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Ethnomathematics examines the relationship between mathematics and cultural practices, highlighting mathematical concepts embedded within diverse cultural contexts. Ijo Temple, located approximately 4 km southeast of Ratu Boko Temple and 18 km east of Yogyakarta, stands as a prominent cultural site in Indonesia. While prior studies have explored mathematical elements within cultural heritage, limited attention has been given to the geometric concepts inherent in Ijo Temple's architecture. This study bridges this gap by analyzing the temple's architectural geometry through an ethnographic lens, guided by four key research questions: "Where do I observe?", "How do I investigate?", "How do I identify significant findings?", and "How do I interpret these findings?". The investigation uncovers various geometric sub-concepts, validated in collaboration with geometry experts. These include (1) planar geometry, encompassing triangles, rectangles, squares, trapezoids, and circles; (2) spatial geometry, such as cubes, rectangular prisms, and cylinders; (3) geometric transformations, including translation, reflection, and dilation; and (4) congruence principles. Beyond contributing to the academic discourse on geometric applications within cultural heritage, this research underscores the potential of culturally contextualized learning to enhance students' mathematical understanding. [ABSTRACT FROM AUTHOR]

Background Cryptococcal meningitis (CM) is responsible for 15%–20% of human immunodeficiency virus (HIV)–associated mortalities. CM prevalence has also increased in other immunocompromised populations of transplant recipients, patients with cancer, and individuals on immunomodulatory medication. Methods This retrospective review included 51 definitive patients with CM hospitalized at a tertiary academic medical center in New York City between 2010 and 2023. We assessed clinical features and outcomes of CM, with additional analysis of factors related to antiretroviral therapy (ART) adherence in HIV-infected cases and immunomodulatory medication history of HIV-negative cases. Results The cohort had a mean (standard deviation) age of 47.1 ± 15.1 years, and was predominantly male (37, 72.5%). Of 32 patients with HIV, 3 (9.4%) were newly diagnosed with HIV at the time of CM hospitalization, 5 (15.6%) had recurrent CM, and 2 (6.3%) had a CM relapse. The majority (30, 93.8%) of patients with HIV were ART nonadherent. Of 19 HIV-negative patients, 8 (42.1%) were solid-organ transplant recipients, 5 (26.3%) had autoimmune conditions of sarcoidosis or systemic lupus erythematosus, and 3 (15.8%) had chronic lymphocytic leukemia. Six (11.8%) patients died during hospitalization, 4 of whom had HIV. Conclusions The burden of CM in people with HIV and immunocompromised patients continues even in settings with accessible standard antifungal treatment though interventions of increased ART adherence for those with HIV and antifungal prophylaxis may improve morbidity and mortality. [ABSTRACT FROM AUTHOR]

The article focuses on establishing efficient methods for deriving airway and alveolar organoids from human bronchoalveolar lavage (BAL) samples. It is reported that these organoids recapitulate diverse cell types found in the lung epithelium, offering versatile models for studying lung diseases and personalized therapeutics.

West Nile virus (WNV) neuroinvasive disease (WNND) occurs in approximately 1 percent of WNV-infected patients and typically presents as encephalitis, meningitis, or acute flaccid paralysis (AFP). WNND remains a difficult inpatient diagnosis, creating significant challenges for prognostication and therapy selection. We characterized the clinical and diagnostic features of WNND cases at two major academic medical centers in New York City in routine clinical practice. We retrospectively reviewed the charts of thirty-six patients with WNND, including twenty-six encephalitis, four meningitis, and six AFP cases. The most common presenting symptoms were fever (86.1%) and gastrointestinal symptoms (38.9%) in addition to altered mental status (72.2%), lethargy (63.9%), gait disturbances (46.2%), and headache (44.4%). Fourteen (48.3%) patients displayed acute magnetic resonance imaging (MRI) findings, particularly T2 hyperintensities in the bilateral thalami, brainstem, and deep white matter. New York State Department of Health WNV CSF IgM testing was utilized for diagnosis in 58.3% of patients; however, just 38.1% had the result by discharge, compared to 85.6% of those who underwent serum IgM testing. The median length of stay was 13.5 days, 38.9% were intubated, and three patients (8.9%) died during acute hospitalization. Our findings underscore the morbidity, mortality, and diagnostic challenges of WNND, suggesting the potential utility of serum IgM testing in combination with confirmatory CSF testing to expedite diagnosis in the acute setting. [ABSTRACT FROM AUTHOR]

This systematic review evaluates the evidence for accuracy of automated analyzers that estimate cerebrospinal fluid (CSF) white blood cell counts (WBC) compared to manual microscopy. Inclusion criteria of original research articles included human subjects, English language, and manual microscopy comparator. PUBMED, EMBASE and Cochrane Review databases were searched through 2019 and QUADAS‐2 Tool was used for assessment of bias. Data were pooled and analyzed by comparison method, using random effects estimation. Among 652 titles, 554 abstracts screened, 104 full‐text review, 111 comparisons from 41 studies were included. Pooled estimates of sensitivity and specificity (n = 7) were 95% (95%‐CI 93%–97%) and 84% (95%‐CI: 64%–96%), respectively. Pooled R2 estimates (n = 29) were 0.95 (95%‐CI: 0.95–0.96); Pooled spearman rho correlation (n = 27) estimates were 0.95 (95% CI 0.95–0.96). Among those comparisons using Bland–Altman analysis (n = 11) pooled mean difference was estimated at 0.98 (95% CI‐0.54–2.5). Among comparisons using Passing‐Bablok regressions (n = 14) the pooled slope was estimated to be 1.05 (95% CI 1.03–1.07). Q tests of homogeneity were all significant with the exception of the Bland–Altman comparisons (I2 10%, p value 0.35). There is good overall accuracy for CSF WBC by automated hematologic analyzers. These findings are limited by the small sample sizes and inconsistent validation methodology in the reviewed studies. [ABSTRACT FROM AUTHOR]

Non-small-cell lung cancer is the leading cause of cancer-related death worldwide (1). Chemotherapies such as the topoisomerase II (TopoII) inhibitor etoposide effectively reduce disease in a minority of patients with this cancer (2,3); therefore, alternative drug targets, including epigenetic enzymes, are under consideration for therapeutic intervention (4). A promising potential epigenetic target is the methyltransferase EZH2, which in the context of the polycomb repressive complex 2 (PRC2) is well known to tri-methylate histone H3 at lysine 27 (H3K27me3) and elicit gene silencing (5). Here we demonstrate that EZH2 inhibition has differential effects on the TopoII inhibitor response of non-small-cell lung cancers in vitro and in vivo. EGFR and BRG1mutations are genetic biomarkers that predict enhanced sensitivity to TopoII inhibitor in response to EZH2 inhibition. BRG1 loss-of-function mutant tumours respond to EZH2 inhibition with increased S phase, anaphase bridging, apoptosis and TopoII inhibitor sensitivity. Conversely, EGFR and BRG1 wild-type tumours upregulate BRG1in response to EZH2 inhibition and ultimately become more resistant to TopoII inhibitor. EGFR gain-of-function mutant tumours are also sensitive to dual EZH2 inhibition and TopoII inhibitor, because of genetic antagonism between EGFR and BRG1. These findings suggest an opportunity for precision medicine in the genetically complex disease of non-small-cell lung cancer., To validate that EZH2 is an important target for non-small-cell lung cancer (NSCLC), we generated a 116-gene lung cancer EZH2 co-expression gene signature (Supplementary Table 1). This signature had predictive [...]

Objective: Emerging variants and sublineages of SARS‐CoV‐2 have differing disease severity, transmissibility, and immune evasion. The neurological conditions associated with the original strain of SARS‐CoV‐2 are well established. Our study assessed the neurological presentations specific to hospitalized patients during the B.1.1.529 (Omicron) variant surge in New York City. Methods: A total of 178 cases with positive RT‐PCR result within 6 weeks before admission, and subsequent development of select neurological conditions during the SARS‐CoV‐2 B.1.1.529 (Omicron) surge between December 1, 2021 and February 28, 2022, were included from 12,800 SARS‐CoV‐2‐positive hospital admissions. Clinical data from acute hospitalizations were compared to findings of inpatient neurological cases with COVID‐19 infections from the initial surge in NYC in the same hospital system. Results: Compared to SARS‐CoV‐2 infections of the original strain, COVID‐19 cases hospitalized during the Omicron surge (B.1.1.529) were associated with incidental and/or asymptomatic COVID‐19 cases (96, 53.9%) and an increased incidence of pre‐existing neurological and immunocompromising conditions. Encephalopathy, seizures, and stroke remained the most prevalent neurological conditions identified in hospitalized COVID‐19 cases during the study period, reflecting a similar distribution of neurological presentations associated with the original strain. Interpretation: In our cohort of 178 admitted SARS‐CoV‐2‐positive patients with select neurological conditions during the Omicron B.1.1.529 surge, 54% of COVID‐19 cases were considered incidental and/or asymptomatic, and the identified neurological conditions resembled those associated with the original SARS‐CoV‐2 strain. Further studies characterizing neurological presentation in Omicron sublineages and other variants are warranted in an ongoing COVID‐19 pandemic. [ABSTRACT FROM AUTHOR]

Acute Respiratory Distress Syndrome (ARDS) and Ulcerative Colitis (UC) are each characterized by tissue damage and uncontrolled inflammation. Neutrophils and other inflammatory cells play a primary role in disease progression by acutely responding to direct and indirect insults to tissue injury and by promoting inflammation through secretion of inflammatory cytokines and proteases. Vascular Endothelial Growth Factor (VEGF) is a ubiquitous signaling molecule that plays a key role in maintaining and promoting cell and tissue health, and is dysregulated in both ARDS and UC. Recent evidence suggests a role for VEGF in mediating inflammation, however, the molecular mechanism by which this occurs is notwell understood. We recently showed that PR1P, a 12-amino acid peptide that binds to and upregulates VEGF, stabilizes VEGF from degradation by inflammatory proteases such as elastase and plasmin thereby limiting the production of VEGF degradation products (fragmented VEGF (fVEGF)). Here we show that fVEGF is a neutrophil chemoattractant in vitro and that PR1P can be used to reduce neutrophil migration in vitro by preventing the production of fVEGF during VEGF proteolysis. In addition, inhaled PR1P reduced neutrophil migration into airways following injury in three separate murine acute lung injury models including from lipopolysaccharide (LPS), bleomycin and acid. Reduced presence of neutrophils in the airways was associated with decreased pro-inflammatory cytokines (including TNF-a, IL-1β, IL-6) andMyeloperoxidase (MPO) in broncho-alveolar lavage fluid (BALF). Finally, PR1P prevented weight loss and tissue injury and reduced plasma levels of key inflammatory cytokines IL-1b and IL-6 in a rat TNBS-induced colitis model. Taken together, our data demonstrate that VEGF and fVEGF may each play separate and pivotal roles in mediating inflammation in ARDS and UC, and that PR1P, by preventing proteolytic degradation of VEGF and the production of fVEGF may represent a novel therapeutic approach to preserve VEGF signaling and inhibit inflammation in acute and chronic inflammatory diseases. [ABSTRACT FROM AUTHOR]

Progression of premalignant lesions is restrained by oncogene-induced senescence. Oncogenic Ras triggers senescence in many organs, including the lung, which exhibits high levels of the angiogenesis inhibitor thrombospondin-1 (TSP-1). The [...]

New discoveries in stem ceil biology are making the biology of solid tissues increasingly complex. Important seminal studies demonstrating the presence of damage-resistant cell populations together with new isolation and characterization techniques suggest that stem cells exist in the adult lung. More detailed in vivo molecular and cellular characterization of bronchioalveolar stem cells (BASCs), other putative lung stem and progenitor cells, and differentiated cells is needed to determine the lineage relationships in adult lung. Lung diseases such as cystic fibrosis or chronic obstructive pulmonary disease, as well as the most common form of lung cancer in the United States, all involve apparent bronchiolar and alveolar cell defects. It is likely that the delicate balance of stem, progenitor, and differentiated cell functions in the lung is critically affected in patients with these devastating diseases. Thus the discovery of BASCs and other putative lung stem cells will lay the foundation for new inroads to understanding lung biology related to lung disease. progenitor cells; bronchiolar; alveolar