Objective To evaluate the biodistribution and radiation-absorbed doses of main organs in healthy people with 13 N-ammonia.Methods Five healthy volunteers underwent whole-body PET and CT scans after injection of 666-814 MBq of 13 N-ammonia.The serial dynamic emission images of each healthy volunteer were acquired.ROI were drawn manually based on the transverse CT images and transferred to the corresponding PET slices.Radiation-absorbed doses were calculated using the medical internal radiation dosimetry (MIRD) method.Results The highest concentrations of 13 N-ammonia were found in the heart,liver and kidneys,followed by pancreas,brain,spleen and stomach.The organ of highest absorbed dose was heart with (7.14±3.63) × 10-3 mGy/MBq.The whole-body absorbed dose was (2.11±0.44) × 10 3 mGy/MBq.The whole-body effective dose was (6.58± 1.23) × 10-3 mSv/MBq.Conclusion As one of the most important myocardial perfusion tracers,the whole-body 13 N-NH3 · H2 O PET appears to be safe for humans.

Objective To explore the effectof cognitive behavioral Intervention on the quality of life and cognitive lever of patients with venous thrombus embolism. Methods 164 patients with Venous Thrombus Embolism were randomly divided into control group and research group, the control group received routine care, The study group received cognitive behavior intervention. The cognitive lever and quality of life score was measured between before and after the intervention. Results Before the intervention, the difference score of living quality and cognitive lever in the two groups has no statistical significance (P > 0.05), and after intervention, the cognition lever and the three aspects of risk factors, anticoagulant knowledge and treatment methods of research group scored (28.47 ± 7.63), (7.38 ± 2.48), (6.82±2.73), (3.64±1.59) points which were significantly higher than the control group scored (20.54±5.49), (4.31±2.14), (3.72±1.62), (2.18±1.36) points (t=7.635, 8.469, 8.822, 6.299, P<0.01),the quality of life and four dimensions of daily life ability, pain, social activities, mental scored ( 37.04 ± 7.08), [9.00 (5.00, 11.00)],(9.04 ± 1.55),(5.52 ± 1.59),(14.00 ± 3.06) points which showed great improvement than the control group scored [49.50(39.75-59.25)], [11.50 (6.75, 16.00)], (10.05 ± 1.65), (7.95 ± 2.19), (19.18 ± 3.88) points. There were significant difference in the quality of life and four dimensions between the two groups. (Z=-3.558,-2.143, t=2.102, 4.274, 4.991, P<0.05 or 0.01). Conclusions The quality of life for the venous thrombus embolism patients were in lower level. The cognitive behavioral intervention could correcting their bad behavior and negative emotions, eventually improve the quality of life of venous thrombus embolism patients.

Humans ; Cardiologists ; Neoplasms/drug therapy* ; Medical Oncology ; Heart ; Oncologists

Since the utilization of anthracyclines in cancer therapy, severe cardiotoxicity has become a major obstacle. The major challenge in treating cancer patients with anthracyclines is minimizing cardiotoxicity without compromising antitumor efficacy. Herein, histone deacetylase SIRT6 expression was reduced in plasma of patients treated with anthracyclines-based chemotherapy regimens. Furthermore, overexpression of SIRT6 alleviated doxorubicin-induced cytotoxicity in cardiomyocytes, and potentiated cytotoxicity of doxorubicin in multiple cancer cell lines. Moreover, SIRT6 overexpression ameliorated doxorubicin-induced cardiotoxicity and potentiated antitumor efficacy of doxorubicin in mice, suggesting that SIRT6 overexpression could be an adjunctive therapeutic strategy during doxorubicin treatment. Mechanistically, doxorubicin-impaired mitochondria led to decreased mitochondrial respiration and ATP production. And SIRT6 enhanced mitochondrial biogenesis and mitophagy by deacetylating and inhibiting Sgk1. Thus, SIRT6 overexpression coordinated metabolic remodeling from glycolysis to mitochondrial respiration during doxorubicin treatment, which was more conducive to cardiomyocyte metabolism, thus protecting cardiomyocytes but not cancer cells against doxorubicin-induced energy deficiency. In addition, ellagic acid, a natural compound that activates SIRT6, alleviated doxorubicin-induced cardiotoxicity and enhanced doxorubicin-mediated tumor regression in tumor-bearing mice. These findings provide a preclinical rationale for preventing cardiotoxicity by activating SIRT6 in cancer patients undergoing chemotherapy, but also advancing the understanding of the crucial role of SIRT6 in mitochondrial homeostasis.