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At least 19 recordsLinked to original sources
PubMed1992

Are intersecting staple lines a hazard in intestinal anastomosis?

To determine the safety of intersecting staple lines, 22 pigs were operated upon with a functional end-to-end enteroanastomosis 40 cm distal to the ligament of Treitz using linear stapling devices. The procedure was repeated on the colon, where a colocolostomy was created. The blood flow at intersecting staple lines and single-row staple lines for each anastomosis was studied with the reference organ method 24 hours after the first operation. The purpose was to evaluate whether there is a reduction in blood flow at the site of intersecting staple lines, causing an increased risk for anastomotic leakage. The reduction in mean blood flow in crossing compared with noncrossing staple lines was 6 percent (-5-17 percent) for small bowel anastomoses and 7 percent (-6-19 percent) for colonic anastomoses. An equivalence test showed that, if a reduction in blood flow exists between crossing and noncrossing staple lines, it is most likely less than 30 percent (P less than 0.001) for both small bowel and colonic anastomoses. This experimental study demonstrates that intersecting staple lines in small bowel and colonic anastomoses do not reduce anastomotic blood flow to a dangerous level.

Anastomosis, Surgical↗
PubMed1992

The value of capture-recapture methods even for apparent exhaustive surveys. The need for adjustment for source of ascertainment intersection in attempted complete prevalence studies.

Almost all reported prevalence studies of which we are aware make exhaustive attempts to find diagnosed individuals and report all affected individuals, but make no attempt to estimate or adjust for missing cases. Yet very simple methods introduced in the planning stage of a prevalence study may enable investigators, or at least those subsequently reading their reports, to derive such adjusted estimates. If investigators keep track of the nature of the ascertainment of cases by source and collect and report data that allow calculation of the number of cases by source intersection, then they, or at least others, may derive estimates of missing cases and of the total population affected, by using readily available analogues of capture-recapture methods developed for wildlife populations censuses. Unfortunately, such methods are often inappropriately disparaged or ignored by epidemiologists. The derived estimates are sensitive to assumptions about dependence or independence ("interaction") of various sources, assumptions that sometimes are unprovable, and these estimates have some uncertainty because of statistical fluctuation. Moreover, most investigators who attempt exhaustive prevalence studies apparently believe that they have ascertained all cases and that there is no need to attempt to adjust for, let alone provide data pertinent to, the number of missing cases or to use a statistical method that will at best imply a certain imprecision to their result. Yet a survey that reports prevalence data without adjustment for, or data on, source intersection in essence makes an estimate of missing cases--zero--while providing no quantitative grounds for that claim. The results of all such surveys should be regarded with skepticism because, at best (if the case reports are accurate), they provide only a lower boundary of prevalence. We illustrate the grounds for these views by analyzing data from an apparently exhaustive prevalence study that used at least 14 distinct sources for ascertainment, including advertising, to find cases. Available limited data on source intersection provided in the report enable the plausible inference that the study missed about 25-40% of cases. We urge that no attempted complete prevalence studies be presented without data on ascertainment by source intersection.

Bias↗
PubMed1992

Computer-assisted morphometry: point, intersection, and profile counting and three-dimensional reconstruction.

The use of computers in morphometry can involve 1) automated image analysis, semiautomated image analysis and point, intersection, intercept and profile counts of two-dimensional images on tissue sections with mathematical extrapolation to the third dimension, 2) direct measurement of volumes, surfaces, lengths, and curvature using x,y,z coordinates of serial sectioned images, or 3) stereologic techniques and serial sections which is a combination of 1 and 2 above. Automated and semiautomated image analysis are generally restricted to specimens that are characterized by differential contrast such as interalveolar septa in the lung or histochemically stained mucous granules in pulmonary epithelium. Point, intersection, and profile counts using hand-held, notebook PCs, portable PCs, or standard PCs and MS-DOS-based application programs are extremely efficient, precise, affordable, and convenient methods of quantitating average values of a population. When morphometric measurements of individual structures are required, computer-assisted three-dimensional reconstruction using x,y,z coordinates of the surface outline from serial sections is a tedious yet precise method. We describe a computer program that efficiently estimates mean caliper diameter, volume, and surface area with less than five percent error with five sections per structure. We also describe a program that does digital image subtraction on serial sections, superimposes digitally generated test systems on biological images, and accumulates point, intersection, and profile counts using a Macintosh II series computer.

Animals↗
PubMed1977

Visual extrapolation of a line segment to the point of its intersection with a straight line. I.

A study is made of the capacity of fifty subjects to estimate the position of the point of intersection between a straight line and the visually extrapolated extension of a line segment at three different angles between the line and the segment: 30 degrees, 60 degrees and 90 degrees. The results show systematic deviations in the estimation of acute angles. The point of intersection of the straight line and the segment is misperceived to be shifted inwards in the angle between them. It is also shown that the set of imaginary extensions of a line segment with a given length, until its intersection with the given straight line, is determined only by the angle between the straight line and the segment and does not depend on the distance between them. Various possible mechanisms which could determine the solution of the task facing the subjects are discussed.

Adult↗
PubMed2026

Generation and validation of a Myh11Dre-Spp1Cre intersectional mouse model for lineage tracing of disease-associated smooth muscle cell states.

BACKGROUND: Phenotypic modulation of vascular smooth muscle cells (VSMCs) is a hallmark of vascular remodeling and cardiovascular disease. Recent lineage-tracing and single-cell transcriptomic studies have identified secreted phosphoprotein 1 (SPP1) as a prominent marker associated with disease-associated VSMC states, particularly those linked to fibrotic remodeling and vascular calcification. However, the cellular origins and fate of SPP1-associated VSMC populations remain incompletely understood. METHODS AND RESULTS: We generated a novel Spp1-rSTOPr-Cre (Spp1Cre) knock-in mouse line in which Cre recombinase is expressed from the endogenous Spp1 locus following Dre-mediated excision of a rox-flanked transcriptional STOP cassette. Correct targeting of the knock-in allele was validated by internal, 5' junction, 3' junction, and long-range PCR analyses, as well as Sanger sequencing. To establish an intersectional lineage-tracing strategy, Spp1Cre mice were crossed with Myh11DreERT2 and Rosa26-RSR-LSL-tdTomato-LSL-eGFP reporter mice, enabling permanent labeling of VSMC-derived populations following activation of the endogenous Spp1 locus. Under physiological conditions, eGFP-positive cells were detected at low frequency within the vascular wall and were predominantly negative for the contractile markers ACTA2 and MYH11. As a proof-of-principle application, eGFP-positive cells markedly expanded within atherosclerotic lesions induced by AAV-PCSK9D377Y and high-fat diet feeding. These lineage-traced cells remained largely ACTA2- and MYH11-negative, consistent with a modulated phenotype. Notably, only a minority of eGFP-positive cells expressed SPP1 or fibronectin at the time of analysis, demonstrating the utility of permanent lineage tracing for tracking cells with a history of endogenous Spp1 activation during vascular remodeling. CONCLUSION: We report the generation and validation of a novel Myh11Dre-Spp1Cre intersectional mouse model for lineage tracing of VSMC-derived populations that have activated the endogenous Spp1 locus. This genetic resource provides a valuable platform for investigating the origin, fate, and phenotypic evolution of Spp1-associated VSMC populations during vascular remodeling and cardiovascular disease.

Animals↗
PubMed1977

Visual extrapolation of a line segment to the point of its intersection with a straight line. II.

The article describes three experiments to study visual extrapolation of a line segment to the point of its intersection with a straight line. Eye movements are shown to play no significant role in solving problems involving visual spatial extrapolation. It is also indicated that systematic mislocations of the point of intersection sought in cases of acute angles are preserved even when the motor response is substituted by verbal estimation. When the test line segment is presented for a very short time (tau =20 ms), the estimations of the subjects manifest great individual differences and considerable dispersion. The results of the experiments show that the ability of visual extrapolation is influenced by different and numerous factors and this ability does not reflect only the functioning of simple detectors for direction in the visual system.

Adult↗
PubMed2025

Intersectionality in a sociogenomic world: How do race, disability, socioeconomic status, and polygenic prediction interact to affect perceptions of educational trajectories?

PURPOSE: Education is important for lifelong skills and economic growth; however, student placement decisions may be shaped by social biases. As genomic information captured via polygenic scores becomes more available, it may also inform student placement decisions. We assessed the intersectional effects of polygenic scores, race, disability, and socioeconomic status on US adults' views of educational trajectories using an online experimental survey design. METHODS: A total of 1367 US adults were randomized to one of 16 conditions and prompted to read a short vignette about a boy named Michael, also depicted in an image. Each condition varied Michael's race (Black/White), disability (wheelchair user/no), socioeconomic status (high/low), and polygenic score (high/low) for educational attainment (EA-PGS). After reading the vignette, the respondents were asked to answer multichoice questions about Michael's immediate and long-term educational trajectories. RESULTS: Variation in Michael's EA-PGS strongly influenced participants' expectations regarding (1) the most appropriate immediate educational program for Michael (ie, general, special, or gifted education), (2) whether he would graduate high school, and, if so, (3) the highest educational degree he would complete in his lifetime (associate, bachelor, master, or PhD). Across these responses, high EA-PGS was associated with more socially desirable outcomes, whereas the opposite was true for low EA-PGS. Depicting Michael in a wheelchair significantly influenced respondents' expectations that his most appropriate immediate educational trajectory would be special. There were significant interactions between Michael's race, disability, socioeconomic status, and the EA-PGS. CONCLUSION: Information about children's EA-PGS may affect their views about their immediate and long-term educational trajectories. The negative effects of low EA-PGS were comparable to those of high EA-PGS. The EA-PGS may be interpreted in ways that compound the existing stereotypes related to a child's race, disability, and socioeconomic status.

Humans↗
PubMed2025

Sex differences in the developing human cortex intersect with genetic risk of neurodevelopmental disorders.

Autism is highly heritable and diagnosed more frequently in males than females. To identify neurodevelopmental processes that might present sex-biased vulnerability, we generated transcriptomic and epigenomic profiles of cell types present in the prenatally developing human cerebral cortex of 27 males and 21 females. By intersecting sex-biased molecular signatures and genes with de novo mutations in male and female autistic probands, we reveal two points of vulnerability contributing to the sex-biased penetrance in neurodevelopmental disorders (NDDs). First, we show that NDD risk genes are biased towards higher expression in females, identifying the NDD gene MEF2C as a critical transcription factor for female-biased expression. Second, we identify a significant contribution of X chromosome genes to NDD pathobiology. We construct a gene regulatory map of X-linked risk genes to enable functional studies of genetic variants that likely disrupt gene expression in the developing brains of autistic males. Together, these results point towards an outsized contribution of the X-chromosome to both the origin of sex differences in the developing human cortex and NDD vulnerability. We propose a model where female-biased vulnerability is driven by coding variation within genes while male-biased vulnerability is driven by noncoding variation in regulatory elements that affect gene expression.

Sex differences↗
PubMed1979

Superior vena cava stenosis at site of intersection of two pacing electrodes.

Superior vena cava obstruction is described in a patient with two endocardial pacing electrodes. At necropsy a severe stenosis of the venous lumen was found at the site of intersection of the two catheters. There was no evidence of thrombus formation. Venous wall stenosis is an unusual complication of transvenous pacing and is probably favoured by the presence of two electrodes.

Constriction, Pathologic↗
PubMed2026

Transposon insertion sequencing of Pseudomonas aeruginosa identifies multiple intersecting pathways essential for extreme colistin resistance.

Colistin is used to treat antibiotic resistant gram-negative infections, including those caused by Pseudomonas aeruginosa (Pa). Using a diverse collection of clinical isolates, we identified BWH047, a colistin-resistant isolate with an extremely high minimum inhibitory concentration (MIC, 1280 µg/mL). To characterize the genes conditionally essential for colistin resistance in BWH047, we employed transposon insertion sequencing and identified 20 gene candidates. In-frame deletion validated 75% of the candidates and identified genes in several new pathways that contribute to colistin resistance in Pa, including algU and wapH. We also identified several candidate genes from previously reported colistin resistance pathways (e.g., arn, pmrAB). We further investigated the impact of a colistin resistance-associated inner membrane DedA-family undecaprenyl phosphate flippase, which we named DpcA (DedA of Pseudomonas necessary for colistin resistance A). Deletion of dpcA in BWH047 restored sensitivity to colistin (MIC = 0.5 µg/mL) and resulted in several unique changes to the structure of lipopolysaccharide (LPS), including production of decreased amounts of the colistin resistance-conferring 4-amino-4-deoxy-L-arabinose (L-Ara4N) modification on lipid A. This work represents a robust analysis of colistin resistance in Pa and identifies intersecting pathways that contribute to extreme phenotypic resistance.

Pseudomonas aeruginosa↗
PubMed1992

Hypothesis: can type IX collagen "glue" together intersecting type II fibers in articular cartilage matrix? A proposed mechanism.

Type IX collagen is crosslinked to the surface of type II collagen molecules, and has been proposed as the glue that binds the collagen network of cartilage matrix. However, there is as yet no evidence that the crosslinks that have been described to date provide interfibrillar connections, and the only mechanism proposed for such connections between intersecting fibers is unlikely on stereochemical grounds. We propose that both type IX collagen and an intermediary molecule are necessary for network stabilization and that proteoglycans are likely candidates for the role of intermediary.

Animals↗
PubMed2026

GLP-1 Receptor Agonist and GIP/GLP-1 Receptor Dual Agonist Therapeutics at the Intersection of Alcohol Use Disorder, Obesity, and Cardiometabolic Dysfunction.

The co-occurrence of metabolic dysfunction and heavy alcohol consumption contributes substantially to global morbidity, particularly through its impact on liver disease progression. Glucagon-like peptide-1 receptor (GLP1R) agonists and glucose-dependent insulinotropic polypeptide receptor (GIPR)/GLP1R dual agonists, currently approved for the treatment of diabetes and obesity and under investigation for metabolic dysfunction-associated steatohepatitis, are considered for repurposing to reduce alcohol consumption and stabilize metabolic health in heavy-drinking populations. This review summarizes existing evidence, highlights ongoing research, and outlines key unanswered questions regarding this therapeutic potential and the paradigm shift toward metabolic circuit-based interventions in addiction treatment. The dual-target GIPR/GLP1R approach could fill a critical gap for individuals struggling with both heavy alcohol consumption and metabolic dysfunction.

Alcohol use disorder↗
PubMed1991

Intersection of the complement and immune systems: a signal transduction complex of the B lymphocyte-containing complement receptor type 2 and CD19.

The complement system augments the humoral immune response, possibly by a mechanism that involves the B lymphocyte membrane receptor, CR2, which binds the C3dg fragment of C3 and triggers several B cell responses in vitro. The present study demonstrates that CR2 associates with a complex of membrane proteins that may mediate signal transduction by ligated CR2. Monoclonal antibodies to CR2 immunoprecipitated from digitonin lysates of Raji B lymphoblastoid cells a membrane complex containing CR2, approximately equimolar amounts of CD19, which is a member of the immunoglobulin superfamily, and three unidentified components: p130, p50, and p20. The complex, which was immunoprecipitated also with anti-CD19, could be dissociated by Nonidet P-40, accounting for its absence in previous studies of CR2. Expression of recombinant CR2 and CD19 in K562 erythroleukemia cells led to formation of a complex that contained not only these two proteins but also p130, p50, and p20, and another component, p14. These unidentified components of the CR2/CD19 complex coimmunoprecipitated with CD19 and not with CR2 from singly transfected cells, indicating primary association with the former. CD19 replicated the capacity of CR2 to interact synergistically with mIgM for increasing free intracellular Ca2+, suggesting that the complex mediates this function of CR2. Therefore, CR2 associates directly with CD19 to become a ligand-binding subunit of a pre-existing signal transduction complex of the B cell that may be representative of a family of membrane protein complexes. This interaction between the complement and immune systems differs from that between immunoglobulin and Clq by involving membrane rather than plasma proteins, and by having complement involved in the afferent phase of the immune response.

Antigens, CD↗
PubMed2026

Intersecting experimental evolution and CRISPR screens to identify novel toxin resistance loci.

Understanding toxin resistance in insects is key to appreciate niche adaptations but remains challenging due to its often-polygenic basis. A well-known example is the specialized association of Drosophila sechellia with noni fruit ( Morinda citrifolia ), which is toxic to most other insects, including the closely-related Drosophila simulans and Drosophila melanogaster . Toxicity of noni is due to its high concentration of octanoic acid (OA), but the mechanisms that determine sensitivity or resistance to OA in different species remain poorly understood. Here, we experimentally-evolved D. simulans with increased OA resistance, identifying multiple loci under selection. Cross-referencing these with a genome-wide, OA-resistance CRISPR screen in a D. melanogaster cell line highlighted two proteins: Kraken, a putative detoxification enzyme expressed in digestive and renal tissues, and Alkbh7, a mitochondrial protein linked to fatty acid metabolism. Both genes show elevated expression in D. sechellia and OA-resistant D. simulans . In D. melanogaster , kraken mutants are more OA-sensitive, while Alkbh7 overexpression increased OA resistance. Importantly, mutation of these genes in D. sechellia reduced OA tolerance. Our identification of genes underlying OA resistance in laboratory and natural contexts demonstrates how complementary, cross-species selection approaches can provide insights into complex mechanisms of toxin susceptibility and adaptation; such methods could also have practical applications in the characterization of natural and artificial insecticides.

Journal Article↗
PubMed2025

Interleukin-6 related signaling pathways as the intersection between chronic diseases and sepsis.

Sepsis is associated with immune dysregulated and organ dysfunction due to severe infection. Clinicians aim to restore organ function, rather than prevent diseases that are prone to sepsis, resulting in high mortality and a heavy public health burden. Some chronic diseases can induce sepsis through inflammation cascade reaction and Cytokine Storm (CS). Interleukin (IL)-6, the core of CS, and its related signaling pathways have been considered as contributors to sepsis. Therefore, it is important to study the relationship between IL-6 and its related pathways in sepsis-related chronic diseases. This review generalized the mechanism of sepsis-related chronic diseases via IL-6 related pathways with the purpose to take rational management for these diseases. IL-6 related signaling pathways were sought in Kyoto Encyclopedia of Genes and Genomes (KEGG), and retrieved protein-protein interaction in the Search for Interaction Genes tool (STRING). In PubMed and Google Scholar, the studies were searched out, which correlating to IL-6 related pathways and associating with the pathological process of sepsis. Focused on the interactions of sepsis and IL-6 related pathways, some chronic diseases have been studied for association with sepsis, containing insulin resistance, Alcoholic liver disease (ALD), Alzheimer disease (AD), and atherosclerosis. This article summarized the inflammatory mechanisms of IL-6 cross-talked with other mediators of some chronic diseases in vitro, animal models, and human experiments, leading to the activation of pathways and accelerating the progression of sepsis. The clinicians should be highlight to this kind of diseases and more clinical trials are needed to provide more reliable theoretical basis for health policy formulation.

Humans↗
PubMed2026

Multiomics: the intersection of personalized nutrition in cardiometabolic diseases.

BACKGROUND: Cardiometabolic diseases are among the leading causes of increasing morbidity and mortality worldwide. However, current population-based dietary recommendations do not sufficiently account for biological differences between individuals and therefore do not have the same effect on everyone. The multiomic approach, which incorporates genomic, epigenomic, transcriptomic, proteomic, metabolomic, and microbiome data, facilitates more accurate classification of disease risk and selection of appropriate nutritional interventions by mapping food-disease relationships across different biological layers. METHODS: Through a narrative synthesis of the current literature, we focused on evidence from multiomic studies to assess their ability to guide personalized nutrition strategies based on individual genetic, metabolic, and microbiome characteristics in cardiometabolic diseases. RESULTS: Recent evidence indicates that metabolomic markers have been reported to provide predictive value in addition to classic risk indicators and to increase the predictive power of models when combined with genetic data. Microbiome research shows that glycemic and lipemic responses can be predicted using algorithms based on gut microbiota. Recent clinical studies show that personalized nutrition plans, which evaluate the microbiome and clinical characteristics together, improve continuous glucose monitoring-based glycemic control, glycated hemoglobin levels, and triglycerides more than the classic Mediterranean diet. CONCLUSION: This review summarizes the current multiomic evidence, discusses the methodological and practical challenges in this field, and highlights future priorities. The integration of digital biomarkers obtained from wearable technologies with multiomic systems and artificial intelligence-supported models, when developed in accordance with ethical and equitable access principles, has the potential to support the transition from the discovery phase to patient-centered clinical applications.

Humans↗
PubMed2025

Interconnected study of molecular pathways: miR-137 as a central element at the intersection of lipid metabolism and prostate carcinogenesis.

OBJECTIVE: To evaluate the roles of miR-137 and its target genes in lipid metabolism and prostate tumorigenesis. METHODS: We used a series of bioinformatic approaches to establish the relationship between miR-137 and its target genes. We mapped the metabolic pathways of interest in the Reactome database and identified the central target genes of miR-137 in this pathway using four platforms: Reactome, miRDB, miRmap, and TargetScan. To assess the expression and association with clinical parameters, we obtained information from the UALCAN, OncoDB, and GEPIA2 databases using a dataset of patients with prostate cancer from The Cancer Genome Atlas. For functional enrichment analysis and construction of the protein-protein interaction network, we used the Kyoto Encyclopedia of Genes and Genomes, Gene Ontology, and STRING. RESULTS: Our in silico study of The Cancer Genome Atlas database revealed that miR-137 is underexpressed in tumor tissues, and its reduction is associated with poor prognosis. An intriguing set of eight genes within the PPARα pathway: PPARGC1A, PPARGC1B, NCOA1, NCOA2, NCOA3, MED1, MED27, and ESRRA displayed synergy, positive correlations, and synchronized expression patterns in adipose, hepatic, and prostatic tissues, all linked to the enigmatic processes of metabolic regulation. Among the highlighted genes, ESRRA was overexpressed in the malignant environment, whereas its counterparts remained underexpressed. The plot was thickened with associations between the expression of NCOA1, NCOA3, and MED27, lymph node involvement, and the overexpression of several genes linked to advanced prostate cancer stages. An intriguing pattern emerged, with patients exhibiting reduced disease-free survival overexpressing NCOA2, NCOA3, MED27, and ESRRA. CONCLUSION: This study elucidates the possibility that miR-137 subtly modulates metabolic genes in prostate cancer, suggesting its latent therapeutic potential as a biomarker for disease progression. BACKGROUND: ■ The reduction of miR-137 in tumor tissues is associated with a worse prognosis. BACKGROUND: ■ miR-137 has eight oncogenically relevant target genes acting in the PPARα lipid pathway. BACKGROUND: ■ NCOA1, NCOA3, MED27, and ESRRA are associated with advanced prostate cancer. BACKGROUND: ■ miR-137 exhibits significant clinical potential by repressing the activation of pathways that influence prostate tumorigenesis in hyperstimulated metabolic environments. BACKGROUND: Prostate cancer progression is sustained by the simultaneous activation of pathways involving lipid uptake and de novo synthesis. In this context, miR-137 inhibits adipogenic differentiation and may reduce lipid uptake by tumor cells by modulating the PPAR/ p160/ESRRA axis, considerably attenuating metabolic effects and suppressing prostate tumorigenesis.

Male↗