Background: Carpenters perform repetitive and forceful upper-limb activities that may increase the risk of lateral Background: Dexmedetomidine and propofol are frequently used intravenous sedatives with distinct molecular targets and effects on arousal networks. Although both agents can achieve clinically comparable sedation, their electroencephalographic manifestations differ in spectral composition, spatial organization, processed index behavior, functional connectivity, and emergence dynamics. These differences are clinically important because simplified depth-of-sedation indices may not represent equivalent neurophysiological states across drug classes. Objective: This structured narrative review aimed to critically synthesize contemporary evidence regarding the raw and processed electroencephalographic signatures associated with dexmedetomidine and propofol sedation in adults. Methods: PubMed/MEDLINE, Scopus, Web of Science, and CENTRAL were searched for English-language human studies and relevant reviews published principally between January 2014 and May 2024. Foundational earlier studies were considered when necessary to explain established propofol EEG mechanisms. Literature selection prioritized direct comparative studies, controlled volunteer investigations, prospective clinical studies, secondary EEG analyses, and mechanistically informative reports addressing spectral power, spectral edge frequency, bispectral index, entropy, coherence, functional connectivity, and emergence trajectories. Findings were organized through a structured thematic synthesis rather than statistical pooling. Results: Dexmedetomidine was commonly associated with increased slow-delta activity accompanied by frontal spindle- or alpha-range oscillations and relative preservation of selected coherence measures. Propofol produced prominent slow-wave activity with concentration- and state-dependent frontal alpha oscillations, reduced faster-frequency activity, and greater disruption of selected long-range cortical interactions. At comparable clinical sedation levels, bispectral index and spectral edge frequency values frequently differed between agents. Evidence concerning entropy, connectivity, and emergence trajectories was informative but less extensively replicated. Conclusion: Dexmedetomidine and propofol produce distinct, context-dependent EEG profiles that should not be interpreted through interchangeable processed-index thresholds. Drug-specific EEG interpretation may improve sedation assessment, but standardized prospective studies linking electrophysiological patterns with patient-centered outcomes remain necessary
ABSTRACT Hepatic tuberculosis can mimic pyogenic liver abscess, particularly in patients with uncontrolled diabetes. Persistent or atypical hepatic lesions unresponsive to antibiotics should prompt tissue diagnosis using histopathology and molecular assays like GeneXpert to ensure timely diagnosis and appropriate management.
Background: Febrile seizures are common neurological events in early childhood, and iron deficiency has been proposed as a biologically plausible contributor to altered neuronal excitability because of its role in neurodevelopment, neurotransmitter synthesis, and cerebral energy metabolism. Objective: To determine whether iron deficiency profiles are associated with prolonged seizure duration among toddlers presenting with their first febrile seizure. Methods: This retrospective observational analytical study reviewed electronic medical records, archived laboratory reports, and paediatric emergency registers from tertiary care hospitals in Central Punjab for children aged 6–36 months presenting with first documented febrile seizure between January 2022 and December 2024. After exclusions, 132 eligible records were analyzed. Iron status was categorized as normal iron status, depleted iron stores, latent iron deficiency, or iron deficiency anemia using integrated hematological indices. Statistical analysis included descriptive statistics, chi-square testing, ANOVA, and binary logistic regression adjusted for age, sex, nutritional status, family history, and peak presenting temperature. Results: Depleted iron stores were identified in 42 children (31.8%), latent iron deficiency in 36 (27.3%), iron deficiency anemia in 29 (22.0%), and normal iron status in 25 (18.9%). Mean seizure duration increased progressively from 3.1 ± 1.2 minutes in children with normal iron status to 5.6 ± 2.0 minutes in those with iron deficiency anemia. Seizures lasting longer than five minutes increased from 12.0% to 48.3% across the same spectrum. Iron profile was significantly associated with prolonged seizure duration (χ² = 11.82; p = 0.008), with latent iron deficiency (adjusted OR = 2.18; 95% CI: 1.04–4.55; p = 0.038) and iron deficiency anemia (adjusted OR = 2.94; 95% CI: 1.31–6.58; p = 0.009) independently associated with higher odds of prolonged seizure. Conclusion: Worsening iron deficiency profiles were significantly associated with prolonged first febrile seizure duration in toddlers, suggesting that latent and overt iron deficiency may represent clinically relevant markers of greater seizure severity during febrile illness
Background: Recurrent urinary tract infections are a frequent clinical problem among premenopausal women and often require preventive strategies that balance recurrence reduction with tolerability and antimicrobial stewardship. Low-dose nitrofurantoin is an established prophylactic option, whereas cranberry extract has been proposed as a non-antibiotic alternative because of its potential anti-adhesive effect against uropathogens. Objective: To compare the efficacy and safety of standardized cranberry extract with low-dose nitrofurantoin for prevention of recurrent urinary tract infections among premenopausal women. Methods: A parallel-group randomized controlled trial was conducted among 80 premenopausal women aged 18–45 years with recurrent urinary tract infections. Participants were randomized to receive either cranberry extract containing 36 mg proanthocyanidins once daily or nitrofurantoin 50 mg once daily for 12 weeks. Outcomes included symptomatic culture-confirmed UTI episodes, time to first recurrence, urinary symptom severity measured by VAS, adherence, and adverse events. The final completer analysis included 72 participants. Results: Mean UTI episodes were lower with nitrofurantoin than cranberry extract (0.38 ± 0.49 vs 0.74 ± 0.65; mean difference 0.36, 95% CI 0.10–0.62; p=0.01). Time to recurrence was longer with nitrofurantoin (10.2 ± 2.1 vs 8.4 ± 2.5 weeks; p=0.003), and VAS reduction was greater (-4.6 ± 1.3 vs -3.6 ± 1.5; p=0.004). Adverse events were numerically higher with nitrofurantoin (27.0% vs 11.4%). Conclusion: Nitrofurantoin provided greater short-term prophylactic efficacy, whereas cranberry extract showed better numerical tolerability and may be considered for selected women prioritizing non-antibiotic prevention.
Brain metastasis is a frequent site of relapse in patients with inflammatory breast cancer (IBC) - a rare, highly aggressive variant of breast cancer. We discovered that soluble E-cadherin (sEcad), an 80-kDa E-cadherin fragment, correlates with increased brain metastasis risk and mortality in metastatic IBC patients. We further demonstrated that sEcad drives brain metastasis in HER2+ and triple-negative IBC mouse models. We hypothesize that sEcad induces specific cytokine production, activating astrocytes and priming the brain microenvironment for metastatic growth. sEcad-high and control IBC cells were injected into SCID/Beige mice to assess brain metastasis burden and survival. Human cytokine array analyzed conditioned medium from sEcad high and control cells. Clinical datasets compared expression and percent brain relapse rates. A brain-permeable CXCR2 inhibitor was tested for efficacy in IBC brain metastases. Multiplex quantitative imaging visualized cells in the brain metastatic microenvironment. Higher serum sEcad levels were independently correlated with reduced overall survival and increased brain metastasis. Cytokine array and ELISA showed increased levels of pro-inflammatory cytokines CXCL1, DKK1 and CXCL8 in conditioned medium from sEcad-overexpressing IBC cells compared with control cells. In patient samples, CXCL1, CXCL8 and CXCR2, the receptor for CXCL1 and CXCL8, were expressed higher in brain metastases and had increased brain metastasis relapse. sEcad promoted reactive astrocytosis in vitro and in vivo, while CXCR2 inhibition reduced this effect. Treating sEcad-high brain metastases with a brain- permeable CXCR2 inhibitor reduced metastasis, lowered burden and prolonged survival in two IBC mouse models. Multiplexed immunofluorescence showed fewer reactive astrocytes in brain metastasis lesions treated with the CXCR2 inhibitor. sEcad drives brain metastasis by promoting an inflammatory brain microenvironment via a targetable CXCL1/CXCL8-CXCR2 axis. Targeting this axis presents a promising therapeutic strategy to block brain metastasis in aggressive breast cancers.
