[Analysis on the status of occupational health of medical radiation workers in China in 2019].

Objective: To grasp the occupational health monitoring of radiation workers in medical institutions across the country, and to discover weak links in the prevention and treatment of occupational radiation diseases. Methods: In 2020 January, according to the monitoring data of the "National Radiation Health Information Platform" (Occupational Radiation Disease and Occupational Health Monitoring Subsystem and Occupational Radiation Disease Reporting Subsystem) , the national occupational health monitoring data from January 1 to December 31, 2019, including the number of radiation workers in medical institutions, occupational health examinations, personal dose monitoring and occupational radiation disease diagnosis, were descriptive analyzed. Results: There were a total of 394436 radiation workers in medical institutions across the country. The number of radiation workers in various provinces was quite different, with a median of 10206, which was positively correlated with the number of permanent residents in each province (r=0.947) . There were 376 personal dose monitoring institutions nationwide, and the personal dose monitoring rate of radiation workers in medical institutions was 96.61% (381045/394436) . There were 419 occupational health inspection institutions for radiation workers across the country, and 269 (64.20%) used software to print physical examination forms. A total of 334455 radiation workers in medical institutions had been subjected to occupational health examinations. The rate of occupational health examinations for radiation workers in medical institutions was 84.79% (334455/394436) . The abnormal rate of chromosomal aberrations in peripheral blood lymphocytes of radiation workers in medical institutions was 0.33% (776/233571) , the detection rate of posterior posterior subcapsular turbidity was 0.63% (2093/334455) , and the abnormality rate of thyroid color ultrasound was 28.49% (14946/52464) . In 2019, a total of 16 cases of occupational radiation diseases were reported. Conclusion: The personal dose monitoring rate and occupational health examination rate of medical radiation workers nationwide are relatively high, but the quality of lymphocyte chromosome aberration analysis, eye lens examination and thyroid color photograph examination needs to be further improved.

Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder.

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of a hematopoietic stem cell. The majority of cases of CML are associated with the (9;22) chromosome translocation that generates the bcr-abl chimeric gene. Alpha interferon (IFN-alpha) treatment induces hematological remission and prolongs life in 75% of CML patients in the chronic phase. It has been shown that mice deficient in interferon consensus sequence binding protein (ICSBP), a member of the interferon regulatory factor family, manifest a CML-like syndrome. We have shown that expression of Bcr-Abl in bone marrow (BM) cells from 5-fluorouracil (5-FU)-treated mice by retroviral transduction efficiently induces a myeloproliferative disease in mice resembling human CML. To directly test whether icsbp can function as a tumor suppressor gene, we examined the effect of ICSBP on Bcr-Abl-induced CML-like disease using this murine model for CML. We found that expression of the ICSBP protein was significantly decreased in Bcr-Abl-induced CML-like disease. Forced coexpression of ICSBP inhibited the Bcr-Abl-induced colony formation of BM cells from 5-FU-treated mice in vitro and Bcr-Abl-induced CML-like disease in vivo. Interestingly, coexpression of ICSBP and Bcr-Abl induced a transient B-lymphoproliferative disorder in the murine model of Bcr-Abl-induced CML-like disease. Overexpression of ICSBP consistently promotes rather than inhibits Bcr-Abl-induced B lymphoproliferation in a murine model where BM cells from non-5-FU-treated donors were used, indicating that ICSBP has a specific antitumor activity toward myeloid neoplasms. We also found that overexpression of ICSBP negatively regulated normal hematopoiesis. These data provide direct evidence that ICSBP can act as a tumor suppressor that regulates normal and neoplastic proliferation of hematopoietic cells.

The SH2 domain of bcr-Abl is not required to induce a murine myeloproliferative disease; however, SH2 signaling influences disease latency and phenotype.

Bcr-Abl plays a critical role in the pathogenesis of chronic myelogenous leukemia (CML). It was previously shown that expression of Bcr-Abl in bone marrow cells by retroviral transduction efficiently induces a myeloproliferative disorder (MPD) in mice resembling human CML. This in vivo experimental system allows the direct determination of the effect of specific domains of Bcr-Abl, or specific signaling pathways, on the complex in vivo pathogenesis of CML. In this report, the function of the SH2 domain of Bcr-Abl in the pathogenesis of CML is examined using this murine model. It was found that the Bcr-Abl SH2 mutants retain the ability to induce a fatal MPD but with an extended latency compared with wild type (wt) Bcr-Abl. Interestingly, in contrast to wt Bcr-Abl-induced disease, which is rapid and monophasic, the disease caused by the Bcr-Abl SH2 mutants is biphasic, consisting of an initial B-lymphocyte expansion followed by a fatal myeloid proliferation. The B-lymphoid expansion was diminished in mixing experiments with bcr-abl/DeltaSH2 and wt bcr-abl cells, suggesting that the Bcr-Abl-induced MPD suppresses B-lymphoid expansion.