal complexes. Methods: Data was collected using the Capes, PubMed, Cochrane Reviews and Virtual Health Library (BVS) databases. Results: The results obtained through bibliographic surveys show the importance of studies of metal complexes against the strain of C. albicans, which have promising inhibitory activities and in some cases, with Minimum Inhibitory Concentration (MIC) values lower than 20µg/mL Discussion: The results obtained through bibliographic surveys show the importance of studies of metal complexes against the strain of C. albicans, which have promising inhibitory activities, and in some cases, with Minimum Inhibitory Concentration (MIC) values lower than 20µg/mL. Conclusion: Highlighting the activity performed by ruthenium complexes and Schiff bases when coordinated to metallic ions arouses great interest in a future study of a complex of this metal with a Schiff base in its coordination site.
Read ArticleTREATMENTS FOR ACUTE LYMPHOBLASTIC LEUKEMIA: A COMPARISON BETWEEN TISAGENLECLEUCEL AND CLOFARABINE
Background: Acute lymphoblastic leukemia (ALL) is a heterogeneous hematological malignancy predominantly affecting individuals under 20 years of age. Traditional chemotherapy, such as clofarabine, has shown efficacy; however, novel immunotherapeutic strategies like tisagenlecleucel (Kymriah®) have significantly altered the treatment paradigm. Aim: This study aimed to perform a comparative analysis of tisagenlecleucel, a CAR-T cell therapy, and clofarabine, a second-generation purine nucleoside analog, evaluating their mechanisms of action, therapeutic benefits, limitations, and clinical applicability across diverse patient populations. Methods: A systematic comparative evaluation was conducted, encompassing pharmacological characteristics, mechanisms of action, treatment protocols, efficacy, safety profiles, and clinical indications of both agents. The analysis considered pharmacokinetic and pharmacodynamic data and included patient demographic variables. Results: Tisagenlecleucel demonstrated high efficacy in refractory B-cell ALL, with durable responses and a blood half-life of 128 days, but with notable immune-related adverse effects such as cytokine release syndrome. Clofarabine, effective across a broader patient population, acts via multiple antitumor mechanisms but carries significant toxicity risks, including infection and sepsis. Discussion: The therapies present distinct clinical profiles: tisagenlecleucel offers targeted immunotherapy with high specificity but requires specialized infrastructure and management of immune toxicities. Clofarabine is more widely accessible and applicable, but is associated with conventional chemotherapy-related side effects. Treatment accessibility and cost differ markedly between the two. Conclusions: Therapy selection should be personalized based on patient-specific factors and institutional resources. Tisagenlecleucel is ideal for pediatric and young adult patients with relapsed/refractory B-cell ALL in CAR-T-capable centers, while clofarabine remains a viable option for broader ALL populations, particularly when genetic therapies are not feasible. Further research is needed to optimize therapeutic strategies and improve access to advanced treatments.
Read ArticleE-SELECTIN AS A BIOMARKER IN FEMALE PATIENTS WITH Β-THALASSEMIA IN AL- NAJAF PROVENCE, IRAQ
E-selectin, as identified (CD62E), is expressed on endothelial cells after stimulation with inflammation cytokines. β-Thalassemia diseases (βT) and early diagnosis are of utmost significance in the entire world population. This study was performed in the Thalassemia Center of the Al-Zahraa Educational Hospital in Al-Najaf Province, Iraq, on sixty-nine with β-thalassemia (54 βT major and 15 βT Intermedia) aged 8-40 years who transfused blood. Compared to 20 healthy volunteers as a control group. In both βT patients and healthy groups were assessed serum E-selectin levels. It was investigated the relationship with RBC, Hb, PCV, WBC, PLT, BMI, splenic status, iron, and ferritin levels. The results revealed a significant (P<0.05) decreased values of HB, RBC, P.C.V, and BMI. In contrast, values of WBC, PLT, Iron, and Ferritin were significantly increased in βT patients as compared to the healthy control groups. A significant (P<0.05) increase in serum E- Selectin level in βT patients (20.55±0.47) ng/ml to compare with the healthy group (9.16±0.50) ng/ml. Furthermore, it was a significant decrease in groups of βT major (19.87±0.42) ng/ml more than in βT intermedia (23±1.42) ng/ml. E-Selectin revealed a significant increase (P<0.05) in progress age and associated with splenectomies and underweight groups compared to splenectomies and the normal weight groups, respectively. Also, E-Selectin levels significantly positively correlated with WBC, PLT value, iron, and Ferritin levels. However, it was no significant with RBC, PCV, Hb. As a conclusion from this study, E- Selectin is an important biomarker in β-thalassemia patients can be identified as the complications associated with iron overload, inflammatory process, and endothelial dysfunction in βT disease.
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