24 research outputs found
Emotional Intelligence as a Factor in Adolescent Hardiness
The article discusses the possibilities of developing emotional intelligence among teachers in order to increase the hardiness of children and adolescents.Π ΡΡΠ°ΡΡΠ΅ ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°ΡΡΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠΌΠΎΡΠΈΠΎΠ½Π°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΈΠ½ΡΠ΅Π»Π»Π΅ΠΊΡΠ° Ρ ΠΏΠ΅Π΄Π°Π³ΠΎΠ³ΠΎΠ² Ρ ΡΠ΅Π»ΡΡ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠΈ ΠΆΠΈΠ·Π½Π΅ΡΡΠΎΠΉΠΊΠΎΡΡΠΈ Π΄Π΅ΡΠ΅ΠΉ ΠΈ ΠΏΠΎΠ΄ΡΠΎΡΡΠΊΠΎΠ²
Dynamics of the chemokine ENA-78/CXCL5 levels in blood serum and skin exudate in patients with atopic dermatitis
Currently, there are only scarce data on dynamics of biologically active substances in the lesions associated with atopic dermatitis. Persistence of microorganisms in atopic dermatitis is high on the skin surface. However, pathophysiological significance of ENA-78/CXCL5 for development of atopic dermatitis was not studied so far. The ENA-78/CXCL5 is known to be produced by endotheliocytes, keratinocytes, eosinophils, fibroblasts to activate neutrophil migration, especially under the influence of LPS-containing microorganisms. The aim of this study was to evaluate the dynamics of ENA-78/CXCL5 chemokine levels in blood serum and skin exudates in the patients with atopic dermatitis, as well as to determine pathophysiological role of the chemokine in pathogenesis of dermatosis. 80 patients with limited and widespread forms of atopic dermatitis and 15 volunteers were under observation. The dynamics of ENA-78/CXCL5 levels was studied in blood sera and skin exudates. Blood samples for the study were drawn at the time periods of exacerbation and remission. Skin exudates were taken from the patients during the exacerbation period using disposable insulin syringes and 20-G disposable needles. In healthy volunteers, the skin exudate was obtained by the βskin windowβ technique as described by V.V. Klimov and coauthors βA method for assessing minimal inflammatory activity of skin in atopic dermatitis in remissionβ. The cell analysis was conducted by flow cytofluorimetry using the LEGEND plex TM Human Proinflammatory Chemokine Panel (USA) according to the manufacturerβs protocol. Serum concentrations of chemokine ENA-78/CXCL5 in adolescents with atopic dermatitis, exceeded the range for healthy volunteers. During remission of dermatitis, the chemokine level did not reach the indices in the control group. In adults, the ENA-78/CXCL5 concentration, both at the onset of symptoms and upon their resolution, was below the control levels. Maximal concentrations of ENA-78/CXCL5 chemokine were detected in the skin exudates. As based on our data on the dynamics of ENA-78/CXCL5 chemokine levels, it could be assumed that this substance may represent a sufficient link in pathogenesis of atopic dermatitis, by causing migration of neutrophils and monocytes to the affected area. The ENA-78/CXCL5 chemokine may be a marker of microbial pathogenesis and cellular damage in atopic dermatitis
Time course of autoantibodies to collagen type I and III in blood serum and skin exudate in atopic dermatitis
In accordance with Clinical Guidelines of the Russian Society of Dermatovenerologists and Cosmetologists, atopic dermatitis is a chronic allergic genetically determined dermatosis of a multifactorial nature. There are, however, some aspects that challenge the allergic nature of dermatosis. For example, according to literature data, not all the patients have increased synthesis of immunoglobulin E, some of them are torpid to antihistamine treatment, and, when examining the skin of some patients with atopic dermatitis, an absolute polymorphism of rashes is revealed, thus being not typical to the reagin-type allergic reactions. According to modern data, autoimmune theory is assumed for the mechanisms of atopic dermatitis. However, objective proofs of this theory have not been presented, thus drawing our attention to the studies of this issue. The aim of this study was to identify autoimmune pathogenetic mechanisms of atopic dermatitis. The study included 40 adolescents and 40 adult patients with limited and extended forms of atopic dermatitis. The patients were evaluated during the period of exacerbation and remission of the disease. Blood and skin exudates samples were taken from all the patients. The control group consisted of 30 practically healthy volunteers in whom skin exudate was obtained by the βskin windowβ technique as proposed by Klimov V.V. et al. βA method for assessing minimal inflammatory activity of skin in atopic dermatitis in remissionβ. Concentrations of IgG autoantibodies to collagen types I and III were determined in blood serum and skin exudate samples applying ELISA techniques with ready-made panels AEA571Hu ELISA Kit for Anti-Collagen Type I Antibody (USA), AEA176Hu ELISA Kit for Anti-Collagen Type III Antibody (USA), according to the manufacturerβs protocols. For the first time, the contents of autoantibodies to skin collagen types I and III in the patients with atopic dermatitis we studied in parallel, i.e., at systemic level and in affected skin. If compared to the group of healthy volunteers, the concentration of autoantibodies to collagen types I and III was found to be increased in all the patients with atopic dermatitis, both during exacerbation and in remission of the disease. The maximal values of autoantibodies to collagen types I and III were recorded in blood serum upon development of clinical symptoms of dermatosis, along with low contents of these antibodies detectable in their skin exudates. Permanently high concentrations of autoantibodies to collagen types I and III in blood serum at exacerbation and remission of atopic dermatitis, and their low level in their skin exudate suggest emergence of circulating and precipitating immune complexes, thus allowing us to consider atopic dermatitis as an autoimmune process
Functional activity of the oral endothelium in persons, with chronic periodontitis during treatment with plasmolifting
Chronic periodontitis as an osteoimmune disease of the oral cavity is accompanied by a change in the functional activity of endotheliocytes. Moreover, abnormal vascularization exacerbates periodontal inflammation, as it promotes the transmigration of a larger number of immunocompetent cells, the influx of inflammatory mediators and cytokines.The aim of our work was to study the functional activity of the endothelium of the vessels of the oral cavity in persons suffering from chronic periodontitis in the treatment of plasmolifting.Materials and methods. Under observation were 30 patients diagnosed with chronic generalized periodontitis of moderate severity at the age of 35 (32.50; 40.00) years, with no severe somatic pathology (main group). The comparison group included 20 people aged 38 (34.00; 45.00) years with no inflammatory diseases in the oral cavity. All patients underwent local anti-inflammatory therapy and sanitation of periodontal pockets, correction of occlusal contacts, curettage, plasma lifting. Oral fluid concentration of soluble adhesion molecules ICAM-1 and VCAM-1, endothelin-1, qualitative and quantitative composition of microflora were determined.Results. After the treatment with plasmolifting, a noticeable relief of the activity of the inflammatory process was observed. In patients with chronic periodontitis, Porphyromonas gingivalis was found in 100 % of cases in a titer of 5.73 (4.9; 6.7) lg (gEq/sample), in 62.5 % β Prevotella intermedia in a titer of 4.5 (3.0; 5.5) lg (gEq/sample). Against the background of therapy, decrease of the occurrence of the microorganism and of the number of microorganisms was observed. The concentration of the soluble form of VCAM-1 in the oral fluid of patients with chronic periodontitis exceeded the values of the control group by 38.3 times (p = 0.000001), and ICAM-1 β by 18.1 times (p = 0.00001). Against the background of plasmolifting therapy, the level of the studied substances decreased, but exceeded the control values by 25.2 and 6.4 times, respectively. The content of endothelin in the oral fluid in patients with periodontitis exceeded the values of healthy individuals by 40.7 % (p = 0.003), during therapy its values decreased, but did not reach the level of healthy volunteers (p = 0.04)
Pathophysiological role of chemokine MIG/CXCL9 in the development of atopic dermatitis
Background. In patients with atopic dermatitis, the persistence of microorganisms on the skin surface is high, which can enhance the expression of MIG/CXCL9, exacerbating inflammation and activating keratinocyte apoptosis, however, the dynamics of this chemokine in atopic dermatitis has not been studied.The aim. To study the concentration of chemokine MIG/CXCL9 in the dynamics of atopic dermatitis and determine its role in the pathogenesis of dermatosis.Materials and methods. The study included 80 patients aged 13 to 44 years with limited and widespread atopic dermatitis and 30 practically healthy volunteers. The therapy of patients, the collection of biological material were carried out in the Regional Dermatovenerologic Dispensary in Chita, laboratory tests were performed at the Chita State Medical Academy in the period from 2018 to 2020. The MIG/CXCL9 level was studied during exacerbation and remission of the disease in blood serum and skin exudate by flow cytofluorimetry using LEGENDplex Human Proinflammatory Chemokine Panel (BioLegend, USA). In healthy volunteers, skin exudate sampling was carried out by the βskin windowβ method. For statistical processing, the Microsoft Excel (Microsoft Corp., USA) application software package and SPSS Statistics 25.0 (IBM Corp., USA) were used.Results. The concentration of chemokine MIG/CXCL9 in the skin exudate is greater than in the blood serum. With a limited form of the disease in adolescents, the level of MIG/CXCL9 in the skin exudate is 8.1 times higher than the control values, with a common form β 9.3 times. In adults with advanced atopic dermatitis, the concentration of chemokine IL/CXCL9 in the skin exudate is 20.8 times higher than the values of the control group.Conclusion. In atopic dermatitis, the level of chemokine MIG/CXCL9 is higher in the cutaneous pathological process. In the pathogenesis of the disease, MIG/ CXCL9 inhibits collagen synthesis and promotes apoptosis of keratinocytes, followed by the formation of hyperreactivity of the skin, its dryness and peeling
ΠΠ·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·Ρ Π½Π΅ΠΊΠΎΡΠΎΡΡΡ ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠΎΠ² ΠΌΡΠΊΠΎΠ·Π°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΈΠΌΠΌΡΠ½ΠΈΡΠ΅ΡΠ° ΠΏΠΎΠ»ΠΎΡΡΠΈ ΡΡΠ° Ρ ΡΡΠΎΠ²Π½Π΅ΠΌ Π²ΠΈΡΠ°ΠΌΠΈΠ½Π° D Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΌ ΠΊΠ°ΡΠΈΠ΅ΡΠΎΠΌ
Aim. To determine the saliva level of immunoregulatory proteins in patients with rampant caries and 25-hydroxyvitamin D (25(OH)D) deficiency and evaluate the association of their concentration with 25(OH)D plasma level.Materials and methods. The study was performed in two groups. The experimental group included 15 patients aged 20β22 years with rampant caries and the 25(OH)D plasma level of < 20 ng / ml. The control group encompassed 15 healthy age-matched volunteers with the 25(OH)D plasma level of 20β100 ng / ml. The concentrations of B7.2 (CD86), free active TGF-Ξ²1, CTLA-4, PD-1, Tim-3, LAG-3, IGFBP-4, and ICAM-1 were assessed using flow cytometry. The levels of LL-37 and secretory immunoglobulin A (sIgA) were measured using ELISA. The Spearmanβs rank correlation coefficient was used to reveal a correlation between the indicated proteins and the 25(OH)D plasma level.Results. A decrease in B7.2 (CD86), PD-1, Tim-3, sIgA, and LL-37 and elevation of IGFBP-4 and ICAM-1 saliva levels were detected in patients with rampant caries and 25-hydroxyvitamin D deficiency. A positive Spearmanβs rank correlation coefficient was revealed between plasma 25(OH)D and saliva levels of free active TGF-Ξ²1, CTLA4, B7.2 (CD86), LL-37, and sIgA. A negative correlation was revealed between 25(OH)Dand ICAM-1.Conclusion. 25(OH)D deficiency in patients with rampant caries is associated with decreased levels of B7.2 (CD86), PD-1, Tim-3, sIgA, and LL-37 and elevated levels of IGFBP-4 and ICAM-1 in the saliva.Β Π¦Π΅Π»Ρ β ΠΎΡΠ΅Π½ΠΈΡΡ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠ½ΡΡ
ΠΌΠΎΠ»Π΅ΠΊΡΠ» Π² ΡΠ»ΡΠ½Π΅ Ρ Π»ΠΈΡ Ρ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π΅Π½Π½ΡΠΌ ΠΊΠ°ΡΠΈΠ΅ΡΠΎΠΌ ΠΈ Π΄Π΅ΡΠΈΡΠΈΡΠΎΠΌ 25(OH)D3 ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΠΈΡΡ Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·ΠΈ ΠΈΡ
Π²Π΅Π»ΠΈΡΠΈΠ½ Ρ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠ΅ΠΉ 25(OH)D3 Π² ΠΊΡΠΎΠ²ΠΈ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ Π΄Π²Π΅ Π³ΡΡΠΏΠΏΡ Π»ΠΈΡ Π² Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ 20β22 Π»Π΅Ρ. Π ΠΎΠ΄Π½Ρ Π²ΠΊΠ»ΡΡΠ΅Π½Ρ 15 ΡΠ΅Π»ΠΎΠ²Π΅ΠΊ Ρ ΠΊΠ°ΡΠΈΠ΅ΡΠΎΠΌ ΠΈ ΡΡΠΎΠ²Π½Π΅ΠΌ 25(OH)D3 ΠΌΠ΅Π½Π΅Π΅ 20 Π½Π³/ΠΌΠ», Π² Π΄ΡΡΠ³ΡΡ (ΠΊΠΎΠ½ΡΡΠΎΠ»ΡΠ½ΡΡ) β 15 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
ΡΠ΅Π»ΠΎΠ²Π΅ΠΊ Ρ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ΠΌ 25(OH)D3 30β100 Π½Π³/ΠΌΠ». Π ΡΠΎΡΠΎΠ²ΠΎΠΉ ΠΆΠΈΠ΄ΠΊΠΎΡΡΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Ρ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ ΡΠ°ΡΡΠ²ΠΎΡΠΈΠΌΡΡ
ΡΠΎΡΠΌ ΠΌΠΎΠ»Π΅ΠΊΡΠ» B7.2 (CD86), Free Active TGF-b1, CTLA-4, PD-1, Tim-3, LAG-3, IGFBP-4, ICAM-1 ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΡΠ»ΡΠΎΠΌΠ΅ΡΡΠΈΠΈ, ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ ΠΊΠ°ΡΠ΅Π»ΠΈΡΠΈΠ΄ΠΈΠ½Π° LL-37, ΡΠ΅ΠΊΡΠ΅ΡΠΎΡΠ½ΠΎΠ³ΠΎ ΠΈΠΌΠΌΡΠ½ΠΎΠ³Π»ΠΎΠ±ΡΠ»ΠΈΠ½Π° A (IgA) ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅ΡΠΌΠ΅Π½ΡΠ½ΠΎΠ³ΠΎ Π°Π½Π°Π»ΠΈΠ·Π°. ΠΠ΅ΠΆΠ΄Ρ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅ΠΌΡΠΌΠΈ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΠΌΠΈ ΡΠ°ΡΡΡΠΈΡΠ°Π½ ΠΊΡΠΈΡΠ΅ΡΠΈΠΉ ΠΊΠΎΡΡΠ΅Π»ΡΡΠΈΠΈ Π‘ΠΏΠΈΡΠΌΠ΅Π½Π°.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π£ Π»ΠΈΡ Ρ ΠΊΠ°ΡΠΈΠ΅ΡΠΎΠΌ ΠΈ Π΄Π΅ΡΠΈΡΠΈΡΠΎΠΌ Π²ΠΈΡΠ°ΠΌΠΈΠ½Π° D Π²ΡΡΠ²Π»Π΅Π½ΠΎ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ Π·Π½Π°ΡΠ΅Π½ΠΈΠΉ Free Active TGF-b1, B7.2 (CD86), PD-1, Tim-3, sIgA, ΠΊΠ°ΡΠ΅Π»ΠΈΡΠΈΠ΄ΠΈΠ½Π° LL-37 ΠΈ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΡΡΠΎΠ²Π½Ρ IGFBP-4 ΠΈ ICAM-1 Π² ΡΠ»ΡΠ½Π΅. ΠΠ±Π½Π°ΡΡΠΆΠ΅Π½ΠΎ Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΏΡΡΠΌΡΡ
ΠΊΠΎΡΡΠ΅Π»ΡΡΠΈΠΎΠ½Π½ΡΡ
ΡΠ²ΡΠ·Π΅ΠΉ ΠΌΠ΅ΠΆΠ΄Ρ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎΠΌ 25(OH)D3 Π² ΠΊΡΠΎΠ²ΠΈ, Ρ ΠΎΠ΄Π½ΠΎΠΉ ΡΡΠΎΡΠΎΠ½Ρ, ΠΈ Π·Π½Π°ΡΠ΅Π½ΠΈΡΠΌΠΈ Free Active TGF-b1, CTLA-4, Π7.2 (CD86), ΡΠ΅ΠΊΡΠ΅ΡΠΎΡΠ½ΠΎΠ³ΠΎ IgA, ΠΏΠ΅ΠΏΡΠΈΠ΄Π° LL-37 β Ρ Π΄ΡΡΠ³ΠΎΠΉ. ΠΠ°ΡΠΈΠΊΡΠΈΡΠΎΠ²Π°Π½Π° ΠΎΡΡΠΈΡΠ°ΡΠ΅Π»ΡΠ½Π°Ρ Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·Ρ ΠΌΠ΅ΠΆΠ΄Ρ Π²Π΅Π»ΠΈΡΠΈΠ½Π°ΠΌΠΈ 25(OH)D3 ΠΈ ICAM-1.ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠ° ΡΠΎΠ½Π΅ Π΄Π΅ΡΠΈΡΠΈΡΠ° Π²ΠΈΡΠ°ΠΌΠΈΠ½Π° D ΠΏΡΠΈ ΠΌΠ½ΠΎΠΆΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠΌ ΠΊΠ°ΡΠΈΠ΅ΡΠ΅ Π² ΡΠΎΡΠΎΠ²ΠΎΠΉ ΠΆΠΈΠ΄ΠΊΠΎΡΡΠΈ ΡΠ΅Π³ΠΈΡΡΡΠΈΡΡΡΡΡΡ Π½ΠΈΠ·ΠΊΠΈΠ΅ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ Free Active TGF-b1, B7.2 (CD86), PD-1, Tim-3, ΡΠ΅ΠΊΡΠ΅ΡΠΎΡΠ½ΠΎΠ³ΠΎ IgA, ΠΊΠ°ΡΠ΅Π»ΠΈΡΠΈΠ΄ΠΈΠ½Π° LL-37 ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ ΠΊΠΎΠ½ΡΡΠΎΠ»Π΅ΠΌ, Π½ΠΎ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½Ρ Π·Π½Π°ΡΠ΅Π½ΠΈΡ IGFBP-4 ΠΈ ICAM-1.
Modulation of functional pendant chains within poly(ethylene glycol) hydrogels for refined control of protein release
Hydrogels are highly attractive delivery vehicles for therapeutic proteins. Their innate biocompatibility, hydrophilicity and aqueous permeability allow stable encapsulation and release of proteins. The release rates also can be controlled simply by altering the crosslinking density of the polymeric network. However, the crosslinking density also influences the mechanical properties of hydrogels, generally opposite to the permeability. In addition, the release of larger proteins may be hindered below critically diminished porosity determined by the crosslinking density. Herein, the physical properties of the hydrogels are tuned by presenting functional pendant chains, independent of crosslinking density. Heterobifunctional poly(ethylene glycol) monomethacrylate (PEGMA) with various end functional groups is synthesized and copolymerized with PEG dimethacrylate (PEGDA) to engineer PEG hydrogels with pendant PEG chains. The pendant chains of the PEG hydrogels consisting of sulfonate, trimethylammonium chloride, and phenyl groups are utilized to provide negative charge, positive charge and hydrophobicity, respectively, to the hydrogels. The release rates of proteins with different isoelectric points are controlled in a wide range by the type and the density of functional pendant chains via electrostatic and hydrophobic interactions
Experimental models of dermatological diseases
This review presents analysis of experimental models of atopic dermatitis, psoriasis, skin symptoms of autoimmune systemic connective tissue diseases, and blistering skin diseases. Presented in the review are experimental models of atopic dermatitis which reproduce various stages and types of disease that allows the investigation of disease pathogenesis. Atopic dermatitis can develop spontaneously in Nc/Nga mice. There are atopic dermatitis models initiated by monoclonal IgE injection or epicutant sensitization under dermal barrier disfunction imitation. Genetically modified atopic dermatitis models - transgenic and knockout mice β are convenient for investigation of disease stages, cytokines, antigen-presenting cells and T-cells influence. We show that the psoriasis models created by genetic engineering methods are the most convenient for investigation of the role of particular cell types and specific factors in the disease development. Up-regulation of adhesion molecules, cytokines, transcription factors, inflammation mediators in both keratinocytes and immune cells of transgenic mice reveals their influence on psoriasis pathogenesis. There are descriptions of skin symptom models of autoimmune systemic connective tissue diseases and blistering skin disease models with and without genetic modifications. Each model demonstrates some peculiarities of pathogenesis and disease symptoms, whereas combined use of the models will allow to study the mechanisms of development of atopic dermatitis, psoriasis, blistering skin diseases and skin lesions under autoimmune systemic connective tissue diseases, that will contribute to the development of modern effective methods of treatment
Effect of helium presence on tungsten-deuterium co-deposited films
Co-deposited W-D, W-He, and mixed W-D-He films 250Β nm thick were investigated. The films were obtained by magnetron sputtering of W in Ar:D2:He =: 1:1:0, 1:0:1, 1:1:0.05, and 1:1:0.2, gas mixtures and at deposition temperatures ofΒ βΌΒ 350Β K, 500Β K, and 800Β K. The films were studied by thermal desorption spectroscopy (TDS) with TmaxΒ =Β 2200Β K using threshold ionization mass spectrometry to separate D2 and He signals. It was found that films obtained in gas mixtures with mixed He-D2 atmospheres contained less total gas atoms than films deposited in pure D2 or He atmospheres. It was found that in mixed W-D-He films, He trapping with high binding energies (TdesΒ >Β 1500Β K) is strongly mitigated