张艳

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04 9月 2019

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Author : 伤口世界

专业特长:擅长各种肿瘤及外周血管疾病的介入治疗，在华南地区率先开展外周动脉疾病腔内治疗，包括主髂动脉闭塞腔内治疗、髂股胭动脉及膝下球囊血管成形术、动脉斑块旋切术、血管腔内流变除栓术、双向:会师等技术完成各类复杂病变的诊治。

学术任职:中华医学会广东省医学会影像分会委员、中国医师协会介入医师分会常务委员、中国医师协会腔内血管学专业委员会青年委员、广东省健康管理学会血管病学专业委员会常委、广东省抗癌协会肿瘤影像与介入诊治专业委员会委员、广东省医疗行业协会伤口管理分会常委

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The Skin Barrier and Moisturization: Function, Disruption, and Mechanisms of Repair 2026-05-18 00:00

Jeffrey Rajkumara Neha Chandana Peter Liob Vivian Shic

a Department of Dermatology, University of Illinois at Chicago College of Medicine, Chicago, IL, USA;

b Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA;

c Department of Dermatology, University of Arkansas for Medical Sciences, Little Rock, AK, USA

Keywords

Skin barrier · Barrier disruption · Moisturizers

Abstract

Background: The anatomic layers of the skin are well-defined, and a functional model of the skin barrier has recently been described. Barrier disruption plays a key role in several skin conditions, and moisturization is recommended as an initial treatment in conditions such as atopic dermatitis. This review aimed to analyze the skin barrier in the context of the function model, with a focus on the mechanisms by which moisturizers support each of the functional layers of the skin barrier to promote homeostasis and repair. Summary: The skin barrier is comprised of four interdependent layers – physical, chemical, microbiologic, and immunologic – which maintain barrier structure and function. Moisturizers target disruption affecting each of these four layers through several mechanisms and were shown to improve transepidermal water loss in several studies. Occlusives, humectants, and emollients occlude the surface of the stratum corneum (SC), draw water from the dermis into the epidermis, and assimilate into the SC, re- spectively, in order to strengthen the physical skin barrier. Acidic moisturizers bolster the chemical skin barrier by sup-porting optimal enzymatic function, increasing ceramide production, and facilitating ideal conditions for commensal microorganisms. Regular moisturization may strengthen the immunologic skin barrier by reducing permeability and subsequent allergen penetration and sensitization. Key Messages: The physical, chemical, microbiologic, and im-munologic layers of the skin barrier are each uniquely impacted in states of skin barrier disruption. Moisturizers target each of the layers of the skin barrier to maintain homeostasis and facilitate repair.
GLP-1 receptor agonists and coronary plaques regression in diabetic patients after acute coronary syndromes 2026-05-16 00:00

Mauro Gitto1,2 · Federica Catapano1,2 · Marco Francone1,2 · Gianluca Mincione1,2 · Vincenzo Scialò1,2 ·Carlo A. Pivato1,2 · Costanza Lisi1,2 · Damiano Regazzoli1,2 · Davide Cao1,2 · Roberta Maria Fiorina1 ·Alessandra Petrelli3,4 · Loredana Bucciarelli4 · Cristian Loretelli3,4 · Gianluigi Condorelli1,2 · Paolo Fiorina3,4,5 · Giulio Stefanini1,2

Received: 4 October 2025 / Accepted: 15 October 2025 / Published online: 4 November 2025 © The Author(s) 2025

Abstract

Background Despite advances in therapeutic strategies a significant proportion of acute coronary syndrome (ACS) patients experience early coronary artery disease (CAD) progression, particularly those with diabetes.

Aim To evaluate CAD progression in diabetic patients treated with glucagon-like peptide 1 receptor agonists (GLP-1Ra) over 1 year after an ACS.

Methods Patients presenting with non–ST-elevation ACS between 2019 and 2022 were enrolled in a prospective registry and underwent serial coronary computed tomography angiography (CCTA) at baseline (after revascularization, during the index hospitalization) and at 1-year follow-up. The primary endpoint was the absolute change (1 year – baseline) in non-culprit lesion plaque burden (ΔPB) on CCTA, with the absolute change in patient percent atheroma volume (ΔPAV) as a key secondary endpoint. A comprehensive lipidomic, metabolomic, and proteomic plasma assessment was also performed in all GLP-1Ra–treated patients and four randomly selected controls.

Results Of 28 diabetic patients, 7 (25%) with 22 coronary plaques were treated with GLP-1Ra, and 21 (75%) with 65 plaques received other antidiabetic agents. In the 1-year observation frame, both ΔPB (-5.8±12.8% vs. -1.1±13.6%, p=0.041) and ΔPAV (-6.1% [-7.3, -1.8] vs. -0.7% [-2.4, 9.8], p=0.039) were significantly lower in GLP-1Ra-treated patients. Total atheroma volume also showed a numerically greater reduction in the GLP-1Ra cohort (0.7 mm³ [-2.5-8.7] vs. 25.0 mm³ [4.8–39.7]), primarily due to a decrease in plaque fibrofatty volume percentage (-2.9±10.1% vs. 1.0±6.8%, p=0.042). Lipi-domic, metabolomic, and proteomic analyses identified reductions in monoacylglycerols and triacylglycerols, increases in diacylglycerols and phosphatidylethanolamine, a shift from carbohydrate metabolism toward lipid metabolism and hormone regulation, and differential expression of proteins involved in complement activation, endothelial function, and cytoskeletal organization in GLP-1Ra–treated patients compared with controls.

Conclusions In diabetic patients with ACS, GLP-1Ra therapy was associated with a significant regression in coronary plaque burden at 1 year, supported by favorable lipidomic, metabolomic, and proteomic changes. These findings suggest a potential role for GLP-1Ra in modifying atherosclerosis progression beyond glycemic control.

Keywords GLP-1 receptor agonists · Diabetes mellitus · Coronary artery disease · Acute coronary syndrome · Plaque regression
Anxiety, social responsiveness, and grit among patients with KCNJ11- related neonatal diabetes compared to unaffected siblings 2026-05-15 00:00

Jui M. Desai1 · Lisa R. Letourneau-Freiberg1 · Kristen E. Wroblewski2 · Megan N. Scott3 · Michael E. Msall4 · Siri Atma W. Greeley1,4

Received: 27 February 2025 / Accepted: 4 October 2025 / Published online: 27 January 2026 © The Author(s) 2026

Abstract

Aims Neonatal diabetes mellitus (NDM) occurs before 6–12 months of age and is commonly caused by activating mutations in KCNJ11 (KCNJ11-NDM) or ABCC8. Because of brain expression of these mutant ATP-dependent potassium channels, a spectrum of divergent neurodevelopmental difficulties have been described, including developmental delay, epilepsy, and neonatal diabetes (DEND). However, information on anxiety, social responsiveness, and grit is limited.

Methods Individuals with KCNJ11-NDM (N= 12) and their unaffected siblings (N=12) were recruited through the Uni-versity of Chicago Monogenic Diabetes Registry and participants or their parent/caregiver completedthe Screen for Adult/ Child Anxiety Related Disorder (SCAARED/SCARED), the Social Responsiveness Scale, Second Edition (SRS-2), and the Grit Scale.

Results Mean SRS-2 scores were significantly different between KCNJ11-NDM and sibling controls (P= <0.001 ), with 7/10 affected participants, and 0 /11 siblings, having scores suggestive of autism spectrum disorder (ASD). Differences in anxiety (P=0.69) and grit (P=0.46) were not significant when compared to sibling controls; however, 58% (7/12) of KCNJ11-NDM participants and 40% (4/10) of sibling controls had scores indicating an anxiety disorder by either self- or parent-report.

Conclusions Our results agree with previous studies suggesting significant difficulties with social functioning in KCNJ11- NDM, with 7/10 participants having scores suggestive of ASD, strongly reinforcing the need for early neurodevelopmental screening to allow for prompt support. Our report adds to the knowledge of this population in finding robust grit scores but with a high level of anxiety in both KCNJ11-NDM and unaffected siblings. Although families affected by KCNJ11-NDM may have a high risk of anxiety disorders, it is encouraging that affected and unaffected children exhibit robust self-resiliency that will help support functioning through the challenges of life. Study of additional individuals will help to clarify specific challenges, long-term outcomes, and best approaches for monitoring and support.

Keywords Diabetes mellitus · Potassium channels · Brain · Anxiety · Resilience · Genetics

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主任医师、教授、博导，南方医科大学第三附属医院（广东省骨科医院）院长

张艳

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主任医师、教授、博导，南方医科大学第三附属医院（广东省骨科医院）院长

张艳

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