Objective To explore the effect of carnosic acid combined with tamoxifen on breast cancer cells and the mechanism.Methods Breast cancer cell lines MCF-7,T47D were divided into 4 groups:PBS was given to control group,carnosic acid(CA)was added to CA group,tamoxifen(TAM)was added to TAM group,and CA+TAM group was treated with carnosic acid and tamoxifen.The proliferation ability was measured by MTT assay,the colony formation capacity was measured by colony formation assay,the invasion ability was measured by Transwell chamber assay,the migration ability was measured by wound-healing assay,the expression of Caspase-8,Caspase-3 and PARP protein were measured by Western blotting.Results CA,TAM and CA+TAM suppressed breast cancer cell proliferation with a dose-dependent manner.Compared with CA group and TAM group,the proliferation inhibitory rate of CA+TAM group was significantly increased(P<0.05).In MCF-7 and T47D cell lines,compared to control group,the rate of colony fromation,number of invasive cells and cell migration rate of CA,TAM,CA+TAM groups were significantly decreased(all P<0.05).These indexes mentioned above in CA+TAM group were significantly lower than those in CA group and TAM group(all P<0.05),but there were no significant differences between CA group and TAM group (all P>0.05).In two breast cancer cell strains,the expression of cleaved Caspase-8 protein between control,CA,TAM and CA+TAM groups was not significantly different(P>0.05).Compared to control group,the expression levels of cleaved caspase-3,cleaved PARP protein in CA,TAM and CA+TAM groups were significantly increased(P<0.05),and these protein levels were significantly higher in CA+TAM group than in CA and TAM group(all P<0.05).But there were no significant differences between CA group and TAM group(all P>0.05).Conclusion Carnosic acid combined with tamoxifen can suppress the proliferation,invasion and migration of breast cancer cells,and its mechanism may be related to the activation of Caspase-3/PARP signaling pathway.

Objective To evaluate the differential diagnostic value of 18F-FDG PET/CT between pancreatic lymphoma (PL) and pancreatic carcinoma (PC).Methods The 18 F-FDG PET-CT data of 16 patients who were pathological diagnosed with PL were retrospectively reviewed and compared with those of 32 consecutive pancreatic cancer patients who were pathologically diagnosed and randomly enrolled.The age,location,diameter and the maximum standard uptake values (SUVmax) of pancreatic lesions,pancreatic ductal dilatation,distal pancreatic atrophy,serum CA19-9 level and extrapancreatic organs involvement were analyzed.Results The 16 patients with PL included 8 men and 8 women,the mean age was (46 ± 17)year,and 11.1％ (1/9) patients had elevated CA19-9.The 32 patients with PC included 15 men and 17 women,the mean age was (61 ± 12)year,and 81.3％ patients had elevated CA19-9.There were no significant differences on gender between the two groups,while the mean age of PL patients was younger than that of PC,elevated CA19-9 was less common than that in PC,and the differences were statistically significant (all P＜0.05).There were 12 cases of diffusive large B cell lymphoma,2 cases of B lymphoblastic lymphoma/leukaemia,1 case of follicular lymphoma and 1 case of dysplastic large T cell lymphoma in 16 PL patients.There was no significant difference on the site of pancreatic lesions between the two groups,but long diameter of PL lesions was larger than that of PC [(6.6 ± 3.3) vs (4.3 ± 1.8) cm,P =0.038].Dilated pancreatic duct and distal parenchyma atrophy in PL were less than those in PC (3/16 vs 17/32,1/16 vs 13/32),and SUVmax of PL lesions was significantly higher than that of PC (12.0 ± 5.5 vs 8.6 ± 3.8),indicating that the differences were statistically significant (all P ＜ 0.05).The cut-off value of SUVmax was 9.95,and Youden's index was 0.406 with the sensitivity and specificity of 68.8％ and 71.9％ for differentiating PL from PC.The incidence of extrapancreatic lesions including bone marrow and kidney and spleen infiltration was significantly more frequent in patients with PL than that in patients with PC(56.3％ vs 6.25％,43.8％ vs 3.1％,50.0％ vs 6.3％),while the incidence of liver metastases was significantly lower than that in PC (12.5％ vs 5.0％),indicating that the differences were statistically significant (all P ＜0.01).There were no significant differences on the incidence of other extrapancreatic lesions.Conclusions PL should be considered in relatively younger patients and manifested as a bulky mass with significant FDG uptake and extrapancreatic involvement of bone,kidney and spleen but without distinct pancreatic ductal dilation or distal parenchymal atrophy or liver metastasis.

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.