Background/Objectives: It is estimated that gestational diabetes mellitus (GDM) affects approximately 14% of pregnant women. This is due to the inability of the body to produce enough insulin for gestation. With greater appearance during the second and third trimesters, GDM has a multifactorial cause including hypertension, cardiovascular issues (CVD), family history both or either type two diabetes mellitus (T2DM) or GDM, obesity, advanced maternal age, and polycystic ovarian syndrome (PCOS). However, it has been suggested that except for genetic predisposition, environmental factors can increase the risk of GDM development to a great extent. The aim of this systematic review and meta-analysis is the examination of different environmental contributors that play a significant role in the development of GDM. Methods: The databases used were PubMed and ScienceDirect. The inclusion criteria were a 10-year duration (2014–2024), English language, research articles, and only humans included. Afterwards, tables were created to summarize the most important information from each article. Forest and funnel plots were created to assess the possibility of a greatly significant difference between each environmental contributor. Results: Initially, 9361 articles were found. After the automation tools were applied, 706 were left. The total number of articles used in the study after the screening process was 26. Through the systematic review analysis, the following risk factors were stated to play a contributing role with GDM: extreme temperatures (both high and low), organophosphorus flame retardants (OFRs), bisphenol A (BPA), selenium (Se), metallic elements, urinary antimony (Sb), trace elements, thiamine and riboflavin, and fine particulate matter PM_2.5. Conclusions: Through this meta-analysis, it can be concluded that there is statistical significance for fine particulate matter PM_2.5, especially in the first (p < 0.001) and second (p < 0.001) trimesters, proving the acknowledged connection between PM_2.5 and GDM pathogenesis during pregnancy. Apart from that, fetal sex can play an important role in the development of GDM, as there is the greatest risk in males (p < 0.001), whereas no correlation between maternal smoking habit and bisphenol A with GDM was found. In conclusion, it can be stated that environmental factors can have a great impact on the development of GDM during the gestational period, but more studies must be carried out to reinforce our outcomes.

Background/Objectives: Orthognathic surgery has evolved with digital advancements, improving precision and predictability. Traditional free-hand techniques rely on surgeon expertise, often leading to variable outcomes. Fully guided approaches integrate computer-assisted surgery, including virtual surgical planning (VSP), CAD/CAM, and dynamic navigation, enhancing accuracy and efficiency. This review compares these approaches, assessing their impact on surgical accuracy, efficiency, and patient outcomes. Methods: A scoping review was conducted across PubMed, MEDLINE, Scopus, Cochrane Library, and Embase databases, focusing on clinical trials and cohort studies. Key parameters analyzed include surgical precision, operative efficiency, complication rates, and functional/aesthetic results. Results: Fully guided techniques achieve sub-millimetric accuracy with mean length deviations ranging from 1.3 mm to 2.4 mm and mean angular deviations between 2.29° and 3.51°. Moreover, these approaches markedly reduce operative time, averaging between 34 min and 1.7 h, and postoperative complications. Digital tools streamline workflow, improving reproducibility and aesthetic outcomes. Free-hand methods remain cost-effective but require greater surgical expertise, often resulting in longer recovery periods and higher variability. Conclusions: Computer-assisted orthognathic surgery enhances precision and efficiency, outperforming free-hand techniques in accuracy and predictability. While free-hand methods remain viable for simpler cases, fully guided approaches optimize surgical execution. Future research should explore hybrid strategies combining digital precision with manual adaptability to further refine surgical techniques.

Purpose: Pancreatic cancer (PC) is a fatal malignancy with an aggressive course derived from the cells of pancreatic tissue. Gestational diabetes mellitus (GDM) is a state of spontaneous hyperglycemia occurring during gestation and has been suggested as a risk factor PC. Women with a history of GDM revealed a risk rate of 7.1% for the development of PC. The current systematic review aims to investigate the correlation between GDM and the degree to the prevalence of PC. Methodology: For this systematic review, the PICO model was prepared to construct and outline the exact questions of the study, a PRISMA flow diagram was prepared and quality assessment was conducted using the Newcastle Ottawa Scale (NOS) for Cohort Studies, the NIH Quality Assessment Tool-Criteria for Case Reports and the Cochrane quality assessment tool for Systematic Reviews and Meta-analysis studies. Result: A total of eight articles were retrieved from the main databases, and a table was created to summarize the information found. Even though the data found were limited, the quality assessment performed revealed that the articles were of high validity. Conclusions: It can be concluded that GDM has an association with the development of PC and can be considered as a risk factor.

Acute myeloid leukemia (AML) continues to carry a dismal prognosis in older adults and those with secondary or high-risk disease, where conventional 7 + 3 chemotherapy has long delivered complete remission rates below 40% and median overall survival often under 6 months. CPX-351 (Vyxeos), a liposomal co-encapsulation of cytarabine and daunorubicin at a fixed synergistic 5:1 molar ratio, was designed to overcome the pharmacokinetic mismatch that undermines the traditional regimen. This review critically examines the preclinical rationale and clinical evidence for CPX-351, with particular attention to whether its nanoparticle platform truly represents a breakthrough or merely an incremental refinement of decades-old cytotoxics. Across phase I–III trials and real-world cohorts, CPX-351 consistently outperformed standard 7 + 3 in its approved populations of newly diagnosed therapy-related AML (t-AML) and AML with myelodysplasia-related changes (AML-MRC) in patients aged 60–75 years. In the pivotal phase III study (n = 309), CPX-351 improved median overall survival from 5.95 to 9.56 months (HR 0.69, 95% CI 0.52–0.90; p = 0.005) and raised the complete remission rate from 33.3% to 47.7%, while facilitating allogeneic transplantation in 34% as opposed to 25% of patients. A five-year follow-up sustained the separation in survival curves, and post-hoc analyses of responders showed median overall survival exceeding 25 months with CPX-351 versus approximately 10 months with 7 + 3 (HR 0.49). Real-world series have reported composite remission rates of 53–60%, measurable residual disease negativity in up to 65% of responders, and median overall survival of 12–20 months, depending on transplant utilization. Despite these gains, the absolute survival benefit remains modest, prolonged cytopenias are universal, and outcomes in TP53-mutated or younger adverse-risk patients are still poor, raising legitimate questions about cost-effectiveness and generalizability. Nonetheless, CPX-351 stands as the first clinically validated example of ratiometric nanomedicine in oncology, proving that reformulating established drugs can yield meaningful progress where novel agents have often failed.

Background. Gestational diabetes mellitus (GDM) induces maternal hyperglycemia, which may alter fetal cardiac structure and function, increasing short- and long-term cardiovascular risks. Purpose. To systematically review the evidence on the fetal cardiac structural and functional effects of GDM, to explore the diagnostic role of novel imaging and biochemical biomarkers, and to summarize the long-term cardiovascular complications associated with GDM. Materials and Methods. A systematic search of PubMed, Scopus, and Cochrane Library was conducted according to the PRISMA guidelines. All studies comparing cardiac outcomes in GDM and non-GDM pregnancies were included. Data on myocardial hypertrophy, diastolic and systolic function, imaging modalities, and biomarkers were extracted and qualitatively synthesized. Results. A total of twelve eligible studies were identified. Fetal cardiac hypertrophy and diastolic and early systolic dysfunction are common among GDM pregnancies and can be detected by dual-gate Doppler and speckle-tracking echocardiography. Abnormalities are observed in indices such as the myocardial performance index, E/A, E/e′ ratios, and global longitudinal and circumferential strain in fetuses and may persist in the neonatal period. Alterations may be more pronounced for the right ventricle compared to the left. Septal hypertrophy is associated with elevated umbilical cord pro-brain natriuretic peptide. The risk of early-onset cardiovascular disease in the progeny of diabetic mothers is 29% higher, as evidenced by population-based cohort data. Conclusions. GDM is linked to fetal cardiac remodeling and an increased long-term cardiovascular risk. Early detection and customized interventions to reduce adverse outcomes may be achieved by integrating advanced echocardiographic techniques and biomarkers into prenatal surveillance.

Background/Objectives: Cytarabine (Ara-C) remains central to acute myeloid leukemia therapy but is limited by unpredictable systemic toxicities. Preclinical studies have long documented multi-organ injury, yet findings remain fragmented. This systematic review synthesizes animal evidence to clarify the spectrum, dose–response patterns, and mechanisms of cytarabine-induced toxicity. Methods: Following PRISMA 2020 guidelines and PROSPERO registration (CRD420251081384), a comprehensive search of PubMed, MEDLINE, Scopus, Cochrane Library and Embase identified eligible in vivo animal studies. Data extraction covered animal models, dosing regimens, routes of administration, histopathological and biochemical endpoints and mechanistic findings. Risk of bias and study quality were assessed using SYRCLE’s tool, CAMARADES checklist and an adapted Newcastle–Ottawa Scale, with reporting benchmarked against ARRIVE 2.0. Results: Eighty-one studies (1964–2024) were included. Cytarabine produced dose- and regimen-dependent toxicities across multiple organs. Neurotoxicity was most frequently reported, followed by intestinal mucositis, ocular injury, alopecia, hepatotoxicity, nephrotoxicity, and developmental anomalies. Mechanistic analyses consistently implicated oxidative stress, inflammatory cascades, apoptosis, and epigenetic dysregulation. Study quality was moderate, with frequent deficiencies in randomization, blinding, and sample-size justification, raising concerns about reproducibility. Cardiotoxicity, despite clinical relevance, was virtually absent from preclinical evaluation. Conclusions: Preclinical evidence suggests cytarabine’s systemic toxicity as a multifactorial process extending beyond rapidly proliferating tissues. While animal studies provide mechanistic insights, methodological weaknesses and translational gaps limit predictive value. Future research must adopt rigorous design, systematically assess underexplored toxicities, and integrate molecular profiling to identify biomarkers and protective strategies.