Objective.This work presents and evaluates a Monte Carlo (MC) -based scatter correction (SC) method developed for the Jagiellonian positron emission tomography (J-PET) scanner, a modular PET system based on plastic scintillators.Approach.The algorithm employs SimSET-based simulations integrated into a time-of-flight ordered-subsets expectation maximization reconstruction framework to estimate scatter contributions. Phantom studies using the NEMA image quality (IQ) phantom and a proof-of-principle human subject scan with the J-PET scanner were analyzed. To accelerate computation, lutetium-yttrium oxyorthosilicate (LYSO) crystals were also assessed in simulations as a surrogate for the native plastic material BC-404.Main results.In phantom experiments, SC improved contrast recovery coefficients by over 20% and reduced background variability by 8.5%, without introducing significant noise. Residual activity in cold regions was also considerably reduced. Substituting LYSO in the simulations decreased runtime by nearly one order of magnitude, while maintaining deviations below 6% in IQ metrics compared to BC-404. Human subject data demonstrated qualitatively reduced residual scatter and improved organ delineation. Quantitative comparison with the commercial PET/CT scanner by General Electric HealthCare (GE) discovery MI Gen 2 showed consistent activity concentration ratios across organs, although higher noise and residual scatter between organs were observed in J-PET, which most likely originates from lower count density.Significance.The proposed MC-based SC method provides robust scatter removal for J-PET, improving quantitative performance and establishing a foundation for advanced correction and reconstruction techniques. These results bring the plastic scintillator-based J-PET scanner closer to enabling clinically relevant quantitative PET imaging.
Colorectal cancer (CRC) incidence is rising in India, yet formal screening programs are lacking, in part due to the perceived low adenoma prevalence. This study aimed at evaluating the impact of quality improvement measures on adenoma detection rate (ADR) in a real world Indian setting and identifying factors associated with adenoma detection. In this single-center study, consecutive patients aged ≥ 18 years undergoing colonoscopy between September 2022 and August 2024 were included. Colonoscopy data from September 2022 to August 2023 served as a retrospective control arm, while those from September 2023 to August 2024 formed the prospective intervention arm, following implementation of standardized quality-focused withdrawal techniques. Of 2260 patients (mean age 47.3 ± 13.8 years, 69
A 69-year-old gentleman without any previous comorbidities presented with complaints of acute-onset low-grade fever, one episode of loss of consciousness, and weakness of both legs with urinary and stool retention for 1 day. He had an episode of generalized tonic-clonic seizure 3 hours after admission. On examination, he had tachycardia and hypotension; Glasgow Coma Scale (GCS) was E3V2M4, and neurological examination was suggestive of bilateral lower limb upper motor neuron lesion in the shock stage. Blood investigation revealed severe hyponatremia, and magnetic resonance imaging (MRI) with contrast of the dorsolumbar spine revealed longitudinally extensive transverse myelitis (LETM). Blood investigation for antineuromyelitis optica (anti-NMO) antibody was negative. Other investigations revealed low serum osmolality, raised urine osmolality, and spot sodium. Cerebrospinal fluid (CSF) viral panel detected human herpesvirus 6 (HHV6). He was treated with a pulse dose of IV methylprednisolone, hypertonic saline, and IV levetiracetam. He had symptomatic improvement and was discharged with a tapering dose of oral prednisolone. He had a complete recovery after 3 months of regular follow-up. Thus, we report a case of HHV6-induced LETM complicated with cerebral salt wasting syndrome and hyponatremic seizures.
BACKGROUND:Triazole resistance in Aspergillus fumigatus is a global public health concern associated with treatment failure, notably in invasive aspergillosis. However, population-level data on triazole resistance from India remain limited, with most reports originating from single-center studies. METHODS:We conducted a multicenter surveillance study to assess the prevalence of triazole resistance among clinical A. fumigatus isolates across India. Antifungal susceptibility testing was performed using the CLSI broth microdilution method (M38-Ed3), and molecular characterization was conducted on resistant isolates. A total of 518 isolates were analyzed: 115 prospectively collected from 13 tertiary-care hospitals from 2015-2020, and 403 archived isolates obtained from the National Culture Collection of Pathogenic Fungi (1994-2020). RESULTS:The overall pooled prevalence of non-wildtype isolates was 4.1% for itraconazole (95% CI: 2.54-6.17%), 3.9% for posaconazole (95% CI: 2.39-5.94%), while 1.4% were resistant to voriconazole (95% CI: 0.55-2.77%). One multi-azole-resistant isolate from an immunocompromised, mold-active triazole-naïve patient carried the TR34/L98H mutation, suggesting environmental acquisition. Prevalence of resistance did not differ significantly across geographic regions or between public and private sector hospitals. Linear regression analysis revealed a significant temporal increase in median MICs of all three licensed triazoles between 1994 and 2020. Approximately 29% of isolates exhibited amphotericin B MICs exceeding the epidemiological cutoff value; however, the clinical significance of this finding remains uncertain. CONCLUSIONS:Azole resistance among clinical A. fumigatus isolates in India remains uncommon (<5%), supporting the continued use of triazoles as first-line therapy. However, the observed temporal increase in triazole MICs underscores the need for sustained national surveillance to detect emerging resistance trends.
Alzheimer’s disease (AD) and related dementias (DEM) involve immunological, vascular, and neurological abnormalities. Circulating L1 cell adhesion molecule (L1CAM/CD171)-enriched extracellular vesicles (NEVs), combined with haematological markers, may reflect multisystem changes associated with disease progression. We evaluated 412 individuals: Controls (n = 161), DEM (n = 61), AD (n = 132), mild cognitive impairment (MCI; n = 27), and other neurological disorders (OND; n = 31). Plasma NEVs were enriched using L1CAM immunocapture and quantified by cluster of differentiation 81 (CD81) enzyme-linked immunosorbent assay (ELISA). Acetylcholinesterase (AChE) activity, total vesicle protein, and lipid content were measured. Statistical analyses included non-parametric testing, correlations, and discriminant modeling integrating cognitive scores and haematological parameters such as hemoglobin (Hb), hematocrit (Hct), mean platelet volume (MPV), and leukocyte subsets. NEV concentrations differed significantly (H = 25.7, p < 0.001): controls 49.0, MCI 63.6, AD 32.9, DEM 35.4, and OND 28.3 ng/mL. NEVs were reduced in AD and DEM but relatively elevated in MCI, indicating a possible early compensatory response, although interpretation is limited by the small MCI sample size. AD showed elevated MPV, neutrophil-lymphocyte imbalance, and mild normocytic anaemia. NEVs in AD had higher protein and reduced AChE activity. NEV-MPV correlations reversed across stages (MCI r = -0.42; AD r = 0.45). Classification accuracy reached 74–83 Circulating L1CAM-enriched extracellular vesicle (NEV; CD81) levels peak in mild cognitive impairment and progressively decline through AD and dementia. The NEV- MPV relationship reverses across disease stages, negative in MCI and positive in AD, indicating dynamic neurovascular coupling. NEV biochemical profiling reveals disrupted protein-lipid composition and reduced AChE activity in AD. Combined NEV and haematological parameters provide a minimally invasive framework for staging the progression of neurodegenerative diseases. A discriminant model integrating MPV, Hct, MCH, and neutrophils achieved diagnostic classification accuracy of 74-83
