Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Autophagy is a conservative lysosome-dependent material catabolic pathway, and exists in all eukaryotic cells. Autophagy controls cell quality and survival by eliminating intracellular dysfunction substances, and plays an important role in various pathophysiology processes. Erectile dysfunction (ED) is a common male disease. It is resulted from a variety of causes and pathologies, such as diabetes, hypertension, hyperlipidemia, aging, spinal cord injury, or cavernous nerve injury caused by radical prostatectomy, and others. In the past decade, autophagy has begun to be investigated in ED. Subsequently, an increasing number of studies have revealed the regulation of autophagy contributes to the recovery of ED, and which is mainly involved in improving endothelial function, smooth muscle cell apoptosis, penile fibrosis, and corpus cavernosum nerve injury. Therefore, in this review, we aim to summarize the possible role of autophagy in ED from a cellular perspective, and we look forward to providing a new idea for the pathogenesis investigation and clinical treatment of ED in the future.

Background Polycyclic aromatic hydrocarbons (PAHs), one of the main components of fine particulate matter (PM_2.5), have a certain impact on ambient air quality, and long-term exposure to PAHs may pose potential health risks to human beings. Objective To identify the distribution characteristics and sources of PAHs in atmospheric PM_2.5 in a district of Taizhou City from 2019 to 2021, and to evaluate the health risks of PAHs to the population in the area through the inhalation pathway. Methods From 2019 to 2021, air PM_2.5 sampling was carried out at a state-controlled surveillance point in a district of Taizhou City for 7 consecutive days on the 10th-16th of each month, the sampling time was 24 h·d⁻¹, and the sampling flow rate was 100 L·min⁻¹. PM_2.5 mass concentration was calculated by gravimetric method. A total of 16 PAHs were determined by ultrasonic extraction-liquid chromatography. Kruskal-Wallis H test was used to compare the distribution charac teristics of PAHs concentrations by years and seasons, characteristic ratio and principal component analysis (PCA) was used to analyze their sources, and a lifetime carcinogenic risk (ILCR) model was used to assess the health risk of PAHs. Results From 2019 to 2021, the annual average concentrations [M (P₂₅, P₇₅)] of ∑PAHs in atmospheric PM_2.5 in the selected district of Taizhou City were 6.52 (2.46, 10.59), 8.52 (4.56, 12.29), and 3.72 (1.51, 7.11) ng·m⁻³, respectively, and the annual benzo[a]pyrene (BaP) excess rates (national limit: 1 ng·m⁻³) were 27.38% (23/84), 47.62% (40/84), and 19.04% (16/84), respectively, both presenting 2020> 2019 > 2021 (P<0.001, P<0.05). The ∑PAHs concentration distribution showed a seasonal variation, with the highest value in winter and the lowest value in summer (P<0.05). Among the atmospheric PM_2.5 samples, the proportion of 5-ring PAHs was the highest, the proportion of 2-3-ring PAHs was the lowest; the proportion of 2-4-ring PAHs showed a yearly upward trend, and the proportion of 5-6-ring PAHs showed yearly downward trend (P<0.05). The characteristic ratio and PCA results suggested that the sources of sampled PAHs were mainly mixed sources such as dust, fossil fuel (natural gas), coal combustion, industrial emissions, and motor vehicle exhaust emissions. The ILCR (R_ILCR) of PAHs by inhalation for men, women, and children were 1.83×10⁻⁶, 2.35×10⁻⁶, and 2.04×10⁻⁶, respectively, and the annual average R_ILCR was 2.07×10⁻⁶, all greater than 1×10⁻⁶. Conclusion For the sampled time period, the main sources of PAHs pollution in atmospheric PM_2.5 in the target district of Taizhou City are dust, fossil fuel (natural gas), coal combustion, industrial emissions, motor vehicle emissions, etc., and PAHs may have a potential carcinogenic risk to local residents.

Objective To explore the clinical features of occupational pneumoconiosis (hereinafter referred to as “pneumoconiosis”) complicated with interstitial lung disease (ILD). Methods A total of 56 patients with pneumoconiosis complicated with ILD were selected as the research subjects using a retrospective study method, and their clinical features were analyzed. Results The main clinical symptoms of the 56 patients were progressive dyspnea, cough, and expectoration, with detection rates of 76.8%, 75.0%, and 55.4%, respectively. The detection rates of hypoxemia and respiratory failure were 67.9% and 32.1% respectively. Among the 35 patients who underwent pulmonary function test, restrictive, mixed, and obstructive ventilatory disorders were detected in 37.1%, 22.9%, and 17.1% of cases, respectively, with a 74.3% detection rate for reduced diffusion capacity. High resolution computed tomography of the chest revealed ground-glass shadows, grid shadow, interlobular thickening, honeycomb shadows and tractive bronchiectasis, with detection rates of 57.1%, 35.7%, 35.7%, 23.2%, and 17.9%, respectively. Lesions were mostly diffusely distributed in both lungs, with a predominance in the lower lungs compared to the mid-upper lungs. Patients complicated with connective tissue disease, including systemic sclerosis, rheumatoid arthritis, systemic lupus erythematosus, polymyositis, and dermatomyositis, accounted for 33.9% (19 cases). Conclusion The clinical symptoms, pulmonary function, and arterial blood gas analysis results of patients with pneumoconiosis complicated with ILD show no specific features. However, a subset of pneumoconiosis patients with ILD also have coexisting connective tissue diseases.

Objective To investigate the clinical characteristics and influencing factors of moderate-to-severe pulmonary ventilation dysfunction in occupational pneumoconiosis (hereinafter referred to as "pneumoconiosis") patients complicated with pulmonary tuberculosis. Methods A total of 136 male pneumoconiosis patients complicated with pulmonary tuberculosis suffering different degrees of pulmonary ventilation dysfunction were selected as the study subjects using the judgmental sampling method. Patients were divided into mild dysfunction and moderate-to-severe dysfunction groups based on the degrees of pulmonary ventilation dysfunction. Clinical data from patients of these two groups were collected, and influencing factors of pulmonary ventilation dysfunction were analyzed. Results The prevalence of mild dysfunction and moderate-to-severe dysfunction among the study subjects was 39.0% and 61.0%, respectively. The proportion of patients with moderate-to-severe pulmonary ventilation dysfunction increased with the progression of pneumoconiosis (P<0.05). Patients in moderate-to-severe dysfunction group had higher rates of dyspnea, elevated C-reactive protein, coexisting chronic obstructive pulmonary disease (COPD), and a history of lung infections within the past two years compared with those in the mild dysfunction group (all P<0.05). The result of multivariate logistic regression analysis showed that the degree of pneumoconiosis, complicated with COPD, and a history of lung infections within the past two years were risk factors for moderate-to-severe pulmonary ventilation dysfunction (all P<0.05). Specifically, higher degree of pneumoconiosis was associated with a greater proportion of moderate-to-severe dysfunction, and patients complicated with COPD or had a history of lung infections within the past two years were more likely to experience severe pulmonary ventilation dysfunction. Conclusion The degree of pneumoconiosis, complicated with COPD, and a history of lung infections within the past two years are influencing factors of moderate-to-severe pulmonary ventilation dysfunction in patients with pneumoconiosis combined with pulmonary tuberculosis. Early detection of pneumoconiosis progression, timely diagnosis of COPD and lung infections, and appropriate treatment such as antifibrotic agents, inhaled bronchodilators, and anti-infective therapies are recommended.

Adipose Tissue ; Cadaver ; Humans ; Vertebral Artery

Objective To employ Logistic regression modeling to analyze the related factors influencing the accuracy of the high performance liquid chromatography (HPLC) determination of preservatives in beverages. Methods The HPLC separation was performed on a Zorbax Eclipse Plus C18 column with methanol-ammonium acetate solution as mobile phase. The external standard method was used to determine 5 beverage preservatives. The influencing factors on the measurement accuracy were statistically evaluated with univariate and multivariate analysis. Results Univariate analysis showed that the recovery rate of the added standard in the determination of coffee beverage preservatives by HPLC was affected by the pretreatment method, and the difference was statistically significant (P<0.05). Multivariate analysis showed that the main influencing factors on the accuracy of determination of sorbic acid was the pretreatment method (OR=5.406, P<0.05), while the sample type was a protective factor (OR=0.134, P<0.05). For the determination of benzoic acid, the main factor influencing the accuracy was the sample type (OR=1.112, P<0.05), while the pretreatment method was a protective factor (OR=0.447, P<0.05). Conclusion Logistic regression analysis can identify risk factors for the accuracy of the determination, and provide statistical modeling support for the experimental optimization.