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Abstract Malaria, though witnessing a decline in prevalence, remains a global health threat. Despite its primarily recognized impact on the hematological system, recent studies shed light on severe cardiac complications, particularly myocarditis, associated with Plasmodium infections. This review examines the literature on malaria-induced myocarditis to elucidate its mechanisms, clinical manifestations, regional perspectives, treatment outcomes, and diagnostic challenges. A literature search spanning PubMed, Scopus, and Web of Science identified relevant studies up to January 2024, encompassing case reports, cohort studies, clinical trials, and experimental studies. The relationship between severe malaria and myocardial involvement is explored, showcasing elevated biomarkers indicative of myocardial damage. Notably, while Plasmodium falciparum is traditionally linked to malaria-induced myocarditis, instances of Plasmodium vivax contributing to cardiac complications are documented. Regional perspectives reveal diverse cases, emphasizing the importance of considering malaria-induced myocarditis in endemic regions and beyond. Treatment outcomes underscore the efficacy of timely antimalarial therapy, advocating for integrated approaches to patient care. Diagnostic challenges, often complicated by overlapping symptoms with other cardiac conditions, highlight the need for heightened clinical suspicion. Addressing therapeutic challenges involves balancing antimalarial drugs, supportive care, and long-term monitoring. Future research directions are outlined, emphasizing the necessity for understanding host-parasite interactions, elucidating molecular mechanisms, and developing targeted diagnostic tools. This review consolidates the current knowledge on malaria-induced myocarditis, emphasizing the significance of continuous vigilance, research, and improved diagnostic approaches to mitigate the impact of this overlooked complication.

Seizures, characterized by excessive electrical discharges in the brain, can lead to severe complications, including cardiac arrhythmias and Takotsubo syndrome, a form of stress-induced cardiomyopathy mimicking acute coronary syndrome. We present a case of a 66-year-old female with epilepsy and postcerebrovascular accident status who experienced a 45-minute seizure resulting in elevated troponin levels and ECG changes. Echocardiography revealed severe hypokinesia and hyperkinesia with a left ventricular ejection fraction of 30%-35%, and coronary angiography was normal, leading to the diagnosis of a variant of Takotsubo syndrome characterized by basal rather than apical dysfunction. The patient showed significant improvement after 96 hours in the coronary care unit following adjusted anti-seizure medications and supportive cardiac care. This case highlights the importance of recognizing and managing cardiac complications such as Takotsubo syndrome in patients with neurological events, emphasizing the need for close collaboration between neurology and cardiology to improve patient outcomes.

In the medical diagnostics domain, pathology and histology are pivotal for the precise identification of diseases. Digital histopathology, enhanced by automation, facilitates the efficient analysis of massive amount of biopsy images produced on a daily basis, streamlining the evaluation process. This study focuses in Stain Color Normalization (SCN) within a Whole-Slide Image (WSI) cohort, aiming to reduce batch biases. Building on published graphical method, this research demonstrates a mathematical population or data-driven method that optimizes the dependency on the number of reference WSIs and corresponding aggregate sums, thereby increasing SCN process efficiency. This method expedites the analysis of color convergence 50-fold by using stain vector Euclidean distance analysis, slashing the requirement for reference WSIs by more than half. The approach is validated through a tripartite methodology: 1) Stain vector euclidean distances analysis, 2) Distance computation timing, and 3) Qualitative and quantitative assessments of SCN across cancer tumors regions of interest. The results validate the performance of data-driven SCN method, thus potential to enhance the precision and reliability of computational pathology analyses. This advancement is poised to enhance diagnostic processes, therapeutic strategies, and patient prognosis.

Background: Lewy body disorders (LBD), encompassing Parkinson disease (PD), PD dementia (PDD), and dementia with Lewy bodies (DLB), are characterized by alpha-synuclein pathology but often are accompanied by Alzheimer’s disease (AD) neuropathological change (ADNC). The medial temporal lobe (MTL) is a primary locus of tau accumulation and associated neurodegeneration in AD. However, it is unclear the extent to which AD copathology in LBD (LBD/AD+) contributes to MTL-specific patterns of degeneration. We employ a MTL subregional segmentation strategy of T1-weighted (T1w) MRI in biomarker-supported or autopsy-confirmed LBD and LBD/AD+ to investigate the anatomic consequences of co-occurring LBD/AD+ pathology on neurodegeneration. Methods: We studied 167 individuals with clinical diagnoses of LBD (PD, n = 124 (74.3 %); PDD, n = 11 (6.6 %); DLB, n = 32 (19.2 %)) with available T1w MRI and AD biomarkers or autopsy evidence of ADNC. Individuals were further biologically classified as LBD/AD+ based on hierarchical evidence of ADNC pathology: 1) AD “intermediate” or “high” by ABC neuropathologic criteria (n = 39 (23.4 %)); 2) positive amyloid PET (n = 2 (1.2 %)); or 3) CSF β-amyloid1-42

In this paper, we discuss the existence and uniqueness of a solution for the implicit two-order fractional integro-differential equation with m-point boundary conditions by applying the Banach fixed point theorem. Moreover, in the paper we establish the four different varieties of Ulam stability (Hyers–Ulam stability, generalized Hyers–Ulam stability, Hyers–Ulam-Rassias stability, and generalized Hyers–Ulam–Rassias stability) for the given problem.

Background: Pre-operative kidney disease was shown to impact peri-operative outcomes of endoscopic BPH surgeries. We aim to assess the effect of novel surgical techniques (Laser Enucleation of the Prostate (LEP) and Laser Vaporization of the Prostate (LVP)) compared to Transurethral Resection of Prostate (TURP), on post-operative outcomes stratified based on kidney function. Methods: The ACS-NSQIP database was reviewed from 2008 to 2021 for 83,020 patients that underwent TURP, LEP, and LVP. Pre-operative variables were compared across kidney function groups: G1(normal/high function); G2-G3(mild/moderate kidney disease); and G4-G5(severe kidney disease). Multivariate logistic regression was performed on 30-day peri-operative complications adjusting for pre-operative variables. Propensity score matching was done between LEP and LVP to TURP. Results: LEP showed a protective effect against UTIs (p < 0.05) in the G1 and G2-G3 categories but lost that protective effect in the G4-G5 category when compared to TURP. It had longer operative time (p < 0.05) across all kidney function groups, and demonstrated shorter hospital stay (p < 0.05) in the G1 and G2-G3 categories compared to TURP. LVP had a persistent protective effect against bleeding (p < 0.05) across all kidney function groups and shorter hospital stay (p < 0.05) when compared to TURP. LVP had a protective effect against return to OR (p < 0.05) in the G1 and G2-G3 kidney function group but lost that protective effect in the G4-G5 category. LVP had significant protective effect against thromboembolic events (p < 0.05) in the G2-G3 category and against cardiac complications (p < 0.05) in the G4-G5 category. Conclusion: LEP and LVP are superior to TURP in terms of post-operative complications. The type of endoscopic surgery technique should be tailored according to patient's pre-operative kidney status and risk. [ABSTRACT FROM AUTHOR]

Malaria, though witnessing a decline in prevalence, remains a global health threat. Despite its primarily recognized impact on the hematological system, recent studies shed light on severe cardiac complications, particularly myocarditis, associated with Plasmodium infections. This review examines the literature on malaria-induced myocarditis to elucidate its mechanisms, clinical manifestations, regional perspectives, treatment outcomes, and diagnostic challenges. A literature search spanning PubMed, Scopus, and Web of Science identified relevant studies up to January 2024, encompassing case reports, cohort studies, clinical trials, and experimental studies. The relationship between severe malaria and myocardial involvement is explored, showcasing elevated biomarkers indicative of myocardial damage. Notably, while Plasmodium falciparum is traditionally linked to malaria-induced myocarditis, instances of Plasmodium vivax contributing to cardiac complications are documented. Regional perspectives reveal diverse cases, emphasizing the importance of considering malaria-induced myocarditis in endemic regions and beyond. Treatment outcomes underscore the efficacy of timely antimalarial therapy, advocating for integrated approaches to patient care. Diagnostic challenges, often complicated by overlapping symptoms with other cardiac conditions, highlight the need for heightened clinical suspicion. Addressing therapeutic challenges involves balancing antimalarial drugs, supportive care, and long-term monitoring. Future research directions are outlined, emphasizing the necessity for understanding host-parasite interactions, elucidating molecular mechanisms, and developing targeted diagnostic tools. This review consolidates the current knowledge on malaria-induced myocarditis, emphasizing the significance of continuous vigilance, research, and improved diagnostic approaches to mitigate the impact of this overlooked complication. [ABSTRACT FROM AUTHOR]

Background: Left atrial (LA) myopathy is thought to be associated with silent brain infarctions (SBI) through changes in blood flow hemodynamics leading to thrombogenesis. 4D‐flow MRI enables in‐vivo hemodynamic quantification in the left atrium (LA) and LA appendage (LAA). Purpose: To determine whether LA and LAA hemodynamic and volumetric parameters are associated with SBI. Study Type: Prospective observational study. Population: A single‐site cohort of 125 Participants of the multiethnic study of atherosclerosis (MESA), mean age: 72.3 ± 7.2 years, 56 men. Field Strength/Sequence: 1.5T. Cardiac MRI: Cine balanced steady state free precession (bSSFP) and 4D‐flow sequences. Brain MRI: T1‐ and T2‐weighted SE and FLAIR. Assessment: Presence of SBI was determined from brain MRI by neuroradiologists according to routine diagnostic criteria in all participants without a history of stroke based on the MESA database. Minimum and maximum LA volumes and ejection fraction were calculated from bSSFP data. Blood stasis (% of voxels <10 cm/sec) and peak velocity (cm/sec) in the LA and LAA were assessed by a radiologist using an established 4D‐flow workflow. Statistical Tests: Student's t test, Mann–Whitney U test, one‐way ANOVA, chi‐square test. Multivariable stepwise logistic regression with automatic forward and backward selection. Significance level P < 0.05. Results: 26 (20.8%) had at least one SBI. After Bonferroni correction, participants with SBI were significantly older and had significantly lower peak velocities in the LAA. In multivariable analyses, age (per 10‐years) (odds ratio (OR) = 1.99 (95% confidence interval (CI): 1.30–3.04)) and LAA peak velocity (per cm/sec) (OR = 0.87 (95% CI: 0.81–0.93)) were significantly associated with SBI. Conclusion: Older age and lower LAA peak velocity were associated with SBI in multivariable analyses whereas volumetric‐based measures from cardiac MRI or cardiovascular risk factors were not. Cardiac 4D‐flow MRI showed potential to serve as a novel imaging marker for SBI. Level of Evidence: 3 Technical Efficacy: Stage 2 [ABSTRACT FROM AUTHOR]

Multiple Myeloma is a hematological malignancy characterized by the proliferation of clonal plasma cells and associated with severe clinical manifestations. Despite advancements in diagnosis and management, Multiple Myeloma remains incurable, necessitating further research into more effective therapies.The primary objective of this review is to provide an informative and critical summary of the Multiple Myeloma microenvironment, and emerging revolutionary therapeutic approaches with potential combination therapy to improve the quality of life for Multiple Myeloma patients.Recent advancements in immunotherapy, particularly immune checkpoint inhibitors (ICIs), have shown improvements in immune response against Multiple Myeloma. ICIs target inhibitory pathways such as PD-1/PD-L1 and CTLA-4, potentially overcoming tumor-induced immunosuppression. Combination therapies integrate ICIs with proteasome inhibitors, immunomodulators, and monoclonal antibodies to enhance the anti-tumor immune response. Additionally, Chimeric Antigen Receptor T-cell (CAR-T) therapy has demonstrated effectiveness against Multiple Myeloma, particularly when coupled with ICIs to decrease resistance and relapse.Although the efficacy of ICIs in treating Multiple Myeloma has been hindered by the complexity of the tumor microenvironment and immune evasion mechanisms, this challenge has led to the exploration of combination therapies. Potential side effects are still a big challenge for newly recognized ICIs and combination treatment.Investigations of new immune checkpoints and the development of targeted therapies against these markers are in progress, creating possibilities for more personalized and effective treatment strategies. Continuous research and robust clinical trials are needed to comprehend the complex dynamics of the Multiple Myeloma microenvironment to develop revolutionary therapeutic targets. [ABSTRACT FROM AUTHOR]

Human pigmentary disorders encompass a broad spectrum of phenotypic changes arising from disruptions in various stages of melanocyte formation, the melanogenesis process, or the transfer of pigment from melanocytes to keratinocytes. A large number of pigmentation genes associated with pigmentary disorders have been identified, many of them awaiting in vivo confirmation. A more comprehensive understanding of the molecular basis of pigmentary disorders requires a vertebrate animal model where changes in pigmentation are easily observable in vivo and can be combined to genomic modifications and gain/loss-of-function tools. Here we present the amphibian Xenopus with its unique features that fulfill these requirements. Changes in pigmentation are particularly easy to score in Xenopus embryos, allowing whole-organism based phenotypic screening. The development and behavior of Xenopus melanocytes closely mimic those observed in mammals. Interestingly, both Xenopus and mammalian skins exhibit comparable reactions to ultraviolet radiation. This review highlights how Xenopus constitutes an alternative and complementary model to the more commonly used mouse and zebrafish, contributing to the advancement of knowledge in melanocyte cell biology and related diseases., (© 2024 The Author(s). Pigment Cell & Melanoma Research published by John Wiley & Sons Ltd.)