Röntgenhoitajien oppimisympäristö työelämässä : Jorvin ja Peijaksen röntgenyksiköiden esittelysivut

Projektimme tarkoituksena oli tuottaa esittelysivut Jorvin ja Peijaksen röntgenyksiköistä ja niiden alaisuuteen kuuluvista perusterveydenhuollon yksiköistä Helsingin ja Uudenmaan sairaanhoitopiirin verkkosivuja varten. Jorvin ja Peijaksen röntgenyksiköt tulivat vuoden 2006 alussa osaksi HUS-Röntgen liikelaitosta. Tästä syntyi tarve kerätä myös kyseisistä yksiköistä tiedot verkkoon tulevia esittelysivuja varten. Pyrimme kehittämään esittelysivujen sisältöä edelleen tarkastelemalla HUS-Röntgeniä röntgenhoitaja-opiskelijan oppimisen kannalta työharjoittelupaikkana ja oppimisympäristönä pedagogisesta, pragmaattisesta ja sosiaalisesta näkökulmasta. Työelämässä tapahtuvassa oppimisessa painotimme myös opiskelijan oman sitoutumisen ja motivaation merkitystä. Esittelysivujen tarkoituksena on auttaa röntgenhoitajaopiskelijoita valitsemaan itselleen juuri sillä hetkellä opintoihinsa sopiva harjoittelupaikka. Röntgenyksiköt ovat verkkosivuilla keskenään helposti vertailtavissa. Sivut palvelevat myös työelämää. Röntgenyksiköt saavat oman työympäristönsä esille ja pystyvät kertomaan eri työskentelymahdollisuuksista potentiaalisille tulevaisuuden työntekijöille. Esittelysivujen sisältämien tietojen mahdollisesti muuttuessa ne ovat helposti päivitettävissä keskitetysti ja sähköisesti verkkoa hallinnoivan henkilön kautta. Esittelysivujen merkitys tulee kasvamaan tulevaisuudessa edelleen kehittyvän tietoyhteiskunnan ja opiskelijoiden kasvavan tietotekniikkaosaamisen myötä. Mahdollisesti tulevaisuudessa uusien HUS-Röntgen liikelaitokseen liittyvien röntgenyksiköiden esittelysivujen tuottaminen oppilastyönä luo hyvät edellytykset esittelysivujen edelleen kehittämiseen

Osteoarthritis and Toll-Like Receptors: When Innate Immunity Meets Chondrocyte Apoptosis

Osteoarthritis (OA) has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis. In particular, chondrocyte-mediated inflammatory responses triggered by the activation of innate immune receptors by alarmins (also known as danger signals) are thought to be involved. Thus, toll-like receptors (TLRs) and their signaling pathways are of particular interest. Recent reports suggest that among the TLR-induced innate immune responses, apoptosis is one of the critical events. Apoptosis is of particular importance, given that chondrocyte death is a dominant feature in OA. This review focuses on the role of TLR signaling in chondrocytes and the role of TLR activation in chondrocyte apoptosis. The functional relevance of TLR and TLR-triggered apoptosis in OA are discussed as well as their relevance as candidates for novel disease-modifying OA drugs (DMOADs).Peer reviewe

Osteoarthritis and Toll-Like Receptors: When Innate Immunity Meets Chondrocyte Apoptosis

Osteoarthritis (OA) has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis. In particular, chondrocyte-mediated inflammatory responses triggered by the activation of innate immune receptors by alarmins (also known as danger signals) are thought to be involved. Thus, toll-like receptors (TLRs) and their signaling pathways are of particular interest. Recent reports suggest that among the TLR-induced innate immune responses, apoptosis is one of the critical events. Apoptosis is of particular importance, given that chondrocyte death is a dominant feature in OA. This review focuses on the role of TLR signaling in chondrocytes and the role of TLR activation in chondrocyte apoptosis. The functional relevance of TLR and TLR-triggered apoptosis in OA are discussed as well as their relevance as candidates for novel disease-modifying OA drugs (DMOADs).Peer reviewe

Niveltulehdusten diagnostiikka

English summar

Cost-effectiveness of routine measuring of serum drug concentrations and anti-drug antibodies in treatment of rheumatoid arthritis patients with TNF-alpha blockers

Peer reviewe

Congestive heart failure : more common as well as an important cardiovascular outcome: reply

Non peer reviewe

Human β-Defensin 2 Expression in Oral Epithelium: Potential Therapeutic Targets in Oral Lichen Planus

Human β-defensin 2 (hBD-2) is a potent antimicrobial peptide that participates in defense against invading bacteria. We recently showed that bacterial components and histamine, through histamine H4 receptor (H4R), are involved in the pathogenesis of the potentially malignant lesion, oral lichen planus (OLP). However, the underlying mechanisms remain unknown. We, therefore, investigated the role of hBD2–histamine crosstalk signaling in promoting OLP pathology. Biopsies from OLP and oral tongue squamous cell carcinoma (OTSCC) patients, and healthy controls were used. Two OTSCC cell lines and normal human oral keratinocytes (HOKs) were used. HBD-2 and other targets were mapped by immunostaining and analyzed by ImageJ2 software. The highly sensitive droplet-digital PCR technology and qRT-PCR were utilized to study the clinically derived and in vitro samples, respectively. H4R was challenged with the specific agonist HST-10 and inverse agonist ST-1007. HBD-2 was highly induced in OLP lesions. In contrast, hBD2 expression was attenuated in OTSCC tissues, while very low levels of hBD-2 messenger RNA (mRNA) were observed in OTSCC cells. Together with tumor necrosis factor-α (TNF-α), histamine upregulated hBD-2 mRNA expression in HOKs. Activation of H4R seems to modulate the expression of epithelial hBD-2. These findings suggest the involvement of hBD-2 in the pathogenesis of OLP and may, thus, be harnessed for therapeutic interventions in OLP

Leg Ulcers Treated with Topical Tacrolimus in Patients with Rheumatoid Arthritis

Non peer reviewe

Activation of NLRP3 Inflammasome in the Skin of Patients with Systemic and Cutaneous Lupus Erythematosus

NLRP3 inflammasome is suggested to contribute to the complex pathogenesis of systemic lupus erythematosus, but its role in cutaneous lupus erythematosus has not been addressed. This study investigated the expression of NLRP3 inflammasome components and levels of type I interferons in the skin of 20 patients with cutaneous lupus erythematosus. Expression of NLRP1/3, adaptor protein ASC (apoptosis-associated speck-like protein), caspase-1, interferon-alpha (IFN-alpha), myxovirus resistance protein (MxA), and interferon-induced proteins 1 and 2 (IFIT 1/2) in the skin was assessed using reverse transcription quantitative real-time PCR (RT-qPCR), western blotting and immunohistochemistry. Serum interferon-a protein levels from 12 patients were measured using digital enzyme-linked immunoassay (ELISA). Interleukin-1 beta expression was significantly upregulated in the lesional skin of patients with cutaneous lupus erythematosus compared with their uninvolved skin. However, NLRP1/3, ASC and caspase-1 were not significantly upregulated compared with the skin of control persons. IFN-alpha and IFN-induced proteins MxA and IFIT1/2 were strongly expressed in cutaneous lupus erythematosus skin. Variability in the expression of NLRP3 inflammasome components among patients suggests heterogeneity of pathological pathways in cutaneous lupus erythematosus.Peer reviewe

Human β-Defensin 2 Expression in Oral Epithelium: Potential Therapeutic Targets in Oral Lichen Planus

Human β-defensin 2 (hBD-2) is a potent antimicrobial peptide that participates in defense against invading bacteria. We recently showed that bacterial components and histamine, through histamine H4 receptor (H4R), are involved in the pathogenesis of the potentially malignant lesion, oral lichen planus (OLP). However, the underlying mechanisms remain unknown. We, therefore, investigated the role of hBD2–histamine crosstalk signaling in promoting OLP pathology. Biopsies from OLP and oral tongue squamous cell carcinoma (OTSCC) patients, and healthy controls were used. Two OTSCC cell lines and normal human oral keratinocytes (HOKs) were used. HBD-2 and other targets were mapped by immunostaining and analyzed by ImageJ2 software. The highly sensitive droplet-digital PCR technology and qRT-PCR were utilized to study the clinically derived and in vitro samples, respectively. H4R was challenged with the specific agonist HST-10 and inverse agonist ST-1007. HBD-2 was highly induced in OLP lesions. In contrast, hBD2 expression was attenuated in OTSCC tissues, while very low levels of hBD-2 messenger RNA (mRNA) were observed in OTSCC cells. Together with tumor necrosis factor-α (TNF-α), histamine upregulated hBD-2 mRNA expression in HOKs. Activation of H4R seems to modulate the expression of epithelial hBD-2. These findings suggest the involvement of hBD-2 in the pathogenesis of OLP and may, thus, be harnessed for therapeutic interventions in OLP