Gotowe bibliografie tematyczne / Actinic keratosis

Gotowa bibliografia na temat „Actinic keratosis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Actinic keratosis"

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Mark, Brady, Jaxon Dawson i Dominic Chase. "The Management of Actinic Keratosis and Squamous Cell Carcinoma". Dermatology and Dermatitis 2, nr 1 (26.02.2018): 01–03. http://dx.doi.org/10.31579/2578-8949/019.

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Background: Actinic keratosis or solar keratosis is a common skin lesion caused by sun damage that progresses to squamous cell carcinoma. It has been suggested that actinic keratosis is in fact SCC in situ. Objective: This literature review was conducted to investigate the differences between actinic keratosis and squamous cell carcinoma and whether actinic keratosis should in fact be managed as squamous cell carcinoma. Methods: A literature review was conducted to assess the differences between actinic keratosis and squamous cell carcinoma. We conducted searches of Pubmed, Cochrane and Medline for articles published between January 1, 2000 and April 30, 2014, using the following search terms: actinic keratosis, solar keratosis, skin cancer, squamous cell carcinoma, dermoscopy, sun exposure, ultra violet radiation, and dysplasia. Studies published in English were selected for inclusion in this review as were additional articles identified from bibliographies. Results: It is difficult to distinguish between both actinic keratosis and squamous cell carcinoma. Perhaps a classification system for actinic keratosis including early in situ SCC type AK1, early in situ SCC type AK2 and in situ SCC type actinic keratosis is needed. Conclusion: Actinic keratosis invades the basement membrane and as such may progress into invasive SCC. Superficially actinic keratoses are not distinguishable from a superficial SCC and as such may go unrecognized or inaccurately diagnosed.
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Ishioka, Priscila, Sílvio Alencar Marques, Amélia Toyomi Hirai, Mariangela E. A. Marques, Sérgio Henrique Hirata i Sérgio Yamada. "Prevalence of precancerous skin lesions and non-melanoma skin cancer in Japanese-Brazilians in Bauru, São Paulo State, Brazil". Cadernos de Saúde Pública 25, nr 5 (maj 2009): 965–71. http://dx.doi.org/10.1590/s0102-311x2009000500003.

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Precancerous lesions and skin cancer are infrequent in Asians, and have received little documentation in the literature. Brazil has the world's largest contingent of Japanese immigrants and their descendants, and 70% live in the State of São Paulo. The prevalence of such skin lesions in Japanese-Brazilians is unknown. This study aimed to assess the prevalence of actinic keratoses and non-melanoma skin cancer in first and second-generation Japanese-Brazilians over 30 years of age, without miscegenation, living in the city of Bauru, São Paulo State, in 2006. Of the 567 Japanese-Brazilians that underwent dermatological examination, actinic keratosis was diagnosed in 76, with a mean age of 68.9 years, and a single case of basal cell carcinoma was detected in a 39-year-old female patient. In Japan, prevalence of actinic keratosis varies from 0.76% to 5%, and the incidence of non-melanoma skin cancer is 1.2 to 5.4/100 thousand. Japanese-Brazilians from Bauru showed a 13.4% prevalence of actinic keratoses and earlier age at onset. Proximity to the Equator and a history of farming contribute to these higher rates. Presence of solar melanosis was associated with a 1.9-fold risk of developing actinic keratosis.
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Campione, Elena, Monia Di Prete, Cosimo Di Raimondo, Gaetana Costanza, Vincenzo Palumbo, Virginia Garofalo, Sara Mazzilli i in. "Topical Treatment of Actinic Keratosis and Metalloproteinase Expression: A Clinico-Pathological Retrospective Study". International Journal of Molecular Sciences 23, nr 19 (26.09.2022): 11351. http://dx.doi.org/10.3390/ijms231911351.

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Actinic keratosis is an intraepithelial proliferation of atypical keratinocytes that could progress into invasive squamous cell carcinoma. Most evidence suggests an important role of the dermal matrix metalloproteinases in the progression of atypical skin epithelial lesions. We evaluated the clinical efficacy of three different therapeutic modalities (a medical device containing 0.8% piroxicam cream and 50+ sunscreen, photodynamic therapy, and ingenol mebutate gel) to treat suspicious actinic keratoses, which were biopsied for histopathological examination and then analyzed for the expression of matrix metalloproteinases by immunohistochemistry. Clinical, dermoscopic, and reflectance confocal microscopy evaluations revealed a gradual decrease in all standard scores validated for actinic keratosis assessment at the end of the treatments. From a histopathological point of view, we documented the substantial restoration of normal skin architecture, while the immunohistochemical evaluation of matrix metalloproteinases showed a reduction in expression in the treated skin lesions compared to the baseline. As actinic keratoses are considered the precursors of squamous cell carcinoma, their treatment is crucial to prevent the development of a more aggressive disease. Our study monitored the evolution of actinic keratoses subjected to three different topical therapies, with the value of correlating clinical and histopathological findings. Moreover, as the matrix metalloproteinases are largely recognized factors involved in the pathogenesis and evolution of actinic keratosis to squamous cell carcinoma, the demonstration by immunohistochemistry of a reduction in their expression after the treatments adds new valuable concern to the field.
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Schmitt, Juliano, i Hélio Miot. "Oral acetylsalicylic acid and prevalence of actinic keratosis". Revista da Associação Médica Brasileira 60, nr 2 (2014): 131–38. http://dx.doi.org/10.1590/1806-9282.60.02.010.

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Objective: To investigate the influence of a regular oral use of acetylsalicylic acid in the prevalence of actinic keratosis. Methods: A case-control study with dermatologic outpatients above 50 years of age assessed between 2009 and 2011. Cases were defined as those who had been under regular use of oral acetylsalicylic acid for more than six consecutive months. The assessment focused on: age, sex, skin-type, tobacco smoking, use of medication, occurrence of individual or family skin cancer, and sunscreen and sun exposure habits. Actinic keratoses were counted in the medial region of the face and upper limbs. Counts were adjusted by co-variables based on a generalized linear model. Results: A total of 74 cases and 216 controls were assessed. The median time of acetylsalicylic acid use was 36 months. Cases differed from controls as to the highest age, highest prevalence of use of angiotensin-converting enzyme inhibitors and fewer keratosis on the face and on the upper limbs (p<0.05). The multivariate model showed that the use of acetylsalicylic acid was associated to lower counts of face actinic keratosis and upper-limb erythematous actinic keratosis (p<0.05), regardless of other risk factors. Conclusion: The regular use of oral acetylsalicylic acid for more than six months was associated to a lower prevalence of actinic keratosis, especially facial and erythematous ones.
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Yu, Hyunseon, Tien Son Ho, Heesung Kang, Youngwoo Bae, Eung Ho Choi, Seung Ho Choi i Byungjo Jung. "Use of digital photography to identify neoplastic skin lesions after labelling by ALA-derived protoporphyrin". Journal of Porphyrins and Phthalocyanines 25, nr 04 (25.02.2021): 307–13. http://dx.doi.org/10.1142/s1088424621500309.

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Actinic keratosis is a premalignant skin lesion that develops into non-melanoma skin cancer. Various imaging techniques have been developed to find the actinic keratosis lesion. In this clinical study, the feasibility of a nonspectroscopic fluorescence imaging system is investigated for spatial assessment of the actinic keratosis lesion. Six patients between the ages of 70 and 80 years old are diagnosed with actinic keratosis by a board-certified dermatologist to obtain biopsy-proven clinical images. The patients were treated with 5-aminolevulinic acid, which is transformed into the protoporphyrin IX. After illuminating ultraviolet-A light on facial lesions, the protoporphyrin IX produces the exogenous fluorescence. The fluorescence is measured using both a hyperspectral camera and an RGB color camera to obtain spectroscopic and nonspectroscopic fluorescence images, respectively. It is found that fluorescence intensity of the actinic keratosis lesion is higher than that of normal skin. Based on combined fluorescence and physiological characteristics, the actinic keratosis lesion is distinguished from the adjacent normal skin area. For delineation of the actinic keratosis lesion, a linear unmixing algorithm is applied to spectroscopic image data and an erythema index is calculated from nonspectroscopic image data. Then, two extracted actinic keratosis lesions are compared for cross-validation. As a result, both spectroscopic and nonspectroscopic fluorescence images demarcate an identical lesion of actinic keratosis. Given the affordability and simplicity, an RGB camera and a 5-ALA photosensitizer can be used as a cost-effective nonspectroscopic imaging modality for accurate assessment of actinic keratosis margins.
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Jeffes, Edward W., i Emily H. Tang. "Actinic Keratosis". American Journal of Clinical Dermatology 1, nr 3 (maj 2000): 167–79. http://dx.doi.org/10.2165/00128071-200001030-00004.

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Berlin, Joshua M. "Actinic Keratosis". Journal of the Dermatology Nurses’ Association 6, nr 1 (2014): 11–14. http://dx.doi.org/10.1097/jdn.0000000000000015.

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&NA;. "Actinic Keratosis". Journal of the Dermatology Nurses’ Association 6, nr 1 (2014): 15–16. http://dx.doi.org/10.1097/jdn.0000000000000024.

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HIROSE, Ryoji. "Actinic keratosis". Skin Cancer 18, nr 2 (2003): 106–17. http://dx.doi.org/10.5227/skincancer.18.106.

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Nicol, Noreen Heer. "Actinic Keratosis". Plastic Surgical Nursing 9, nr 2 (1989): 49–55. http://dx.doi.org/10.1097/00006527-198900920-00003.

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Więcej źródeł

Rozprawy doktorskie na temat "Actinic keratosis"

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Stritt, Andrea Christina. "Photodynamic therapy in the treatment of actinic keratosis /". Bern : [s.n.], 2008. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Haque, T. "Development of novel pyrrolobenzodiazepines for treatment of skin cancer and actinic keratosis". Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1464117/.

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The pyrrolobenzodiazepines (PBDs) are members of a family of DNA minor-groove binding anticancer agents. Some PBD compounds have very potent in vitro cytotoxicity and in vivo antitumour activities. Topical dosage forms in some cases offer more advantages than oral or parenteral dosage forms as more localised delivery of drug is possible with comparatively lower side effects. However, there are only a few anticancer topical formulations currently available for the treatment of skin cancer. Therefore, the main objective of this project was to develop topical formulations using PBD compounds for the palliative treatment of late stage melanoma patients, and for the treatment of non-melanoma skin cancers and potentially actinic keratosis. In order to develop suitable topical formulations for PBD compounds, a number of formulations were initially evaluated using anthramycin, a model PBD compound. In addition, the permeation and retention of the penetration enhancers (solvents) in human skin were also evaluated. Single solvent analysis results showed that Transcutol® and propylene glycol (PG) were the most highly permeable solvents. For all formulations, anthramycin absorption was comparatively higher in PG:PGML (propylene glycol monolaurate) (90:10). A focussed library of PBD C8-conjugates and a PBD-dimer (SJG-136) were also evaluated using dimethyl sulphoxide as a solvent. Potential topical efficacy was confirmed for a number of the compounds based on skin flux values and in vitro potency data. KMR-04-175 and KMR-28-24 were ranked as the most topically effective PBD conjugates. SJG-136 which has reached Phase II clinical trials, also showed higher skin absorption values compared with the other PBD compounds (except for KMR-28-24). This is the first report describing the preparation and evaluation of topical formulations of PBD compounds. The results are encouraging and suggest that topical formulations of PBD compounds could be efficacious for the topical treatment of skin cancers and potentially actinic keratosis.
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Azimi, Ali. "PROTEOMIC ANALYSIS OF ACTINIC KERATOSIS, BOWEN’S DISEASE AND CUTANEOUS SQUAMOUS CELL CARCINOMA". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20449.

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Cutaneous squamous cell carcinoma (cSCC), premalignant actinic keratosis (AK) and Bowen’s disease (BD) are highly prevalent, heterogeneous keratinocytic skin lesions (KSLs). Discrepancies between clinical presentations and histologic analyses of KSLs frequently lead to misdiagnoses or delayed diagnoses. Biomarkers that can accurately stratify KSLs by their malignant potential are urgently needed to support a paradigm shift in skin cancer care to personalised, precision medicine. In this thesis, a liquid chromatography tandem mass spectrometry (MS) platform was employed to conduct comprehensive proteomic profiling of formalin-fixed and paraffin embedded samples of normal skin and KSLs. Using complementary MS approaches, namely information dependent acquisition (IDA) and sequential windowed acquisition of all theoretical fragment ion mass spectra (SWATH-MS), 3574 proteins were quantified overall allowing the identification of novel protein signatures for KSL subtypes. Proteomic findings were further investigated in silico using transcriptome databases, and several interesting targets were confirmed by immunohistochemistry. Distinct proteome profiles corresponding to subcategories of cSCC and precursor lesions were found, demonstrating the potential of MS-based approaches to deliver reliable diagnostics and disease staging. The bioinformatic analysis provided new insights into molecular pathways disrupted in different KSLs. The successful application of a non-invasive tape-stripping method for proteome sampling of KSLs was also demonstrated. This work represents the most comprehensive proteome study of KSLs to date. The identification of deferentially altered proteins and molecular pathways between subtypes of KSLs will inform the development of diagnostic, therapeutic and disease staging strategies. Further exploration and implementation of the approaches described herein could have a major impact on patient outcomes and reduce the cost burden of KSLs.
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Sáenz, Sardà Xavier. "Progression pathways of squamous cell carcinoma associated with actinic damage: From cancer field to actinic keratosis and invasive squamous cell carcinoma". Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667918.

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Se pensaba que la progresión de una queratosis actínica (AK) a carcinoma escamoso infiltrante (SCC) de piel ocurría siempre y cuando la neoplasia intra-epidérmica ocupara todo el espesor de la epidermis como ocurre en la vía clásica (CP) descrita en el cáncer de cérvix. Sin embargo, el carcinoma escamoso infiltrante cutáneo puede aparecer directamente desde una displasia que sólo ocupe el tercio inferior de la epidermis (AK I, vía diferenciada o DP). Esta segunda vía de progresión se ha descrito en el SCC de vulva y de cavidad oral , cuyo comportamiento biológico es además más agresivo. Esta tesis empezó revisando todos los casos correspondientes a biopsias quirúrgicas, obtenidas mediante el BioBanco del Hospital Germans Trias y Pujol, de tres años consecutivos correspondientes al período 2004-2007. Seleccionamos 503 casos de SCC cutáneo, de los que finalmente estudiamos 196. La mayor parte mostraron AK I en superficie (63.8%) o en los bordes (77.9%), concluyendo así que la invasión directa desde AK I (DP) es la forma más frecuente de progresión a SCC cutáneo. Este estudio fue el primero que se propuso investigar la prevalencia de la CP y DP en la transformación de la AK en SCC infiltrante aportando evidencias de su existencia. Estos hallazgos se publicaron en J Eur Acad Dermatol Venereol. 2014 Oct; 29(5):991-7.). La siguiente etapa del estudio consistió en la realización de una matriz de tejidos (TMA) de las biopsias ya estudiadas y se segregaron los casos con SCC entre los originados por DP y los originados por CP. En total se realizaron ocho TMA que supusieron 756 cores a evaluar. Mediante el uso de técnicas de inmunohistoquímica se evidenció que la transición epitelio-mesénquima participa en la transformación de AK I en SCC (DP) mientras que una capacidad proliferativa mayor facilita la extensión intra-epidérmica en la vía clásica y se hallaron diferencias significativas en cuanto a la expresión de CD31 (angiogénesis) y MMP (metaloproteinasas) hallándose estos marcadores elevados en los tumores que progresan por DP, lo que junto con la transición epitelio-mesenquima podría facilitar la progresión local. Una parte de estos resultados han sido publicados en la revista J Eur Acad Dermatol Venereol. 2018 Apr; 32(4):581-586). Tambien se procedio al uso de técnicas de CISH para el estudio de miRNA hallándose los tumores surgidos por DP expresan mayores niveles de miRNA31 tanto en su intensidad como en su extensión. En la siguiente etapa se estudió la extensión de la atipia queratinocitaria por el epitelio de los anejos estando esta presente en el 25.9% de los casos y, de ellos, la infiltración del carcinoma escamoso directamente adyacente a la basal folicular estaba presente en el 58% de los casos. En consecuencia, seria altamente recomendable indicar la profundidad de la extensión folicular en el diagnóstico histológico de biopsias incisionales, dado el riesgo de recurrencia e infiltración que ello implica, así como las derivadas terapéuticas que conlleva. Los hallazgos han sido publicados en la revista J Eur Acad Dermatol Venereol. 2018 Oct; 32(10):1657-1661). Consideramos que la serie de estudios que conforman esta tesis proporcionan conocimiento nuevo sobre las vías de progresión del SCC cutáneo y de sus lesiones precursoras. Se ha establecido que existen al menos dos vías de progresión de SCC a AK, se ha introducido el concepto de DP en la carcinogénesis cutánea, se han hallado bases moleculares que explican la progresión a través de ambas vías y se ha constatado el riesgo de la extensión folicular en la AK. Todos estos estudios han supuesto en algunos ámbitos un cambio de paradigma y tienen relevancia tanto en el diagnóstico como en el tratamiento de las AK.
It was thought that the progression of an actinic keratosis (AK) to invasive squamous cell carcinoma (SCC) occurred as long as the intra-epidermal neoplasm occupied the entire thickness of the epidermis as in the classical pathway (PC) described in cervix cancer. However, cutaneous infiltrative squamous carcinoma can appear directly from a dysplasia that only occupies the lower third of the epidermis (AK I, differentiated pathweay or DP). This second pathway of progression has been described in SCC of the vulva and oral cavity, whose biological behavior is more aggressive. This thesis began by reviewing all cases corresponding to surgical biopsies, obtained through the BioBanco of the Germans Trias and Pujol Hospital, for three consecutive years corresponding to the period 2004-2007. We selected 503 cases of cutaneous SCC, of ​​which we finally studied 196. Most showed AK I on the surface (63.8%) or on the edges (77.9%), thus concluding that the direct invasion from AK I (DP) is the most frequent form of progression to cutaneous SCC. This study was the first one that was proposed to investigate the prevalence of CP and DP in the transformation of AK into infiltrating SCC, providing evidence of its existence. These findings were published in J Eur Acad Dermatol Venereol. 2014 Oct; 29 (5): 991-7.). The next stage of the study consisted in the realization of a tissue microarrays (TMA) of the biopsies already studied and the cases with SCC were segregated between those originated by DP and those originated by CP. In total, eight TMAs were performed, which involved 756 cores to be evaluated. Through the use of immunohistochemical techniques it was demonstrated that the epithelial-mesenchymal transition participates in the transformation of AK I into SCC (DP) while a greater proliferative capacity facilitates the intra-epidermal extension in the classical pathway and significant differences were found in to the expression of CD31 (angiogenesis) and MMP (metalloproteinases), these markers being elevated in tumors that progress through DP, which together with the epithelium-mesenchymal transition could facilitate local progression. A part of these results have been published in the journal J Eur Acad Dermatol Venereol. 2018 Apr; 32 (4): 581-586). We also proceeded to the use of CISH techniques for the study of miRNA, finding that tumors arising from DP express higher levels of miRNA31 both in their intensity and in their extension. In the next stage the extension of the keratinocyte atypia among adnexal structures was studied, being present in 25.9% of the cases and, of them, the infiltration of the squamous carcinoma directly adjacent to the follicular basal was present in 58% of the cases. Consequently, it would be highly advisable to indicate the depth of follicular extension in the histological diagnosis of incisional biopsies, given the risk of recurrence and infiltration that this implies, as well as the therapeutic derivatives that it entails. The findings have been published in the journal J Eur Acad Dermatol Venereol. 2018 Oct; 32 (10): 1657-1661). We consider that the series of studies that make up this thesis provide new knowledge about the pathways of cutaneous SCC progression and its precursor lesions. It has been established that there are at least two pathways of progression from SCC to AK, the concept of PD has been introduced in cutaneous carcinogenesis, molecular bases have been found that explain the progression through both pathways and the risk of follicular extension in the AK. All these studies have led to a paradigm shift in some areas and are relevant both in the diagnosis and treatment of AKs.
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Werner, Ricardo Niklas [Verfasser]. "Systematic review of the natural course of actinic keratosis and their relation to squamous cell carcinoma / Ricardo Niklas Werner". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1057869708/34.

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Buinauskaitė, Evelina. "AKTININĖS KERATOZĖS FOTODINAMINIO GYDYMO SKIRTINGOMIS RAUDONOSIOS ŠVIESOS DOZĖMIS VEIKSMINGUMAS". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2014. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2014~D_20140618_233345-93532.

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Šio tyrimo tikslas buvo įvertinti aktininės keratozės klinikinius ypatumus ir fotodinaminio gydymo skirtingomis raudonosios šviesos dozėmis veiks-mingumą. Aktininė keratozė – tai ikinavikinė odos liga, pasireiškianti ilgalaikio saulės poveikio srityse, o jos diagnozė nustatoma remiantis klinikiniu vaizdu. Histologinis tyrimas atliekamas tik neaiškiais atvejais. Vis tik pasitaiko diagnozavimo klaidų ir nesuta¬pimo atvejų tarp tyrėjų dermatologų bei dermatopatologų. Šiame darbe įvertinome ir nustatėme AK klinikinės raiškos ypatumus bei jų sąsajas su histologiniais požymiais, o taip pat AK klinikinio tyrimo jautrumą ir specifiškumą, remiantis histologinio tyrimo duomenimis. Nuo 0,025 iki 20 proc. atvejų AK transfor¬muojasi į plokščiųjų ląstelių karcinomą. Aktininę keratozę rekomenduojama gydyti, nes prognozuoti, kuri AK plis iš epidermio į gilesnius odos sluoksnius ir taps plokščiųjų ląstelių karcinoma, neįmanoma. Veiksmingas bei saugus būdas gydyti AK yra vietinio poveikio foto¬dinaminis gydymas, tačiau jo trūkumas – skausmas procedūros metu. Atlikę perspektyvųjį tyrimą, įvertinome aktininės keratozės klinikinės raiškos ypatumus po fotodinaminio gydymo su 5-aminolevulino rūgštimi. Nustatėme skausmą procedūros metu įtakojančius veiksnius. Nustatėme šio gydymo dviejomis raudonosios šviesos dozėmis veiksmingumą po dvejų metų stebėjimo bei AK atkrytį prognozuojančius veiksnius. Pateikėme praktines šio AK gydymo rekomendacijas.
The aim of this study was to evaluate clinical characteristics of actinic keratosis and the efficacy of photodynamic treatment with different red light doses. The diagnosis of AK is based upon its typical clinical aspects. However, there are data stating that diagnosing single AKs clinically is not precise and that there are even interobserver disagreements between dermatologists and dermatopathologists. In this study we assessed the clinical peculiarities of AK and its correlation with histological characteristics. We assessed the sensitivity and specificity of AK clinical diagnosis based on histopathological analysis. In 0.025% to 20% cases AK transforms into squamous cell carcinoma. It is impossible to predict which AK will spread from the epithelium into the deeper layers of the skin. Therefore, treatment of actinic keratosis is recommended in all cases. Topical photodynamic treatment is safe and effective therapy for AK but pain is the limitation of the procedure. We performed a prospective within-patient study and evaluated the clinical pecularities of actinic keratosis after photodynamic treatment. We assessed the factors that influence pain during the treatment. We assessed the efficacy of photodynamic treatment with different red light doses for actinic keratosis after two-years follow-up. Factors that influence the recurrence of AK were evaluated. Follow-up data for two years was used to formulate the practical recommendations of the study.
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Ashton, Kevin John. "Genetic Aberrations in Non-Melanoma Skin Cancer". Thesis, Griffith University, 2002. http://hdl.handle.net/10072/367012.

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Genetic changes are hallmarks of cancer development involving the activation and/or inactivation of oncogenes and tumour suppressor genes, respectively. In non-melanoma skin cancer (NMSC) development, the initiation of genetic mutations results from exposure to solar ultraviolet radiation. Non-melanoma skin cancers are comprised of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Several related cutaneous lesions also exist, of which solar keratoses (SK) are widely accepted as a precursor dysplasia to SCC development. The study of recurrent genetic changes present within NMSC and SK should help reveal causative mutations in skin cancer development. Such analysis could also elucidate links in the genetic similarity of these dysplasia. The rapid screening of numerical changes in DNA sequence copy number throughout the entire genome has been made possible by the advent of comparative genomic hybridisation (CGH). This technique enables the identification of net gains and loss of genetic material within a tumour DNA sample. Chromosomal regions of recurrent gain or loss identify loci containing putative oncogenes and tumour suppressor genes, respectively with potential roles in NMSC tumourigenesis. Used in conjunction with tissue microdissection and universal degenerate PCR techniques this can enable the elucidation of aberrations in small histologically distinct regions of tumour. Such a technique can utilize archival material such as paraffin embedded tissue, which is the major source of neoplastic material available for cancer research. This study used the CGH technique to investigate aberrations in BCC, SCC and SK samples. The screening of copy number abnormalities (CNAs) in BCC revealed that although these tumours were close to diploid and generally genetically stable, they did contain several recurrent aberrations. The loss of genetic material at 9q was identified in a third of BCC tumours studied. This is characteristic of inactivation of the PTCH tumour suppressor gene, a known attribute in some sporadic BCC development. Validation of this loss was performed via loss of heterozygosity, demonstrating good concordance with the CGH data. In addition the over-representation of the 6p chromosome arm was revealed in 47% of biopsies. This novel CNA is also commonly observed in other cutaneous neoplasias, including Merkel cell carcinoma and malignant melanoma. This suggests a possible common mechanism in development and or promotion in these cutaneous dysplasias, the mechanisms of which have yet to be clearly defined. In contrast to BCC, numerical genetic aberrations in SCC and SK were much more frequent. Several regions of recurrent gain were commonly shared between both dysplasias including gain of 3q, 4p, 5p, 8q, 9q, 14q, 17p, 17q and 20q. Common chromosomal regions of loss included 3p, 8p, 9p, 11p, 13q and 17p. In addition loss of chromosome 18 was significantly observed in SCC in comparison to SK, a possible defining event in SK progression to SCC. The identification of shared genetic aberrations suggests a clonal and genetic relationship between the two lesions. This information further supports the notion for re-classification of SK to an SCC in situ or superficial SCC. Finally, the CNAs detected have been similarly observed in other squamous cell-derived tumours, for example cervical and head and neck SCC. This provides further evidence to common mechanisms involved in the initiation, development and progression of SCC neoplasia. This study has identified a number of recurrent chromosomal regions, some of which are novel in NMSC development. The further delineation of these loci should provide additional evidence of their significance and degree of involvement in NMSC tumourigenesis. The identification of the cancer-causing genes mapped to these loci will further demarcate the genetic mechanisms of BCC and SCC progression. An understanding of the events involved in skin cancer formation and progression should shed additional light on molecular targets for diagnostics, management and therapeutic treatment.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
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Costa, Sabrina dos Santos [UNESP]. "Proliferação celular e expressão da cicloxigenase-2 como parâmetros prognósticos na ceratose actínica e no carcinoma de células escamosas cutâneo em cães". Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/89218.

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Este estudo apresenta uma análise comparativa da taxa de proliferação celular e da expressão da enzima cicloxigenase-2 na pele de cães saudáveis e acometidos por ceratose actínica e carcinoma de células escamosas cutâneo (CCE). O objetivo foi avaliar o prognóstico destes cães utilizando-se a imunorreatividade a COX-2 e o índice de proliferação celular. Foram analisados 20 amostras de pele de cães, sendo 10 casos de ceratose actínica (G1) e 10 de CCE cutâneo (G2). Os dados epidemiológicos e as características clínicas e histopatológicas foram estudados. A taxa de proliferação celular foi avaliada por meio de índice mitótico (IM) e imunomarcação para MIB-1. A expressão da enzima cicloxigenase foi pesquisada por exame imunoistoquímico. Os cães da raça Pit Bull foram os mais acometidos em G1 e G2 e a média de idade foi 4,3 (±0,8) anos e 5,6 (±1,7) anos, respectivamente. Os valores médios do índice mitótico foram 0,4; 4,6 (±3,6) e 4,9 (±2,6) em G0, G1 e G2, respectivamente. Não houve diferença estatística entre G1 e G2, mas sim em relação ao G0. Houve imunomarcação para COX-2 em G1 e G2, a média dos escores foi 8,16 (±3,51) e 8,56 (±1,03), respectivamente. Não houve imunomarcação nas amostras de G0 e não houve diferença estatística entre G1 e G2, mas sim em relação ao G0 (p>0,05). A média da porcentagem de células imunomarcadas para Ki-67 em G0, G1 e G2 foi 0,4; 15,77 (± 8,81) e 17,71 (± 12,21), respectivamente. Não houve diferença entre G1 e G2, mas sim destes em relação ao G0 (p>0,05). A ceratose actínica se comportou como o CCE cutâneo, revelando não ser uma lesão pré-neoplásica, mas sim o estágio inicial da neoplasia propriamente dita.
This research presents a comparative analysis of cell proliferation index and cyclooxigenase-2 expression in skin of healthy and with actinic keratosis and cutaneous squamous cell carcinoma (SCC) dogs. The goal was to evaluate the prognosis of these dogs by COX-2 immunorreactivity and cell proliferation index. Skin sections from 20 dogs were evaluated, which 10 were actinic keratosis (G1) and 10 cutaneous SCC (G2). Epidemiological information, clinical and histopathological aspects were evaluated. Cell proliferation index hás been stimated by mitotic index (MI) and MIB-1 staining. Cyclooxigenase-2 expression has been analyzed by immunohistochemistry study. Pit Bull dogs were the main affected in G1 and G2 and the mean age was 4,3 (±0,8) years old and 5,6 (±1,7) years old, relatively. MI mean values were 0,4; 4,6 (±3,6) and 4,9 (±2,6) in G0, G1 and G2, relatively. There was no statistical difference between G1 and G2, but it did with G0. There was positive staining for COX-2 in G1 and G2, the score mean value was 8,16 (±3,51) and 8,56 (±1,03), relatively. There was no positive staining in G0 samples and neither statistical difference between G1 and G2, but it did with G0 (p>0,05). The positive cells for Ki-67 mean percentage in G0, G1 and G2 was 0,4; 15,77 (± 8,81) and 17,71 (± 12,21), relatively. There was no difference between G1 and G2, but it did with G0 (p>0,05). Actinic keratosis behavior was similar to cutaneous SSC, demonstrating that it is not a pre-neoplastic disease, but, in fact, the initial of neoplasm.
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Costa, Sabrina dos Santos. "Proliferação celular e expressão da cicloxigenase-2 como parâmetros prognósticos na ceratose actínica e no carcinoma de células escamosas cutâneo em cães /". Jaboticabal : [s.n.], 2009. http://hdl.handle.net/11449/89218.

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Orientador: Mário Roberto Hatayde
Banca: Mirela Tinucci Costa
Banca: Andrigo Barboza De Nardi
Resumo: Este estudo apresenta uma análise comparativa da taxa de proliferação celular e da expressão da enzima cicloxigenase-2 na pele de cães saudáveis e acometidos por ceratose actínica e carcinoma de células escamosas cutâneo (CCE). O objetivo foi avaliar o prognóstico destes cães utilizando-se a imunorreatividade a COX-2 e o índice de proliferação celular. Foram analisados 20 amostras de pele de cães, sendo 10 casos de ceratose actínica (G1) e 10 de CCE cutâneo (G2). Os dados epidemiológicos e as características clínicas e histopatológicas foram estudados. A taxa de proliferação celular foi avaliada por meio de índice mitótico (IM) e imunomarcação para MIB-1. A expressão da enzima cicloxigenase foi pesquisada por exame imunoistoquímico. Os cães da raça Pit Bull foram os mais acometidos em G1 e G2 e a média de idade foi 4,3 (±0,8) anos e 5,6 (±1,7) anos, respectivamente. Os valores médios do índice mitótico foram 0,4; 4,6 (±3,6) e 4,9 (±2,6) em G0, G1 e G2, respectivamente. Não houve diferença estatística entre G1 e G2, mas sim em relação ao G0. Houve imunomarcação para COX-2 em G1 e G2, a média dos escores foi 8,16 (±3,51) e 8,56 (±1,03), respectivamente. Não houve imunomarcação nas amostras de G0 e não houve diferença estatística entre G1 e G2, mas sim em relação ao G0 (p>0,05). A média da porcentagem de células imunomarcadas para Ki-67 em G0, G1 e G2 foi 0,4; 15,77 (± 8,81) e 17,71 (± 12,21), respectivamente. Não houve diferença entre G1 e G2, mas sim destes em relação ao G0 (p>0,05). A ceratose actínica se comportou como o CCE cutâneo, revelando não ser uma lesão pré-neoplásica, mas sim o estágio inicial da neoplasia propriamente dita.
Abstract: This research presents a comparative analysis of cell proliferation index and cyclooxigenase-2 expression in skin of healthy and with actinic keratosis and cutaneous squamous cell carcinoma (SCC) dogs. The goal was to evaluate the prognosis of these dogs by COX-2 immunorreactivity and cell proliferation index. Skin sections from 20 dogs were evaluated, which 10 were actinic keratosis (G1) and 10 cutaneous SCC (G2). Epidemiological information, clinical and histopathological aspects were evaluated. Cell proliferation index hás been stimated by mitotic index (MI) and MIB-1 staining. Cyclooxigenase-2 expression has been analyzed by immunohistochemistry study. Pit Bull dogs were the main affected in G1 and G2 and the mean age was 4,3 (±0,8) years old and 5,6 (±1,7) years old, relatively. MI mean values were 0,4; 4,6 (±3,6) and 4,9 (±2,6) in G0, G1 and G2, relatively. There was no statistical difference between G1 and G2, but it did with G0. There was positive staining for COX-2 in G1 and G2, the score mean value was 8,16 (±3,51) and 8,56 (±1,03), relatively. There was no positive staining in G0 samples and neither statistical difference between G1 and G2, but it did with G0 (p>0,05). The positive cells for Ki-67 mean percentage in G0, G1 and G2 was 0,4; 15,77 (± 8,81) and 17,71 (± 12,21), relatively. There was no difference between G1 and G2, but it did with G0 (p>0,05). Actinic keratosis behavior was similar to cutaneous SSC, demonstrating that it is not a pre-neoplastic disease, but, in fact, the initial of neoplasm.
Mestre
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Ashton, Kevin John, i K. Ashton@griffith edu au. "Genetic Aberrations in Non-Melanoma Skin Cancer". Griffith University. School of Health Science, 2002. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20030818.122305.

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Genetic changes are hallmarks of cancer development involving the activation and/or inactivation of oncogenes and tumour suppressor genes, respectively. In non-melanoma skin cancer (NMSC) development, the initiation of genetic mutations results from exposure to solar ultraviolet radiation. Non-melanoma skin cancers are comprised of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Several related cutaneous lesions also exist, of which solar keratoses (SK) are widely accepted as a precursor dysplasia to SCC development. The study of recurrent genetic changes present within NMSC and SK should help reveal causative mutations in skin cancer development. Such analysis could also elucidate links in the genetic similarity of these dysplasia. The rapid screening of numerical changes in DNA sequence copy number throughout the entire genome has been made possible by the advent of comparative genomic hybridisation (CGH). This technique enables the identification of net gains and loss of genetic material within a tumour DNA sample. Chromosomal regions of recurrent gain or loss identify loci containing putative oncogenes and tumour suppressor genes, respectively with potential roles in NMSC tumourigenesis. Used in conjunction with tissue microdissection and universal degenerate PCR techniques this can enable the elucidation of aberrations in small histologically distinct regions of tumour. Such a technique can utilize archival material such as paraffin embedded tissue, which is the major source of neoplastic material available for cancer research. This study used the CGH technique to investigate aberrations in BCC, SCC and SK samples. The screening of copy number abnormalities (CNAs) in BCC revealed that although these tumours were close to diploid and generally genetically stable, they did contain several recurrent aberrations. The loss of genetic material at 9q was identified in a third of BCC tumours studied. This is characteristic of inactivation of the PTCH tumour suppressor gene, a known attribute in some sporadic BCC development. Validation of this loss was performed via loss of heterozygosity, demonstrating good concordance with the CGH data. In addition the over-representation of the 6p chromosome arm was revealed in 47% of biopsies. This novel CNA is also commonly observed in other cutaneous neoplasias, including Merkel cell carcinoma and malignant melanoma. This suggests a possible common mechanism in development and or promotion in these cutaneous dysplasias, the mechanisms of which have yet to be clearly defined. In contrast to BCC, numerical genetic aberrations in SCC and SK were much more frequent. Several regions of recurrent gain were commonly shared between both dysplasias including gain of 3q, 4p, 5p, 8q, 9q, 14q, 17p, 17q and 20q. Common chromosomal regions of loss included 3p, 8p, 9p, 11p, 13q and 17p. In addition loss of chromosome 18 was significantly observed in SCC in comparison to SK, a possible defining event in SK progression to SCC. The identification of shared genetic aberrations suggests a clonal and genetic relationship between the two lesions. This information further supports the notion for re-classification of SK to an SCC in situ or superficial SCC. Finally, the CNAs detected have been similarly observed in other squamous cell-derived tumours, for example cervical and head and neck SCC. This provides further evidence to common mechanisms involved in the initiation, development and progression of SCC neoplasia. This study has identified a number of recurrent chromosomal regions, some of which are novel in NMSC development. The further delineation of these loci should provide additional evidence of their significance and degree of involvement in NMSC tumourigenesis. The identification of the cancer-causing genes mapped to these loci will further demarcate the genetic mechanisms of BCC and SCC progression. An understanding of the events involved in skin cancer formation and progression should shed additional light on molecular targets for diagnostics, management and therapeutic treatment.
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Książki na temat "Actinic keratosis"

1

Actinic keratosis. Basel: Karger, 2015.

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Soyer, H. P., T. W. Prow i G. B. E. Jemec, red. Actinic Keratosis. S. Karger AG, 2014. http://dx.doi.org/10.1159/isbn.978-3-318-02763-1.

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Piérard, Gérald E., Claudine Franchimont i Philippe Delvenne. Thousand and One Facets of Actinic Keratosis. Nova Science Publishers, Incorporated, 2013.

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Publications, ICON Health. Actinic Keratosis: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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Favour, Chika. Aldara: The Perfect Treatment for Different Skin Diseases Genital Warts, Actinic Keratosis and Skin Cancer. Independently Published, 2019.

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Wisozk, Sasha. IMIQUIMOD CREAM: An Immunomodulatory Medication Used to Treat Actinic Keratosis, Minor Form of Skin Cancer and Genital Warts. Independently Published, 2019.

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DuBuque, David. ALDARA CREAM: Effective Medication for the Treatment of Trifling Form of Skin Cancer, Actinic Keratosis, and Genital Warts. Independently Published, 2019.

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Bright, Doctor Amos. Aldara Cream: The Fast and Most Effective Medication for Treating Skin Cancer, Actinic Keratosis and Genital Warts in No Time. Independently Published, 2019.

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Robins, MD Perry. Understanding Actinic Keratoses (What you need to know). Physicians Continuing Education Corp., 2002.

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Green, Adèle C., Catherine M. Olsen i David J. Hunter. Skin Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0015.

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Skin cancer is one of the few types of cancer for which exposure to the major carcinogen, solar ultraviolet (UV) radiation, is strongly implicated on the basis of descriptive epidemiologic data alone. There are three major forms of skin cancer considered in this chapter—melanoma, basal cell carcinoma (BCC), and squamous cell carcinoma (SCC)—and each appears to have different causal relations to the pattern and total amount of sun exposure. High-intensity UV exposure and long-term UV exposure appear to be involved differentially in the various skin cancers and their subtypes. Underlying molecular mechanisms are becoming better understood, though many aspects like the cells of origin and the exact roles of intermediate lesions like actinic keratoses and nevi remain unclear. Because exposure of skin to UV radiation is modifiable, skin cancers are substantially preventable.
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Części książek na temat "Actinic keratosis"

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Green, Adèle C. "Epidemiology of Actinic Keratoses". W Actinic Keratosis, 1–7. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366525.

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Esmann, Solveig. "Patients' Perspectives on Actinic Keratosis". W Actinic Keratosis, 8–13. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366530.

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Wei, Jerry, Lai Fong Kok, Scott N. Byrne i Gary M. Halliday. "Photodamage: All Signs Lead to Actinic Keratosis and Early Squamous Cell Carcinoma". W Actinic Keratosis, 14–19. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366531.

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Frazer, Ian H. "The Actinic Keratosis Virome: Can We Prevent Squamous Cell Carcinoma with a Vaccine?" W Actinic Keratosis, 28–35. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366532.

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Wells, James W. "Do Actinic Keratoses and Superficial Squamous Cell Carcinomas Have a Specific Immunoprofile?" W Actinic Keratosis, 36–41. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366533.

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Handoko, Herlina Y., Blake Ferguson i Graeme J. Walker. "Mouse Models for Actinic Keratosis and Squamous Cell Carcinoma". W Actinic Keratosis, 42–48. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366534.

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Jenni, Daniella, i Günther F. L. Hofbauer. "Keratinocyte Cancer and Its Precursors in Organ Transplant Patients". W Actinic Keratosis, 49–57. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366535.

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Wheller, Laura, i H. Peter Soyer. "Clinical Features of Actinic Keratoses and Early Squamous Cell Carcinoma". W Actinic Keratosis, 58–63. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366536.

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Massone, Cesare, i Lorenzo Cerroni. "The Many Clinico-Pathologic Faces of Actinic Keratosis: An Atlas". W Actinic Keratosis, 64–69. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366538.

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Zalaudek, Iris, i Giuseppe Argenziano. "Dermoscopy of Actinic Keratosis, Intraepidermal Carcinoma and Squamous Cell Carcinoma". W Actinic Keratosis, 70–76. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000366539.

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Streszczenia konferencji na temat "Actinic keratosis"

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Kammerer, Susanne. "Fern extract reverses severe actinic keratosis lesions". W EADV Congress 2022, redaktor Peter van de Kerkhof. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/96eeb9d2.

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Thecua, E., C. Vicentini, A.-S. Vignion, F. Lecomte, P. Deleporte, L. Mortier, R. M. Szeimies i S. Mordon. "Light emitting fabric for photodynamic treatment of actinic keratosis". W SPIE BiOS, redaktorzy Bernard Choi, Haishan Zeng i Nikiforos Kollias. SPIE, 2017. http://dx.doi.org/10.1117/12.2252201.

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Cho, Yong-Jin, Youngwoo Bae, Eung-Ho Choi i Byungjo Jung. "5-ALA induced fluorescent image analysis of actinic keratosis". W BiOS, redaktorzy Nikiforos Kollias, Bernard Choi, Haishan Zeng, Reza S. Malek, Brian J. Wong, Justus F. R. Ilgner, Kenton W. Gregory i in. SPIE, 2010. http://dx.doi.org/10.1117/12.843050.

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Seoni, Silvia, Kristen M. Meiburger, Federica Veronese, Vanessa Tarantino, Elisa Zavattaro, Massimo Salvi, Nicola Michielli, Bruno De Santi, Filippo Molinari i Paola Savoia. "Non-invasive analysis of actinic keratosis using a cold stimulation and near-infrared spectroscopy". W 2019 41st Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2019. http://dx.doi.org/10.1109/embc.2019.8857279.

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Litniewski, Jerzy, Hanna Piotrzkowska-Wroblewska, Andrzej Nowicki i Elzbieta Szymanska. "Statistics of envelope of ultrasonic backscatter from Basal Cell Carcinoma and Actinic Keratosis lesion". W 2014 IEEE International Ultrasonics Symposium (IUS). IEEE, 2014. http://dx.doi.org/10.1109/ultsym.2014.0474.

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Takayama, Ryoko, Toshiyuki Ishiwata, Shin-ichi Ansai, Tetsushi Yamamoto, Yoko Matsuda, Seiji Kawana i Zenya Naito. "Abstract 5531: Lumican as a novel differential diagnostic maker for Bowen's disease and actinic keratosis". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5531.

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Sun, Chi-Kuang, Yi Pan, Pei-Che Wu, Sheng-Tse Chen i Yi-Hua Liao. "Clinical applicability of in vivo harmonic generation microscopy for the diagnosis and grading of actinic keratosis (Conference Presentation)". W Photonics in Dermatology and Plastic Surgery 2020, redaktorzy Bernard Choi i Haishan Zeng. SPIE, 2020. http://dx.doi.org/10.1117/12.2541484.

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Vignion-Dewalle, Anne-Sophie, Claire Vicentini, Gregory Baert, Elise Thécua, Fabienne Lecomte, Laurent Mortier i Serge R. Mordon. "Photodynamic therapy for actinic keratosis: a trend towards a decrease in irradiance without loss of efficacy for a better tolerability". W 17th International Photodynamic Association World Congress, redaktor Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2528112.

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Anand, Sanjay, Anton Yasinchak, Mukul Govande, Sajina Shakya i Edward V. Maytin. "Painless versus conventional photodynamic therapy for treatment of actinic keratosis: comparison of cell death and immune response in a murine model". W Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXVIII, redaktorzy David H. Kessel i Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2511646.

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Darvin, M. E., M. Klemp, M. Weinigel, M. C. Meinke, K. Konig i J. Lademann. "In vivo imaging for detection and discrimination of actinic keratosis and squamous cell carcinoma from healthy human skin using two-photon tomography". W 2016 International Conference Laser Optics (LO). IEEE, 2016. http://dx.doi.org/10.1109/lo.2016.7549987.

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Raporty organizacyjne na temat "Actinic keratosis"

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5% fluorouracil cream is the best first-line treatment for actinic keratosis skin lesions. National Institute for Health Research, czerwiec 2019. http://dx.doi.org/10.3310/signal-000775.

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