The impact of electromagnetic radiation emitted by LCD monitors on selected blood cell counts - in vitro studies

2017 ◽  
Vol 1 (7) ◽  
pp. 99-103
Author(s):  
Magdalena ZAWADZKA
Keyword(s):  
Blood Cell ◽  
Electromagnetic Radiation ◽  
In Vitro Studies ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
The Impact

scholarly journals The Impact of Electromagnetic Radiation of Different Parameters on Platelet Oxygen Metabolism – In Vitro Studies

2015 ◽  
Vol 24 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Małgorzata Lewicka ◽  
Gabriela Henrykowska ◽  
Krzysztof Pacholski ◽  
Artur Szczęsny ◽  
Maria Dziedziczak-Buczyńska ◽  
...  
Keyword(s):  
Electromagnetic Radiation ◽  
Oxygen Metabolism ◽  
In Vitro Studies ◽  
The Impact

MO020AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE, CYTOPENIA AND POSTTRANSPLANT OUTCOMES: A RETROSPECTIVE ANALYSIS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Pieter Schellekens ◽  
Djalila Mekahli ◽  
Rudi Vennekens ◽  
Isabelle Meyts ◽  
Dirk Kuypers ◽  
...  
Keyword(s):  
Overall Survival ◽  
Kidney Disease ◽  
Blood Cell ◽  
The Other ◽  
Transplant Recipients ◽  
Total White Blood Cell ◽  
Polycystic Kidney ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
The Impact

Abstract Background and Aims Autosomal dominant polycystic kidney disease (ADPKD), the most common monogenetic inherited kidney disease, has been reported to be associated with distinct cytopenias. The pathophysiological mechanism behind this association and its clinical implications are unknown. Sparse and conflicting data have suggested a tendency to greater vulnerability for cancer and infections in ADPKD renal transplant recipients as compared to their non-ADPKD counterparts. Furthermore polycystin expression has been demonstrated in lymphocytes in vitro with impact on lymphocyte function. From this background, cytopenia could be hypothesized to be directly induced by the molecular PKD defects and to impact on outcome in affected patients. The main interest of the current study is to confirm the association between ADPKD and cytopenia in a well-defined clinical cohort of patients at the time of kidney transplantation. Furthermore, the impact of ADPKD and cytopenia on posttransplant outcomes is studied. Method Baseline (pre-transplantation) and follow-up data from all patients who underwent a first renal transplantation between 01/04/1964 and 01/09/2019 at the Leuven University Hospitals were retrieved from the renal transplantation database. Results 4103 patients were included: 611 ADPKD and 3492 non-ADPKD. Immediately before transplantation, significant differences in total white blood cell (6.33 +/- 2.59 ADPKD versus 7.17 +/- 2.21 non-ADPKD; p<0.0001), neutrophil (4.04 +/- 1.59 versus 4.54 +/- 1.88; p<0.0001), lymphocyte (1.45 +/- 0.05 versus 1.57 +/- 0.68; p<0.0001), basophil (0.041 +/- 0.084 versus 0.046 +/- 0.048; p<0.0001), eosinophil (0.23 +/- 0.24 versus 0.29 +/- 0.33; p<0.0001) and thrombocyte counts (203.00 +/- 67.21 versus 230.18 +/- 76.00; p<0.0001) between ADPKD and non-ADPKD patients were observed. After multiple linear regression analysis, ADPKD remained significantly associated with total white blood cell, neutrophil, monocyte and thrombocyte counts. In terms of post-transplant outcomes, significant univariate differences between ADPKD and non-ADPKD transplant recipients in favor of the ADPKD patients were observed for overall survival, time to first rejection and time to transplant failure. On the contrary, a significantly faster onset of the first posttransplant malignancy and infection was observed in ADPKD as compared to non-ADPKD. Furthermore, the numbers of posttransplant infections and malignancies tended to be higher in the ADPKD patient cohort, the number of transplant rejections was significantly lower. While pre-transplantation lymphopenia was univariately associated with lower overall survival, none of the other post-transplant outcomes was associated with lymphopenia, nor with any of the other blood cell counts. After multivariate Cox proportional hazard regression analysis, ADPKD remained significantly associated with time to first rejection (p=0.0310; HR 0.632) and overall survival (p<0.0001; HR 0.512). None of the blood cell count variables retained significance in the multivariate outcome models. Conclusion This large retrospective single center study confirmed the association between cytopenia and ADPKD immediately before kidney transplantation. Furthermore, ADPKD was also associated with differences in posttransplant outcomes. In multivariate survival analysis, the impact of ADPKD on outcomes outweighed that of other variables, amongst others the blood cell counts. From this, it is tempting to speculate that ADPKD influences outcome through a disease-related impact on blood cells, however many more factors are most probably involved. The hypothesis that cytopenia could be an extra-renal manifestation of ADPKD, directly linked to its genetic basis, and its impact on outcome warrant further investigation.

In vitro effect of blood cell counts on multiple-electrode impedance aggregometry in dogs

2017 ◽  
Vol 78 (12) ◽  
pp. 1380-1386 ◽  
Author(s):  
Katherine J. Nash ◽  
Lenore M. Bacek ◽  
Pete W. Christopherson ◽  
Elizabeth A. Spangler
Keyword(s):  
Blood Cell ◽  
Electrode Impedance ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Impedance Aggregometry ◽  
Vitro Effect ◽  
Multiple Electrode

Splenomegaly with Increased Erythroblast Numbers During Erythropoietic Stress Caused by Ambient Low-Temperature in Mice.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4602-4602
Author(s):  
Shun Maekawa ◽  
Hitomi Iemura ◽  
Hiroshi Miyazaki ◽  
Takashi Kato
Keyword(s):  
Low Temperature ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Conflicts Of Interest ◽  
Normal Serum ◽  
Enhanced Production ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Peripheral Erythrocyte

Abstract Abstract 4602 Erythropoietic stress such as hypoxia has been well described in mammals. These conditions decrease oxygen supply and then enhance production of erythropoietin (EPO) regulates production of red blood cells. Moreover, spleen becomes the main organ of erythropoiesis due to limited marrow space. Here, we describe a new erythropoietic stress, ambient low-temperature. It has been reported that peripheral blood cell counts are affected by ambient low-temperature in several vertebrates. Cold-acclimated rat and chicken exhibit polycythemia (Dveci et al, J Comp Physiol, 2001; Yahav S, Poult Sci, 1997). The response is considered to increase demand of tissues for oxygen, and then enhance metabolic rate and capacity for heat production to acclimate to ambient low-temperature. However, the physiological mechanisms had not been investigated. First, we examined peripheral erythrocyte levels in C57BL/6 mice putting into 5°C ambient. Hematocrits increased from 48% to a plateau of 53% after fourteen days. Likewise, hemoglobin concentration, initially 15 g/dl, rose to 17 g/dl. Reticulocyte production index significantly increased from 4% to 8% after seven days. These data suggested that mice exposed to low-temperature enhanced production of erythrocytes, so we next examined the anatomy and cell composition of their spleens. On day 5, spleens were about 6 mg/g of body weight, two-fold those on day 0. They gradually decreased to their initial weights on day 14. Flow cytometry showed 38% more Ter119+ splenocytes and four-fold more CD71 high Ter119+ early erythroblasts than normal. These values also gradually declined to their initial numbers by day 14. The results suggested the elevated red blood cell counts were due to an increase in production. To test erythropoietic activity in serum, we used an erythrocyte colony-forming assay. Serum from mice kept at low-temperature showed no ability to stimulate CFU-E colony formation in vitro. However, a combination of the serum with EPO (0.5 U/ml) increased CFU-E numbers 1.5 to 2 times that of a combination of normal serum plus EPO or EPO alone. Whether inducible factors account for these effects is the focus of future investigation. Our findings suggest a low-temperature environment is an erythropoietic stress that may offer insights into the adaptive physiology of red blood cell production in mice. Disclosures: No relevant conflicts of interest to declare.

The Role of Stathmin, a Regulator of Mitosis, in Hematopoiesis

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3453-3453
Author(s):  
Charmaine A. Ramlogan-Steel ◽  
Jason C. Steel ◽  
Hassana Fathallah ◽  
Camelia Iancu-Rubin ◽  
Manoocher Soleimani ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Megaloblastic Anemia ◽  
Platelet Production ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
The Mean

Abstract Abstract 3453 Introduction Stathmin is a 17KDa cytosolic protein that plays an important role in the regulation of microtubule dynamics, mitotic spindle formation, cell cycle progression and cell differentiation. Stathmin knockout (KO) mice were initially reported to have a normal phenotype but were subsequently shown to develop an age-related neurological phenotype with axonopathy evident in both central and peripheral nervous systems. These mice were also shown to have a defect in recovery from acute ischemic renal injury. We had previously shown that stathmin plays an important role in the differentiation and proliferation of megakaryocytes (MK) and that down-regulation of stathmin is necessary for the maturation of MK and platelet production in vitro. In this study, we investigated the role of stathmin in megakaryopoiesis and hematopoiesis in vivo using the stathmin KO mouse as an experimental model. Results Stathmin KO mice had lower platelet (PLT) counts at 3 weeks of age when compared to WT mice. The WT mice had a mean PLT count of 662 ± 27 K/μL while KO mice had a mean PLT count of 543 ± 37 K/μL. This correlated with larger and fewer MK in the bone marrow of KO mice (WT: 4.2 ± 0.7 MK/40X field; KO: 3.6 ± 0.2 MK/40X field). Furthermore, in the spleen, there was a 10 fold decrease in the number of MK in KO mice compared to WT mice (6.6 ± 0.6 vs 0.7 ± 0.1 MK/40X field). By 8 weeks, PLT counts and MK size and numbers in the bone marrow and spleen were similar in WT and KO mice. Interestingly, by 16 weeks, the mean PLT of KO mice became significantly higher than that of WT and by 40 weeks, the mean PLT count of KO mice was 1379 ± 100K/μL compared to 1045 ± 120K/μL in WT mice (P<0.05). Microscopic analysis of the bone marrow at 46 weeks of age showed approximately 50% more MK in KO mice compared to WT mice. Differences in red blood cell counts (RBC) were also observed. While at 3 weeks, there were no significant differences between the 2 groups, at 8 weeks, KO mice had significantly lower RBC counts, hemoglobin levels (Hb) and hematocrit (HCT). This trend continued until the last measurement recorded at 40 weeks. Mean RBC in WT mice was 10.5 ± 0.1M/μL compared to 8.9 ± 0.2M/μL in KO mice. The mean corpuscular volume (MCV) and the red blood cell distribution width (RDW) were consistently higher in KO mice than in WT mice. No significant differences were noted in white blood cell counts. Bone marrow cell counts were significantly lower in KO mice when compared to WT mice at different ages from 3–40 weeks. Progenitor cell assays from 10–12 week old animals have shown that bone marrow from KO mice produce significantly fewer BFU-E and Pre-B colonies while no differences were observed in CFU-GMs. Conclusions The phenotypic characteristics of stathmin KO mice confirmed our prior in vitro findings that suggested a role for stathmin in megakaryopoiesis. We expected to see a decrease in the number of platelets and MK coupled with an increase in MK size. This was confirmed in stathmin KO mice at 3 weeks of age. However, we did not expect to see the marked increase in the number of platelets and MK that was observed as the mice aged. The exact mechanism for this has not been identified. Interestingly, the stathmin KO mice exhibited characteristic features of megaloblastic anemia including mild anemia and a significant increase in MCV and RDW. The megaloblastic anemia that is seen in the presence of B12 and folate deficiency results from interference with DNA synthesis resulting in asynchronous maturation of the nucleus and the cytoplasm. We believe a similar phenomenon is occurring in the stathmin KO mice. The deficiency of stathmin results in aberrant exit from mitosis, thereby delaying nuclear maturation and resulting in the megaloblastic features. Thus, the deficiency of stathmin in the KO mice results in two hematopoietic phenotypes that are seen in humans, megaloblastic anemia and thrombocytosis. It is unclear whether mutations of stathmin in humans might result in similar phenotypes. This is a question that will require further investigation. Future studies will investigate the compensatory mechanisms that result in the switch from decreased to increased platelet production as the mice age. Furthermore, examining the effects of hematopoietic stress (e.g. response to chemotherapy or bleeding) in stathmin KO mice might also elucidate a role for stathmin in the recovery from hematopoietic injury as was seen in acute ischemic renal injury. Disclosures: No relevant conflicts of interest to declare.

An Alternative Elastase-mediated Degradation of Fibrinogen and Fibrin Observed in a Patient with Herpes Simplex Encephalitis and Pneumonia

1996 ◽  
Vol 76 (02) ◽  
pp. 184-186 ◽  
Author(s):  
Kenji lijima ◽  
Fumiyo Murakami ◽  
Yasushi Horie ◽  
Katsumi Nakamura ◽  
Shiro Ikawa ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Blood Cell ◽  
White Blood Cell ◽  
Herpes Simplex Encephalitis ◽  
Pmn Elastase ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Sds Page ◽  
White Blood Cell Counts ◽  
Pmn Élastase

SummaryA 74-year-old female developed pneumonia following herpes simplex encephalitis. Her white blood cell counts reached 28,400/μl, about 90% of which consisted of granulocytes. The polymorphonuclear (PMN) elastase/α1-arantitrypsin complex levels increased and reached the maximum of 5,019 ng/ml, indicating the release of a large amount of elastase derived from the granulocytes. The mechanism of PMN elastase release was most likely to be granulocyte destruction associated with phagocytosis. The cleavage of fibrinogen and fibrin by PMN elastase, independent of plasmin, was indicated by the presence of the fragments in immunoprecipitated plasma from the patient corresponding to elastase-induced FDP D and DD fragments and the absence of fragments corresponding to plasmin-induced FDP D and DD fragments on SDS-PAGE. These findings suggested that the large amount of PMN elastase released from the excessive numbers of granulocytes in this patient with herpes simplex encephalitis and pneumonia, induced the cleavage of fibrinogen and fibrin without the participation of plasmin.

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