Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transfusion of platelet concentrates was used to establish a thrombocytosis of approximately three times normal platelet levels in male rats. This thrombocytosis resulted in a rebound thrombocytopenia to 60% of normal counts. Examination of the small acetylcholinesterase (ACh-E) positive cells of the marrow at this time showed a reduction to 50% of normal levels without significant changes in control animals. A second group of experiments indicated that this suppression developed as early as the third day posttransfusion, persisted until day 7, and returned to baseline levels by day 9. Incorporation of 75SeM indicated that the reduction in platelet count was due to decreased platelet production. Little or no changes were observed in the hematocrit or WBC. This evidence supports the hypothesis that these cells are early cells in the megakaryocytic series. They are the earliest cells of the series seen to be affected by thrombocytosis. Feedback control by platelets or platelet extracts of this cell population may represent one level of regulation of megakaryopoiesis.
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PMID:Thrombocytosis-induced suppression of small acetylcholinesterase-positive cells in bone marrow of rats. 50 41

Recombinant human erythropoietin (rHuEpo) was tested for its ability to stimulate rat megakaryopoiesis in vivo. Groups of Sprague-Dawley rats were injected with rHuEpo at a daily dose of 20, 80, or 200 U for 5 days. Significant thrombocytosis (a 30 to 40% increase over the control level) was found only in the rats that received 200 U/day, but some changes in the megakaryopoietic parameters were observed not only in the rats given 200 U/day, but also in those receiving 80 or 20 U/day. rHuEpo induced a dose-dependent elevation of megakaryocyte ploidy, with the maximum 45% increase in the mean ploidy over the control level seen in rats given 200 U/day. The size of the marrow megakaryocytes also increased dose-dependently. rHuEpo did not increase bone marrow megakaryocyte numbers, but it increased those in the spleen in a dose-dependent manner. A change of these parameters was seen as early as day 1 at 24 h after initiating the Epo injections at a time when significant thrombocytosis was already present. Moreover, a significant increase in the ratio of small acetylcholinesterase-positive bone marrow cells was also found, with the greatest response noted on day 1. Administration of a large dose of iron did not alter the thrombopoietic effect of rHuEpo. These results suggest that the in vivo administration of rHuEpo stimulates the maturation of mature as well as immature megakaryocytes already present in the bone marrow.
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PMID:Effects of short-term administration of recombinant human erythropoietin on rat megakaryopoiesis. 155 21

Essential thrombocythemia (ET) in an 11-year-old dog was characterized by persistently high platelet counts (range, 4.19 X 10(6)/microliters to 4.95 X 10(6)/microliters, abnormal platelet morphology, marked megakaryocytic hyperplasia in the bone marrow, absence of circulating megakaryoblasts, and history of splenomegaly and gastrointestinal bleeding. Increased numbers of megakaryocytes and megakaryoblasts (15% to 20%) in the bone marrow were confirmed by a positive acetylcholinesterase reaction. Another significant finding was the presence of a basophilia in blood (4,836/microliters) and bone marrow. The marked persistent thrombocytosis, absence of reactive (secondary) thrombocytosis, abnormal platelet morphology, and quantitative and qualitative changes in the megakaryocytic series in the bone marrow suggested the presence of a myeloproliferative disease. Cytochemical and ultrastructural findings aided in the diagnosis of ET. The dog was treated with radiophosphorus. The results was a rapid decline in the numbers of megakaryoblasts and megakaryocytes in the bone marrow and platelets and basophils in the peripheral blood. The dog died unexpectedly of acute necrotizing pancreatitis and diabetes mellitus before a complete remission was achieved.
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PMID:Probable essential thrombocythemia in a dog. 271 60

The DNA content of rat bone marrow megakaryocytes (MK) was studied by Feulgen photometry following splenectomy and sham operation, respectively. The DNA measurements were preceded by acetylcholinesterase staining for identification of the 2N-8N MK. The number of 2N-8N MK decreased to minimum values, while the number of 16N-64N MK increased to maximum values about 4 days following both splenectomy and sham operation. However, the changes were somewhat more pronounced following splenectomy than sham operation. The total MK number did not change significantly. Platelet production, measured by 35S incorporation into platelets, increased during the first 2 days and remained high for 6-7 days, increasing the platelet counts. All values were about normal 30 days after surgery, except for a minor thrombocytosis following splenectomy. The early, highly significant thrombocytosis, following both splenectomy and general surgery, is caused by increased production of platelets due to the surgical trauma. This is caused by a direct action on bone marrow MK by transforming 2N-8N MK into higher ploidy classes. Lack of splenic platelet pooling may influence the grade and duration of the early thrombocytosis after splenectomy. The late, long-lasting, minor thrombocytosis, which occurs after splenectomy but not after sham operation, can be explained by the removal of the splenic platelet pool.
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PMID:The effect of splenectomy on platelet formation and megakaryocyte DNA content in rats. 660 56

Megakaryocytopoiesis was evaluated in the marrow of mice after they had been injected with rabbit anti-mouse platelet serum (RAMPS) or a thrombocytopoiesis-stimulating factor (TSF or thrombopoietin). For controls, other mice were injected with normal rabbit serum or saline. All materials were given as single intraperitoneal injections; at frequent intervals of up to seven days the mice were killed. RAMPS caused severe thrombocytopenia in mice with significant rebound-thrombocytosis following five to seven days later. TSF did not significantly increase platelet counts of mice. Both RAMPS and TSF increased the proportion of the small acetylcholinesterase positive (SAChE+) cells in the marrow of mice which was elevated 3-fold above control values at 8-10 h after treatment. The percentage of SAChE+ cells returned to control levels by 48 h and to below control values by 64-168 h. These data indicate that both exogenous TSF and endogenously produced TSF released in response to acute thrombocytopenia caused a transitory increase in the percentage of SAChE+ cells in mice.
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PMID:Effects of antiplatelet serum and thrombopoietin on the percentage of small acetylcholinesterase-positive cells in bone marrow of mice. 730 23

Aplasia cutis congenita affecting the elbows, knees, hips, and gluteal area was observed in a female newborn, product of a twin pregnancy. One of the twins was a fetus papyraceous detected at 15 weeks of pregnancy. During the course of the pregnancy, maternal thrombocytosis was diagnosed and treated with aspirin. alpha-Fetoprotein was elevated in maternal serum and amniotic fluid, and a distinct electrophoretic acetylcholinesterase band was seen in amniotic fluid. These findings are in agreement with the classification of aplasia cutis congenita as proposed by Frieden et al in which type V is related to the presence of a fetus papyraceous or placental infarcts. The findings in the present case may be explained by the effect of the dead twin on the surviving fetus and the extensive denuded skin areas. Long-term follow-up of the infant showed that the lesions were cured, most of them with minimal scars. Increased risk for aplasia cutis congenita should be considered when elevated maternal and amniotic fluid alpha-fetoprotein and a distinct electrophoretic band of acetylcholinesterase are found. Especially when one of the twins is dead.
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PMID:Aplasia cutis congenita, elevated alpha-fetoprotein, and a distinct amniotic fluid acetylcholinesterase electrophoretic band. 751 37

In this study, the protein which stimulates proplatelet formation (PPF) of megakaryocytes was purified from normal human plasma using 7 steps procedures. Two different protease inhibitors were identified based on their amino acid sequences, i.e. antithrombin III (AT III) and C1 inhibitor. They were included in high density lipoprotein (HDL). HDL was necessary for AT III to be active in PPF in vitro. The biological effects of the AT III/HDL or thrombin-AT III (TAT)/HDL were studied in vitro. PPF of murine megakaryocytes was stimulated by negative control (BSA) (1.8 +/- 0.3%), AT III (2.0 +/- 0.4%), HDL (1.2 +/- 0.9%), AT III/HDL (14.8 +/- 2.1%) or TAT/HDL (23.3 +/- 3.5%), respectively. TAT/HDL also had a synergistic effect with the mpl ligand, judging by the acetylcholinesterase (AchE) expression of murine megakaryocytes (2.7 fold increase). In vivo subcutaneous administration of AT III alone or TAT for 3 days significantly stimulated thrombocytosis (136% and 144%, respectively, p<0.05) and AT III/HDL showed rapid and further stimulation (150%, p <0.01). These results and the previous studies indicate that megakaryocytopoiesis is regulated by the mpl ligand, while a protease/protease inhibitor complex such as TAT, which is involved in the coagulation cascade associated with platelet consumption, might be one of the regulators in platelet production.
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PMID:Purification of proplatelet formation (PPF) stimulating factor: thrombin/antithrombin III complex stimulates PPF of megakaryocytes in vitro and platelet production in vivo. 1124 59

The effect of malignant tumor growth on host's megakaryocytopoiesis and platelet production was studied in mice bearing transplantable Dalton's lymphoma. Tumor growth was paralleled by thrombocytosis, neutrophilia, and anemia. Platelet 51Cr half-life was normal but incorporation of 75Selenomethionine into circulating platelets was significantly enhanced in the tumor bearers suggesting stimulated thrombopoiesis while platelet life span remained unchanged. Megakaryocytes and their precursors, the small acetyl cholinesterase positive cells, were found in increased numbers in the bone marrow (BM) and particularly in the spleen where five to eight-fold rise was observed at the log phase of tumor growth. In addition, a remarkable increase in the number of megakaryocyte progenitors (CFU-MK and MK CFU-S) was observed both in the BM and spleen. Stimulation of these progenitors was more pronounced in the spleen than in the marrow, and the change was noticeable even from the third day of tumor bearing. Therefore, the results suggest that thrombocytosis associated with the growth of this experimental lymphoma was due to accelerated platelet production following stimulated megakaryocytopoiesis especially in the spleen.
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PMID:Stimulation of megakaryocytopoiesis and platelet production during growth of an experimental lymphoma. 1127 30