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PubMedDate not supplied

[Angioimmunoblastic lymphadenopathy: a pathogenetic intersection between dysimmune, viral and lymphomatous diseases].

Angioimmunoblastic lymphadenopathy (AIL) still is a clinico-pathological syndrome with little known physiopathology. The advent of molecular biology has improved our understanding of this syndrome by characterization of the clonal cell. With this technique, combined with cytogenetics and immunohistochemistry, three pathological states have been individualized: 1) true AIL without evidence of monoclonal proliferation; 2) transformed AIL, and 3) AIL-like T-cell lymphoma. This clinical complex can be integrated in an evolutive continuum, starting with simple lymphoid hyperplasia and ending with frank malignant T-cell lymphoma.

Antibodies, Monoclonal↗
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↗
PubMed2026

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

Understanding toxin resistance in insects is key to appreciating 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 other insects, including Drosophila simulans and Drosophila melanogaster. The main noni toxin is octanoic acid (OA), but the mechanisms that determine sensitivity or resistance to OA in different species remain unclear. 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. Mutation of these genes in D. sechellia reduced OA tolerance. Our identification of genes contributing to OA resistance in laboratory and natural contexts demonstrates how complementary selection approaches can provide insights into complex mechanisms of toxin susceptibility and adaptation. Such methods could have practical applications in the characterization of natural and artificial insecticides.

Animals↗
PubMed1975

[Use of scanning electron microscopy for studying the intersection of lymphocytes with tumor cells].

With the aid of steroscan microscopy it was found that the state of surface membranes of the cells under study showed a significant change during the interaction of lymphocytes of BALB/C mice--bearers of methylcholantrene-induced sarcoma--with autologous tumour cells. Lymphocytes separated from the autologous tumour cells by a millipore filter formed long cytoplasmic processes which passed through the filter pores and came into close contact with tumour cells. Tumour cells acquired a spherical shape, and became swollen; "openings" appeared in the surface membrane, and this led to cell lysis.

Animals↗
PubMed1992

[Effect of immunosuppressants FK506 and rapamycin on the function of progesterone receptor: protein "p59-HBI", intersection between immunology and endocrinology?].

In the absence of hormonal ligand, inactive, heterooligomeric, 8-10S steroid receptor complexes include a p59 protein (apparent M(r) approximately 59 kDa) bound to th heat shock protein hsp90 (apparent M(r) approximately 90 kDa), which itself binds to the ligand binding domain LBD of the receptor molecule, p59 is thus an hsp binding immunophilin HBI, which, through its interaction with a chaperone, may intervene in several cellular functions. We report that, in cell-free experiments at 0 degrees C, FK506 and rapamycin do not release p59 nor hsp90 from the 9.5S rabbit uterus progesterone receptor, suggesting that the binding of p59 to hsp90 does not interfere with the rotamase site of HBI. There is no "transformation/activation" of the receptor, but an up to 2 fold increase in progesterone agonist and antagonist binding to the receptor is observed. It is suggested that a functional interaction between HBI and receptor activity may be mediated by hsp90.

Animals↗
PubMed1991

[Dental treatment concepts on a point of intersection].

Dentists appear to plan the treatment of one and the same patient very differently. Each dentist uses both professional and relational concepts, but the differences in treatment plans are in this article just partially explained.

Dental Care↗
PubMedDate not supplied

Attention, the intersection of cost and quality in health care.

A method for assessing health care technology that models the demand on the clinician's attention exerted by patients' data (diagnostic and therapeutic) can provide a means for simultaneously reducing the cost and improving the quality of health care. The attentional demand exerted by patients' data can be measured by the amount of uncertainty in the data. Uncertainty can be expressed mathematically by the concept of entropy in information theory.

Health Services Needs and Demand↗