scholarly journals Skin inflammation driven by differentiation of quiescent tissue-resident ILCs into a spectrum of pathogenic effectors

2018 ◽  
Author(s):  
Piotr Bielecki ◽  
Samantha J. Riesenfeld ◽  
Monika S. Kowalczyk ◽  
Maria C. Amezcua Vesely ◽  
Lina Kroehling ◽  
...  
Keyword(s):  
Steady State ◽  
Latent Dirichlet Allocation ◽  
Cell Lineage ◽  
Skin Inflammation ◽  
Plastic Type ◽  
Disease Induction ◽  
Lineage Mapping ◽  
Type 3

Psoriasis pathology is driven by the type 3 cytokines IL-17 and Il-22, but little is understood about the dynamics that initiate alterations in tissue homeostasis. Here, we use mouse models, single-cell RNA-seq (scRNA-seq), computational inference and cell lineage mapping to show that psoriasis induction reconfigures the functionality of skin-resident ILCs to initiate disease. Tissue-resident ILCs amplified an initial IL-23 trigger and were sufficient, without circulatory ILCs, to drive pathology, indicating that ILC tissue remodeling initiates psoriasis. Skin ILCs expressed type 2 cytokines IL-5 and IL-13 in steady state, but were epigenetically poised to become ILC3-like cells. ScRNA-seq profiles of ILCs from psoriatic and naïve skin of wild type (WT) and Rag1-/- mice form a dense continuum, consistent with this model of fluid ILC states. We inferred biological “topics” underlying these states and their relative importance in each cell with a generative model of latent Dirichlet allocation, showing that ILCs from untreated skin span a spectrum of states, including a naïve/quiescent-like state and one expressing the Cd74 and Il13 but little Il5. Upon disease induction, this spectrum shifts, giving rise to a greater proportion of classical Il5- and Il13- expressing “ILC2s” and a new, mixed ILC2/ILC3-like subset, expressing Il13, Il17, and Il22. Using these key topics, we related the cells through transitions, revealing a quiescence-ILC2-ILC3s state trajectory. We demonstrated this plasticity in vivo, combining an IL-5 fate mouse with IL-17A and IL-22 reporters, validating the transition of IL-5–producing ILC2s to IL-22– and IL-17A–producing cells during disease initiation. Thus, steady-state skin ILCs are actively repressed and cued for a plastic, type 2 response, which, upon induction, morphs into a type 3 response that drives psoriasis. This suggests a general model where specific immune activities are primed in healthy tissue, dynamically adapt to provocations, and left unchecked, drive pathological remodeling.

scholarly journals Functional characterization of thousands of type 2 diabetes-associated and chromatin-modulating variants under steady state and endoplasmic reticulum stress

2020 ◽  
Author(s):  
Shubham Khetan ◽  
Susan Kales ◽  
Romy Kursawe ◽  
Alexandria Jillette ◽  
Steven K. Reilly ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Endoplasmic Reticulum ◽  
Steady State ◽  
Er Stress ◽  
Transcriptional Activity ◽  
Chromatin Accessibility ◽  
Stress Conditions ◽  
Gwas Snps

AbstractA major goal in functional genomics and complex disease genetics is to identify functional cis-regulatory elements (CREs) and single nucleotide polymorphisms (SNPs) altering CRE activity in disease-relevant cell types and environmental conditions. We tested >13,000 sequences containing each allele of 6,628 SNPs associated with altered in vivo chromatin accessibility in human islets and/or type 2 diabetes risk (T2D GWAS SNPs) for transcriptional activity in ß cell under steady state and endoplasmic reticulum (ER) stress conditions using the massively parallel reporter assay (MPRA). Approximately 30% (n=1,983) of putative CREs were active in at least one condition. SNP allelic effects on in vitro MPRA activity strongly correlated with their effects on in vivo islet chromatin accessibility (Pearson r=0.52), i.e., alleles associated with increased chromatin accessibility exhibited higher MPRA activity. Importantly, MPRA identified 220/2500 T2D GWAS SNPs, representing 104 distinct association signals, that significantly altered transcriptional activity in ß cells. This study has thus identified functional ß cell transcription-activating sequences with in vivo relevance, uncovered regulatory features that modulate transcriptional activity in ß cells under steady state and ER stress conditions, and substantially expanded the set of putative functional variants that modulate transcriptional activity in ß cells from thousands of genetically-linked T2D GWAS SNPs.

New Fine Structure within the Adult Hematopoietic Stem Cell Compartment Revealed by Longterm Analysis of Mice Repopulated with Single Cells or Their In Vitro Generated Clonal Progeny.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1720-1720
Author(s):  
Brad Dykstra ◽  
David Kent ◽  
Lindsay McCaffrey ◽  
Kristin Lyons ◽  
Merete Kristiansen ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Single Cells ◽  
Myeloid Cells ◽  
Hematopoietic Stem ◽  
Type 3

Abstract Assessments of hematopoietic stem cell (HSC) repopulating activity in vivo have historically relied on calculated average longterm (12–16 wk) progeny outputs using non-purified transplants, thereby precluding definitive clonal assignments of donor-derived cells. Viral marking circumvents this problem, but has not been used for large scale surveys. Heterogeneity observed in the repopulation patterns has generally been inferred to reflect stochastic processes. We now report the in vivo repopulation kinetics of 89 individual longterm repopulating cells (LTRCs) before (n=49) and after (n=40) 4 days of clonal growth in vitro. LTRCs were defined here as cells whose WBC progeny could be detected at levels of ≥1% for at least 16 wk in sublethally irradiated Ly5-congenic W41/W41 hosts. Recipients were transplanted with either freshly isolated, single lin−Rho−SP LTRCs or 4-day clones generated from similar cells in serum-free cultures (+ 300 ng/ml SF, 20 ng/ml IL-11 & 1ng/ml Flt3-L). 4, 8, 12, 16, and 24 wk post-transplant, blood samples were stained for donor-derived B, T, and myeloid cells using a procedure that identifies donor/recipient doublets and Ly6g/Mac1low cells (which have features of lymphoid rather than myeloid WBCs) to exclude false-positive myeloid events. Four distinct patterns of repopulation were revealed. Type 1 showed a delayed production of predominantly myeloid WBCs (low or undetectable before 12 wk) that increased progressively (reaching 0.4–15% of all WBCs by 16 wk). Type 2 showed a robust multilineage repopulation that remained stable or increased over time (6–84% of all WBCs at 16 wk). Type 3 also showed an initially robust pattern of multilineage repopulation (peak numbers of WBCs at 8–12 wk and 1–51% at 16 wk), but the contribution of donor-derived myeloid cells was transient (<0.5% by 16 wk). Type 4 showed a lymphoid-restricted pattern (myeloid contribution <0.5% at all time points), with repopulation levels peaking at 8 wk and decreasing thereafter (1–22% at 16 wk). Persisting granulopoiesis, indicated by a high proportion of donor-derived cells in the Ly6g/Mac1+SSChi population at 16–24 wk, clearly distinguished the type 1 and 2 patterns from types 3 and 4 which showed near or complete cessation of donor-derived granulopoiesis beyond 12 wk. Preliminary secondary transplant experiments show that donor-derived LTRCs (with and without longterm granulopoietic activity) were exclusively generated in primary recipients with type 1 and 2 repopulation patterns. Amongst the freshly isolated LTRCs, 18% (9/49) were type 1, 41% (20/49) were type 2, 22% (11/49) were type 3, and 18% (9/49) were type 4. In contrast, 4-day clones derived from cells of the same phenotype and containing LTRC activity showed a marked decrease in type 1 and type 2 activity with a corresponding increase in type 3 and type 4 activity: type 1 = 5% (2/41), type 2 = 18% (7/40), type 3 = 28% (11/40) and type 4 = 50% (20/40). Collectively, these data identify a new hierarchy of four biologically discrete states within the compartment of cells currently defined as LTRCs. Proliferation of LTRCs either in vitro or in vivo appears to induce an irreversible transition from one state to another (from Type 1 to 2 to 3 to 4), suggesting the existence of intrinsic molecular correlates for each of these states and specific mechanisms that underlie their sequential appearance.

Daratumumab, a Novel Therapeutic Human CD38 Monoclonal Antibody, Induces Killing of Refractory Patient-Derived Multiple Myeloma Cells, Growing in a Novel Humanized Mouse MM Model

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 940-940
Author(s):  
Willy A Noort ◽  
Richard W.J. Groen ◽  
Reinier Raymakers ◽  
Linda Aalders ◽  
Frans M Hofhuis ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Tumor Cells ◽  
Research Funding ◽  
Humanized Mouse ◽  
Myeloma Cells ◽  
Tumor Load ◽  
Type 3

Abstract Abstract 940 The evolution of multiple myeloma (MM) is a multi-step process during which mature B cells acquire genetic mutations in multiple genes, which typically takes place in the bone marrow (BM) microenvironment. This, together with the difficulty to culture MM in vitro or to grow MM in vivo in animal models has been the main reason during past decades for poor progress in preclinical research with patient-derived myeloma (pMM) cells. Recently, we developed a unique human-mouse hybrid model that allows engraftment and outgrowth of pMM cells by implementing a technology that is based on first generating a human bone environment in immune deficient mice (Groen et al. 2012) and that is subsequently capable of supporting growth of injected pMM cells. The model offers the opportunity (1) to study the pathobiology of myeloma, and (2) to evaluate, preclinically, new therapeutics for MM treatment, including antibody testing against pMM cells, obtained from patients who acquired resistance to conventional and novel drugs. Daratumumab (DARA) is a human CD38 antibody with broad-spectrum killing activity. Daratumumab induces effective killing of MM tumor cells via complement dependent cytolysis (CDC), ADCC (antibody dependent cellular cytolysis) and ADCP (antibody-dependent phagocytosis). DARA represents a novel promising treatment for MM and other hematological malignancies and is currently tested in Phase I/II clinical trials. In these clinical studies the adverse events have been manageable and marked reductions in paraprotein and bone marrow plasma cells have been observed. In the current study, we asked whether DARA was able to inhibit growth of refractory tumor cells in our human-mouse hybrid model. To this end, immune-deficient RAG2−/−gc−/−-mice were implanted subcutaneously with biphasic calcium phosphate (BCP) particles (2–3 mm) loaded with culture expanded human mesenchymal stromal cells (MSCs). Eight weeks later, the humanized scaffolds in mice (n=45) were injected with 0.5–5×106 pMM cells obtained from different refractory, MM patients. The pMM cells were gene-marked with a GFP-luciferase lentiviral construct for imaging of viable tumor cells. Bioluminescent imaging (BLI) was used to follow myeloma outgrowth in time and to visualize the effect of treatment. The pMM cells were obtained from patients at diagnosis (type 1); at end stage disease, after a history of MPT (melphalan, prednisone, thalidomide, type 2); or from a patient refractory to chemotherapy with bortezomib (BORT), adriamycine and dexamethasone (DEX) (type 3). Mice carrying the pMM cells received similar treatment as the patients or were treated with DARA in a dose range of 1x 50 μg (low dose (LD)) or 2 to 3x 200 μg/mouse (high dose (HD)). BLI showed that the type 1 pMM-bearing mice responded well to all treatments, including DARA; type 2-bearing pMM mice showed no reduction in tumor growth after chemotherapy, but DARA treatment (LD) resulted in an almost complete elimination of circulating MM cells, as assessed with a CD138 antibody, in blood and BM. In a second experiment, type 2-pMM bearing mice were treated with a high DARA dose early (day 34, 50 and 72, 3 times HD, tumor size/BLI signal <200 cmp/cm2) or late (day 50 and 72, 2 times HD, tumor size/BLI signal >8000 cpm/cm2). A significant reduction of overall tumor load, as measured with BLI was observed, which interestingly did not differ between the high and low tumor load group. A reduction of circulating tumor cells (CD138+) was observed for both conditions, which was most obvious in the early treated mice and in agreement with the observations in the first experiment. Type 3 (resistant) pMM-bearing mice showed only a minor response to DEX and BORT, but were highly sensitive to melphalan. When DEX- and BORT-treated mice were treated with a single injection of DARA, this resulted in a complete remission in 3 out of 4 mice and a reduction of the tumor load by 50% in the fourth BORT-treated mouse. In conclusion, our results demonstrate that DARA is effective against multiple myeloma cells derived from therapy- naïve or -refractory patients grafted in a humanized mouse model. In addition, this humanized MM model can be used to study the potential and mechanism of action of DARA in vivo. This novel MM model might be used to predict responsiveness of myeloma patients to particular treatments. Disclosures: Groen: Genmab BV: Research Funding. Raymakers:Novartis: Consultancy. Lammerts van Bueren:Genmab BV: Employment. Parren:genmab: Employment. Mutis:genmab: Research Funding. Martens:Genmab BV: Research Funding.

scholarly journals The use of SGLT2 inhibitors in achieving glycaemic control in maturity-onset diabetes of the young type 3

2021 ◽  
Vol 2021 ◽  
Author(s):  
Arunan Sriravindrarajah ◽  
Amelia Fernandes ◽  
Ted Wu ◽  
Samantha Hocking
Keyword(s):  
Glycaemic Control ◽  
Sglt2 Inhibitor ◽  
Sglt2 Inhibitors ◽  
List Type ◽  
Maturity Onset Diabetes ◽  
Rapid Improvement ◽  
Onset Diabetes ◽  
Type 3

Summary Maturity-onset diabetes of the young type 3 (MODY3) accounts for approximately 50% of cases of MODY. First-line treatment with sulfonylureas has been well established for individuals with MODY3. In contrast, the use of sodium-glucose co-transporter 2 (SGLT2) inhibitors in the treatment of individuals with MODY3 remains unclear. This case illustrates the in vivo effect of an SGLT2 inhibitor in a 30-year-old woman with MODY3 with poor glycaemic control despite the treatment with supramaximal doses of sulfonylurea and metformin. The addition of a SGLT2 inhibitor resulted in a rapid improvement in glycaemic control without any hypoglycaemic episodes. This case suggests that SGLT2 inhibitors may be an effective and potent treatment option in addition to sulfonylureas for individuals with MODY3. Learning points Maturity-onset diabetes of the young type 3 (MODY3) arises from mutations in the hepatocyte nuclear factor-1alpha gene, which controls the expression of sodium-glucose co-transporter 2 (SGLT2) in the kidneys. Paradoxically, despite individuals with MODY3 having reduced expression of SGLT2, SGLT2 inhibitors induce higher glycosuria in individuals with MODY3 compared to individuals with type 2 diabetes mellitus. SGLT2 inhibitors may be an effective treatment for achieving glycaemic control in individuals with MODY3.

scholarly journals A mathematical model of rat ascending Henle limb. III. Tubular function

2010 ◽  
Vol 298 (3) ◽  
pp. F543-F556 ◽  
Author(s):  
Alan M. Weinstein
Keyword(s):  
Mathematical Model ◽  
Tubular Function ◽  
Proton Secretion ◽  
Luminal Membrane ◽  
Catalytic Role ◽  
Type 3

K+ plays a catalytic role in AHL Na+ reabsorption via Na+-K+-2Cl− cotransporter (NKCC2), recycling across luminal K+ channels, so that luminal K+ is not depleted. Based on models of the ascending Henle limb (AHL) epithelium, it has been hypothesized that NH4+ may also catalyze luminal Na+ uptake. This hypothesis requires that luminal NH4+ not be depleted, implying replenishment via either direct secretion of NH4+, or NH3 in parallel with a proton. In the present work, epithelial models of rat medullary and cortical AHL (Weinstein AM, Krahn TA. Am J Physiol Renal Physiol 298: F000–F000, 2009) are configured as tubules and examined in simulations of function in vitro and in vivo to assess the feasibility of a catalytic role for NH4+ in Na+ reabsorption. Modulation of Na+ transport is also examined by peritubular K+ concentration and by Bartter-type transport defects in NKCC2 (type 1), in luminal membrane K+ channels (type 2), and in peritubular Cl− channels (type 3). It is found that a catalytic role for NH4+, which is significant in magnitude (relative to K+), is quantitatively realistic, in terms of uptake via NKCC2, and in terms of luminal membrane ammonia backflux. Simulation of a 90% NKCC2 defect is predicted to double distal Na+ delivery; it is also predicted to increase distal acid delivery (principally as NH4+). With doubling of medullary K+, the model predicts a 30% increase in distal Na+ delivery, but in this case there is a decrease in AHL acidification. This effect of peritubular K+ on proton secretion appears to be akin to type 3 Bartter's pathophysiology, in which there is decreased peritubular HCO3− exit, cytosolic alkalinization, and a consequent decrease in luminal proton secretion by NHE3. One consequence of overlapping and redundant roles for K+ and NH4+, is a blunted impact of luminal membrane K+ permeability on overall Na+ reabsorption, so that type 2 Bartter pathophysiology is not well captured by the model.

Subclassified Acutely Dissociated Cells of Rat DRG: Histochemistry and Patterns of Capsaicin-, Proton-, and ATP-Activated Currents

2000 ◽  
Vol 84 (5) ◽  
pp. 2365-2379 ◽  
Author(s):  
Jeffrey C. Petruska ◽  
Jintana Napaporn ◽  
Richard D. Johnson ◽  
Jianguo G. Gu ◽  
Brian Y. Cooper
Keyword(s):  
Cell Types ◽  
Long Duration ◽  
Calcitonin Gene ◽  
Dissociated Cells ◽  
Type 3 ◽  
Current Signatures ◽  
Current Signature

We used a “current signature” method to subclassify acutely dissociated dorsal root ganglion (DRG) cells into nine subgroups. Cells subclassified by current signature had uniform properties. The type 1 cell had moderate capsaicin sensitivity (25.9 pA/pF), powerful, slowly desensitizing (τ = 2,300 ms), ATP-activated current (13.3 pA/pF), and small nondesensitizing responses to acidic solutions (5.6 pA/pF). Type 1 cells expressed calcitonin gene–related peptide immunoreactivity (CGRP-IR), manifested a wide action potential (7.3 ms), long duration afterhyperpolarization (57.0 ms), and were IB4 positive. The type 2 cell exhibited large capsaicin activated currents (134.9 pA/pF) but weak nondesensitizing responses to protons (15.3 pA/pF). Currents activated by ATP and αβ-m-ATP (51.7 and 44.6 pA/pF, respectively) had fast desensitization kinetics (τ = 214 ms) that were distinct from all other cell types. Type 2 cells were IB4 positive but did not contain either substance P (SP) or CGRP-IR. Similar to capsaicin-sensitive nociceptors in vivo, the afterhyperpolarization of the type 2 cell was prolonged (54.7 ms). The type 3 cell expressed, amiloride-sensitive, rapidly desensitizing (τ = 683 ms) proton-activated currents (127.0 pA/pF), and was insensitive to ATP or capsaicin. The type 3 cell was IB4 negative and contained neither CGRP nor SP-IR. The afterhyperpolarization (17.5 ms) suggested nonnociceptive function. The type 4 cell had powerful ATP-activated currents (17.4 pA/pF) with slow desensitization kinetics (τ = 2,813 ms). The afterhyperpolarization was prolonged (46.5 ms), suggesting that this cell type might belong to a capsaicin-insensitive nociceptor population. The type 4 cell did not contain peptides. The type 7 cell manifested amiloride-sensitive, proton-activated currents (45.8 pA/pF) with very fast desensitization kinetics (τ = 255 ms) and was further distinct from the type 3 cell by virtue of a nondesensitizing amiloride-insensitive component (6.0 pA/pF). Capsaicin and ATP sensitivity were relatively weak (4.3 and 2.9 pA/pF, respectively). Type 7 cells were IB4 positive and contained both SP and CGRP-IR. They exhibited an exceptionally long afterhyperpolarization (110 ms) that was suggestive of a silent (mechanically insensitive) nociceptor. We concluded that presorting of DRG cells by current signatures separated them into internally homogenous subpopulations that were distinct from other subclassified cell types.

scholarly journals DC mobilization from the skin requires docking to immobilized CCL21 on lymphatic endothelium and intralymphatic crawling

2011 ◽  
Vol 208 (10) ◽  
pp. 2141-2153 ◽  
Author(s):  
Orna Tal ◽  
Hwee Ying Lim ◽  
Irina Gurevich ◽  
Idan Milo ◽  
Zohar Shipony ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Steady State ◽  
Skin Inflammation ◽  
Collagen Iv ◽  
Lymph Flow ◽  
Lymphatic Endothelium ◽  
Wild Type ◽  
Random Migration ◽  
And Migration

Dendritic cells (DCs) must travel through lymphatics to carry skin antigens into lymph nodes. The processes controlling their mobilization and migration have not been completely delineated. We studied how DCs in live mice respond to skin inflammation, transmigrate through lymphatic endothelium, and propagate in initial lymphatics. At steady state, dermal DCs remain sessile along blood vessels. Inflammation mobilizes them, accelerating their interstitial motility 2.5-fold. CCR7-deficient BMDCs crawl as fast as wild-type DCs but less persistently. We observed discrete depositions of CCL21 complexed with collagen-IV on the basement membrane of initial lymphatics. Activated DCs move directionally toward lymphatics, contact CCL21 puncta, and migrate through portals into the lumen. CCR7-deficient DCs arrive at lymphatics through random migration but fail to dock and transmigrate. Once inside vessels, wild-type DCs use lamellipodia to crawl along lymphatic endothelium and, sensing lymph flow, proceed downstream. DCs start drifting freely only in collecting lymphatics. These results demonstrate in vivo that the CCL21–CCR7 axis plays a dual role in DC mobilization: promoting both chemotaxis and arrest of DCs on lymphatic endothelium. Intralymphatic crawling, in which DCs combine active adhesion-based migration and directional cues from lymph flow, represents a new step in DC mobilization which may be amenable to regulation.

scholarly journals The transcription factor Bcl11b is specifically expressed in group 2 innate lymphoid cells and is essential for their development

2015 ◽  
Vol 212 (6) ◽  
pp. 865-874 ◽  
Author(s):  
Yong Yu ◽  
Cui Wang ◽  
Simon Clare ◽  
Juexuan Wang ◽  
Song-Choon Lee ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Lineage ◽  
Influenza Virus Infection ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Effector Cytokines ◽  
Group 2

Group 2 innate lymphoid cells (ILCs), or ILC2s, are a subset of recently identified ILCs, which play important roles in innate immunity by producing type 2 effector cytokines. Several transcription factors have been found to have critical functions in the development of both ILC2s and T cells. We report here that Bcl11b, a transcription factor essential in T cell lineage commitment and maintenance, is specifically expressed in progenitors committed to the ILC2 lineage and is required for ILC2 development. The Bcl11b gene is expressed in ∼28% of ILC progenitors (ILCPs; common helper innate lymphoid progenitors or ILCPs expressing either ID2 or promyelocytic leukemia zinc finger, respectively). Both in vitro and in vivo, these Bcl11b-expressing early ILCPs generate only ILC2s. Inactivation of Bcl11b causes a complete loss of ILC2 development from hematopoietic progenitors, which is confirmed upon immune challenge with either papain administration or influenza virus infection.

FUNCTIONAL STATUS AND ADAPTIVE POTENTIAL IN FOREIGN STUDENTS WITH DIFFERENT TYPES OF VEGETATIVE REGULATION DURING TUITION

2020 ◽  
pp. 118-126
Author(s):  
A.M. Satarkulova
Keyword(s):  
Heart Rate ◽  
Foreign Students ◽  
Autonomic Regulation ◽  
The Body ◽  
Functional Changes ◽  
Different Types ◽  
Type 3 ◽  
Adaptive Abilities

The assessment and dynamic control over students’ status is a very important task. It allows timely detection of prenosological status prior to pathology and health maintenance in students. The objective of the paper is to assess the adaptive abilities of the body, to analyze changes in heart rate variability indicators in students with various types of autonomic regulation, to identify prenosological status and precursory pathological symptoms. Materials and Methods. The study enrolled 302 students from India, aged 21.54±1.43. Programming complex «Psychophysiologist» was used to register the main HRV parameters within 5 minutes. Health status was evaluated according to the index of functional changes and the scale of functional states. Results. N.I. Shlyk (2009) distinguished two groups of students with different types of autonomic regulation: type 1 (53 %) with moderate and type 2 (5 %) with marked characteristics of central regulation profile, type 3 (35 %) with moderate and type 4 (7 %) with marked characteristics of autonomous regulation profile. Main parameters of HRV and adaptation potential were defined for each student.All the parameters characterized functional and health status. Conclusions. It was shown that 82 % of trial subjects (type 1), 53 % (type 2), 94 % (type 3) and 95 % (type 4) demonstrated satisfactory adaptation and their physiological processes were at an optimal level. 18 % of students (type 1) demonstrated reduced adaptive abilities of the body. Moreover, they were under moderate stress. 47 % of subjects (type 2) were also under a significant stress, which was proven by excessively high SI, low SDNN and TP, and an increased index of functional changes. 5 % of students (type 4) revealed dysfunctional characteristics in the heart rhythm, peculiar to pathology. Keywords: foreign students, heart rate variability, types of autonomic regulation, adaptation potential, functional status. Оценка состояния студентов и динамический контроль за ним является важной задачей, поскольку позволяет своевременно выявлять у студентов донозологические состояния, предшествующие патологии, и способствовать сохранению здоровья. Цель. Оценка адаптивных возможностей организма, анализ изменений показателей вариабельности сердечного ритма у студентов с различными типами вегетативной регуляции, выявление донозологических состояний и ранних признаков патологии. Материалы и методы. В исследовании участвовало 302 студента в возрасте 21,54+1,43 года из Индии. Регистрировались основные параметры ВСР в течение 5 мин с использованием программно-аппаратного комплекса «Психофизиолог». Состояние и уровень здоровья оценивались по индексу функциональных изменений и шкале функциональных состояний. Результаты. По способу, предложенному Н.И. Шлык, выделены группы студентов с различными типами вегетативной регуляции: I (53 %) и II типы (5 %) – с умеренным и выраженным преобладанием центрального контура регуляции соответственно, III (35 %) и IV типы (7 %) – с умеренным и выраженным преобладанием автономного контура регуляции соответственно. У каждого из студентов определены основные параметры ВСР и адаптационного потенциала, характеризующие функциональное состояние и уровень здоровья. Выводы. Показано, что для 82 % обследуемых с I типом, 53 % со II типом, 94 % c III типом и 95 % с IV типом регуляции характерно состояние удовлетворительной адаптации, физиологические процессы сохраняются на оптимальном уровне. В группе студентов I типа у 18 % студентов адаптивные возможности организма снижены, выявлено состояние умеренного напряжения. У 47 % обследуемых II типа также зафиксировано состояние резко выраженного напряжения, индикатором которого является чрезмерно высокое значение SI, низкие величины SDNN и ТP, повышенное значение индекса функциональных изменений. В группе студентов с IV типом у 5 % учащихсяв регуляции ритма сердца выявлены дисфункциональные признаки, характерные для патологии. Ключевые слова: иностранные студенты, вариабельность сердечного ритма, типы вегетативной регуляции, адаптационный потенциал, функциональное состояние.

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