Rationale: Older adults spend the majority of their time in sedentary behaviours (SB). High amounts of SB have been correlated with reduced cognitive performance. Long periods of time spent sitting results in excessive glycemic variability, potentially contributing to cognitive decline. Reducing/replacing SB with short intermittent bouts of light physical activity have shown positive effects on glycemic variability. Thus, interrupting prolonged sitting with bouts of light physical activity may regulate blood glucose and thus mitigate cognitive decline.
Purpose: This study intends to investigate the appropriate interval frequency of post-prandial SB reduction, by light physical activity needed to optimize total and incremental area under the curve for glucose response in overweight older adults at risk for glucose intolerance with mild cognitive impairment in both lab and free-living environments. Second, this study aims to investigate the acute impact of reducing SB on glycemic variability and its relationship with cognition.
Hypothesis: First, there will be a dose-dependent response of more frequent interruptions of SB (more frequent intervals of light physical activity) with better glycemic control. Second, reducing SB will result in less glycemic variability, which will translate into better levels of cognitive performance.
Methods: Generalized linear mixed models with random intercepts will be used to evaluate the differential effects of the experimental conditions on the selected outcomes.

开始日期2025-12-01

申办/合作机构

University of Western Ontario

NCT06143202 / Not yet recruitingN/AIIT

Feasibility of Continuous Glucose Monitor Use In Hospitalized Youth

This study is assessing the feasibility of a continuous glucose monitor during hospital admissions in youth with hyperglycemia due to diabetes or other underlying conditions that requires frequent glucose monitoring, through pediatric patient/family and nursing staff feedback on their perspectives and usability of the system in the hospital will be assessed through surveys. In addition, retrospective glycemic comparisons between CGM data and POC will be conducted.

开始日期2025-02-15

申办/合作机构

University of Colorado Denver

[+2]

ACTRN12624000861550 / Not yet recruitingN/AIIT

The impact of an interprofessional exercise program on improving glycaemic management in children and adolescents with type 1 diabetes.

开始日期2025-02-03

申办/合作机构

Southern Cross University

100 项与高血糖相关的临床结果

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100 项与高血糖相关的转化医学

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0 项与高血糖相关的专利（医药）

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92,364

项与高血糖相关的文献（医药）

2025-08-01·Neural Regeneration Research

Interconnections between diabetic corneal neuropathy and diabetic retinopathy: diagnostic and therapeutic implications

Article

作者: Ning, Faith Teo En ; Yu, Mingyi ; Liu, Yu-Chi ; Liu, Chang

Diabetic corneal neuropathy and diabetic retinopathy are ocular complications occurring in the context of diabetes mellitus. Diabetic corneal neuropathy refers to the progressive damage of corneal nerves. Diabetic retinopathy has traditionally been considered as damage to the retinal microvasculature. However, growing evidence suggests that diabetic retinopathy is a complex neurovascular disorder resulting from dysfunction of the neurovascular unit, which includes both the retinal vascular structures and neural tissues. Diabetic retinopathy is one of the leading causes of blindness and is frequently screened for as part of diabetic ocular screening. However, diabetic corneal neuropathy is commonly overlooked and underdiagnosed, leading to severe ocular surface impairment. Several studies have found that these two conditions tend to occur together, and they share similarities in their pathogenesis pathways, being triggered by a status of chronic hyperglycemia. This review aims to discuss the interconnection between diabetic corneal neuropathy and diabetic retinopathy, whether diabetic corneal neuropathy precedes diabetic retinopathy, as well as the relation between the stage of diabetic retinopathy and the severity of corneal neuropathy. We also endeavor to explore the relevance of a corneal screening in diabetic eyes and the possibility of using corneal nerve measurements to monitor the progression of diabetic retinopathy.

2025-05-01·Current Diabetes Reviews

Stem Cells Reprogramming in Diabetes Mellitus and Diabetic Complications: Recent Advances

Article

作者: Madkor, Hafez R. ; Abd El-Maksoud, Mostafa S. ; Ibrahim, Islam M. ; Ali, Fares E.M. ; Abd El-Aziz, Mostafa K.

Background:The incidence of diabetes mellitus (DM) is dramatically increasing worldwide, and it is expected to affect 700 million cases by 2045. Diabetes influences health care economics, human quality of life, morbidity, and mortality, which were primarily seen extensively in developing countries. Uncontrolled DM, which results in consistent hyperglycemia, may lead to severe life-threatening complications such as nephropathy, retinopathy, neuropathy, and cardiovascular complications.Methodology:In addition to traditional therapies with insulin and oral anti-diabetics, researchers have developed new approaches for treatment, including stem cell (SC) therapy, which exhibits promising outcomes. Besides its significant role in treating type one DM (T1DM) and type two DM (T2DM), it can also attenuate diabetic complications. Furthermore, the development of insulin-producing cells can be achieved by using the different types of SCs, such as embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), and multiple types of adult stem cells, such as pancreatic, hepatic, and mesenchymal stem cells (MSC). All these types have been extensively studied and proved their ability to develop insulin-producing cells, but every type has limitations.Conclusion:This review aims to enlighten researchers about recent advances in stem cell research and their potential benefits in DM and diabetic complications.

2025-05-01·Current Diabetes Reviews

Association of the Immunity Genes with Type 1 Diabetes Mellitus

Article

作者: Bakkali, Mohammed ; Khaiz, Youssef ; Al Idrissi, Najib ; Ahid, Samir

:Type 1 diabetes mellitus (T1D) is a complicated illness marked by the death of insulin- producing pancreatic beta cells, which ultimately leads to insulin insufficiency and hyperglycemia. T lymphocytes are considered to destroy pancreatic beta cells in the etiology of T1D as a result of hereditary and environmental factors. Although the latter factors are very important causes of T1D development, this disease is very genetically predisposed, so there is a significant genetic component to T1D susceptibility. Among the T1D-associated gene mutations, those that affect genes that encode the traditional Human Leukocyte Antigens (HLA) entail the highest risk of T1D development. Accordingly, the results of decades of genetic linkage and association studies clearly demonstrate that mutations in the HLA genes are the most associated mutations with T1D. They can, therefore, be used as biomarkers for prediction strategies and may even prove to be of value for personalized treatments. Other immunity-associated genetic loci are also associated with higher T1D risk. Indeed, T1D is considered an autoimmune disease. Its prevalence is rising globally, especially among children and young people. Given the global rise of, and thus interest in, autoimmune diseases, here we present a short overview of the link between immunity, especially HLA, genes and T1D.

1,209

项与高血糖相关的新闻（医药）

2024-10-31

·PipelineReview

BridgeBio Oncology Therapeutics (BBOT) Announces First Patient Dosed with First-in-Class BBO-10203, a RAS:PI3Kα Breaker, in the Phase 1 BREAKER-101 Trial for Advanced Solid Tumors

SOUTH SAN FRANCISCO, CA, USA I October 30, 2024 I TheRas, Inc. d/b/a BridgeBio Oncology Therapeutics (“BBOT” or the “Company”), a clinical-stage biopharmaceutical company focused on RAS-pathway malignancies, has announced that the first patient has been dosed with BBO-10203 in the BREAKER-101 trial. BBO-10203 is a first-in-class orally bioavailable RAS:PI3Ka breaker that blocks the interaction between RAS and PI3Kα to inhibit PI3Kα-AKT signaling in tumors, without directly inhibiting the catalytic activity of PI3Kα. “I am thrilled to partner with BBOT to bring a potentially transformable new therapeutic to the clinic,” said Dr. Minal Barve, Chief Medical Officer and Principal Investigator at Mary Crowley Cancer Research, Dallas, TX. “BBO-10203 represents a first-in-class drug with potential to address high unmet medical needs and change the landscape of cancer care. We look forward to evaluating BBO-10203 in the BREAKER-101 trial.” BBO-10203 was designed to bind covalently and selectively to the RAS-binding domain (RBD) of PI3Kα. This selective inhibition is agnostic to the mutational status of PI3Kα and RAS, and in preclinical models, results in complete inhibition of RAS-driven pAKT signal at single digit nanomolar concentration. Additionally, no hyperglycemia was observed in preclinical species treated with BBO-10203. The discovery of BBO-10203 was the result of a collaboration between the RAS Initiative at Frederick National Laboratory, Lawrence Livermore National Laboratory, and BBOT. “BBO-10203 is a first-in-class program that inhibits the interaction of the two most mutated oncogenes in human cancer, and it will allow us to test, for the first time, the importance of RAS-coordinated activation of the MAPK and AKT signaling pathways,” said Pedro Beltran, PhD, Chief Scientific Officer of BBOT. “The discovery of BBO-10203 was made possible by the dedicated collaboration between academic, national laboratory, and industry experts that synergized to advance medicines for patients suffering from cancer.” The BREAKER-101 trial will enroll patients globally with locally advanced or metastatic HER2-positive breast cancer, HR-positive/HER2-negative breast cancer, KRAS mutant advanced colorectal cancer, and KRAS mutant advanced non-small cell lung cancer. “There is a tremendous opportunity to improve the standard of care in oncology by inhibiting oncogenic pAKT signaling without the metabolic side effects observed with kinase inhibitors, and the initiation of the Phase 1 study of BBO-10203 marks an important milestone in this regard,” said Yong (Ben) Ben, MD, Chief Medical and Development Officer of BBOT. “The second IND within six months of establishing BBOT clearly demonstrates our team’s capability in advancing our novel programs into the clinic. This novel mechanism and scientific rationale behind it will allow tremendous combination opportunities that optimally inhibit both pAKT and pERK – an approach we hope will bring unprecedented benefit to patients with RAS-driven cancers.” About TheRas, Inc. d/b/a BridgeBio Oncology Therapeutics (BBOT) BridgeBio Oncology Therapeutics (BBOT) is a clinical-stage biopharmaceutical company advancing a next generation pipeline of novel small molecule therapeutics targeting RAS and PI3K malignancies. Initially formed as a subsidiary of BridgeBio, BBOT completed a $200M private financing with external investors in 2024 with the goal of improving outcomes for patients with cancers driven by the two most prevalent oncogenes in human tumors. For more information visit bridgebiooncology.com . SOURCE: BridgeBio Oncology Therapeutics

临床1期

2024-10-28

·奇点网

BMJ：这套控糖方案真的太牛了！中山一院团队证实，“强化-简化”疗法可以帮助80%的初诊2型糖尿病患者持久控制血糖丨临床大发现

*仅供医学专业人士阅读参考糖尿病，真要命。前不久，帝国理工学院的研究人员发现，到50岁时，1/3的糖尿病患者会患至少3种慢病，这些疾病会伴随他们至少20年，并缩减了起码11年的寿命[1]。从分子机制层面来看，高血糖会导致β细胞被活活饿死[2]，会导致胰腺细胞中促癌KRAS突变暴增[3]，会让巨噬细胞成促进动脉粥样硬化病变[4]，会促进抑癌蛋白p53的降解[5]，还会导致肺部树突状细胞抗原提呈能力降低[6]，等等。难怪牛津大学的研究人员发现，2型糖尿病患者确诊后如果及时采取强化血糖控制，与全因死亡风险降低10%-20%相关[7]。然而，遗憾的是，尽管采取了各种降糖治疗措施，半数以上的患者血糖控制仍不充分[8]。这表明，早期糖尿病患者亟需更有效的治疗策略。近日，由中山大学附属第一医院的李延兵领衔的研究团队，在顶级医学期刊《英国医学杂志》（BMJ）上发表一篇重磅研究成果[9]。她们基于一项临床研究发现，在接受为期2-3周的短期胰岛素强化治疗（SIIT）控制住血糖之后，启动为期48周的利格列汀+二甲双胍“简化”治疗，可以帮助80%以上的新确诊2型糖尿病患者控制住血糖，而对照组的这一比例只有60%。不难看出，李延兵团队给新确诊的2型糖尿病患者提供了一种更有效的新选择。可以预见，这种方法有望帮助糖尿病患者减少并发症，并提升患者的生活/生命质量。 ▲ 论文首页截图据统计，在2021年，全球20-79岁人群的糖尿病流行率达到10.5%，累计近5.4亿人患病[10]。对于早期的2型糖尿病而言，已经有研究发现，短期胰岛素强化治疗（SIIT）可以有效控制住血糖水平，消除高血糖毒性，改善β细胞功能和胰岛素敏感性。遗憾的是，SIIT的疗效难以持久，一般在SIIT之后，约70%患者会达到缓解，到一年之后缓解率只有50%，到第二年年底仅剩约40%[11]。这意味着，在SIIT之后，需要一套策略，帮助维持SIIT的效果。正是在这种情况下，李延兵团队提出了一种“强化-简化”策略，并开展了这项多中心随机对照试验。她们将SIIT作为初始疗法，然后使用简化的口服抗糖尿病药物作为维持疗法。她们推测这个方案可以改善新确诊2型糖尿病和严重高血糖患者的血糖控制，并保护患者的β细胞功能。在2017年12月至2020年12月期间，研究人员共筛选出464名患者，其中412名符合条件（平均年龄为46.8岁，平均BMI为25.8）。所有患者的HbA1c（11.0%）、空腹血糖（11.4mmol/L）和餐后两小时血糖（20.5mmol/L）浓度均较高。所有患者按1:1:1:1的比例，随机分成4组并都接受了2-3周的SIIT治疗，其中有39名患者失访。随后四组患者分别接受为期48周的利格列汀、二甲双胍、利格列汀+二甲双胍或单纯生活方式调整（对照组）治疗。最终，有321名患者完成了48周的随访（各组患者数量如下图所示）。 ▲ 研究流程图所有患者接受SIIT后，空腹血糖从11.4mmol/L降至5.9mmol/L，餐后两小时血糖从20.5mmol/L降至13.8mmol/L，HbA1c从11.0%降至9.2%（均P<0.001）。此外，患者的血脂状况也有所改善，β细胞功能和胰岛素敏感性均有所恢复，各组之间无显著差异。在接受为期48周的简化口服抗糖尿病药物治疗之后，71%（266/373）的患者在第48周达到了HbA1c<7.0%的主要终点。四组第48周时达到HbA1c<7.0%的患者比例分别为：利格列汀+二甲双胍组80%（78/97），利格列汀组72%（63/88），二甲双胍组73%（69/95），对照组60%（56/93）。经多重比较调整后，利格列汀+二甲双胍组与对照组的差异有统计学意义（P=0.003），而利格列汀组与对照组、二甲双胍组与对照组的差异没有统计学意义（分别为P=0.12和P=0.09）。此外，利格列汀+二甲双胍组、利格列汀组和二甲双胍组的患者中，分别有70%（68/97）、68%（60/88）和68%（65/95）的HbA1c达到了<6.5%，而对照组的这一数据仅为48%（45/93）。 ▲ 四组数据比较从安全性数据来看，在整个治疗期间均未发生严重低血糖事件。简化口服抗糖尿病药物治疗的耐受性良好。最常见的不良反应是胃肠道副作用，二甲双胍组（16/103；16%）和利格列汀+二甲双胍组（18/103；17%）的发生率，均高于利格列汀组（7/103；7%）和对照组（4/103；4%）。利格列汀+二甲双胍组有3人因胃肠道副作用而退出，二甲双胍组有5人。没有参与者死亡。基于以上研究成果，研究人员认为，她们提出的“强化-简化”方案著改善了新确诊2型糖尿病患者的血糖水平。简单来说，SIIT快速消除了高血糖毒性（平均空腹血糖从11.4mmol/L降至5.9mmol/L），改善了β细胞功能，而且这些降糖益处通过简化的口服药物治疗方案得到了很好的维持。这项研究结果意味着，在管理早期糖尿病时，这种“强化-简化”方案值得推荐。研究人员还认为，这项原理性研究也为今后的探索提供了一个新的领域：在“强化”阶段中，可探索可在门诊环境中应用、更切实可行的强化方法；在“简化”阶段，也可考虑使用更方便的药物。参考文献： [1].Gregg EW, Pratt A, Owens A, et al. The burden of diabetes-associated multiple long-term conditions on years of life spent and lost. Nat Med. 2024;30(10):2830-2837. doi:10.1038/s41591-024-03123-2 [2].Zhang E, Mohammed Al-Amily I, Mohammed S, et al. Preserving Insulin Secretion in Diabetes by Inhibiting VDAC1 Overexpression and Surface Translocation in β Cells. Cell Metab. 2019;29(1):64-77.e6. doi:10.1016/j.cmet.2018.09.008 [3].Hu CM, Tien SC, Hsieh PK, et al. High Glucose Triggers Nucleotide Imbalance through O-GlcNAcylation of Key Enzymes and Induces KRAS Mutation in Pancreatic Cells. Cell Metab. 2019;29(6):1334-1349.e10. doi:10.1016/j.cmet.2019.02.005 [4].Edgar L, Akbar N, Braithwaite AT, et al. Hyperglycemia Induces Trained Immunity in Macrophages and Their Precursors and Promotes Atherosclerosis. Circulation. 2021;144(12):961-982. doi:10.1161/CIRCULATIONAHA.120.046464 [5].Su Y, Luo Y, Zhang P, et al. Glucose-induced CRL4COP1-p53 axis amplifies glycometabolism to drive tumorigenesis. Mol Cell. 2023;83(13):2316-2331.e7. doi:10.1016/j.molcel.2023.06.010 [6].Nobs SP, Kolodziejczyk AA, Adler L, et al. Lung dendritic-cell metabolism underlies susceptibility to viral infection in diabetes. Nature. 2023;624(7992):645-652. doi:10.1038/s41586-023-06803-0 [7].Adler AI, Coleman RL, Leal J, Whiteley WN, Clarke P, Holman RR. Post-trial monitoring of a randomised controlled trial of intensive glycaemic control in type 2 diabetes extended from 10 years to 24 years (UKPDS 91). Lancet. 2024;404(10448):145-155. doi:10.1016/S0140-6736(24)00537-3 [8].Wang L, Gao P, Zhang M, et al. Prevalence and Ethnic Pattern of Diabetes and Prediabetes in China in 2013. JAMA. 2017;317(24):2515-2523. doi:10.1001/jama.2017.7596 [9].Liu L, Ke W, Li H, et al. Intense simplified strategy for newly diagnosed type 2 diabetes in patients with severe hyperglycaemia: multicentre, open label, randomised trial. BMJ. 2024;387:e080122. Published 2024 Oct 15. doi:10.1136/bmj-2024-080122 [10].Sun H, Saeedi P, Karuranga S, et al. IDF Diabetes Atlas: Global, regional and country-level diabetes prevalence estimates for 2021 and projections for 2045 [published correction appears in Diabetes Res Clin Pract. 2023 Oct;204:110945. doi: 10.1016/j.diabres.2023.110945]. Diabetes Res Clin Pract. 2022;183:109119. doi:10.1016/j.diabres.2021.109119 [11].Kramer CK, Zinman B, Retnakaran R. Short-term intensive insulin therapy in type 2 diabetes mellitus: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2013;1(1):28-34. doi:10.1016/S2213-8587(13)70006-8 本文作者丨BioTalker

临床结果临床研究

2024-10-28

·美通社

男性健康日培养良好运动习惯提升整体健康水平

--美纳里尼"自由随心爱力随行"骑行活动圆满举行深圳 2024年10月28日 /美通社/ -- 10月28日是第25个男性健康日，今年的主题为："人口发展高质量，男性健康全周期"，呼吁全社会关注男性健康，推广疾病科普，提升疾病诊疗率，提升男性全生命周期健康水平，提高人口质量。积极响应关爱男性健康和全民健身号召，美纳里尼联合KEEP、海王星辰共同发起"自由随心爱力随行"关爱男性健康伴侣骑行活动，开展大规模线上骑行的同时，于10月27日、29日，在深圳和上海组织线下公益骑行活动。中华医学会男科学分会青委、广东省医学会男科分会青委副主委、深圳市医学会男科分会秘书长段永刚教授、海王星辰医药连锁集团有限公司副总裁张妙、美纳里尼中国首席执行官陈家麟与KEEP运动专家、骑行达人和企业代表，共同出席并参与骑行仪式，并携手男性健康领域专家一起推广公益科普，呼吁公众对男性健康领域的关注，也号召男性保持良好运动习惯，从而提升自身整体健康水平。 "近年来，男性健康疾病的发病率呈每年递增趋，前列腺疾病、性功能障碍、不育症等男性健康疾病，对患者身心及家庭和谐造成影响，更对公共卫生事业形成挑战。"陈家麟表示，"美纳里尼深耕男性健康领域十余年，致力于通过不同形式的行业协作创新与探索，帮助患者获得更好的诊疗帮助。很荣幸我们此次的骑行活动得到了行业专家、KEEP和海王星辰的大力支持，在男性健康日这一重要节点，让更多男性动起来，迈出提升健康新一步。" 男性健康，是家庭幸福与社会和谐的基石健康是全面建成小康社会的重要内涵，也是家庭幸福、社会和谐的重要基石。在"健康中国2030"这一宏伟蓝图的指引下，国家积极致力于人民的身心健康与整体生活质量的全面提升。然而，随着工作节奏、生活方式的快速变化，男性在家庭和社会中面临更大压力，健康"男"题逐渐浮出水面。勃起功能障碍（ED）和早泄（PE）是两种最常见的男性健康疾病。中国初级卫生保健基金会关爱男性健康公益基金发布的《男性健康与伴侣幸福手册》中表明，在中国，40岁以上男性ED的发病率达41%，且随着年龄增长，发病率逐渐升高；超1/3的男性患有PE [2] ，且多数PE患者伴随ED共病发生 [1] 。深圳市医学会男科分会秘书长段永刚教授段永刚教授表示："两性健康关系是和谐健康中国的重要基石之一。男性健康疾病的病因和发病机制复杂，‘三高'（高血压、高血糖、高血脂）、前列腺相关疾病，抑郁等心理问题却可能导致两性生活不尽如人意，同时，男性健康疾病往往伴随发生，互相影响、相互加重，亟需男性及伴侣的重视。如果出现疑似症状，可以采用国际勃起功能指数问卷简化版（IIEF-5）进行自测，并第一时间去医院进一步检查、确诊。" 指南推荐，5型磷酸二酯酶抑制剂（PDE5i）和选择性5-羟色胺再摄取抑制剂（SSRI）是治疗ED和PE的推荐治疗药物，其安全性和有效性已经经过长时间的市场验证 [2] 。"男性健康疾病在治疗方面，有多种手段可供选择，从包括生活方式、心理干预在内的基础治疗，到药物治疗、中医治疗、手术治疗，以及各种治疗方式的联合。通过规范化的治疗，绝大多数男性健康疾病患者都可以达到满意的治疗效果。"段永刚教授表示，"患者在治疗时，也要将伴侣和家庭等社会因素引入疾病管理中，并加强情感沟通和心理疏导，这样有助于稳固两性和谐关系，对治疗结果也能带来积极影响。" 自由随心，良好运动习惯塑造活力健康现代人的绝大多数时间都是以坐卧为主，而久坐及缺乏运动等不健康的生活方式也是男性健康疾病，如ED的风险因素之一 [3-4] 。一项研究表明，经常运动的中青年男性比缺乏运动的中青年男性，具有更好的勃起功能、性欲以及更高的性交满意度 [3] 。良好的生活习惯（如戒烟戒酒、适度运动及规律性生活等）不仅对勃起功能有益，而且对整体健康有益。部分 ED 患者经过有效的干预或基础治疗，甚至可以恢复正常的勃起功能 [4] 。海王星辰医药连锁集团有限公司副总裁张妙 "海王星辰扎根社区、赋能社区，通过社区辐射更广泛的受众，这非常符合我们此次骑行活动的宗旨。我们希望通过此次活动，与专业合作伙伴一起推广健康的生活方式，提升社区整体健康水平，帮助更多有需要的患者及公众。"张妙提到。"男性健康疾病具有隐私性强的特点，患者往往隐忍就医，耽误了病情。而家门口的连锁药店可以为患者提供更便捷的药物可及性和综合服务。因此，海王星辰将倡导并推行专业的药师服务作为我们重点打造的服务领域，助力患者获得更多疾病认知，并且提供初步诊断。" 美纳里尼中国首席执行官陈家麟陈家麟认为，"作为男性健康领域的领导者，美纳里尼通过完善的产品组合，成熟的应用经验和深刻的市场洞察，为男性及其伴侣提供优质药物和综合解决方案。我们希望从疾病科普、生活方式、诊疗模式、药物可及性等多方面着手，全面提升男性健康疾病的诊断率和就诊率，助力中国伴侣之间的自然健康两性生活。" 除深圳、上海两地的线下骑行外，此次"自由随心爱力随行"关爱男性健康伴侣骑行活动也在KEEP APP端开展为期三周的线上骑行活动，将健康生活、保持运动习惯的理念传递给更广泛的人群，让更多人关注男性健康日，关爱男性健康和伴侣幸福。参考文献：《男性健康与伴侣幸福手册》. 中国初级卫生保健基金会关爱男性健康公益基金. 晏斌,郭博达,赵明,等.ED-PE共病中西医结合多学科诊疗指南(2024版)[J].中国男科学杂志,2024,38(05):3-12. 杨林.你想雄风不减吗?运动起来[J].大众健康,2023,(02):108-109. 勃起功能障碍诊断与治疗指南[J].中华男科学杂志,2022,28(08):722-755.