IntroductionMalaria continues as a public health threat through symptomatic/febrile cases, asymptomatic and low-density infections of Plasmodium falciparum, P. vivax, and their mixed infections. Mixed infections have not been studied much regarding their burden, clinical manifestations, and implications, and therefore, this study was conducted.MethodsFebrile patients were recruited from four patient-care settings from June to November 2020 through the collection of dried blood spots (DBS) and their paired microscopy and/or rapid diagnostic test (RDT) data. Polymerase chain reaction (PCR)-based molecular diagnosis of both parasite species was performed from genomic DNA isolated from the DBS. Clinico-demographic details were recorded from patients from one of the sites, wherein patients with mixed infections were telephonically followed for subsequent clinical development.ResultsOut of the 1030 samples collected and analyzed, 27% (280) were infected with P. falciparum and/or P. vivax: 188 (18%) mono-P. falciparum, 6 (0.5%) mono-P. vivax and 86 (8%) mixed. None of the infections were detected by microscopy and/or RDT, meaning that all 27% were febrile sub-microscopic infections with 8% burden of mixed infections. The quality of microscopic slides was found to be unsatisfactory when a sub-sample of slides was cross-examined by level 1-competent microscopists. None of the nine mixed-infection patients from Gandhi Medical College and Hospital (GMCH) reported recurrences or any clinical development during the 12-month follow-up. No clinically/statistically significant difference was observed between mono- and mixed infections.ConclusionsA high 27% febrile sub-microscopic Plasmodium infections with 8% mixed infections represent a significant challenge for malaria elimination, considering the quality of microscopy and the fact that Madhya Pradesh is classified under category 1 in the National Strategic Plan for malaria elimination 2023-2027.
Background: Paraquat (PQ) a synthetic weedicide is often consumed with the intent to commit suicide. PQ can accumulate in the lungs and kidneys through redox reactions, tubular necrosis. Literature on PQ-acute kidney injury (PQ-AKI) is limited. Materials and Methods: We reviewed data on patients referred to nephrology services to manage PQAKI between June 2014 and June 2024. We analyzed epidemiological data, clinical features, and outcomes. Results: Four hundred patients were analyzed. The mean age was 30 +/- 11 for 6. 2% of all cases with AKI during the period. Oligoanuria and deranged kidney function were reasons for referral. The majority were in stage 3 AKI (75%), of whom 45% received hemodialysis (HD). The mortality rate (75%) was associated with consumption quantity, gender, and multiorgan failure. Conclusion: PQ-AKI is an important contributor to AKI in this region and is associated with high mortality. Quantity of consumption, gender, multiorgan failure, and latency in seeking medical care were associated with outcomes.
Recent advancements in neurobiology have shifted the understanding of addiction and reward-processing disorders from purely behavioral or genetic frameworks toward an epigenetic paradigm. This systematic review synthesizes current research on the epigenetic and transgenerational reprogramming of the brain’s reward system, specifically focusing on how environmental stressors, substance exposure, and nutritional factors alter gene expression without modifying the underlying DNA sequence. The review highlights critical mechanisms such as DNA methylation, histone acetylation, and non-coding RNA regulation within the mesolimbic dopamine pathway. Evidence from both animal models and longitudinal human studies suggests that these molecular "scars" can be inherited across generations, predisposing offspring to heightened vulnerability to substance use disorders (SUDs) and altered hedonic responses. Central to this phenomenon is the reprogramming of the germline, which facilitates the transmission of paternal and maternal environmental experiences to subsequent generations. Bridging the gap between molecular biology and clinical practice, this paper introduces Clinical Counseling Guidelines designed for mental health professionals. These guidelines emphasize the importance of "epigenetic literacy" in trauma-informed care, advocating for interventions that leverage neuroplasticity to reverse adverse epigenetic marking. Key recommendations include personalized lifestyle modifications, targeted mindfulness-based cognitive therapy, and family-centered psychoeducation that addresses the hereditary nature of reward system dysregulation. By integrating transgenerational perspectives into counseling, clinicians can provide more comprehensive support that breaks the cycle of inherited neurobiological vulnerability. Keywords: DNA, RNA, neurology, methylation, biochemical
Background Mucosal barrier injury–laboratory confirmed bloodstream infections (MBI-LCBI) represent an endogenous subset of central line–associated bloodstream infections (CLABSIs), particularly in immunocompromised patients. Misclassification may distort surveillance metrics and infection prevention strategies. This study aimed to estimate the proportion of MBI-LCBI among CLABSIs and explore sources of variability. Methods A PRISMA-compliant systematic review and meta-analysis (PROSPERO: CRD420261281159) was conducted using MEDLINE and EMBASE (2013–2026). Observational studies reporting MBI-LCBI (per 2013 NHSN criteria) among CLABSIs were included. Random- effects meta-analysis (REML) with logit transformation was performed. Heterogeneity, prediction intervals (PI), small-study effects, and subgroup analyses (pediatric and geographic) were evaluated. Results Twenty-seven studies (n = 44,106) were included. The exploratory pooled proportion of MBI- LCBI among CLABSIs was 40.3% (95% CI: 30.4%–51.1%), with extreme heterogeneity (I²=99.7%). The 95% PI ranged from 6.5% to 86.8%, indicating substantial variability across settings. Small-study effects were significant (p = 0.0002); excluding studies with < 200 participants reduced the estimate to 29.0% (95% CI: 18.2%–42.8%), with persistent heterogeneity. Pediatric estimates were comparable (38.8%), while geographic variation was not a significant moderator. Conclusions MBI-LCBI may represent a clinically important but highly variable proportion of CLABSIs. Given substantial heterogeneity and small-study effects, pooled estimates should be interpreted cautiously. Accurate differentiation of MBI-LCBI is essential for reliable surveillance, antimicrobial decision-making, and context-specific infection prevention strategies.
Complement Factor H (CFH) is a key regulator of the alternative complement pathway, and mutations in its gene are commonly associated with atypical hemolytic uremic syndrome (aHUS). Typically linked to renal thrombotic microangiopathy (TMA), CFH also interacts with coagulation factors, suggesting its role in thrombosis. We describe a 22-year-old male with AKI, nephrotic-range proteinuria, and anuria. Renal biopsy revealed chronic TMA. A CT revealed partial thrombosis of the right internal jugular vein (IJV). Thrombophilia workup was unremarkable. Genetic testing identified a pathogenic heterozygous CFH mutation (c.3572C>T; p.Ser1191Leu). This case illustrates an unusual CFH deficiency with venous thrombosis in the absence of traditional risk factors. Structural similarities between CFH and β2-glycoprotein I may underlie its anticoagulant function. Complement dysregulation should be considered in the differential diagnosis of unexplained thrombosis, particularly when associated with renal dysfunction.
