Purpose: Cancer survivors are at increased risk of diabetes mellitus (DM). Additionally, the prevalence of obesity, which is also a risk factor for DM, is increasing in cancer survivors. We investigated the associations between weight change after cancer diagnosis and DM risk. Materials and Methods: This retrospective cohort study used data from the Korean National Health Insurance Service. Participants who were newly diagnosed with cancer from 2010 to 2016 and received national health screening before and after diagnosis were included and followed until 2019. Weight change status after cancer diagnosis was categorized into four groups: sustained normal weight, obese to normal weight, normal weight to obese, or sustained obese. Cox proportional hazard analyses were performed to examine associations between weight change and DM. Results: The study population comprised 264,250 cancer survivors. DM risk was highest in sustained obese (adjusted hazard ratios [aHR], 2.17; 95% confidence interval [CI], 2.08 to 2.26), followed by normal weight to obese (aHR, 1.66; 95% CI, 1.54 to 1.79), obese to normal weight (aHR, 1.29; 95% CI, 1.21 to 1.39), and then sustained normal weight group (reference). In subgroup analyses according to cancer type, most cancers showed the highest risks in sustained obese group. Conclusion Obesity at any time point was related to increased DM risk, presenting the highest risk in cancer survivors with sustained obesity. Survivors who changed from obese to normal weight had lower risk than survivors with sustained obesity. Survivors who changed from normal weight to obese showed increased risk compared to those who sustained normal weight. Our finding supports the significance of weight management among cancer survivors.

Purpose: Cancer survivors are at increased risk of diabetes mellitus (DM). Additionally, the prevalence of obesity, which is also a risk factor for DM, is increasing in cancer survivors. We investigated the associations between weight change after cancer diagnosis and DM risk. Materials and Methods: This retrospective cohort study used data from the Korean National Health Insurance Service. Participants who were newly diagnosed with cancer from 2010 to 2016 and received national health screening before and after diagnosis were included and followed until 2019. Weight change status after cancer diagnosis was categorized into four groups: sustained normal weight, obese to normal weight, normal weight to obese, or sustained obese. Cox proportional hazard analyses were performed to examine associations between weight change and DM. Results: The study population comprised 264,250 cancer survivors. DM risk was highest in sustained obese (adjusted hazard ratios [aHR], 2.17; 95% confidence interval [CI], 2.08 to 2.26), followed by normal weight to obese (aHR, 1.66; 95% CI, 1.54 to 1.79), obese to normal weight (aHR, 1.29; 95% CI, 1.21 to 1.39), and then sustained normal weight group (reference). In subgroup analyses according to cancer type, most cancers showed the highest risks in sustained obese group. Conclusion Obesity at any time point was related to increased DM risk, presenting the highest risk in cancer survivors with sustained obesity. Survivors who changed from obese to normal weight had lower risk than survivors with sustained obesity. Survivors who changed from normal weight to obese showed increased risk compared to those who sustained normal weight. Our finding supports the significance of weight management among cancer survivors.

Purpose: Cancer survivors are at increased risk of diabetes mellitus (DM). Additionally, the prevalence of obesity, which is also a risk factor for DM, is increasing in cancer survivors. We investigated the associations between weight change after cancer diagnosis and DM risk. Materials and Methods: This retrospective cohort study used data from the Korean National Health Insurance Service. Participants who were newly diagnosed with cancer from 2010 to 2016 and received national health screening before and after diagnosis were included and followed until 2019. Weight change status after cancer diagnosis was categorized into four groups: sustained normal weight, obese to normal weight, normal weight to obese, or sustained obese. Cox proportional hazard analyses were performed to examine associations between weight change and DM. Results: The study population comprised 264,250 cancer survivors. DM risk was highest in sustained obese (adjusted hazard ratios [aHR], 2.17; 95% confidence interval [CI], 2.08 to 2.26), followed by normal weight to obese (aHR, 1.66; 95% CI, 1.54 to 1.79), obese to normal weight (aHR, 1.29; 95% CI, 1.21 to 1.39), and then sustained normal weight group (reference). In subgroup analyses according to cancer type, most cancers showed the highest risks in sustained obese group. Conclusion Obesity at any time point was related to increased DM risk, presenting the highest risk in cancer survivors with sustained obesity. Survivors who changed from obese to normal weight had lower risk than survivors with sustained obesity. Survivors who changed from normal weight to obese showed increased risk compared to those who sustained normal weight. Our finding supports the significance of weight management among cancer survivors.

PURPOSE: We evaluated patterns of tumor recurrence after nephron sparing surgery for sporadic renal cell carcinoma MATERIALS AND METHODS: From December 1992 to October 1997, 20 patients(21 renal units) underwent nephron sparing surgery(partial nephrectomy, wedge resection, enucleation) for sporadic renal cell carcinoma at our department. Mean postoperative followup period was 25.4+/-0.3 months. All patients were evaluated with a medical history, physical examination, blood chemistry, chest x-ray, abdominal CT every 6 months. The clinical course and outcome for patients who had recurrence after nephron sparing surgery were reviewed retrospectively. We also reviewed 122 patients who underwent radical nephrectomy at the same period for patterns of tumor recurrence. RESULTS: Renal cell carcinoma were recurred after nephron sparing surgery in 3 patients (15%, 3/21 renal units:14.2%). Local tumor recurrence with(1) or without(1) metastatic disease developed in 2 patients(10%). Metastatic disease without local tumor recurrence developed in 1 patient(5%). One patient with only local recurrence had positive resection margin. Initial pathological tumor stage and period to tumor recurrence were T3a and 4 months for patient with local recurrence, T2 and 10 months for patient with local recurrence and brain metastasis, T2 and 12 months for patient with lung metastasis without local recurrence. Renal cell carcinoma recurred after radical nephrectomy in 8 patients(6.6%). Local recurrence was none and all recurrent tumors were distant metastasis. CONCLUSIONS: The incidence of metastatic disease after nephron sparing surgery for renal cell carcinoma was not different from that occurring after radical nephrectomy but the incidence of local tumor recurrence after nephron sparing surgery was greater than that occurring after radical nephrectomy. Nephron sparing surgery must be done with enough negative resection margin.
Brain ; Carcinoma, Renal Cell* ; Chemistry ; Follow-Up Studies ; Humans ; Incidence ; Lung ; Neoplasm Metastasis ; Nephrectomy ; Nephrons* ; Physical Examination ; Recurrence* ; Retrospective Studies ; Thorax ; Tomography, X-Ray Computed

To see the inhibitory mechanism of gentamicin in response to electrical field stimulation (EFS) using the rat bladder smooth muscle, atropine or guanethidine was treated but had no effect. Methylsergide, a non-selective 5-HT1, 5-HT2 receptor antagonist was also treated but had on effect. Kinase inhibitors, such as chelerythrine (PKC inhibitor), ML-9 (MLCK inhibitor), or Y27632 (rho kinase inhibitor) were pretreated before gentamicin treatment, but did not have effect. For U73122, a phospholipase C (PLC) inhibitor however, the inhibitory effect to gentamicin was significantly attenuated in all frequencies given by the EFS. Therefore gentamicin induced inhibitory effect on EFS response in rat bladder smooth muscle was not mediated by the activation of adrenergic, cholinergic, or serotonergic receptor. The inhibition of gentamicin might be mediated through the PLC dependent pathway, but not through the PKC, MLCK or rho kinase dependent pathway.
Animals ; Atropine ; Gentamicins* ; Guanethidine ; Muscle, Smooth* ; Phosphotransferases ; Rats* ; rho-Associated Kinases ; Type C Phospholipases ; Urinary Bladder*

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Objectives: The association between statin use and depression is well studied, but the studies on the association of statin use and bipolar disorders are limited. Thus, we aimed to investigate the effects of taking statin on risk of bipolar disorder using national claims data of South Korea. Methods: A total of 5713871 subjects who did not take statin and were not diagnosed with bipolar disorder before the health examination were included. Among eligible subjects, 315537 subjects started taking statin within 1 year after taking the health examination and 5398334 subjects did not. After 9 years of follow-up, the incidence of bipolar disorder was determined for each group. Results: Compared to subjects who were not exposed to statin, subjects who were exposed to statin showed a greater incidence of bipolar disorder and an increased risk of bipolar disorder (hazard ratio [HR]: 1.66; 95% confidence interval [CI]: 1.58 to 1.75), and after adjusting for age, sex, low income, regular exercise, smoking, drinking, diabetes mellitus, hypertension, body mass index, cholesterol and depression (adjusted HR: 1.32; 95% CI: 1.24 to 1.40). Conclusions This result showed an increased risk of bipolar disorder after taking statin, but the underlying biological mechanism needs further investigations. This study has clinical implications for patients taking statins, which require early assessment and response in addition to drug treatment and lifestyle modification, considering the possibility that unhealthy lifestyle habits may appear as part of the mood symptoms of bipolar disorder.

Abnormal aggregation of α-synuclein is a key element in the pathogenesis of several neurodegenerative diseases, including Parkinson’s disease (PD), dementia with Lewy bodies, and multiple system atrophy. α-synuclein aggregation spreads through various brain regions during the course of disease progression, a propagation that is thought to be mediated by the secretion and subsequent uptake of extracellular α-synuclein aggregates between neuronal cells. Thus, aggregated forms of this protein have emerged as promising targets for disease-modifying therapy for PD and related diseases. Here, we generated and characterized conformation-specific antibodies that preferentially recognize aggregated forms of α-synuclein. These antibodies promoted phagocytosis of extracellular α-synuclein aggregates by microglial cells and interfered with cell-to-cell propagation of α-synuclein. In an α-synuclein transgenic model, passive immunization with aggregate-specific antibodies significantly ameliorated pathological phenotypes, reducing α-synuclein aggregation, gliosis, inflammation, and neuronal loss. These results suggest that conformation-specific antibodies targeting α-synuclein aggregates are promising therapeutic agents for PD and related synucleinopathies.