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Introduction: Individuals who experience bullying victimization are at increased risk for future health and social problems. Despite this, studies show that not all bullying victims are in ill health, suggesting the importance of investigating protective factors that could counteract the adverse effects. The present study focused on investigating the moderating effects of emotional competence (EC) in the relationship between cyber-bullying victimization (CV) and mental health among adolescents., Methods: Responses from 6403 adolescents aged 12 to 18 (1925 male, 4478 female, M age  = 16.35, SD = 1.46) with no missing data were used for analysis. The cross-sectional data analyzed in the present study was a part of a large longitudinal online survey conducted by the University of Tokyo in Japan. Participants were recruited among adolescent users of a social networking service widely used in Japan for communication., Results: Results of regression analysis showed significant direct effects of CV on psychological distress/self-esteem, confirming the adverse effects of victimization. Results also suggested that high intrapersonal EC weakened the relationship between CV and psychological distress, whereas high interpersonal EC strengthened the relationship. There were no significant interactions between CV and EC in predicting self-esteem., Conclusions: Intrapersonal and interpersonal EC may play differential moderating roles in the relationship between CV and psychological distress, the former by buffering the effect and the latter by exacerbating it. Interventions targeting abilities to handle one's own emotions may help decrease distress among adolescents with CV experiences., Competing Interests: Declaration of competing interest None., (Copyright © 2020 The Foundation for Professionals in Services for Adolescents. Published by Elsevier Ltd. All rights reserved.)

Background: Upper urinary tract neuroendocrine carcinoma (UUT-NEC) is extremely rare and has a poor prognosis. Although a few cases of successful treatment have been reported, no treatment has shown established efficacy., Patients and Methods: We analyzed 70 UUT-NEC patients, including 68 with small cell neuroendocrine carcinoma (SCNEC) and large cell neuroendocrine carcinoma (LCNEC) reported between 1985 and 2017 and 2 treated at our hospital., Results: Median patient age was 66 years, 58.6% were men, and 60% were of Asian descent. Most UUT-NECs were SCNEC (68; 95.7%), whereas LCNEC was very rare (2; 2.9%). More than half of the patients had accompanying other histological components, the most common being urothelial carcinoma (51.5%), whereas 41.4% had NEC alone. Of the 70 patients, 27 underwent additional therapy (e.g., chemotherapy and radiotherapy) along with surgery. Median survival was 15 months. In univariate analysis, stages T1-2 disease showed better prognosis than stages T3-4 (P < 0.001). Additional treatment (e.g., chemotherapy and radiotherapy) significantly improved prognosis (P = 0.014). Moreover, platinum-based chemotherapy also was associated with improved prognosis (P = 0.017). For platinum-based chemotherapy, multicollinearity with additional treatments was strong, and, thus, these data were not included in the analysis. Multivariate analysis revealed pathological stage (T1-2 vs. T3-4; P = 0.003) and additional treatment (P = 0.028) to be independent predictors of improved prognosis., Conclusion: Although UUT-NEC has a poor prognosis, additional treatment along with surgery and therapeutic intervention and stage T1-2 disease are independent factors to improve prognosis., (Copyright © 2018. Published by Elsevier Ltd.)

A 55-year-old man presented with tumor microembolism manifesting as characteristic patterns of pulmonary perfusion on lung scanning. He had a 2-week history of dyspnea and general fatigue. Echocardiography demonstrated right ventricular enlargement. Computed tomography of the chest was normal. Lung perfusion imaging showed multiple subsegmental peripheral defects, which were characteristic of tumor embolism. Ultrasonography and computed tomography of the abdomen revealed multiple enlargement of the lymph nodes. Upper gastrointestinal panendoscopy showed gastric cancer. At 10 days after admission, he suffered cardiac arrest and died despite resuscitative efforts. Histological examination revealed pulmonary arterial obstruction with tumor cells, and poorly differentiated adenocarcinoma in the stomach and lymph nodes. This case emphasizes the need to include tumor microembolism in the differential diagnosis of dyspnea, even if there is no evidence of an underlying malignant tumor.

A cognitive bias task (CBT) delineates two different cognitive selection mechanisms in the prefrontal cortex. To identify functional anatomy of context-dependent reasoning, we used technetium-99mhexamethyl- propyleneamine oxime (99mTc HM-PAO) single photon emission computed tomography (SPECT) and statistical parametric mapping. Twelve right-handed men 20-24 years old were instructed to look at a target card and then select the choice card (among two) that they preferred (modified CBT; mCBT). They also selected a choice card 2 weeks later without prior presentation of a target card (control task). In both tasks, 99mTc HM-PAO was injected intravenously about 15 s after initiation of the mCBT or control task. Brain images were obtained using a gamma camera and reconstructed by a UNIX-based workstation. Statistical analysis compared all activated images to control images. Results associated with P values of less than 0.01 (Z score > 2.36) were depicted on T1-weighted magnetic resonance images. All subjects preferred choices more similar to the target. SPECT activation occurred bilaterally in the dorsolateral prefrontal cortices and middle temporal gyri during performance of the CBT. Additionally, the left inferior prefrontal cortex and left fusiform gyrus showed significant activation compared with the control task. A neural network linking the temporal and prefrontal cortices prominently seen in the left hemisphere participates in context-dependent reasoning. Knowledge of such neural systems is essential for understanding prefrontal lobe function and dysfunction.

Progressive deterioration of left ventricular function is a characteristic feature of the heart failure state and is often speculated to result from ongoing loss of viable myocytes. We previously showed that in dogs with chronic heart failure, cardiocyte death through apoptosis occurs in the border region of fibrous scars (old infarcts). In the present study we examined the structural integrity of cardiocytes in regions bordering fibrous scars using transmission electron microscopy. Morphometric studies were performed using left ventricular tissue obtained from ten dogs with chronic heart failure produced by intracoronary microembolizations. Mitochondrial number increased significantly with proximity to the scar, while mitochondrial size decreased leading to a gradual decrease in mitochondrial volume fraction. Severe injury to mitochondria was present in only 5% of organelles in myocytes far from the scar but increased markedly to 28-41% in myocytes adjacent to or incorporated within the scar. Similarly, severe myofibrillar abnormalities were present in only 3% of myocytes that were far from the scar but increased significantly to 12-73% in myocytes adjacent to or incorporated within the scar. These results indicate that in dogs with chronic heart failure, constituent myocytes of left ventricular regions bordering fibrous scars manifest heterogeneity in the extent of degeneration. The extent of degeneration is greatest in myocytes closest to the scar and least in myocytes far from the scar. We postulate that this wavefront of myocyte degeneration is a dynamic process that may lead to progressive expansion of the scar through loss of viable myocytes and ultimately may contribute, in part, to the progressive left ventricular dysfunction that characterizes the heart failure state.

It is often speculated that progressive deterioration of left ventricular function in heart failure is due to ongoing loss of viable cardiocytes. In this study, we examined the possibility that cardiocyte loss in heart failure may be due, in part, to apoptosis, an active process of gene-directed cellular self-destruction. Studies were performed in left ventricular tissue obtained from 10 dogs with chronic heart failure produced by multiple intracoronary microembolizations (left ventricular ejection fraction 27 +/- 1%) and from 5 normal dogs. Evidence for cardiocyte apoptosis was based on transmission electron microscopy criteria and on in situ immunohistochemical labeling of nuclear DNA fragmentation. There was no evidence of apoptotic cardiocytes in normal dogs. Features of cardiocyte apoptosis were observed in dogs with heart failure primarily in regions bordering old infarcts. Electron microscopic features of cardiocyte apoptosis included (1) intact sarcolemma and inner organelles in the presence of compaction and segregation of nuclear chromatin into sharply delineated masses that about the nuclear envelope, (2) intact sarcolemma in the presence of cytoplasm shrinkage, blebbing, and nuclear fragmentation, and (3) intact sarcolemma in the presence of complete disorganization of inner organelles and disappearance of nucleolemma. A count of all of the apoptotic bodies positively labeled for nuclear DNA fragments showed that 11% were of cardiocyte origin confirmed by positive labeling with striated muscle antimyosin antibody. We conclude that morphological and biochemical features of cardiocyte apoptosis exist in the left ventricular myocardium of dogs with chronic heart failure.

We examined the incidence and severity of abnormalities of contractile structures of residual viable cardiomyocytes in the left ventricular free wall, septum and right ventricular free wall of 10 dogs with chronic heart failure produced by multiple intracoronary microembolizations and in septal biopsies of 13 patients with chronic heart failure. The abnormalities were evaluated by transmission electron microscopy and classified as either (i) type-1, defined as complete interruption of myofibrils; (ii) type-2, defined as disconnection of end-sarcomeres from the intercalated disc; or (iii) type-3, sarcomere abnormalities defined as Z-bands irregularities and/or focal myofilament disarray. In the left ventricular free wall of dogs, type-1 abnormalities were present in 33 +/- 8% of myocytes, type-2 in 26 +/- 8%, and type-3 in 63 +/- 9%. The incidence of a type-3 abnormality but not type-1 or type-2 was greater in the left ventricular wall compared with the septum and right ventricular wall (P < 0.05). Among abnormal myocytes, 29 +/- 3% of myofibrils were interrupted, 18 +/- 4% of end-sarcomeres were disconnected from the intercalated disc and 12 +/- 2% of sarcomeres were abnormal. The severity of a type-1 but not type-2 or type-3 abnormalities was greater in the left ventricular wall compared with the septum and right ventricular wall. A similarly high incidence of abnormalities was observed in septal myocytes of patients. The results indicate that abnormalities of contractile structures are common among viable myocytes of the failing heart. The incidence of these abnormalities is sufficiently high to warrant serious consideration of their potential role in the progression of left ventricular dysfunction that characterizes the heart failure state.