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Obesity predisposes to cancer and a virtual universality of nonalcoholic fatty liver disease (NAFLD). However, the impact of hepatic steatosis on liver metastasis is enigmatic. We find that while control mice were relatively resistant to hepatic metastasis, those which were lipodystrophic or obese, with NAFLD, had a dramatic increase in breast cancer and melanoma liver metastases. NAFLD promotes liver metastasis by reciprocal activation initiated by tumor-induced triglyceride lipolysis in juxtaposed hepatocytes. The lipolytic products are transferred to cancer cells via fatty acid transporter protein 1, where they are metabolized by mitochondrial oxidation to promote tumor growth. The histology of human liver metastasis indicated the same occurs in humans. Furthermore, comparison of isolates of normal and fatty liver established that steatotic lipids had enhanced tumor-stimulating capacity. Normalization of glucose metabolism by metformin did not reduce steatosis-induced metastasis, establishing the process is not mediated by the metabolic syndrome. Alternatively, eradication of NAFLD in lipodystrophic mice by adipose tissue transplantation reduced breast cancer metastasis to that of control mice, indicating the steatosis-induced predisposition is reversible.Prader-Willi syndrome (PWS) is a developmental disorder caused by loss of maternally imprinted genes on 15q11-q13, including melanoma antigen gene family member L2 (MAGEL2). The clinical phenotypes of PWS suggest impaired hypothalamic neuroendocrine function; however, the exact cellular defects are unknown. Here, we report deficits in secretory granule (SG) abundance and bioactive neuropeptide production upon loss of MAGEL2 in humans and mice. Unbiased proteomic analysis of Magel2pΔ/m+ mice revealed a reduction in components of SG in the hypothalamus that was confirmed in 2 PWS patient-derived neuronal cell models. Mechanistically, we show that proper endosomal trafficking by the MAGEL2-regulated WASH complex is required to prevent aberrant lysosomal degradation of SG proteins and reduction of mature SG abundance. Importantly, loss of MAGEL2 in mice, NGN2-induced neurons, and human patients led to reduced neuropeptide production. Thus, MAGEL2 plays an important role in hypothalamic neuroendocrine function, and cellular defects in this pathway may contribute to PWS disease etiology. Moreover, these findings suggest unanticipated approaches for therapeutic intervention.Diabetes is a risk factor for myocardial infarction, and outcomes after myocardial infarction are worse among diabetics compared with nondiabetics. Diabetes is associated with impaired Heme clearance. Here, we determined whether heme toxicity and impaired heme clearance contribute to diabetic myocardial infarction injury and assessed IL-10 as a therapeutic agent for diabetic myocardial infarction. Plasma-free hemoglobin was significantly elevated in diabetic mice compared with nondiabetic mice after myocardial infarction. Infarct size had strong correlation to the level of plasma-free hemoglobin. Hemoglobin and reactive iron deposition within the infarct zone were also demonstrated in diabetic MI. IL-10 significantly reduced infarct size and improved cardiac function in diabetic mice. Moreover, IL-10 improved capillary density, reduced apoptosis, and decreased inflammation in the border zone of the infarcted hearts, findings that were partially inhibited by Tin protoporphyrin (a heme oxygenase-1 inhibitor). https://www.selleckchem.com/products/triparanol-mer-29.html IL-10 upregulated CD163, the hemoglobinhaptoglobin scavenger receptor, and heme oxygenase-1 in THP-1-derived and primary human CD14+ macrophages. IL-10 significantly protected against ischemic injury when HL-1 cardiomyocytes were cotreated with hemoglobin. Together, our findings indicate that IL-10 is cardioprotective in diabetic myocardial infarction via upregulation of heme clearance pathways. These findings implicate heme clearance as a potentially novel therapeutic direction for diabetic myocardial infarction.IgG4-related disease (IgG4-RD) is a rare autoimmune fibrosis disease characterized by elevated serum IgG4 and tissues as well as organs infiltrated with IgG4-positive cells, resulting in swelling and damage.It is currently treated as first-line treatment with glucocorticoids. Autoimmune hemolytic anemia (AIHA) is also a relatively rare disease that caused by autoreactive erythrocyte antibodies. Although both are autoimmune-related diseases, they rarely overlap. The relationship between them is not clear. A case of IgG4-RD combined with AIHA is reported. The patient has shortness of breath, cough, and sputum after physical activity. Physical examination showed appearance of anemia, yellow staining of skin and sclera, palpable neck and multiple swollen lymph nodes. Laboratory examination, bone marrow biopsy, and lymph node biopsy confirmed the diagnosis. Therefore, clinicians should develop ideas and raise awareness of such diseases.Coping style is a cognitive or behavioral strategy taken by individuals in the face of stress. Positive coping style is of great significance for improving the physical and mental outcomes of elderly patients with urinary incontinence. Accurate assessment of coping styles for the elderly patients with urinary incontinence can provide reference for the subsequent development of intervention measures. The existing coping style assessment tools for elderly incontinence at home and abroad include specific scale of incontinence, relevant psychological assessment scale, and universal scale. In a word, the progress in the studies on relevant assessment tools is slow, and it mainly focuses on the assessment of female population. The assessment content is relatively single and lacks of pertinence and systematization. In the future, a comprehensive scale with strong adaptability should be developed based on the characteristics of elderly incontinence patients in China. To investigate the status and the related factors of nursing behaviors for pressure injury, and to provide the evidence for standardizing pressure injury management. A total of 1 039 clinical nursing staff from 4 general hospitals in Changsha from December 1 to 30, 2017 were selected by a stratified random sampling procedure. Nurses' demographic information such as age, gender, title, educational attainment, and department were collected. We investigated the status of nursing behaviors on pressure injury by a self-designed questionnaire, assessed nurses' knowledge of pressure injury and nurses' attitude of pressure injury using the Pressure Ulcer Knowledge Test and Attitude towards Pressure Ulcer Prevention Instrument, respectively, compared the nursing behaviors on pressure injury with different backgrounds, used multiple linear regression to analyze the influential factors for nursing behaviors on pressure injury, and conducted the Pearson correlation analysis for nurses' knowledge, attitude, and behaviors on the pressure injury.
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