Clinical studies of combined therapy of Lidomex and Keratinamin in atopic dermatitis. Adding statistics of atopic dermatitis in the department of dermatology, Kagawa Medical School.

1990 ◽  
Vol 52 (1) ◽  
pp. 124-130 ◽  
Author(s):  
MASATAKA NISHIMOTO
Keyword(s):  
Atopic Dermatitis ◽  
Medical School ◽  
Clinical Studies ◽  
Combined Therapy

Effectiveness of probiotics in combined therapy of atopic dermatitis

2017 ◽  
pp. 77-80
Author(s):  
S.M. Nedelska ◽  
◽  
O.D. Kuznietsova ◽  
O.O. Shevchenko ◽  
I.A. Kizilova ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Combined Therapy

New possibilities of external therapy for atopic dermatitis based on the use of natural silicon oxide

2020 ◽  
pp. 44-51
Author(s):  
Sh. Z. Мavlyanova ◽  
A. I. Ismogilov ◽  
J. B. Mullakhanov ◽  
A. U. Burkhanov ◽  
Sh. Khonkhodjaev
Keyword(s):  
Atopic Dermatitis ◽  
Clinical Studies ◽  
Silicon Oxide ◽  
Pathological Process ◽  
Symptom Scale ◽  
New Approaches ◽  
Anti Inflammatory

The article presents new approaches to the external therapy of atopic dermatitis using a moisturizing, toning, anti-inflammatory cream «Fatiderm». Clinical studies have shown that Fatiderm cream helps to reduce the severity of the dermatological index of the symptom scale, eliminate subjective sensations, and improve the dynamics of the skin pathological process.

scholarly journals CDK4/6 inhibitors: a novel strategy for tumor radiosensitization

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Yilan Yang ◽  
Jurui Luo ◽  
Xingxing Chen ◽  
Zhaozhi Yang ◽  
Xin Mei ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Clinical Studies ◽  
Cell Cycle Progression ◽  
Combined Therapy ◽  
Small Sample ◽  
Combination Strategies ◽  
Novel Strategy ◽  
Underlying Mechanisms

Abstract Recently, the focus of enhancing tumor radiosensitivity has shifted from chemotherapeutics to targeted therapies. Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors are a novel class of selective cell cycle therapeutics that target the cyclin D-CDK4/6 complex and induce G1 phase arrest. These agents have demonstrated favorable effects when used as monotherapy or combined with endocrine therapy and targeted inhibitors, stimulating further explorations of other combination strategies. Multiple preclinical studies have indicated that CDK4/6 inhibitors exhibit a synergistic effect with radiotherapy both in vitro and in vivo. The principal mechanisms of radiosensitization effects include inhibition of DNA damage repair, enhancement of apoptosis, and blockade of cell cycle progression, which provide the rationale for clinical use. CDK4/6 inhibitors also induce cellular senescence and promote anti-tumor immunity, which might represent potential mechanisms for radiosensitization. Several small sample clinical studies have preliminarily indicated that the combination of CDK4/6 inhibitors and radiotherapy exhibited well-tolerated toxicity and promising efficacy. However, most clinical trials in combined therapy remain in the recruitment stage. Further work is required to seek optimal radiotherapy-drug combinations. In this review, we describe the effects and underlying mechanisms of CDK4/6 inhibitors as a radiosensitizer and discuss previous clinical studies to evaluate the prospects and challenges of this combination.

scholarly journals Complementary use of topical bitter melon for atopic dermatitis

2012 ◽  
Vol 2 (1) ◽  
pp. 7 ◽  
Author(s):  
Dai Park ◽  
Nguyen P. Tran ◽  
Jerald M. Duncan ◽  
D. Betty Lew
Keyword(s):  
Atopic Dermatitis ◽  
Traditional Medicine ◽  
Complementary Medicine ◽  
Clinical Studies ◽  
Skin Disorder ◽  
Momordica Charantia ◽  
Bitter Melon ◽  
Community Interest ◽  
Comparison Trial ◽  
Pruritic Skin

<em>Momordica charantia</em> (bitter melon) is popular in systems of traditional medicine to treat a variety of diseases including atopic dermatitis, which is an inflammatory, chronically relapsing skin disorder characterized by dry, scaly, pruritic skin. While there is growing community interest in adopting bitter melon as a complementary medicine, there are no clinical studies looking at its use for atopic dermatitis. Here we report a case of a 6-yearold female with severe refractory atopic dermatitis that responded to treatment with topical bitter melon in an open half-side comparison trial.

scholarly journals Vitamin E in Atopic Dermatitis: From Preclinical to Clinical Studies

Dermatology ◽  
2020 ◽  
pp. 1-12
Author(s):  
Cheryl Wei Ling Teo ◽  
Shawn Han Yueh Tay ◽  
Hong Liang Tey ◽  
Yee Wei Ung ◽  
Wei Ney Yap
Keyword(s):  
Oxidative Stress ◽  
Atopic Dermatitis ◽  
Vitamin E ◽  
Clinical Studies ◽  
Review Article ◽  
Adjunctive Treatment ◽  
Future Research ◽  
Future Prospects ◽  
Contact Allergen ◽  
The Relationship

<b><i>Background:</i></b> Oxidative stress and inflammation are some of the proposed mechanisms involved in the pathogenesis of atopic dermatitis (AD). Current pharmacotherapeutic approaches are effective yet they are not without adverse effects. Vitamin E has great potential as an adjunctive treatment for AD owing to its antioxidant and anti-inflammatory bioactivities. <b><i>Summary:</i></b> This review article summarizes the current available evidence from cellular, animal and clinical studies on the relationship between vitamin E and AD. The future prospects of vitamin E are also discussed. Vitamin E in practice does not show any toxicity to humans within a range of reasonable dosage. Albeit rarely, vitamin E as a contact allergen should be considered. Collectively, this review envisaged vitamin E as an adjunctive treatment for AD patients. Future research on the distinct effects of different vitamin E isoforms as well as their delivery system in skin disorders is needed.

scholarly journals Barrier-Restoring Therapies in Atopic Dermatitis: Current Approaches and Future Perspectives

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Y. Valdman-Grinshpoun ◽  
D. Ben-Amitai ◽  
A. Zvulunov
Keyword(s):  
Atopic Dermatitis ◽  
Inflammatory Disease ◽  
Clinical Studies ◽  
Skin Barrier ◽  
Future Perspectives ◽  
Barrier Dysfunction ◽  
Gene Encoding ◽  
Promising Strategy ◽  
Topical Treatments ◽  
Barrier Repair

Atopic dermatitis is a multifactorial, chronic relapsing, inflammatory disease, characterized by xerosis, eczematous lesions, and pruritus. The latter usually leads to an “itch-scratch” cycle that may compromise the epidermal barrier. Skin barrier abnormalities in atopic dermatitis may result from mutations in the gene encoding for filaggrin, which plays an important role in the formation of cornified cytosol. Barrier abnormalities render the skin more permeable to irritants, allergens, and microorganisms. Treatment of atopic dermatitis must be directed to control the itching, suppress the inflammation, and restore the skin barrier. Emollients, both creams and ointments, improve the barrier function of stratum corneum by providing it with water and lipids. Studies on atopic dermatitis and barrier repair treatment show that adequate lipid replacement therapy reduces the inflammation and restores epidermal function. Efforts directed to develop immunomodulators that interfere with cytokine-induced skin barrier dysfunction, provide a promising strategy for treatment of atopic dermatitis. Moreover, an impressive proliferation of more than 80 clinical studies focusing on topical treatments in atopic dermatitis led to growing expectations for better therapies.

scholarly journals Effective Menin inhibitor-based combinations against AML with MLL rearrangement or NPM1 mutation (NPM1c)

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Warren Fiskus ◽  
Steffen Boettcher ◽  
Naval Daver ◽  
Christopher P. Mill ◽  
Koji Sasaki ◽  
...  
Keyword(s):  
Fusion Protein ◽  
Cell Line ◽  
Cell Lines ◽  
Clinical Studies ◽  
Combined Therapy ◽  
Npm1 Mutation ◽  
In Vivo Efficacy ◽  
Clinical Responses ◽  
A Cell

AbstractTreatment with Menin inhibitor (MI) disrupts the interaction between Menin and MLL1 or MLL1-fusion protein (FP), inhibits HOXA9/MEIS1, induces differentiation and loss of survival of AML harboring MLL1 re-arrangement (r) and FP, or expressing mutant (mt)-NPM1. Following MI treatment, although clinical responses are common, the majority of patients with AML with MLL1-r or mt-NPM1 succumb to their disease. Pre-clinical studies presented here demonstrate that genetic knockout or degradation of Menin or treatment with the MI SNDX-50469 reduces MLL1/MLL1-FP targets, associated with MI-induced differentiation and loss of viability. MI treatment also attenuates BCL2 and CDK6 levels. Co-treatment with SNDX-50469 and BCL2 inhibitor (venetoclax), or CDK6 inhibitor (abemaciclib) induces synergistic lethality in cell lines and patient-derived AML cells harboring MLL1-r or mtNPM1. Combined therapy with SNDX-5613 and venetoclax exerts superior in vivo efficacy in a cell line or PD AML cell xenografts harboring MLL1-r or mt-NPM1. Synergy with the MI-based combinations is preserved against MLL1-r AML cells expressing FLT3 mutation, also CRISPR-edited to introduce mtTP53. These findings highlight the promise of clinically testing these MI-based combinations against AML harboring MLL1-r or mtNPM1.

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