To thoroughly implement the strategic deployment outlined in the Opinions of the Central Committee of the Communist Party of China and the State Council on Promoting the Inheritance and Innovative Development of Traditional Chinese Medicine regarding research on dominant diseases of traditional Chinese medicine and to uphold the development philosophy of equal emphasis on traditional Chinese medicine and western medicine，the China Association of Chinese Medicine has fully played a leading academic role by systematically organizing and conducting a series of academic youth salons on clinical dominant diseases of traditional Chinese medicine. On September 13，2024，the 36^th Youth Salon on Clinical Dominant Diseases was successfully held in Nanjing，focusing on the advantages of traditional Chinese medicine and the integrative traditional Chinese medicine and western medicine in the diagnosis and treatment of erectile dysfunction （ED）. The conference brought together leading experts from traditional Chinese medicine，western medicine，and interdisciplinary fields，facilitating in-depth multidisciplinary discussions that led to key consensus on optimizing traditional Chinese medicine treatment protocols for ED，researching and developing new drugs of traditional Chinese medicine，and advancing interdisciplinary development in traditional Chinese medicine. This salon systematically sorted out the clinical strengths and distinctive features of traditional Chinese medicine in the diagnosis and treatment of ED. Based on current research foundations and clinical needs，it identified key directions for future scientific layout and scientific research tackling： （1） Standardization of syndrome differentiation system of traditional Chinese medicine for ED. （2） Optimization and standardization of intervention methods of integrated traditional Chinese medicine and western medicine. （3） High-quality clinical research guided by evidence-based medicine. （4） In-depth analysis of the pharmacological mechanisms of traditional Chinese medicine in the treatment of ED. （5） Clinical translation and application promotion of new drugs of traditional Chinese medicine. （6） Interdisciplinary integration and innovation in traditional Chinese medicine. For each research direction，key focus areas，expected objectives，and clinical value were further refined，along with the establishment of a scientifically sound priority funding level evaluation system. Therefore，building on the series of salons on the ED-focused dominant diseases of traditional Chinese medicine，this paper provides standardized guidance for clinical practice of traditional Chinese medicine in ED management，effectively contributing to the high-quality development of traditional Chinese medicine. It serves as a valuable reference for national scientific and technological strategic layout， research and development decision-making in new drugs of traditional Chinese medicine，research topic planning，and clinical guideline formulation.

Phosphodiesterase type 5(PDE5)participates in the physiological functions of multiple organs by regulating the nitric oxide(NO)-cyclic guanosine monophosphate(cGMP)pathway.As a long-acting PDE5 inhibitor,tadalafil has been used clinically for over 20 years and is approved for the treatment of male erectile dysfunction and lower urinary tract symptoms associated with benign prostatic hyperplasia.Furthermore,tadalafil maintains cGMP levels by inhibiting PDE5,thereby activa-ting the downstream NO-cGMP signaling pathway to exert multiple effects,including relaxing smooth muscle,exerting antioxidant actions,regulating apoptosis,and modulating metabolism.Clinical evidence indicates that tadalafil shows promising therapeutic potential in multi-organ system diseases such as pulmonary arterial hypertension,heart failure,type 2 diabetes,cognitive impair-ment,female infertility,and fetal growth restriction.This article systematically reviews the action mechanisms and research pro-gress of tadalafil in treating diseases beyond erectile dysfunction,aiming to summarize its potential for cross-disease system clini-cal applications and provide references for optimizing treatment strategies for patients with chronic diseases.

Erectile dysfunction(ED)is a common sexual dysfunction in adult males.With the accelerated pace of modern life and lifestyle changes,the prevalence of ED and its associated comorbidities have been steadily rising.Problems such as premature ejaculation,hypertension,hyperlipidemia,diabetes,prostate diseases,and infertility all interact with and aggravate ED,thereby endangering the overall health of men.Phosphodiesterase type 5 inhibitors(PDE5i)is the first-line pharmacotherapy for ED.Tadalafil,currently the only long-acting PDE5i approved for clinical use,has received mar-keting authorization in China for the treatment of ED since 2005.In 2013,the once-a-day continuous regimen was intro-duced as a novel treatment paradigm.And the indication was expanded to ED coexisting with benign prostatic hyperplasia in 2019.Accumulating clinical experience and evidence-based data consistently demonstrate its efficacy and safety across ED and ED-related comorbidities.This review summarizes the pharmacological profile of tadalafil and the latest clinical evi-dence on the management of ED and ED-related comorbidities,aiming to provide a reference for clinical practice.

With the breakthroughs in computer hardware and the advancement of software engineering, artificial intelligence (AI) has exerted a profound impact across various domains, including the medical field. In the realm of urological experimental research, studies have endeavored to employ AI models for the assessment of sperm quality, encompassing routine semen analysis, sperm morphology, and sperm DNA integrity testing. Moreover, AI is beginning to play a role in other urological diagnostic areas, such as pathology, radiology, and genetic testing. The purpose of this article is to summarize the research progress in AI applications within urological laboratory diagnostics, to discuss the current limitations and bottlenecks in AI detection, and to provide a reference for the further application of AI in the urological diagnostic and treatment framework.

Objective:To explore the effect of ginsenoside Rg1 on spermatogenic dysfunction in mice caused by diabetes and its mechanism of action.Methods:Eighteen male C57BL mice were randomly divided into control group, the model group and the ginsenoside Rg1 group by completely random method, with 6 mice in each group. Type 2 diabetes models were established in the model group and the ginsenoside Rg1 group by a high-fat diet combined with intraperitoneal injection of streptozotocin, while control group was injected with the same amount of normal saline. After successful modeling, control group was given a regular diet for 8 weeks, while the model group and ginsenoside Rg1 group were given a high-fat diet for 8 weeks. The ginsenoside Rg1 group was also treated with ginsenoside Rg1 medication. Reproductive hormone levels were detected by enzyme-linked immunosorbent assay test kits, and Western blotting was used to detect the expressions of apoptosis-related proteins (Bcl2 protein, Caspase-3 protein, Bax protein), autophagy-related proteins (P62, LC3Ⅰ, LC3Ⅱ, Beclin1), β-Catenin protein, mTOR protein, LAMP1 protein and transcription factor EB. The body weight, blood glucose levels, testicular index of mice in each group were compared, as well as the testicular injury status.Results:The body weight [(18.77±1.14) g], testosterone level [(141.07±8.47) ng/L], follicle-stimulating hormone level [(9.19±0.74) U/L], and luteinizing hormone level [(1 497.91±99.57) pg/L] of mice in the model group were significantly lower than those in the control [(31.57±2.35) g, P<0.001; (171.50±11.76) ng/L, P<0.001; (12.46±1.54) U/L, P<0.001; (1 807.29±92.76) pg/L, P<0.001]; fasting blood glucose level [(20.82±1.11) mmol/L], glycosylated hemoglobin (12.67%±1.03%), the testis index (0.65%±0.03%) were significantly higher than those in the control [(6.40±1.34) mmol/L, P<0.001; 5.17%±1.17%, P<0.001; 0.48%±0.04%, P<0.001]. Compared with the model group, the body weight [(22.62±0.92) g, P=0.023], testosterone level [(172.63±9.20) ng/L, P<0.001], follicle-stimulating hormone level [(12.37±1.15) U/L, P<0.001], and luteinizing hormone level [(1 847.80±108.80) pg/L, P<0.001] of mice in the ginsenoside Rg1 group increased significantly, fasting blood glucose level [(18.63±1.14) mmol/L, P=0.017], glycosylated hemoglobin (8.50%±1.05%, P<0.001) and testicular index (0.54%±0.02%, P<0.001) decreased significantly. Compared with the control, the expressions of P62 ( P=0.039), LC3Ⅱ/LC3Ⅰ( P<0.001), Beclin1 ( P=0.002) and mTOR ( P=0.036) in the testicular tissue of mice in the model group all increased, the expression of β-Catenin ( P<0.001), LAMP1 ( P=0.005), transcription factor EB ( P<0.001) all decreased. Compared with the model group, the expressions of autophagy-related proteins P62 ( P=0.048), LC3Ⅱ/LC3Ⅰ( P<0.001) , Beclin1 ( P=0.023) and mTOR ( P=0.005) in the ginsenoside Rg1 group all decreased, while the expression of β-Catenin ( P=0.001), LAMP1 ( P=0.011) and transcription factor EB ( P=0.022) all increased. Transmission electron microscopy detected a decrease in the number of autophagosomes in the testicles of mice in the model group, and it improved after drug intervention. The HE staining showed that the testes of mice in the model group exhibited phenotypes such as the shedding and disorganization of spermatogenic cells, while ginsenoside Rg1 was able to improve these phenotypes. Conclusion:Ginsenoside Rg1 can improve testicular injury caused by diabetes in mice by regulating autophagy.

Chronic epididymitis (CE) is a long-standing inflammatory condition of the epididymis caused by unresolved acute infections, chronic infections, medication use, or other factors. Clinically, it is characterized by persistent dull pain or a dragging sensation in one or both sides of the scrotum. The disease course typically exceeds three months and is marked by insidious onset and recurrent episodes. Current studies suggest that CE may disrupt the epididymal microenvironment through multiple pathological processes, including local inflammatory responses, oxidative stress, fibrotic remodeling, and autophagy. These alterations impair sperm maturation, transport, and capacitation, thereby contributing to male reproductive dysfunction and infertility. This review summarizes the major etiologies and pathophysiological characteristics of CE and its impact on male reproductive function. It focuses on the roles of inflammatory cytokines and related signaling pathways, oxidative stress mechanisms, and fibrotic progression in the pathogenesis of CE. Moreover, it explores targeted therapeutic strategies based on these mechanisms, aiming to provide a theoretical basis for identifying key molecular targets and signaling pathways involved in CE-induced male reproductive impairment.

With the breakthroughs in computer hardware and the advancement of software engineering, artificial intelligence (AI) has exerted a profound impact across various domains, including the medical field. In the realm of urological experimental research, studies have endeavored to employ AI models for the assessment of sperm quality, encompassing routine semen analysis, sperm morphology, and sperm DNA integrity testing. Moreover, AI is beginning to play a role in other urological diagnostic areas, such as pathology, radiology, and genetic testing. The purpose of this article is to summarize the research progress in AI applications within urological laboratory diagnostics, to discuss the current limitations and bottlenecks in AI detection, and to provide a reference for the further application of AI in the urological diagnostic and treatment framework.

Objective:To explore the effect of ginsenoside Rg1 on spermatogenic dysfunction in mice caused by diabetes and its mechanism of action.Methods:Eighteen male C57BL mice were randomly divided into control group, the model group and the ginsenoside Rg1 group by completely random method, with 6 mice in each group. Type 2 diabetes models were established in the model group and the ginsenoside Rg1 group by a high-fat diet combined with intraperitoneal injection of streptozotocin, while control group was injected with the same amount of normal saline. After successful modeling, control group was given a regular diet for 8 weeks, while the model group and ginsenoside Rg1 group were given a high-fat diet for 8 weeks. The ginsenoside Rg1 group was also treated with ginsenoside Rg1 medication. Reproductive hormone levels were detected by enzyme-linked immunosorbent assay test kits, and Western blotting was used to detect the expressions of apoptosis-related proteins (Bcl2 protein, Caspase-3 protein, Bax protein), autophagy-related proteins (P62, LC3Ⅰ, LC3Ⅱ, Beclin1), β-Catenin protein, mTOR protein, LAMP1 protein and transcription factor EB. The body weight, blood glucose levels, testicular index of mice in each group were compared, as well as the testicular injury status.Results:The body weight [(18.77±1.14) g], testosterone level [(141.07±8.47) ng/L], follicle-stimulating hormone level [(9.19±0.74) U/L], and luteinizing hormone level [(1 497.91±99.57) pg/L] of mice in the model group were significantly lower than those in the control [(31.57±2.35) g, P<0.001; (171.50±11.76) ng/L, P<0.001; (12.46±1.54) U/L, P<0.001; (1 807.29±92.76) pg/L, P<0.001]; fasting blood glucose level [(20.82±1.11) mmol/L], glycosylated hemoglobin (12.67%±1.03%), the testis index (0.65%±0.03%) were significantly higher than those in the control [(6.40±1.34) mmol/L, P<0.001; 5.17%±1.17%, P<0.001; 0.48%±0.04%, P<0.001]. Compared with the model group, the body weight [(22.62±0.92) g, P=0.023], testosterone level [(172.63±9.20) ng/L, P<0.001], follicle-stimulating hormone level [(12.37±1.15) U/L, P<0.001], and luteinizing hormone level [(1 847.80±108.80) pg/L, P<0.001] of mice in the ginsenoside Rg1 group increased significantly, fasting blood glucose level [(18.63±1.14) mmol/L, P=0.017], glycosylated hemoglobin (8.50%±1.05%, P<0.001) and testicular index (0.54%±0.02%, P<0.001) decreased significantly. Compared with the control, the expressions of P62 ( P=0.039), LC3Ⅱ/LC3Ⅰ( P<0.001), Beclin1 ( P=0.002) and mTOR ( P=0.036) in the testicular tissue of mice in the model group all increased, the expression of β-Catenin ( P<0.001), LAMP1 ( P=0.005), transcription factor EB ( P<0.001) all decreased. Compared with the model group, the expressions of autophagy-related proteins P62 ( P=0.048), LC3Ⅱ/LC3Ⅰ( P<0.001) , Beclin1 ( P=0.023) and mTOR ( P=0.005) in the ginsenoside Rg1 group all decreased, while the expression of β-Catenin ( P=0.001), LAMP1 ( P=0.011) and transcription factor EB ( P=0.022) all increased. Transmission electron microscopy detected a decrease in the number of autophagosomes in the testicles of mice in the model group, and it improved after drug intervention. The HE staining showed that the testes of mice in the model group exhibited phenotypes such as the shedding and disorganization of spermatogenic cells, while ginsenoside Rg1 was able to improve these phenotypes. Conclusion:Ginsenoside Rg1 can improve testicular injury caused by diabetes in mice by regulating autophagy.

Chronic epididymitis (CE) is a long-standing inflammatory condition of the epididymis caused by unresolved acute infections, chronic infections, medication use, or other factors. Clinically, it is characterized by persistent dull pain or a dragging sensation in one or both sides of the scrotum. The disease course typically exceeds three months and is marked by insidious onset and recurrent episodes. Current studies suggest that CE may disrupt the epididymal microenvironment through multiple pathological processes, including local inflammatory responses, oxidative stress, fibrotic remodeling, and autophagy. These alterations impair sperm maturation, transport, and capacitation, thereby contributing to male reproductive dysfunction and infertility. This review summarizes the major etiologies and pathophysiological characteristics of CE and its impact on male reproductive function. It focuses on the roles of inflammatory cytokines and related signaling pathways, oxidative stress mechanisms, and fibrotic progression in the pathogenesis of CE. Moreover, it explores targeted therapeutic strategies based on these mechanisms, aiming to provide a theoretical basis for identifying key molecular targets and signaling pathways involved in CE-induced male reproductive impairment.

Erectile dysfunction(ED)is a common sexual dysfunction in adult males.With the accelerated pace of modern life and lifestyle changes,the prevalence of ED and its associated comorbidities have been steadily rising.Problems such as premature ejaculation,hypertension,hyperlipidemia,diabetes,prostate diseases,and infertility all interact with and aggravate ED,thereby endangering the overall health of men.Phosphodiesterase type 5 inhibitors(PDE5i)is the first-line pharmacotherapy for ED.Tadalafil,currently the only long-acting PDE5i approved for clinical use,has received mar-keting authorization in China for the treatment of ED since 2005.In 2013,the once-a-day continuous regimen was intro-duced as a novel treatment paradigm.And the indication was expanded to ED coexisting with benign prostatic hyperplasia in 2019.Accumulating clinical experience and evidence-based data consistently demonstrate its efficacy and safety across ED and ED-related comorbidities.This review summarizes the pharmacological profile of tadalafil and the latest clinical evi-dence on the management of ED and ED-related comorbidities,aiming to provide a reference for clinical practice.