Literatura académica sobre el tema "Dermatologi a"

Antihistamin merupakan obat yang sering dipakai dibidang dermatologi, terutama untuk kelainan kronik dan rekuren. Antihistamin adalah zat yang dapat mengurangi atau menghalangi efek histamin terhadap tubuh dengan jalan memblok reseptor histamin. Bilastine dan rupatadine merupakan dua buah antihistamin terbaru yang dipakai dibidang dermatologi. Bilastin termasuk antagonis reseptor H1 generasi kedua terbaru yang paling aman dan tidak memiliki efek terhadap kardiovaskuler. Rupatadin adalah antihistamin H1 generasi kedua terbaru selain memiliki efek terhadap histamin juga memiliki efek terhadap platelet activating factor.

Pendahulan: Ester asam fumarat oral (FAE) merupakan senyawa yang menarik dalam bidang dermatologi. FAE bekerja pada sel kulit dan jaringan sitokin. Sejauh ini hanya campuran dimethylfumarate (DMF) dan monoethylfumarate (MEF) yang telah mendapatkan persetujuan untuk perawatan oral psoriasis jenis plak sedang hingga parah. Tujuan: Untuk mengetahui penggunaan Ester asam fumarat oral (FAE) dalam tatalaksana di bidang dermatologi Metode: Artikel disusun menggunakan metode literature review, melibatkan 34 literatur bersumber dari buku dan jurnal. Hasil: DMF tampaknya menjadi komponen aktif utama. Penting untuk menekankan perbedaan antara asam fumarat dan ester asam fumarat. Formulasi asam fumarat tersedia sebagai suplemen kesehatan dan sering dipasarkan sebagai obat alternatif alami untuk mengobati psoriasis. Namun buruk diserap oleh usus dan diekskresikan melalui urin tanpa memiliki efek terapi apa pun. Pembahasan: Meskipun mode aksi FAE dan mekanisme kerja dalam terapi psoriasis masih belum jelas, bukti menunjukkan bahwa itu tidak ada hubungannya dengan siklus Krebs dan senyawa aktif utama DMF.Ada bukti bahwa FAE tidak hanya efektif dan aman pada psoriasis tetapi juga penyakit non-infeksi granulomatosa seperti granuloma annulare, necrobiosis lipoidica, dan sarkoidosis. Penelitian in vitro dan hewan menunjukkan beberapa aktivitas dalam melanoma ganas juga. Simpulan: Ester asam fumarat oral (FAE) banyak digunakan dalam beberapa kasus dermatologi Kata kunci: Asam fumarat, dermatologi, psoriasis, sarkoidosis

Patients whose psychopathology is expressed in cutaneous lesions often consult a dermatologist rather than a psychiatrist. Dermatologists may not be interested in working with these difficult patients. The need for liaison dermatology is becoming more widely recognized. This article discusses the place of psychiatric consultation in the dermatology setting, and describes the common dermatologic presentations of psychopathology: cutaneous delusions, obsessive-compulsive symptoms, expressions of depression, and dermatitis-artefacta. Diagnostic criteria for these conditions are outlined and a treatment approach, within the competence of the interested dermatologist, is offered.

Retinoid merupakan salah satu senyawa aktif yang paling luas penggunaannya di bidang dermatologi, yaitu sebagai anti-akne, anti-aging dan depigmenting agent. Penggunaan retinoid dapat menimbulkan iritasi pada kulit yang dapat diminimalkan dengan cara pemakaian konsentrasi dan frekuensi yang dinaikkan bertahap. Selain itu, retinoid memiliki potensi teratogenik sehingga harus dihindari penggunaannya pada wanita hamil dan usia produktif.

Retinoid merupakan salah satu senyawa aktif yang paling luas penggunaannya di bidang dermatologi, yaitu sebagai anti-akne, anti-aging dan depigmenting agent. Penggunaan retinoid dapat menimbulkan iritasi pada kulit yang dapat diminimalkan dengan cara pemakaian konsentrasi dan frekuensi yang dinaikkan bertahap. Selain itu, retinoid memiliki potensi teratogenik sehingga harus dihindari penggunaannya pada wanita hamil dan usia produktif.

Retinoid merupakan salah satu senyawa aktif yang paling luas penggunaannya di bidang dermatologi, yaitu sebagai anti-akne, anti-aging dan depigmenting agent. Penggunaan retinoid dapat menimbulkan iritasi pada kulit yang dapat diminimalkan dengan cara pemakaian konsentrasi dan frekuensi yang dinaikkan bertahap. Selain itu, retinoid memiliki potensi teratogenik sehingga harus dihindari penggunaannya pada wanita hamil dan usia produktif.

Background Over half of dermatologic conditions are seen by nondermatologists, yet medical students receive little dermatology education. Medical students in the clinical years of training at our institution felt insecure in their physical diagnosis skills for dermatologic conditions. Objective The objective of this study was to implement dermatology-focused curricula within the Internal Medicine (IM) Core Clerkship to increase student confidence in diagnosing skin diseases. Methods Two dermatology-focused sessions were integrated into the IM Clerkship. A faculty dermatologist leads students on a dermatology-focused physical diagnosis “Skin Rounds”, where patients are seen at the bedside and students practice describing skin lesions and forming a differential diagnosis. Students also participate in a case-based active learning session. A dermatologist selects images of common skin conditions that students describe utilizing appropriate terminology and offer a differential diagnosis. The impact of these sessions was assessed through survey-based student feedback and by comparing the results from the IM Shelf Exam before and after intervention. Results A total of 74 students completed the skin rounds survey (32% response rate). About 99% ( n = 73) of students felt that skin rounds were effective and useful, and 92% ( n = 68) of students reported that they felt more confident in describing skin lesions afterward. A total of 43 students completed the case-based learning session survey (37% response rate), and 98% ( n = 42) of students strongly agreed or agreed that the session was effective and useful. Performance on the dermatologic questions of the IM Shelf Exam was analyzed. While not statistically significant at P < 0.05, students improved from an average of 77% correct responses before intervention to 79% afterward ( P = 0.60). Conclusions Our case-based and bedside teaching interventions were met with high satisfaction from medical students and increased their confidence in describing skin lesions. This intervention can serve as a model to improve dermatology education and can be adapted to utilize the IM clerkship to address curriculum inadequacies at other institutions.

Human skin forms a biologically active barrier and maintains vital protective functions through continuous regeneration of cells within its outermost layer, the epidermis. In healthy skin, renewal of epithelial cells is a tightly regulated process in which the epidermal growth factor receptor (EGFR or HER1) and its various ligands are involved. The biological role of other EGFR family members (HER2–4) in normal and diseased human skin has gained less interest. The purpose of this work was to investigate the expression and contribution of different HERs in cultured epidermis and psoriatic skin. Epidermal regeneration was studied by fluorescence imaging of a skin explant model exposed to anti-psoriatic drugs, HER ligands or HER-blocking molecules. EGFR, HER2 and HER3 were all markedly expressed with an in vivo-like immunostaining pattern in cultured neoepidermis, whereas only low amounts of HER4 were detected at protein and mRNA levels. Re-epithelialization was associated with receptor activation. Application of HER-selective tyrosine kinase inhibitors and monoclonal antibodies reduced the proliferative activity, receptor phosphorylation and radial outgrowth from normal skin explants. Similar anti-dynamic effects were obtained with HER kinase inhibition of neoepidermis generated from psoriatic skin. Among the HER receptors, EGFR seemed to be the dominant subtype during epithelialization in vitro although HER2 and HER3 were also involved. HER2 probably functioned as a co-receptor for the kinase-deficient HER3 in neoepidermis. In vivo, expression of HER4 mRNA was detected in normal and uninvolved psoriatic skin but was virtually absent in lesional skin, a potentially important finding for HER signalling in psoriasis. This thesis demonstrates the utility of combined dynamic and biochemical analyses of re-epithelialization and highlights the role of EGFR and other HERs for epidermal growth. It also underscores the potential of HER-directed inhibition to control hyperproliferative states of the epidermis.

Positive patch test reactions to gold are commonly seen in dermatology clinics, but it is veryunusual for the patients to actually have any clinical symptoms. It is also common with irritantreactions that are not linked to adaptive immunity. Therefore, a deeper understanding of themechanisms underlying allergic contact dermatitis (ACD) reaction, and the search for acomplementing diagnostic tool, is important. In paper I we included three subject groups; one with morphologically positive patch testreactions to gold sodium thiosulphate (GSTS, the gold salt used in patch testing), one withnegative patch tests, and one with irritant reactions to gold. Blood samples were collected andexamined regarding the proliferation rate and which cytokines were secreted after culturingwith GSTS. We saw that the cultured lymphocytes from the allergic donors proliferated at asignificantly higher rate than the two other subject groups, and that the cells secreted cytokinesof both Th1 (Interferon (IFN) -g and Interleukin (IL) -2) and Th2 (IL-13 and IL-10) types. Theallergic donors secreted significantly higher levels of IFN-g, IL-2 and IL-13 than the two othersubject groups. Both the negative and irritant subject groups showed suppressed levels of thecytokines as compared with the unstimulated cultures, demonstrating the immunosuppressingeffects of gold. We also examined whether any of the analyzed markers, alone or combined, could be usedas an aid for diagnosing ACD to gold. We found that the IFN-g assay yielded the highestsensitivity (81.8 %) and specificity (82.1 %), and also identified 87.5 % of the irritant group asnon-allergic. In paper II we decided to investigate what cell types and subsets that reacted to the goldstimulation. We analyzed proliferation rate and expression of CD45RA, CD45R0, cutaneouslymphocyte-associated antigen (CLA) and the chemokine receptors CXCR3, CCR4 andCCR10. Similar to what has previously been published about nickel (Ni) allergy, the cells fromthe gold-allergic subjects that reacted to the GSTS stimulation expressedCD3+CD4+CD45R0+CLA+. However, contrary to findings in studies on Ni-reactive cells, wesaw no differences between allergic and non-allergic subjects regarding any of the chemokine receptors studied. In conclusion, we found that analysis of IFN-g might be a useful complement to patchtesting, possibly of interest in avoiding the need for repeated tests to rule out irritant reactions.We also saw that the cells that proliferated in response to gold were memory T-cells expressingCD4 and CLA, the marker for skin-homing. However, these cells did not express elevatedlevels of any of the chemokine receptors analyzed, showing that there are both similarities anddifferences between the mechanisms for Ni allergy and gold allergy.

Hereditary ichthyosis is a collective name for many dry and scaly skin disorders ranging in frequency from common to very rare. The main groups are autosomal recessive lamellar ichthyosis, autosomal dominant epidermolytic hyperkeratosis and ichthyosis vulgaris, and x-linked recessive ichthyosis. Anhidrosis, ectropion and keratodermia are common symptoms, especially in lamellar ichthyosis, which is often caused by mutations in the transglutaminase 1 (TGM1) gene. The aim of this work was to study patients with different types of ichthyosis regarding (i) the patho-aetiology (TGM1 and electron microscopy [EM] analysis), (ii) skin signs and symptoms (clinical score and subjective measure of disease activity), (iii) quality of life (questionnaires DLQI, SF-36 and NHP and face-to-face interviews) and (iv) a search for new ways of topical treatment. Patients from Sweden and Estonia with autosomal recessive congenital ichthyosis (n=83) had a broader clinical spectrum than anticipated, but a majority carried TGM1 mutations. Based on DNA analysis and clinical examinations the patients were classified into three groups, which could be further subdivided after EM analysis. Our studies indicate that patients with ichthyosis have reduced quality of life as reflected by DLQI and by some domains of SF-36, by NHP and the interviews. All the interviewees reported that their skin disease had affected them negatively to varying degrees during their entire lives and that the most problematic period was childhood. All patients with ichthyosis use topical therapy. In a double-blind study creams containing either 5% urea or 20% propylene glycol were found inferior to a cream formulation containing lactic acid 5% and propylene glycol 20% both regarding clinical improvement and thinning of the skin barrier. Improved topical therapy may reduce the need of more toxic, oral drugs. Future studies should elucidate whether this increases the quality of life of ichthyosis patients, especially if combined with more detailed information about the aetiology and inheritance of the diseases.

Malignant melanoma is one of the most rapidly increasing cancers and accounts for about three-quarter of all skin cancer deaths worldwide. Despite compelling evidence that ultraviolet (UV) irradiation causes melanoma the knowledge how various wavelength spectra affect the balance between proliferation and apoptosis controlling the homeostasis of the melanocyte population is still limited. The aim of this thesis was to elucidate the regulation of UVA/B induced apoptotic signaling in human epidermal melanocytes in vitro in relation to redox alterations and antioxidant photoprotection. UVA irradiation induced changes in plasma membrane stability, decreased cell proliferation and increased apoptosis. In comparison, melanocyte plasma membrane was markedly resistant to UVB irradiation although apoptosis was triggered. Thus, UVA irradiation should not be overlooked as an etiologic factor in melanoma development. Further, after irradiation with UVA/B we found alterations in redox state manifested by a reduction of intracellular GSH levels, translocation of nuclear factor-κB from the cytosol to the nucleus, an increase of γ-glutamylcysteine synthetase, the rate-limiting enzyme in GSH synthesis, and an increased apoptosis frequency. α-Tocopherol provided photoprotection through several modes of action affecting redox alterations and signaling, stabilizing the plasma membrane, and decreased proliferation and apoptosis rate, while β-carotene did not show the same protective capacity. Altogether, α-tocopherol might be a useful substance in protecting melanocytes from UV induced damage. We demonstrate UVA/B irradiation to activate the intrinsic pathway of apoptosis in melanocytes where translocation of Bcl-2 family proteins to the mitochondria modulates the apoptosis signal. Interestingly, the anti-apoptotic Bcl-2 family proteins generally thought to be attached to membranes, were localized in the cytosol before UV irradiation and translocated to the mitochondria in the surviving population, which might be a critical event in preventing apoptotic cell death. Lysosomal cathepsins were released to the cytosol acting as pro-apoptotic mediators upstream of activation and translocation of Bax to the mitochondria. When melanocytes were exposed to UVA, p53 participated in apoptosis regulation through interaction with Bcl-2 family proteins, while UVB induced p53-transcriptional activity and apoptosis involving lysosomal membrane permeabilization. Thus, depending on the UV wavelength p53 mediated apoptosis in melanocytes by transcriptional dependent or independent activity. These results emphasize p53 as an important pro-apoptotic component in the regulation of apoptosis. This thesis gives new insight in the harmful and various effects of different wavelengths within the UV spectrum on human melanocytes in vitro. Improved knowledge of the apoptosis regulatory systems in melanocytes might lead to a better understanding of the formation of pigment nevi and malignant melanoma and, in the future, provide better strategies to prevent and eliminate tumor development and progression.

Keloids are a fibroproliferative disorder of unknown etiology developing in the skin after injury or spontaneously. The aim of this thesis is to gain deeper insight into the role of TGF-β and its signaling pathway proteins, SMADs, in the pathogenesis of keloids and describe the gene expression profile in different keloid sites in the search for potential target genes for future treatment. Further aim is to develop an instrument to describe the quality of life of patients with keloids. We find cultured keloid fibroblasts to express an increased level of TGF-β1 mRNA and a decreased level of TGF-β3 mRNA compared to control skin. Keloid derived fibroblasts exhibit significantly decreased mRNA levels of TGF-β receptor type II (TβRII) and the ratio of TβRI/TβRII mRNA expression is increased. This suggests that a certain expression pattern of TGF-β subtypes and receptors may be important in keloid pathogenesis. Analysis of keloid derived fibroblasts reveal decreased SMAD3 mRNA expression and decreased ratio of SMAD2/SMAD3 mRNA implicating a disturbed SMAD signaling. Keloid fibroblasts up-regulate SMAD4 protein after stimulation with TGF-β1 and display diminished levels of the inhibitory proteins SMAD6 and 7. This may contribute to unlimited and deregulated TGF-β signaling leading to increased extracellular matrix production (ECM). The gene expression pattern is described in fibroblasts from different keloid sites using microarrays covering the whole human genome. This study reveals 105 regulated genes (79 genes are up- and 26 down-regulated) resulting in a unique gene expression profile in different sites of keloids, where progression or regression of the keloid process took place. In cells from the central part of keloids with clinical signs of regression, an up-regulation of apoptosis inducing genes as ADAM12 and ECM degrading genes as MMP19 is found. These genes may contribute to regression of keloids and might be possible future target genes for treatment. Overexpression of apoptosis inhibitors as AVEN and down-regulation of angiogenesis inhibiting genes as PTX3 found at the active margin of keloids may be responsible for the invasive character of the keloid margin. We develop a disease specific questionnaire to measure the quality of life of patients with keloids. We find two scales, psychological and physical impairment, describing the dimensions of quality of life in patients with scars. These two scales are independent of each other and show a high test-retest reliability. Single items which clinically characterize the disease show correlations to these scales. The results of this study demonstrate for the first time a severe impairment of quality of life of patients suffering from keloids and hypertrophic scars. In conclusion the described alteration in TGF-β expression and its receptors, the disrupted SMAD signaling pathway and the unique gene expression patterns in different keloid sites provide new knowledge on ECM formation and degradation in keloids. Regulatory genes in ECM homeostasis may be future target genes for keloid prevention, regression and treatment. The disease specific quality of life instrument of patients with keloids and scars is a useful tool to estimate success in future therapeutic efforts over time.

Myelomatose (benmargskreft) er en blodsyk dom som rammer ca 200 nordmenn årlig. Sykdommen kan ikke kureres og karakteriseres av symptomer som benmargssvikt og infeksjonstendenns, men kanskje først og fremst av sykelig nedbrytning av skjelettet. Pasientene rammes i høy utstrekning av benbrudd, hvirvelsammenfall og skjelettsmerter. Mekanismene for bennedbrytning og vekstkontroll står sentralt i avhandlingsarbeidet som består av fem artikler om cytokiners rolle i myelomatose. Cytokiner er signalsubstanser som benyttes i celle-celle-kommunikasjon. Det er sannsynligvis ubalanse av cytokiner som forårsaker den sykelige nedbrytningen av bensubstansen.

Det første delarbeidet omhandler funnet av hepatocyttvekstfaktor (HGF) som er uttrykt hos nesten alle pasienter med myelomatose Dette påvises med forskjellige teknikker og det benyttes bl a en separasjonsmetode for myelomceller basert på Ugelstadkuler som ble utviklet ved IKM i 1993. Videre påvises forhøyede nivåer av HGF i serum fra pasienter. Et interessant funn er at HGF reseptor også er uttrykt i pasientprøver, hvilket kan tale for at myelomceller kan ha en selvstimulerende (autokrin) funksjon.

I det andre delarbeidet vises en dyremodell for myelomatose i immundefekte mus. Et hovedpoeng er at det lar seg gjøre å få vekst av myelomceller i musebenmarg med påvisbare tegn til patologisk bennedbrytning på røntgen og ved histologisk undersøkelse. Musene har forhøyede nivåer av HGF i serum. Benlesjonene ble karakterisert ved hjelp av histomorfometri. Denne undersøkelse viste 99% reduksjon av de bendannende cellene (osteoblaster) og 33% reduksjon av bennedbrytende celler (osteklaster).

I tredje delarbeidet viser man at HGF induserer interleukin (IL)-11-produksjon i osteoblaster. IL-11 er en kjent påskynder av benresorpsjon og osteoklastaktivator. Et interessant fenomen er at HGF ser ut til å være bundet til heparansulfat på cellemembranen og at slikt membranbundet HGF virker bedre enn løselig HGF. Effekten av HGF potensieres av cytokinene TGF-beta og IL-1. En styrke ved arbeidet er at såvel ferskisolerte pasientceller som cellelinjer viser identiske mønstre. Arbeidet angir en mulig måte som HGF kan befremme bennedbrytning.

I fjerde delarbeid vises at cytokinet IL-15 forhindrer programmert celledød (apoptose) i myelomcellelinjen OH-2. Det var fra før kjent at myelomceller relativt hyppig lar seg stimulere av cytokinet IL-6, som fortsatt er den mest anerkjente myelomvekstfaktoren. IL-15 var tilnærmet like potent antiapoptotisk som IL-6, og befremmet også kortvarig proliferasjon. IL-15s effekt kunne potensieres av TNF-alfa

I femte delarbeid påvises at cytokinet benmorfogent protein (BMP)-4 hemmer vekst av myelomceller. BMP-4 befremmer bendannelse. Effekten av BMP-4 kom fram i IL-6-stimulerte cellelinjer og pasientprøver. Effekten skyldtes såvel induksjon av apoptose som stopp i cellesyklus G1-fase. Dette er et mulig viktig funn siden man kan tenke seg at pasienter med myelomatose kunne behandles med BMP-4 eller lignende substanser. På slik måte ville såvel skjelettnedbrytningen som myelomcellevekst kunne påvirkes gunstig.

Arbeidet bidrar til forståelse av molekylære mekanismer for bendestruksjon og myelomcellevekst og ble veiledet av profesor dr. med. Anders Waage. Henrik Hjorth-Hansen har vært stipendiat i Den norske kreftforening, og undersøkelsen ble dessuten støttet av Kreftfondet ved RiT og Blix’ legat.

Diabetic nephropathy (DN) is associated with morbidity and mortality due to cardiovascular disease and renal failure. This study focused on the impact of glycemic control on the development of DN and the metabolic consequences of DN. The euglycemic hyperinsulinemic clamp technique was used to assess insulin sensitivity and insulin clearance. Two different registries, the Diabetes Incidence Study in Sweden (DISS) and the Swedish Childhood Diabetes Registry, as well as questionnaires and data from medical records were used to study diabetic complications in population-based cohorts.

Microalbuminuria is an early marker of DN and may also be associated with impaired insulin sensitiv-ity in diabetic and non-diabetic subjects. We studied the relationship between insulin sensitivity and the degree of albuminuria in patients with type 1 diabetes and micro- or macroalbuminuria but normal glomerular filtration rate (GFR). We did not find a direct quantitative association between the degree of albuminuria and insulin resistance, arguing against a cause-effect relationship.

With progression of DN, a decline in GFR is seen. Patients with severe renal failure have both im-paired insulin sensitivity and insulin clearance. We studied insulin sensitivity and insulin clearance in type 1 diabetes patients with three different degrees of renal involvement (none, only albuminuria, and slightly reduced GFR, ~40-70 ml/min/1.73 m2, respectively). A clear reduction in insulin sensitivity in vivo, but not in insulin clearance, was seen in the group with reduced GFR, and concomitant changes in the levels of PTH, IGF-1, IL-6 and TNF-α were found. In parallel, cellular insulin sensitivity and insulin degradation were examined in vitro, in subcutaneous fat cells but no differences were found between the three groups of patients.

To study the occurrence of renal involvement in patients with modern diabetes treatment we moni-tored a cohort of young adults from the DISS-registry with onset of diabetes in 1987-88 at age 15-34 years. We found that ~7% of the patients had signs of renal involvement, i.e. incipient nephropathy (5%) and overt nephropathy (2%), after a median follow-up of ~9 years and the strongest risk markers were poor glycemic control (HbA1c) and high blood pressure. Patients with type 2 diabetes were most prone to have renal involvement in this age group.

Retrospectively, we studied 94 patients diagnosed with type 1 diabetes in 1981-1992 at age 0-14 years at the Umeå University Hospital. Incipient nephropathy and background retinopathy occurred in 18 and 45%, respectively, of the patients, during ~12 years of follow-up. Glycemic control, also during the first five years of diabetes, was a strong risk marker. Young age at onset of diabetes prolonged the time to development of microvascular complications.

Conclusion: Despite modern diabetes treatment some patients with diabetes develop renal involvement within the first ten years. Inadequate glycemic control, also early in the disease, is a risk marker as well as type 2 diabetes and high blood pressure. In patients with type 1 diabetes and diabetic neph-ropathy a slightly reduced GFR, but not albuminuria, is associated with insulin resistance. Concomi-tant changes in insulin-antagonistic hormones and cytokines may be involved.

Pressemelding:

Behandling av type 2 diabetes har trolig best effekt i en tidlig fase av sykdommen. Dette skriver assistentlege Elisabeth Qvigstad (36) fra Grimstad i doktoravhandlingen sin ved Norges teknisk-naturvitenskapelige universitet NTNU. Arbeidet kan bidra til at det utvikles nye medisiner mot diabetes.

Avhandlingen tar utgangspunkt i type 2 diabetes, som rammer 105-120 000 nordmenn. Tidligere forskning i form av celle- og dyreforsøk har vist at vedvarende høye nivåer av fettsyrer i blodet og langvarig stimulering av insulinfrigjøring kan svekke funksjonen til de insulinproduserende beta-cellene i bukspyttkjertelen. Avhandlingen ville teste om lignende forhold er til stede hos mennesker og om korrigerende tiltak ville bedre insulinfrigjøringen ved type 2 diabetes.

Nivået av frie fettsyrer hos personer med type 2 diabetes er oftest forhøyet. Langvarig faste hos friske gir også forhøyet fettsyrenivå og kan ses på som en modellsituasjon for type 2 diabetes. Qvigstad fant redusert insulinfrigjøring hos friske forsøkspersoner etter 58 timer faste.

Fettsyrenivået i blod under testing ble senket ved hjelp av et nikotinsyrederivat hos friske personer og personer med type 2 diabetes. Hos friske påvirket ikke medikamentet insulinfrigjøring eller -følsomhet. Imidlertid virket behandlingen positivt på insulinfrigjøring hos de diabetikerne som hadde best blodsukker-kontroll. Derimot, når type 2 diabetikere reduserte fett i kosten, ga dette ingen utslag på insulinfrigjøringen, men noe nedsatt insulinfølsomhet. Nivået av fettvevshormoner (leptin, adiponectin) ble redusert. Den egne insulinfrigjøringen ble hemmet med medikamentet diazoxid, og insulininjeksjoner ble brukt som erstatning. Insulinfrigjøringen økte uten å endre insulinbehov eller blodsukkerkontroll sammenliknet med placebo. Disse resultatene tyder på at "betacelle-hvile" er gunstig ved type-2 diabetes.

Qvigstads doktorgradsarbeid bidrar til økt forståelse av betydningen av fettsyrer for insulinfrigjøring og insulinfølsomhet hos friske og ved type 2 diabetes. I tillegg støtter funnene betydningen av "betacelle-hvile», som kan bidra til utvikling av nye medisiner mot diabetes.

http://www.ntnu.no/doktorgrader/dr.med/02.03/qvigstad.htm

The purpose of the study was to:

• Study the effect of vascular gas bubbles on the brain and lung

• Study changes in the endothelial function caused by gas bubbles

• Study the preventive effects of monoclonal anti-C5a antibody on functional changes caused by gas bubbles

It is important to reveal any changes in the function of the endothelium caused by gas bubbles, as the endothelium probably plays an important role in the development of decompression sickness (DCS). Furthermore, we followed up previous studies using monoclonal anti-C5a antibody trying to prevent damages caused by gas bubbles. In order to prevent damages causes by gas bubbles and maybe prevent DCS, the mechanisms behind have to be revealed. This thesis is part of an ongoing project that for several years has tried to bring to light the “secrets” of DCS.

In 2016, more than 76,380 new melanoma cases were diagnosed and 10,130 people were expected to die from skin cancer in the United States (one death per hour) [1]. A recent study demonstrates that the economic burden of skin cancer treatment is substantial and, in the United States, the cost was increased from $3.6 billion in 2002–2006 to $8.1 billion in 2007–2011 [2]. Monitoring moderate and high-risk patients and identifying melanoma in the earliest stage of disease should save lives and greatly diminish the cost of treatment. In this project, we are focused on detection and monitoring of new potential melanoma sites with medium/high risk patients. We believe those patients have a serious need and they need to be motivated to be engaged in their treatment plan. High-risk patients are more likely to be engaged with their skin health and their health care providers (physicians). Considering the high morbidity and mortality of melanoma, these patients are motivated to spend money on low-cost mobile device technology, either from their own pocket or through their health care provider if it helps reduce their risk with early detection and treatment. We believe that there is a role for mobile device imaging tools in the management of melanoma risk, if they are based on clinically validated technology that supports the existing needs of patients and the health care system. In a study issued in the British Journal of Dermatology [2] of 39 melanoma apps [2], five requested to do risk assessment, while nine mentioned images for expert review. The rest fell into the documentation and education categories. This seems like to be reliable with other dermatology apps available on the market. In a study at University of Pittsburgh [3], Ferris et al. established 4 apps with 188 clinically validated skin lesions images. From images, 60 of them were melanomas. Three of four apps tested misclassified +30% of melanomas as benign. The fourth app was more accurate and it depended on dermatologist interpretation. These results raise questions about proper use of smartphones in diagnosis and treatment of the patients and how dermatologists can effectively involve with these tools. In this study, we used a MATLAB (The MathWorks Inc., Natick, MA) based image processing algorithm that uses an RGB color dermoscopy image as an input and classifies malignant melanoma versus benign lesions based on prior training data using the AdaBoost classifier [5]. We compared the classifier accuracy when lesion boundaries are detected using supervised and unsupervised segmentation. We have found that improving the lesion boundary detection accuracy provides significant improvement on melanoma classification outcome in the patient data.