No abstract available.
Polycythemia Vera* ; Polycythemia* ; Thrombocythemia, Essential*

No abstract available.
Myocardial Infarction* ; Polycythemia Vera* ; Polycythemia*

A study on 16 patients (male: 14; ages of 50-78) with the primary polycythemia vera treated by the specific guidelines has shown that the number of erythrocyte in patients with polycythemia vera after a duration of suffering the disease was increased, followed by gradual reduction and was at low level at last. The specific clinical signs can change comprised the number of hypertension can be reduced, the number of thrombocyte, and leukocyte can be slightly increased and should be treated in the first stage and second stage but should not be treated in the third stage
Polycythemia Vera ; Erythrocytes

No abstract available.
Adult* ; Cerebral Infarction* ; Humans ; Polycythemia Vera* ; Polycythemia*

Polycythemia vera (PV) was first described nearly 120 years ago. In the subsequent century, the clinical syndrome of PV, its natural history, its treatment, and many critical pathogenetic features of the disease were characterized. The discovery of the Janus-associated kinase - 2 mutation JAK2 V617F and the characterization of its role in myeloproliferative neoplasms have substantially changed the diagnostic paradigm for PV, and have potential to lead to new therapy and new pathogenetic insights.
Natural History ; Phosphotransferases ; Polycythemia ; Polycythemia Vera

No abstract available.
Liver Cirrhosis* ; Liver* ; Polycythemia Vera* ; Polycythemia*

No abstract available.
Polycythemia Vera* ; Renal Artery Obstruction*

MPS comprised 4 disease's forms, such as: Chronic myelogenous leukemia (CLM), polycythemia vera (PV), essential thrombocytothemia (ET) and idiopathic myelofibrosis (IMF). From 1985 to May-2001 at Friendship hospital, authors have followed up a group of 86 patients with MPS and some remarks had been drawn out: Some disease's forms of MPS can transform each other, such as: +PV transformed in to CML: 10.00%; +PV transformed in to ET: 16.67%; +IMF transformed in to CML: 66.67%; +ET transformed in to CLM: 8.0%. Some case in MPS, although have not yet truly transformed, but have some changes, as such: +ET with concomitantly increasing erythrocytes: 4.0%; +IMF with concomitantly increasing platelets: 33.33%; +CML with concomitantly increasing platelets: 21.43%; Authors have also mentioned many interesting issues about the way of transformation, the last diagnosis for those disease's forms and the prognosis of these transformations
Leukemia, Myeloid ; Polycythemia Vera ; Syndrome

No abstract available.
Cerebral Infarction ; Diffusion Magnetic Resonance Imaging ; Polycythemia ; Polycythemia Vera

OBJECTIVETo detect the activity of autophagy and explore the impact on survival and proliferation of HEL cells and hematopoietic cells of polycythemia vera （PV） patients with JAK2 V617F mutation.

METHODSFlow cytometry, AO staining and Western blot methods were used to detect the autophagy activity and the expression of LC3-Ⅱ protein of JAK2 V617F+ HEL cells and hematopoietic cells of 12 newly diagnosed PV patients with JAK2 V617F mutation. HEL cells and bone marrow cells of 3 PV patients were treated with rapamycin or 3-MA to induce and inhibit autophagy, respectively. CellTiter Glo(R) method was used to detect the proliferation activity of cells.

RESULTSThere was higher level of mean LC3-Ⅱ fluorescence intensity in HEL cells (159 389 ± 29 001) than that in K562 cells (96 047 ± 24 134) (P=0.044). The formation of autophagosome in HEL cells is more than that in K562 cells detected by microscope. What's more, the level of mean LC3-Ⅱ fluorescence intensity in 12 PV patients' myeloid cells (92 842 ± 4 250) was higher than that of 15 healthy volunteers (86 633 ± 2 504) (P=0.001). The expression of LC3-Ⅱ protein was higher in PV patients' peripheral blood cells than that in healthy volunteers detected by Western blot. After treated with rapamycin 12, 24, 48 h, the activity of autophagy in HEL cells and bone marrow cells of 3 PV patients were increased and the proliferation activity was higher than the control group, the proliferation activity at 48 h were (101 413 ± 3 720), (18 744 ± 1 015), respectively. However, after treated with 3-MA 12, 24, 48 h, the activity of autophagy was decreased and the proliferation activity was lower than the control group, the proliferation activity at 48 h were (5 732 ± 166), (5 371 ± 56), respectively.

CONCLUSIONThere is high basical activity of autophagy in JAK2 V617F+ HEL cells and hematopoietic cells of PV patients with JAK2 V617F mutation. Up-regulated autophagy promotes proliferation of JAK2 V617F⁺ HEL cells and bone marrow cells of PV patients with JAK2 V617F mutation. Decreased autophagy inhibits proliferation of JAK2 V617F+ HEL cells and bone marrow cells of PV patients with JAK2 V617F mutation.