Educational interventions and their effects on healthcare professionals' digital competence development: A systematic review.

INTRODUCTION: The digitalisation of healthcare requires that healthcare professionals are equipped with adequate digital competencies to be able to deliver high-quality healthcare. Continuing professional education is needed to ensure these competencies. OBJECTIVE: This systematic review aimed to identify and describe the educational interventions that have been developed to improve various aspects of the digital competence of healthcare professionals and the effects of these interventions. METHODS: A systematic literature review following the Joanna Briggs Institute's guidelines for Evidence Synthesis was conducted. Five electronic databases (CINAHL, PubMed, ProQuest, Scopus and Medic) up to November 2023 were searched for studies. Two researchers independently assessed the eligibility of the studies by title, abstract and full text and the methodological quality of the studies. Data tabulation and narrative synthesis analysis of study findings were performed. The PRISMA checklist guided the review process. RESULTS: This review included 20 studies reporting heterogeneous educational interventions to develop the digital competence of healthcare professionals. The participants were mainly nurses and interventions were conducted in various healthcare settings. The length of the education varied from a 20-minute session to a six-month period. Education was offered through traditional contact teaching, using a blended-learning approach and through videoconference. Learning was enhanced through lectures, slide presentations, group work, case studies, discussions and practical exercises or simulations. Educational interventions achieved statistically significant results regarding participants' knowledge, skills, attitudes, perception of resources, self-efficacy or confidence and output quality. CONCLUSIONS: The findings of this review suggest that digital competence education of nurses and allied health professionals would benefit from a multi-method approach. Training should provide knowledge as well as opportunities to interact with peers and instructors. Skills and confidence should be enhanced through practical training. Adequate organisational support, encouragement, and individual, needs-based guidance should be provided.

Healthcare professionals' digital health competence and its core factors; development and psychometric testing of two instruments.

BACKGROUND: Healthcare professionals' digital health competence is an important phenomenon to study as healthcare practices are changing globally. Recent research aimed to define this complex phenomenon and identify the current state of healthcare professionals' competence in digitalisation but did not include an overarching outlook when measuring digital health competence of healthcare professionals. OBJECTIVES: The purpose of this study was to develop and psychometrically validate two self-assessed instruments measuring digital health competence and factors associating with it. METHODS: The study followed three phases of instrument development and validation: 1) conceptualisation and item pool generation; 2) content validity testing and pilot study; and 3) construct validity and reliability testing. The conceptual background of the instruments was based on individual interviews conducted with healthcare professionals (n = 20) and previous systematic reviews. A total of 17 experts assessed the instrument's content validity. Face validity was evaluated by a group of healthcare professionals (n = 20). Data collection from 817 professionals took place in spring-summer 2022 in nine organisations. Construct validity was confirmed with exploratory factor analysis. Cronbach's alpha was used to assess the internal consistency of the instruments. RESULTS: The instrument development and validation process resulted in two instruments: DigiHealthCom and DigiComInf. DigiHealthCom included 42 items in 5 factors related to digital health competence, and DigiComInf included 15 items in 3 factors related to educational and organisational factors associated with digital health competence. The DigiHealthCom instrument explained 68.9 % of the total variance and the factors' Cronbach alpha values varied between 0.91 and 0.97. The DigiComInf instrument explained 59.6 % of the total variance and the factors' Cronbach alpha values varied between 0.76 and 0.88. CONCLUSIONS: The two instruments gave valid and reliable results in psychometric testing. The instruments could be used to evaluate healthcare professionals' digital health competence and associated factors.

Blister fluid and serum cytokine levels in severe sepsis in humans reflect skin dysfunction.

BACKGROUND: Knowledge of sepsis-related end-organ inflammation in vivo is limited. We investigated the cytokine response in skin and in serum in sepsis and its relation to multiorgan failure (MOF) and survival. METHODS: Cytokines were analysed in serum and in suction blister fluid of intact skin of 44 patients with severe sepsis and 15 healthy controls. Blister fluid and serum samples were collected within 48 h of the first sepsis-induced organ failure. This is a substudy of a larger follow-up study on wound healing in sepsis. RESULTS: Cytokine levels were higher in patients with sepsis vs. controls (interleukin [IL]-10, blisters: 65.9 vs. 4.3 pg/ml, P < 0.001, serum: 25.7 vs. 4.5 pg/ml, P = 0.004; IL-6, blisters: 41.9 vs. 0.03 pg/ml, P < 0.001, serum: 45.5 vs. 2.1 pg/ml, P < 0.001). Patients with MOF had higher levels of IL-10 (116.4 vs. 21.3 pg/ml, P = 0.015), IL-4 (0.7 vs. 0.07 pg/ml, P = 0.013) and basic fibroblast growth factor (bFGF) (25.9 vs. 9.5 pg/ml, P = 0.027) in blister fluid than patients without MOF. In blister fluid, survivors had lower levels of IL-10 (43.3 vs. 181.9 pg/ml, P = 0.024) and bFGF (15.8 vs. 31.9 pg/ml, P = 0.006) than non-survivors. In serum, survivors had higher levels of vascular endothelial growth factor (VEGF) (152.2 vs. 14.7 pg/ml, P = 0.012) and lower levels of IL-6 (38.5 vs. 91.1 pg/ml, P = 0.011) than non-survivors. The blister fluid levels of bFGF, TNF and VEGF did not correlate with the serum levels. CONCLUSIONS: Cytokine responses in skin blister fluid in patients with sepsis differed from those in healthy controls.

Dermal expression of laminin-332 and type IV collagen in humans with severe sepsis.

BACKGROUND: An intact basement membrane at the dermal-epidermal junction is essential to the viability of the skin. The effect of sepsis on the basement membrane is unknown. METHODS: Skin biopsies were used to study basement membrane structure in severe sepsis (Day 1). Subsequent biopsies were taken on Day 8 and at 3 months in the survivors. Immunohistochemical staining was undertaken using laminin-223 and type IV collagen. Twenty patients with severe sepsis and four control subjects were included in the analysis. RESULTS: Intensive care unit mortality was 4/20, and total 30-day mortality was 5/20. Exactly, 7/17 of patients with severe sepsis exhibited weak or absent laminin-332 expression and 11/15 exhibited weak or absent type IV collagen expression compared with 0/4 of control subjects on Day 1 in intact skin. The proportion of sepsis patients with weak or absent laminin-332 expression was 5/11 on Day 8 and fell to 1/7 at 3 months. The proportion of sepsis patients with weak or absent type IV collagen expression was 10/11 on Day 8 and 4/7 at 3 months. CONCLUSION: These findings suggest that basement membrane formation may be compromised in patients with severe sepsis.

Increased expression of glucocorticoid receptor beta in lymphocytes of patients with severe atopic dermatitis unresponsive to topical corticosteroid.

BACKGROUND: Variable response to topical glucocorticoid therapy occurs in the treatment of severe atopic dermatitis (AD). Glucocorticoid receptor (GR)-beta does not bind glucocorticoids but antagonizes the activity of the classic GRalpha, and could thus account for glucocorticoid insensitivity. OBJECTIVES: To investigate GRalpha and GRbeta mRNA and protein expression in lymphocytes of patients with AD before and after treatment with topical corticosteroids. METHODS: Blood was collected from 11 healthy donors, 10 patients with mild AD and 13 patients with severe AD. mRNA was isolated from peripheral blood mononuclear cells. Expression of GRalpha and GRbeta mRNA was determined by reverse transcriptase-polymerase chain reaction and quantitated. Expression of the GRs was confirmed by Western blot analysis. RESULT: The expression of GRalpha mRNA was detected in all subjects. GRbeta mRNA was detected in four out of 11 healthy volunteers, five out of 10 patients with mild AD and 11 out of 13 patients with severe AD. The incidence of GRbeta mRNA expression was higher in patients with severe AD (85%) than in patients with mild AD (50%), and significantly higher than in healthy volunteers (36%, P = 0.033). Four of the 13 patients with severe AD showed a 3.3-13.2-fold increase in the expression of GRbeta mRNA during a 2-week treatment with topical corticosteroids. In these patients the response to topical corticosteroids was poor. CONCLUSIONS: Expression of GRbeta is increased during topical corticosteroid treatment in the lymphocytes of patients with AD and, in particular, glucocorticoid-insensitive AD is associated with increased expression of GRbeta.

Keratinocytes cultured from patients with Hailey-Hailey disease and Darier disease display distinct patterns of calcium regulation.

BACKGROUND: Hailey-Hailey disease (HHD) (OMIM 16960) and Darier disease (DD) (OMIM 124200) are dominantly inherited acantholytic skin diseases, respectively, caused by mutations in the genes encoding the Golgi secretory pathway Ca2+-ATPase (SPCA1, ATP2C1) and the sarco/endoplasmic reticulum Ca2+-ATPase type 2 (SERCA2, ATP2A2) genes. OBJECTIVES: To investigate calcium regulation in keratinocytes cultured from patients with HHD and DD by measuring intracellular calcium resting levels and the cellular responses to ATP and thapsigargin. METHODS: The study was carried out using keratinocyte cultures established from four patients with HHD and four with DD. Calcium concentrations were measured with fluorescence ratio imaging using fura-2 loading. RESULTS: Control and HHD keratinocytes displayed approximately the same Ca2+ levels in resting phase, while DD keratinocytes showed elevated Ca2+ levels. Application of ATP caused less pronounced elevation of intracellular calcium concentration ([Ca2+]i) in both HHD and DD keratinocytes than in control cells. HHD keratinocytes did not lower their [Ca2+]i as efficiently as control keratinocytes after treatment with thapsigargin. In addition, DD keratinocytes were practically incapable of lowering their [Ca2+]i after treatment with thapsigargin. CONCLUSIONS: The results demonstrate that the defects in SPCA1 and SERCA2 calcium ATPases result in distinct patterns of calcium metabolism. This is also supported by the different clinical features of the diseases.

Effect of jaundice and its resolution on wound re-epithelization, skin collagen synthesis, and serum collagen propeptide levels in patients with neoplastic pancreaticobiliary obstruction.

BACKGROUND: Wound and anastomotic healing is considered to be delayed in patients with obstructive jaundice. The study was designed to find out whether the healing of experimental suction blister wounds, skin collagen synthesis, and serum procollagen levels are affected by obstructive jaundice, and if biliary drainage may cause any alterations in these processes. PATIENTS AND METHODS: Suction blisters were induced on 24 patients with obstructive jaundice caused by neoplastic pancreaticobiliary obstruction and 17 control patients with the corresponding condition without jaundice, to compare healing parameters and collagen synthesis between the groups. A second set of suction blisters were induced on 13 formerly jaundiced patients after the resolution of jaundice and on 14 control patients, to find out whether drainage or time modifies healing or collagen synthesis. By using this model, it is possible to evaluate the re-epithelization and inflammation on wound healing and to assess the baseline skin collagen synthesis. The healing of suction blisters was followed up by measuring water evaporation and blood flow in the wound. Blister fluids and serum samples were collected to study collagen propeptides. RESULTS: Healing of the blister wound was unaffected by obstructive jaundice. Drainage had no effect on healing. The baseline synthesis of type I and type III collagen in the skin was decreased in jaundiced patients. Biliary drainage improved the synthesis. Serum type III procollagen propeptide levels were elevated in jaundiced patients, but began to normalize after drainage. CONCLUSION: Healing of an experimental blister wound is not disturbed by obstructive jaundice. The decreased baseline skin collagen synthesis is partly restored by the resolution of jaundice. The results indicate that cell protein synthesis is disturbed earlier than cell dynamics in obstructive jaundice. The elevated serum PIIINP levels, which are most likely to be related to early fibrosis in liver, decreased after drainage.

Immunohistological distribution of the tight junction components ZO-1 and occludin in regenerating human epidermis.

BACKGROUND: Molecular characterization of tight junction proteins during the past few years has provided novel methods for studying these specialized junctions. Tight junctions have recently been characterized in the granular cell layer of human epidermis, and the role of these junctions in the epidermal barrier is now being re-evaluated. OBJECTIVES: To investigate the expression of tight junction components during the re-epithelialization of suction blisters and the regeneration of the corneal layer after tape stripping. METHODS: Suction blisters were induced in eight healthy volunteers, and skin biopsies were taken 4 or 6 days afterwards. The restoration of epidermal barrier function was evaluated by measuring water evaporation (WE) from the wound area. Tape stripping was performed on three volunteers to remove the corneal layer. The tissues were immunolabelled using indirect immunofluorescence or the avidin-biotin method. RESULTS: Prior to the biopsies, WE from the blister wounds was markedly elevated in comparison with normal skin. In the epidermis surrounding the blister, occludin and ZO-1 were expressed in the granular cell layer only. In the hyperproliferative zone adjacent to the border of the blister, the expression of ZO-1 was redistributed into several spinous cell layers, while occludin expression was restricted to the upper epidermis. In the leading edge of migrating keratinocytes, both proteins were expressed exclusively in the most superficial layer of keratinocytes. Double labelling for ZO-1 and involucrin showed expression of both proteins in the same layers of hyperproliferative keratinocytes, while the expression patterns were clearly different in the migrating keratinocytes. CONCLUSIONS: Tight junctions of regenerating epidermis may provide a functional barrier prior to regeneration of the corneal layer.

Modulation of collagen synthesis and mRNA by continuous and intermittent use of topical hydrocortisone in human skin.

BACKGROUND: Glucocorticoids have been shown to downregulate collagen synthesis in human skin in vivo, thereby contributing to skin atrophy. OBJECTIVES: To compare the effects of continuous and intermittent use of topical hydrocortisone on skin collagen synthesis and, furthermore, to elucidate the mechanism of collagen synthesis reduction induced by hydrocortisone. METHODS: Collagen propeptides reflecting the synthesis rate of type I and III collagens were studied from suction blister fluids in nine healthy subjects after 3 weeks of continuous (twice daily) or intermittent (on three consecutive days weekly) topical hydrocortisone treatment and 2 weeks after the termination of treatment. Type I collagen mRNA was studied in the same subjects from skin biopsies by using in situ hybridization (ISH) after 3 weeks of treatment. RESULTS: Three weeks of continuous treatment decreased the types I and III collagen propeptides in suction blister fluid by 89% and 82%, respectively, while intermittent treatment resulted in a corresponding decrease of 53% and 50%. ISH studies from skin biopsies showed type I collagen mRNA to be markedly reduced in fibroblasts after continuous and intermittent steroid treatment. After a 2-week drug-free interval, the synthesis rate was completely restored in both areas, and some subjects even showed upregulation of synthesis in previously steroid-treated skin. CONCLUSIONS: Continuous hydrocortisone for 3 weeks markedly decreases collagen propeptides and corresponding mRNA in human skin. Intermittent hydrocortisone has a less marked effect on the collagen synthesis rate.

Smoking affects collagen synthesis and extracellular matrix turnover in human skin.

BACKGROUND: Smoking is associated with premature facial wrinkling and aberrant wound healing, but the underlying mechanisms of skin injury are poorly understood. OBJECTIVES: To compare the in vivo collagen synthesis and degradation in the skin of smokers and non-smokers. METHODS: The study population consisted of 47 current smokers and 51 individuals who had never smoked from northern Finland. Suction blisters were induced in the sun-protected upper inner arm of the study subjects, after which suction blister fluid (SBF) was collected for analyses of the levels of aminoterminal procollagen propeptides of type I and III collagens (PINP and PIIINP, respectively), matrix metalloproteinase (MMP)-8 and tissue inhibitor of MMP (TIMP)-1. PINP, PIIINP and TIMP-1 were also determined from serum samples. The levels of active and pro MMP-1 were assessed from deep-frozen skin biopsies by Western blotting. RESULTS: The synthesis rates of type I and III collagens were lower by 18% and 22%, respectively, in the SBF of the smokers compared with the non-smokers. The levels of MMP-8 were higher by 100% in the SBF of the smokers. The levels of MMP-1 in the skin biopsies did not differ significantly between the groups. The levels of TIMP-1 in SBF were 14% lower in the smokers than in the non-smokers, whereas the serum concentrations of TIMP-1 did not differ between the groups. CONCLUSIONS: Smoking decreases the synthesis rates of type I and III collagens in skin in vivo and alters the balance of extracellular matrix turnover in skin.

Type I collagen turnover and cross-linking are increased in irradiated skin of breast cancer patients.

BACKGROUND AND PURPOSE: The effects of radiation therapy on the turnover and structure of type I collagen were studied in irradiated and contralateral skin of 18 breast cancer patients without clinically evident fibrosis. MATERIALS AND METHODS: The rates of on-going type I collagen synthesis and degradation were assessed by the aminoterminal propeptide of type I procollagen (PINP) and by two different assays (ICTP and SP4) for the carboxyterminal telopeptide of type I collagen in the soluble tissue extracts, respectively. Also, TIMP-1, TIMP-2 and the MMP-2/TIMP-2 complex were measured in the tissue extracts. Insoluble skin matrices, containing the cross-linked type I collagen fibres, were heat-denatured and digested with trypsin. Then, the variants of the carboxyterminal telopeptide of type I collagen were separated by high performance liquid chromatography (HPLC). The major histidinohydroxylysinonorleucine (HHL)-cross-linked variant was quantified by the SP4 assay, and the minor pyridinoline analogue (PA)-cross-linked telopeptide was quantified by the ICTP assay. RESULTS: Both the synthesis and degradation of type I collagen were increased (r=0.906; P<0.001) on the irradiated side, whereas the concentration of the MMP-2/TIMP-2 complex was decreased. In the insoluble tissue digests, the HHL-cross-linked telopeptides of type I collagen, also, when expressed/tissue hydroxyproline, were increased in the irradiated skin. TIMP-1, TIMP-2 or PA-cross-linked telopeptides of type I collagen showed no differences between the two sides. CONCLUSIONS: Radiotherapy induces a long-term increase in the turnover of type I collagen and leads to the accumulation of cross-linked type I collagen in skin.

Radiation therapy induces tenascin expression and angiogenesis in human skin.

In analysing radiation-induced connective tissue changes, we studied tenascin expression, elastic fibres, angiogenesis and physio-mechanical properties in irradiated and contralateral healthy skin of radiotherapy-treated breast cancer patients. Skin biopsies were obtained from a radiotherapy-treated skin area and a corresponding non-treated skin area. Haematoxylin-eosin and Verhoeff stainings as well as immunohistochemical stainings for tenascin and factor VIII were performed. Epidermal and total skin thickness, together with the amount of elastic tissue calculated by computerized digital image analysis, were measured. Suction blisters were induced on both skin areas. Transepidermal water loss was analysed. Skin elasticity was also measured. Tenascin expression was found to be increased in irradiated human skin. In haematoxylin-eosin and factor VIlI-stained sections, an increase in the number of blood vessels was detected. Although skin stiffness measured by an elastometer was increased in irradiated skin, no marked difference in the elastic fibres could be found between treated and non-treated skin. The increased tenascin expression could be due to activation of cytokines as a result of irradiation. An increase in angiogenesis could be caused by an activation of angiogenetic factors by irradiation or due to direct radiation damage on blood vessel walls. Our findings suggest that the effects of irradiation tend to accumulate in the dermal parts of skin. The higher skin stiffness values measured by elastometer in irradiated skin could be due to an accumulation of dermal connective tissue as a result of irradiation.

Effects of glucose on collagen mRNA levels and collagen secretion in EAhy 926 endothelial cell line.

Diabetes mellitus (DM) is a complex metabolic disease associated with increased accumulation of extracellular matrix by endothelial cells and contributing to vascular complications of long-standing diabetes. On the other hand, DM is also associated with decreased accumulation of extracellular matrix in granulation tissue, which is suggested to be a consequence of impaired angiogenesis. The role of hyperglycemia in these situations is not fully understood. We examined the effects of high glucose concentrations on the gene expression and secretion of various collagens in cultured EAhy 926 endothelial cells. EAhy 926 endothelial cells expressed alpha 1(I) collagen mRNA at a low level and small amount of the corresponding peptide was secreted from the cells; mRNA was not affected but peptide secretion was increased by elevated glucose concentration. mRNAs for type III and VI collagens were not detected in the endothelial cells Furthermore, high glucose concentration in long term had no morphological effects on cultured endothelial cells but increased the expression of type IV collagen, which could rather be beneficial for angiogenesis in a healing wound. Our results suggest that high glucose concentration per se may contribute to increased accumulation of extracellular matrix in blood vessels but probably is not responsible for decreased angiogenesis and granulation tissue formation in diabetic patients.

Effects of glucose on collagen mRNA levels and collagen secretion in EAhy 926 endothelial cell line.

Diabetes mellitus (DM) is a complex metabolic disease associated with increased accumulation of extracellular matrix by endothelial cells and contributing to vascular complications of long-standing diabetes. On the other hand, DM is also associated with decreased accumulation of extracellular matrix in granulation tissue, which is suggested to be a consequence of impaired angiogenesis. The role of hyperglycemia in these situations is not fully understood. We examined the effects of high glucose concentrations on the gene expression and secretion of various collagens in cultured EAhy 926 endothelial cells. EAhy 926 endothelial cells expressed alpha1(I) collagen mRNA at a low level and small amount of the corresponding peptide was secreted from the cells; mRNA was not affected but peptide secretion was increased by elevated glucose concentration. mRNAs for type III and VI collagens were not detected in the endothelial cells. Furthermore, high glucose concentration in long term had no morphological effects on cultured endothelial cells but increased the expression of type IV collagen, which could rather be beneficial for angiogenesis in a healing wound. Our results suggest that high glucose concentration per se may contribute to increased accumulation of extracellular matrix in blood vessels but probably is not responsible for decreased angiogenesis and granulation tissue formation in diabetic patients.