Relevant bibliographies by topics / Abnormalies

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Abnormalies'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Abnormalies"

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Mironov, S. P., N. A. Es'kin, V. G. Golubev, et al. "Ultrasound Diagnosis of Tendon and Nerve Pathology." N.N. Priorov Journal of Traumatology and Orthopedics 11, no. 3 (2004): 3. http://dx.doi.org/10.17816/vto20041133.

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Ultrasoumd image of tendons and peripheral nerves was described. Sonographic criteria of tendon injury and pathology: dislocation, degenerative changes, ruptures including intratendinous, i.e. longitudinal, partial, total as well as inflammation, tumors and postoperative complications was given. Sonographic peculiarities of diagnosis on injury, compression and constriction of nerve in tunnel osteofibrosis of extremity was presented. Presence of that pathology was confirmed by clinical and electophysiological examination and verified intraoperatively. Ultrasonography may be used for diagnosis of congenital abnormalies, nerve injury and neurogenic tumors. Authors emphasize the importance of participation of experi­enced examiner in interpretation of ultrasonograms.
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Tijana, Durmic, Djelic Marina, Antic Milena, Gavrilovic Tamara, and Zdravkovic Marija. "O-24 Periodical screening for cardiovascular abnormalies in elite athletes: utility of preparticipation examination." British Journal of Sports Medicine 50, Suppl 1 (2016): A13—A14. http://dx.doi.org/10.1136/bjsports-2016-097120.24.

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Garcia, Joe G. N., Harold L. James, Steve Zinkgraf, and Marc B. Perlman. "Lower Respiratory Tract Abnormalies in Rheumatoid Interstitial Lung Disease: Potential Role of Neutrophils in Lung Injury." American Review of Respiratory Disease 136, no. 4 (1987): 811–17. http://dx.doi.org/10.1164/ajrccm/136.4.811.

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Sycheva, Elena G., Niso M. Nazarova, Olga V. Burmenskaya, Vera N. Prilepskaya, and Dmitry Yu Trofimov. "The occurrence of human papillomavirus types in the formation of neoplastic transformation of the epithelium of the cervix in “lesser abnormalies”." Gynecology 22, no. 1 (2020): 19–22. http://dx.doi.org/10.26442/20795696.2020.1.200015.

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Aim. To assess the frequency of human papillomavirus (HPV) occurrence according to the IARC classification in patients with lesser abnormalie of cervical epithelial lesions and analyze their role in the formation of SIL.
 Materials and methods. The study included 129 HPV-positive women aged 1845 years (average age 34 to 11 years) with cytological conclusion NILM, ASCUS or LSIL. Patients are divided into 3 groups depending on the results of the cytological smear: 1 group (NILM/HPV) 66 (51.2%), 2 group (ASCUS/HPV) 28 (21.7%), 3 group (LSIL/HPV) 35 (27.1%). During dynamic observation for 24 months. A comprehensive clinical-laboratory examination was carried out, including HPV-typing, cytological examination, extended colposcopy every 6 months, sighting biopsy of the cervix (according to the indications).
 Results. According to the results of the pathomorphological study, squamous intraepithelial lesions neoplasia (cervical intraepithelial neoplasia CIN+) was verified in 59 (71.9%) of the results of the study: LSIL (CIN I) 53 (64.6%), HSIL (CIN IIIII) 6 (4.6%). The morphological diagnosis of LSIL (CIN I) was established in 1 group (NILM/HPV+) in 20 (55.6%), 2 groups (ASCUS/HPV+) 9 (32%), 3 group (LSIL/HPV) 24 (68.6%); HSIL (CIN IIIII) in group 1 2 (5.6%), in 2 group 3 (10.7%) and in the 3 group 1 (2.9%).
 Conclusions. In patients with lesser abnormalies of cervical lesions in the formation of CIN+ participated HPV group 1 in 79.1%, groups 2A in 5.5%, groups 2B in 15.4% of cases. The HPV high carcinogenic risk (group 1) was involved in the formation of HSIL (CIN IIIII). The neoplastic transformation of the cervical epithelium of the studied patients was caused by the persistence of HPV 16, 58, 39, 18, 51, 68, 56, 82, 35, 52, 53, 35 types.
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Cicinelli, E., P. C. Mitola, B. Indellicati, et al. "Double Vagina Double Cervix and Uterine Septum Mimicking a Simple Septate Uterus: Role of Cervical Abnormalies at Hysteroscopy with Vaginoscopic Approach as Diagnostic Sign." Journal of Minimally Invasive Gynecology 20, no. 6 (2013): S136. http://dx.doi.org/10.1016/j.jmig.2013.08.467.

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Mossafa, Hossein, Hamid Belaouni, Veronique Saada, Christine Fourcade, J. Pierre Hurst, and Driss Chaoui. "High Frequency of the JAK2 V617F Mutation in Patients with Trisomy of Chromosome 9." Blood 112, no. 11 (2008): 1749. http://dx.doi.org/10.1182/blood.v112.11.1749.1749.

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Abstract The previous studies assessing the relationship of cytogenetic abnormalities to JAK2 status have not shown any significant associations, although numbers have generally been too small to make a definitive comment. We therefore assessed the JAK2 V617F mutation status of 337 patients from 39 centers (175 males, 161 females; median age at time of study 71 years old, range 32–98). Patients were classified as follows: 100 with typical MDS, 10 with 5q- syndrome, 17 with AREB-2, 2 with RARS, 13 with RARS-T, 23 with MPD/MDS, 12 with CMML, 142 with typical MPDs, 5 with hypereosinophilic syndrome (HES), 7 with AML with multi-lineage dysplasia from Ph- MPD, 10 with aCML Ph- or MPD/MDS-u and 25 with typical CML Ph+. Bone marrow or blood derived genomic DNA was screened for the JAK2 mutation. The JAK2 V617F mutation was found in 109/337 pts (32%): typical MPD-Ph− (47%) cases, MDS (4.5%), 5q- syndrome (60%), AREB-2 (64%), CMML (42%), MDS/MPD (36%). A clonal cytogenetic abnormality was detected by R-banding in 159/337 cases (47%). The JAK2 mutation was associated with a chromosomal abnormality in 81/159 cases (51%). The most common chromosome abnormality associated with JAK2 mutation was the gain of chromosome 9 (n= 22, Associated with JAK2 mutation: 19/22 cases 86%). The second most common abnormality was partial deletion of 20q (n=30, Associated with JAK2 mutation: 19/30 cases 63%). The partial or complete loss of chromosome 7 (n=16, Associated with JAK2 mutation: 6/11), deletion of 5q- (n=10, Associated with JAK2 mutation: 6/10), gain of chromosome 8 (n=11, Associated with JAK2 mutation: 7/11), partial deletion of 11q (n=8, Associated with JAK2 mutation: 5/8), partial deletion of 12p (n=6 Associated with JAK2 mutation 4/6), partial deletion of 13q (n=5, Associated with JAK2 mutation: 4/5). Patients with trisomy 9 and JAK2 mutation were classified as follows : polycytemia vera (PV) n=4 (100% JAK2 mutated), essential thrombocytemia (ET) n=3 (100% JAK2 mutated), idiopathic myelofibrosis (IMF), n=2 (100% JAK2 mutated), MPD/MDS, n=3 (67% JAK2 mutated), secondary AML post MDS, n=1 (JAK2 mutated), atypical MPD, n=6 (100% JAK2 mutated), MMCL, n=1(JAK2 mutated). The V617 mutation was not found in the case of de novo AML, and 2 typical MDS cases. 9 males, 10 females, the median age: 68 years old, range 40–98 years old, median white cell count (WCC) 11 G/l, range 2.4–50.7 G/l (13/19 pts> 10G/l), median hemoglobin 13.5 g/dl, range 9–20.2 g/dl (5/19 pts> 17g/dl), median platelet count 667G/l range 9–1769 G/l (9/19 pts> 500 G/l). The BCR/ABL transcript (multiplex PCR) was not detected in all of these cases. In this study the gain of chromosome 9 associated with JAK2 V617F mutation was the most frequent chromosome abnormality (100%) observed in typical MPDs and atypical syndrome such as MDS/MPD. In summary, previous studies assessing the relationship of cytogenetic abnormalies to JAK2 status did not show any significant association (ref). The del(20q), del(13q), trisomy 8 and del(5q) are known to be recurring non-specific cytogenetic abnormalities, and some of them are also detectable in patients with JAK2 mutation positive or negative. We describe here a significant association the JAK2 V617F mutation and trisomy of chromosome 9 that was detected in a cohort of patients with gain of chromosome 9. Clearly, in addition to PV, IMF, and ET these associations were found in other disease entities, high frequency in the case of atypical MPDs particularly in the case of aCML. Previously, Campbell et al. reported 10 patients with a trisomy 9, in typical MPDs, all of them were V617F+. A longer follow-up and morphological diagnosis is however necessary to determine the prognostic signification of JAK2 mutation and +9 in the cases of classic myeloproliferative syndromes and atypical syndrome such as MDS/MPD overlap syndrome.
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Dikarev, A. V., V. G. Dikarev, and N. S. Dikareva. "COMPARATIVE ANALYSIS OF THE FREQUENCY OF CYTOGENETIC ABNORMALIES IN THE ROOT APICAL MERISTEM OF SPRING BARLEY (HORDEUM VULGARE L.) CULTIVAE SEEDLINGS, CONTRASTING IN THEIR LEAD TOLERANCE." PROCEEDINGS ON APPLIED BOTANY, GENETICS AND BREEDING 177, no. 1 (2016): 52–68. http://dx.doi.org/10.30901/2227-8834-2016-1-52-68.

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Kusumawati, Enike Dwi, Syam Rahadi, Sugeng Santoso, and Dyah Lestari Yulianti. "Pengaruh Lama Thawing yang Berbeda pada Suhu 25 oC Terhadap Kualitas Semen Beku Sapi Ongole." Jurnal Ilmu dan Teknologi Peternakan Tropis 6, no. 1 (2019): 119. http://dx.doi.org/10.33772/jitro.v6i1.6538.

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ABSTRAK Penelitian ini bertujuan untuk mengetahui pengaruh lama thawing yang berbeda pada suhu 250C untuk mendapatkan kualitas spermatozoa semen beku sapi ongole yang optimal. Penelitian dilakukan di Laboratorium Fakultas Peternakan Universitas Kanjuruhan Malang. Metode Penelitian yang digunakan adalah metode percobaan dengan menggunakan Rancangan Acak Lengkap (RAL) Faktorial. Setiap perlakuan thawing diberikan ulangan sebanyak 10 sampel semen beku sapi ongole. Hasil penelitian menunjukkan bahwa perlakuan dengan lama thawing 7, 15, 30 detik pada suhu 25oC memberikan perbedaan pengaruh yang sangat nyata (p<0.01) pada motilitas, viabilitas dan abnormalitas spermatozoa semen beku sapi ongole. Motilitas tertinggi diperoleh pada perlakuan P3 dengan rata-rata sebesar 40,8%, viabilitas tertinggi diperoleh pada perlakuan P3 dengan rata-rata sebesar 82,39%, sedangkan abnormalitas terendah diperoleh pada perlakuan P3 dengan rata-rata sebesar 11,95%. Berdasarkan penelitian ini maka dapat disimpulkan bahwa thawing pada suhu 25oC dengan lama waktu 30 detik memberikan kualitas spermatozoa yang paling baik sehingga disarankan untuk melakukan thawing pada suhu 25oC dengan lama waktu 30 detik. Kata kunci: abnormalias, mortalitas, ongole, thawing, viabilitas ABSTRACT This study aims to determine the effect of different thawing time at 250C to get the sperm quality of frozen semen ongole bull. Research conducted at the Laboratory of Animal Husbandry Faculty Kanjuruhan University of Malang. The method of study by using Completely Randomized Design (CRD) factorial. Any treatment given repeated thawing of frozen samples of 10 times. The study show that treatment with time thawing 7 (P1), 15 (P2), 30 (P3) seconds at 25oC gives a very significant difference (P<0.01) on motility, viability and abnormalities of ongole Bull sperm. The highest motility and viability were obtained at P3 (40,8%) and (82,39%), while the lowest abnormalities obtained on P3 (11,95%). Based on this research it can be concluded that thawing at 25oC with 30 seconds to give the best quality sperm that is recommended for thawing. Keywords: abnormality, motility, ongole, thawing, viabilit
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Kusumawati, Enike Dwi, Syam Rahadi, Sutantri Nurwathon, and Dyah Lestari Yulianti. "Kualitas Post Thawing Spermatozoa Kambing Peranakan Etawa (PE) pada Suhu 37oC dengan Waktu yang Berbeda." Jurnal Ilmu dan Teknologi Peternakan Tropis 6, no. 2 (2019): 246. http://dx.doi.org/10.33772/jitro.v6i2.7152.

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ABSTRAKPenelitian ini dilakukan di laboratorium Fakultas Peternakan Universitas Kanjuruhan. Materi Penelitian yang digunakan adalah semen kambing PE beku yang didapatkan dari Balai Besar Inseminasi Buatan (BBIB) Singosari Kabupaten Malang. Metode penelitian yang digunakan adalah metode percobaan dengan rancangan acak lengkap (RAL). Perlakuan thawing menggunakan air dengan suhu 37°C selama 7, 15, dan 30 detik dengan 10 kali ulangan. Variabel yang diamati yaitu motilitas, viabilitas, dan abnormalitas spermatozoa. Hasil penelitian menunjukkan bahwa motilitas dan viabilitas perlakuan pencairan waktu 30 detik pada 37°C (P3) memberikan hasil terbaik adalah motilitas tertinggi 35%, viabilitas tertinggi 65,88%, dan abnormalitas terendah dengan pencairan 30 detik pada 37°C (P3) 18,392% . Namun, perlakuan tidak menunjukkan perbedaan yang signifikan (P>0,05) pada motilitas dan viabilitas tetapi memberikan perbedaan yang sangat signifikan pada abnormalitas (P<0,01). Kesimpulan dari penelitian ini adalah bahwa perlakuan lama thawing mempengaruhi motilitas, viabilitas, dan abnormalitas spermatozoa.Kata Kunci: kambing, motilitas, peranakan etawa, spermatozoa, viabilitasABSTRACTThis study was carried out in the laboratory of Animal Husbandry Faculty Kanjuruhan University. The research material used was frozen sperm PE goat obtained from the Center for Artificial Insemination (BBIB) Singosari Malang. The research method used was an experimental method with a completely randomized design (CRD). The thawing treatment uses water with a temperature of 37 °C for 7, 15, and 30 seconds with 10 replications. The variables observed were motility, viability, and abnormalities of sperm.The result showed that time thawing treatment of 30 seconds at 37°C (P3) was the highest average motility 35%, the highest average viability 65,881%, and the lowest average abnormality with thawing 7 seconds at 37°C (P1) 18,392%. However, the treatment didn’t show significant different (P>0,05) on motility and viability but it gave highly significant different on abnormality (P<0,01). The conclusion of this research is that the treatment of time thawing influence motility, viability and increase abnormality.Keywords: abnormality, etawa filial, goat, motility, sperm, viability
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Bernardi, Simona, Paola Tononi, Sergio Marin Vargas, et al. "Genomic Analisys of Notch Mutations in a Case of Alagille Syndrome with Acute Lymphoblastic Leukemia." Blood 124, no. 21 (2014): 5338. http://dx.doi.org/10.1182/blood.v124.21.5338.5338.

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Abstract Alagille syndrome (ALGS), or arteriohepatic dysplasia, is a congenital multisystem disease due to Notch signalling pathway mutations, most commonly affecting JAGGED-1 (ALGS type 1), and more rarely NOTCH-2 (ALGS type 2), leading to hepatic, lung, renal and ocular dysfunction (chronic cholestasis, peripheral pulmonary artery stenosis, dysplastic kidneys pigmentary retinopathy), and skeletal abnormalies (minor vertebral segmentation, characteristic facies, posterior embryotoxon/anterior segment defects). ALGS is an autosomal dominant disease, but it is characterized also by variable penetrance and clinical expression and somatic/germline mosaicism. A 20-year-old man with ALGS was admitted to the University Hospital of Verona because of pancytopenia. Following analyses led to the diagnosis of Philadelphia chromosome/bcr-abl-negative, CD10-positive, B-lineage acute lymphoblastic leukemia (common B-ALL). In order to identify the genetic components involved in this complex phenotype, we sequenced the exome of a bone marrow sample collected from the patient. By genome interpretation with Knome pipeline applied to the reference genome UCSC hg19, we found missense variants both in NOTCH-2 (E38K) and JAGGED-1 (P871R) genes that are mainly involved in the syndrome, although their effect on protein function was predicted not to be deleterious. However, we detected putative damaging mutations in genes such as PAX5 (R38H) and NOTCH-1 (K1821N), which might be strongly related to the observed disease. In fact, PAX5 is a member of PAX protein family of transcription factors implicated into regulation of early development that binds NOTCH-2 and likely altering its functionality. On the other hand, NOTCH-1 is involved in cell growth and proliferation and thus the predicted alteration of function of the corresponding protein may have an important role in neoplastic transformation. Disclosures Martinelli: Novartis: Consultancy, Speakers Bureau; BMS: Consultancy, Speakers Bureau; Pfizer: Consultancy; ARIAD: Consultancy.
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Dissertations / Theses on the topic "Abnormalies"

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West, Jessica. "Ability and Abnormality." UNF Digital Commons, 2016. https://digitalcommons.unf.edu/etd/638.

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This thesis addresses questions relating to perceptions of abilities and abnormalities found in everyday life. Abilities in this paper range from a total lack of ability to function in extreme disability to a level of ability expected by society to enhanced and radically enhanced abilities and their place in the realm of abnormality. We begin by establishing the differences between abilities and enhancements. Following this is a discussion regarding the ethical concerns of human enhancement. After this we turn to a discussion of abnormality and the social experience of abnormality. These discussions lead into establishing a basis for how many abilities are considered abnormal. This is then followed by a discussion that specifically addresses whether or not individuals who voluntarily undergo non-therapeutic enhancement may be subject to oppressive measures.
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Smith, Keith Charles. "Reproductive abnormalities in ewes." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319129.

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Goatly, Alison. "FOXP1 abnormalities in lymphoma." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611626.

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Sullivan, Courtney R. "Bioenergetic Abnormalities in Schizophrenia." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1523629996205968.

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Martini, Elena. "Chromosomal abnormalities in human gametes." Maastricht : Maastricht : UPM, Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8529.

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Schouten, Hendricus Constantinus. "Chromosomal abnormalities in hematological malignancies." Maastricht : Maastricht : Datawyse ; University Library, Maastricht University [Host], 1991. http://arno.unimaas.nl/show.cgi?fid=5640.

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Haynes, Andrew Paul. "Metabolic abnormalities in uraemic neutrophils." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305133.

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Bedwell, A. E. "Immunological abnormalities of rheumatoid arthritis." Thesis, University of Bristol, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372005.

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Poulogiannis, George. "Genome abnormalities in colorectal cancer." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612117.

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Pazzi, Paolo. "Haemostatic abnormalities in canine spirocercosis." Diss., University of Pretoria, 2012. http://hdl.handle.net/2263/25886.

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Spirocerca lupi (S. lupi) is a nematode that infects the dog’s oesophagus resulting in an inflammatory fibroblastic nodule that progresses to a sarcoma in approximately 25% of cases. Inflammation, coagulation and cancer are exquisitely intertwined and inflammatory changes are known to lead to coagulation abnormalities. The nature and degree of haemostatic alterations in canine spirocercosis are unknown. Evidence of inflammation in dogs with clinical spirocercosis is provided by pyrexia, leucocytosis, increased serum interleukin 8 and C-reactive protein as well as severe inflammatory infiltrates on histopathology of nodules. This study aimed to determine if haemostatic abnormalities exist in canine spirocercosis, and hypothesised that the severity of abnormalities could be used to differentiate non-neoplastic from neoplastic spirocercosis. Thirty-nine client-owned S. lupi-infected dogs and 15 healthy age- and sex-matched control dogs were included in this study. Blood samples were collected at the time of diagnosis. A complete blood count, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, antithrombin (AT) activity, D-dimer concentration and thromboelastography (TEG) analysis were performed. Hypercoagulability was based on the maximum amplitude (MA) value derived from TEG. Inflammatory parameters were also determined and included C-reactive protein (CRP) and fibrinogen concentrations. The S lupi-infected dogs were divided into a non-neoplastic group (n=24) and a neoplastic group (n=15). Data were compared using the Kruskal-Wallis Test and Dunn’s multiple comparisons applied post-hoc. Correlation was determined using Spearman’s correlation. Hypercoagulabilty was found in the neoplastic and non-neoplastic spirocercosis cases. In addition, the neoplastic group was significantly more hypercoagulable than the non-neoplastic group, and the non-neoplastic group was significantly more hypercoagulable than the control group. The median fibrinogen concentration was significantly higher in the neoplastic group compared to the non-neoplastic group, but there was no significant difference between the non-neoplastic and control group. The median CRP concentration was significantly higher in the neoplastic group compared to the non-neoplastic group, with no significant difference between the non-neoplastic and control group. Compared to the control group the median AT activity was significantly decreased in both the non-neoplastic and neoplastic groups. No significant difference was found between the infected groups. Across the non-neoplastic and neoplastic groups, MA showed positive linear correlation with CRP and fibrinogen. The study showed that spirocercosis is associated with a hypercoagulable state that becomes progressively more severe with neoplastic transformation. Overlap did exist between the median MA values of the non-neoplastic and neoplastic groups, but an MA of >76 mm provided a specificity of 96% and sensitivity of 73% for the differentiation of disease state. Thromboelastography might therefore be used as an adjunctive assay to support the suspicion of neoplastic transformation of the oesophageal nodule as well as to determine the overall haemostatic status of the patient. The MA correlated positively with the indicators of inflammation (CRP&fibrinogen) supporting the hypothesis that an inflammatory state induced by the S. lupi nodule is at least partly responsible for the hypercoagulability. The link between inflammation, coagulation and neoplastic transformation in spirocercosis warrants further investigation to elucidate the exact factors resulting in the hypercoagulable state, whether clinically relevant complications develop and whether or not specific therapy should be instituted to prevent thrombotic sequelae.<br>Dissertation (MMedVet)--University of Pretoria, 2012.<br>Companion Animal Clinical Studies<br>unrestricted
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Books on the topic "Abnormalies"

1

Living with Scoliosis. ABDO Publishing Company, 2014.

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Seligman, Martin E. P. Abnormality. W. W. Norton & Co., 1998.

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Endre, Czeizel. Multiple congenital abnormalities. Akadémiai Kiadó, 1988.

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Shimokawa, Hiroaki, ed. Coronary Vasomotion Abnormalities. Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-7594-5.

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Epker, Bruce N. Dentofacial deformities: Integrated orthodontic and surgical correction. C.V. Mosby, 1986.

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Epker, Bruce N. Dentofacial deformities: Integrated orthdontic and surgical correction. C.V. Mosby, 1986.

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C, Fish Leward, ed. Dentofacial deformities: Integrated orthodontic and surgical correction. Mosby, 1986.

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P, Stella John, and Fish Leward C, eds. Dentofacial deformities: Integrated orthodontic and surgical correction. 2nd ed. Mosby, 1995.

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The psychology of abnormality. Harcourt Brace College Publishers, 1996.

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Abnormalities of intestinal motility. R.G. Landes, 1992.

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Book chapters on the topic "Abnormalies"

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Levesque, Roger J. R. "Abnormality." In Encyclopedia of Adolescence. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1695-2_471.

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Levesque, Roger J. R. "Abnormality." In Encyclopedia of Adolescence. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-33228-4_471.

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Banyard, Philip, and Andrew Grayson. "Abnormality." In Introducing Psychological Research. Macmillan Education UK, 2008. http://dx.doi.org/10.1007/978-1-349-99578-3_8.

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Levesque, Roger J. R. "Abnormality." In Encyclopedia of Adolescence. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32132-5_471-2.

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Wolbring, Gregor. "Abnormality." In Encyclopedia of Global Bioethics. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-09483-0_1.

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Hangay, George, Severiano F. Gayubo, Marjorie A. Hoy, et al. "Abnormality." In Encyclopedia of Entomology. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_10.

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Wolbring, Gregor. "Abnormality." In Encyclopedia of Global Bioethics. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-05544-2_1-1.

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Ong, Peter, and Hiroaki Shimokawa. "Epidemiology of Coronary Microvascular Dysfunction." In Coronary Vasomotion Abnormalities. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7594-5_5.

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Takahashi, Jun, and Hiroaki Shimokawa. "Epidemiology of Vasospastic Angina." In Coronary Vasomotion Abnormalities. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7594-5_1.

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Satoh, Kimio, and Hiroaki Shimokawa. "Pathophysiology and Molecular Mechanisms of Coronary Artery Spasm." In Coronary Vasomotion Abnormalities. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7594-5_2.

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Conference papers on the topic "Abnormalies"

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Drouet, L., B. Baudin, F. Ch Baumann, and J. P. Caen. "SERIC ANGIOTENSIN CONVERTING ENZYME : AN ENDOTHELIAL CELL MARKER (application to thrombo-embolic pathology)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644205.

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As a blood marker of endothelium, we investigated the seric activity of Angiotensin Converting Enzyme (ACE) at rest and after stimulation either by local venostasis or dDAVP infusion. dDAVP did not induce any significant change in ACE contrarily to venostasis. Searching for an endothelial abnormality implicated in the genesis of Deep Vein Thrombosis (DVT) we applied the local venostasis test to patients affected by recurrent DVT. Patients, divided in 3 groups (group I : documented history of recurrent DVT, group II : only one DVT or recurrent superficial venous thrombosis, group III : history of arterial thrombo embolism), and controls were screened for ACE as well as for plasmatic fibrinolytic activity and von Willebrand factor (vWF) level. Two types of abnormalities of seric ACE activity were found : low basal level in group I and low response to venostasis in groups I and III : group II did not differ from controls. This suggests an endothelial lesion participating to the etiology of some recurrent DVT and supports the measurement of seric ACE to discriminate some patients at high risk of DVT. Measures of fibrinolytic and ACE activities are not redundant since the two types of ACE abnormalities were not individually encountered in the same patients and were independent from abnormalities of the fibrinolytic system
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Kneis, Janine, and Maicol Peterson Gandolphi de Almeida. "Sensoriamento Automobilístico Usando Redes Sem Fio e Alerta de Falhas por Voz Sintetizada." In Computer on the Beach. Universidade do Vale do Itajaí, 2021. http://dx.doi.org/10.14210/cotb.v12.p149-154.

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This paper proposes a sensing system for vehicles using an auto- motive scanner with wireless connection for sending data. The connection to the scanner provides data that is sent to a cell phone via a Bluetooth connection and to the cloud . In order to provide a response to the driver as soon as an abnormality appears, an appli- cation was created to emit a synthesized voice warning. The results showed that the driver, through the synthesized voice messages and the system interface, was previously able to become aware of the abnormalities of the vehicle and carry out preventive maintenance.
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Briët, E., L. Engesser, E. J. P. Brommer, A. W. Broekmans, and R. M. Bertina. "THROMBOPHILIA:ITS CAUSES AND A ROUGH ESTIMATE OF ITS PREVALENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642945.

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Idiopathic venous thrombosis and embolism have gained widespread interest since the discovery that, deficiencies of antithrombin III, protein C, and protein S are associated with familial venous thrombophilia. The purpose of our study was to obtain an estimate of the prevalence of this syndrome and to establish the etiology in as many cases as possible.We collaborated with specialists from 37 Dutch hospitals, covering about 10% of the Dutch population. A history as well as blood samples were obtained from 113 unrelated cases with familial thrombophilia and from 90 isolated cases. Assuming that each proband in a family with thrombophilia has an average of four affected relatives, a rough estimate of the prevalence of familial thrombophilia in The Netherlands is 40 cases per 100.000. The prevalence of non-familial thrombophilia is probably lower.In 35 out of the 113 familial cases we established a diagnosis of hereditary antithrombin III deficiency (n=5), protein C deficiency (type I: n=9; type II: n=4), protein S deficiency (n=15) and dysfibrinogenemia (n=2). In 36 cases we found no abnormality at all and in the remaining 42 cases abnormalities were found in one or more of the following: heparin cofactor II, factor V, factor VII, factor VIII, von Willebrand factor, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor, alpha 2 antiplasmin and histidine rich glycoprotein. In most of these cases, however, the hereditary nature of the abnormalities could not be demonstrated and the causal relationships remain to be established.In the 90 isolated cases, we diagnosed hereditary deficiencies of anti thrombin III, protein C and protein S each in one case and a lupus anticoagulant in two cases. In 54 cases no abnormality was found and in the remaining 31 cases various abnormalities were found in one or more of the proteins mentioned above.We conclude that the syndrome of thrombophilia is not rare but its true prevalence needs to be established by more rigorous means. An etiological diagnosis can be made with confidence in only one third of the familial cases and in less than 10 percent of the isolated cases.
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Ngo, K. Y., D. Lynch, J. Gitscher, N. Ciavarella, Z. Ruggeri, and T. Zimmerman. "HOMOZYGOUS AND HETEROZYGOUS COMPLETE DELETIONS OF THE VON WILLEBRAND FACTOR GENE CODING REGION IN SEVERE VON WILLEBRAND DISEASE AND CARRIERS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643931.

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Severe von Willebrand disease (vWD) is characterized by undetectable levels of von Willebrand factor (vWF), or trace amounts, in plasma and tissue stores. We have studied the genomic DNA of ten affected individuals from five families with this disorder using two cDNA probes. One probe extended from 175 base pairs of the 5’ untranslated region to the nucleotides encoding amino acid 618 of pro-vWF; the second extended from the nucleotides encoding amino acid 2225 of pro-vWF to 100 bp into the 3’ untranslated region. Three variants of the disorder were identified. Southern blots of restriction endonuclease digests and slot blots of undigested genomic DNA showed complete homozygous deletion of the vWF gene coding region in four affected siblings, three of whom had developed allo-antibodies. Gene dosage analysis performed with slot blots and laser densitometry were consistent with complete heterozygous deletions in both parents. The second variant was characterized by a complete heterozygous deletion of the vWF gene coding region in the propositus and one asymptomatic parent, suggesting that a different type of genetic abnormality was inherited from the other parent and that the patient was doubly heterozygous for distinct genetic abnormalities affecting vWF. In a third variant, no abnormalities could be detected. These techniques should prove useful in identifying carriers of severe vWD and also defining patients at risk of developing allo-antibodies to vWF.
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Sas, G. "DEFECTS IN SERINE PROTEASE INHIBITORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643714.

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Several serine protease inhibitorsof plasma inhibit the activated coagulation enzymes but only antithrombin III(AT-III)and heparin cofactor II (HC-II) are implicated in the pathogenesisof the familial thrombosis. Since thefirst publication (1965) many thrombophilic families with reduced AT-III synthesis have been investigated. These studies have proved that the disorder is associated with a high risk forvenous thrombosis and the inheritanceis autosomal dominant. The AT-III activity in the plasma of the affected patients is about 50% of the normalvalue.In recent years the heterogeneity of the inherited AT-III deficiency has been verified. The various AT-III abnormalities are not mere interestingrarities but they provide naturally occurring models for the solution of theoretical problems such as the function of AT-III molecule, the physiological significance of heparin, etc. Furthermore, the clinical manifestationof the particular variants greatly differs from symptomless abnormality tosevere thrombotic cases.In the majority of cases, reduced functional activity is accompanied with a parallel decrease of antigen concentration of AT-III. This is the characteristic feature of the quantitative or Type I ("classical")AT-III deficiency. By means of crossed immunoelectrophoresis, electro-focussing and recombinant DNA techniques the heterogeneity of this group has been established. In one subgroup (Type la) AT-III molecules are normal as regards their biochemical characteristics. In Type lb, subnormal AT-IIIquantity is accompanied with decreased heparin affinity. Differentiation of these subgroups has practical consequences: therapeutic concentrations of heparin apparently does not decrease AT-III level in the plasma of patients with Type lb AT-III deficiency.The other main form is the qualitative deficiency of AT-III (Type II) which is characterised by reduced functional activity at normal antigen concentration. In general, two populations of AT-III molecules can be detected in the blood of these patients: a normal and an abnormal one. Up till now at least 24 different abnormalities were found and designatedwith toponymes. These disorders can be classified with relatively simple laboratory methods such as functional anti-IIaXaFirstDepartment of Medicine, Postgraduate Medical University, Budapest, Hungary.arin cofactor activity, crossed immunoelectrophoresiswith and without heparin, heparin-affinity chromatography. Type na is characterised by profound structural changes of the molecule,variably: reflected in reduced inactivation of F Ha and F Xa, abnormal heparin-AT-III reaction and aberrant immunochemical structure Seven different abnormalities fall into this group (Budapest I, Tokyo, MalmÖ, Chicago, Milano, Trento and Northwick Park). The last three abnormalities are very similar.In Type lib an isolated defect of protease inactivation can be detected and an isolated disturbance of the active centre ofthe molecule is assumed.Until now 6 apparently different variants belonging to this group have been described. (Aalborg, Vicenza, Denver, Hvidovre, Charleville, Milano 2.) Type lie abnormality is characterised by an isolated defect of the heparin-AT-III reaction. In these cases a disturbance of the heparin binding site(s) is assumed. Eleven families with this type of abnormality have been recorded (Ann Arbor, Basel, Paris 1 and 2, Toyama* Tours, Padova I and 2, Algers, Fontainebleu and Budapest 2). This subgroup is heterogeneous in respect ofheparin affinity: in the majority of cases the abnormal AT-III molecules have no heparin affinity at all while in rare cases (such as Basel, Budapest 2) they have reduced affinity.TheType lie AT-III deficiency has several distinctive features compared with the other subtypesJClinically, the thromboembolic complications are rare: in 4 families thrombosis has notoccurred at all. Only one member in each of 4 other families had thrombosis. In 3 families homozygous patients suffered severe thrombosis in young age and/or in unusual localisations (intraarterial, intracardiac, etc.) butthe other heterozygous members were free of thrombotic symptoms. No increased intravascular coagulation could be detected in Type lie heterozygous cases incontrast to the "classical" AT-III deficiency.These observations suggest a different mechanism and clinical manifestation of the deficiency of progressiveserine protease inactivation and of heparin cofactor activity. In case of progressive inactivation, reduction of 50% of the activity predisposes mainly to venous thrombosis as a consequence of the hypercoagulability of theblood. The isolated reduction of heparin cofactor activity seems to bringabout thrombosis in any part of the vascular system, but only if this reduction is as severe as that of the coagulant factors in case of coagulopathies.In accordance with this finding, rare cases of HCII deficiency give rise to thrombosis in both the arteries and the veins. Heparin cofactor activities may play an important role in the antithrombotic mechanism along theendothelial surface of the whole vascular system.
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Cooper, S. M., R. G. Malia, F. E. Preston, S. L. B. Duncan, AR B. Smith, and M. Greaves. "CLINICAL AND LABORATORY FEATURES ASSOCIATED WITH LUPUS ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644231.

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Recent evidence suggests a relationship between the presence of lupus anticoagulant and elevated titres of antibody to cardiolipin. Also an association with thrombotic tendency and with a high incidence of first trimester spontaneous abortion or second and third trimester fetal death has been noted. In order to investigate the relationship between anticardiolipin (aCL) antibodies and coagulation test abnormalities we have studied 12 subjects with systemic lupus erythematosus (SLE),10 with history of venous thrombosis, 30 with unexplained prolongation of clotting times and 34 with a poor obstetric history. Coagulation tests applied were: KCCT using two ’incomplete’ thromboplastin preparations and corrections with 20%/50% normal plasma; one-stage prothrombin time (OSP); dilute Russell’s viper venom time (DRVVT, including the platelet neutralisation procedure) and the heat stability test. IgG and IgM aCL antibody were assayed by enzyme-linked immunosorbent assay as described elsewhere. Abnormalities in more than one coagulation test were detected in 4 subjects with SLE (33%), 4 with thrombosis (40%), 6 with poor obstetric history (18%) and 10 with unexplained prolonged KCCT (33%). The DRVVT was most sensitive to the presence of lupus anticoagulant. Detectable aCL antibody was present in 12 subjects (IgG in 6, IgM in 4, both in 3), including some from each group. 2 had IgG aCL antibody and normal coagulation tests (1 SLE, 1 poor obstetric history). No coagulation or immunological abnormality was detected in 30 healthy non-pregnant and 13 healthy pregnant controls. Our data indicate the requirement for a comprehensive methodological approach for the detection of aCL antibodies/lupus anticoagulant and the clinical importance of such an approach.
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Gandrille, S., P. Priollet, L. Capron, M. Roncato, J. N. Fiessinger, and M. Aiach. "ASSOCIATION OF HEREDITARY DYSFIBRINOGENEMIA WITH PROTEIN C DEFICIENCY IN TWO PATIENTS WITH THROMBOTIC TENDENCY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644309.

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An abnormal fibrinogen was found to be associated with protein C deficiency in two unrelated patients. Both were symptomatic, one having severe complicated atherosclerosis, the other recurrent venous thrombosis. In both cases, the two abnormalities coexisted in several members of the family. The two abnormal fibrinogens (Poitiers and Argenteuil) were purified from the patients' plasma and compared to fibrinogens purified from several normal subjects. Polymerisation was abnormal in both cases in presence of reptilase and thrombin.The kinetic of proteolysis by plasmin was studied during 24 hours using SDS-polyacrylamide gel electrophoresis. In the first case, the appearance of fibrinogen degradation products (FDPs) was slightly delayed. The most sliking abnormalities were observed with fibrinogen Argenteuil which still contains "early" FDPs (X and Y) at 24 h while the normal fibrinogens were all completely degraded.The stimulating effect of fibrin on plasminogen activation by tPA was studied after insolubilization of the purified fibrinogen according to the SOFIA technique described by Angles-Cano (Anal. Biochem. 1985, 153, 201). Only fibrinogen Argenteuil was found to have a decreased catalytic effect on plasmin formation.Thrombin binding by fibrin clots, studied according to Ha-verkate (Thromb. Haemostas. 1986, 55, 131) was found decreased in fibrinogen Poitiers and normal in fibrinogen Argenteuil.Conclusion: In these two cases of hereditary dysfibrinoge-nemia least one of the natural antithrombotic function elicited by fibrinogen-fibrin transformation was found to be strongly abnormal . Both fibrinogens presented abnormal lysis by plasmin, particularly fibrinogen Argenteuil in which Tibnn degradation was also reduced. This functional abnormality have already been described in patients with thrombotic tendency. It is however difficult to conclude, as in both families the dysfibrinogenemia was associated with protein C deficiency.
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Fuzimoto, T., K. Fuzimura, and A. Kuramoto. "MEASUREMENT OF PLATELET IONIZED CALCIUM IN PATIENTS WITH MYELOPROLIFERATIVE DISORDERS BY AEQUORIN METHOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644573.

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In myeloproliferative disorders(MPD), bleeding tendency and thrombosis are encountered occasionally in the presence of high platelet counts. It has been reported that there are some abnormalities of membrane glycoprotein or arachidonate metabolism in platelets of MPD. We measured the intracellular change of calcium levels[Cai2+] after stimulation in platelets of the patients with MPD by Aequorin method. Eleven cases of chronic myelogenous leukemia(CML), 7 cases of polycythemia vera(PV), 4 cases of essential thrombocythemiaCET^ and 12 normal adults were studied, and as stimulators 0.5 U/ml thrombin and 2.5 μg/ml collagen were used. In the patients with CML, PV and ET, maximum intracellular calcium level was significantly lower and the reaction period reaching to the peak calcium level(the arrival time) was significantly prolonged than the normals after thrombin stimulation. On collagen stimulation, maximum[Cai2+] level in patient with CML and PV was significantly lower and the arrival time in patient with CML and ET was significantly prolonged than the normals. No correlation was found between maximum [Cai2+] level and maximum aggregation rate or platelet counts in those patients. The increasing rate of intracellular calcium levels after stimulation with A23187 in the presence of various concentration of extracellular calcium was proved lower in CML than in the normal. [45Ca2+] uptake rate into the CML platelets after thrombin stimulation showed lower rate compaired with normals. These results suggest that platelets in patients with MPD have some abnormalities of calcium influx mechanism. We already reported that platelet membrane glycoprotein (GP)IIIa was increased significantly in MPD platelets. The study is going to examine the relationship between this membrane abnormality and impaired calcium influx in MPD.
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Batlle, J., M. F. López-Fernández, C. López-Berges, R. Sánchez, L. G. Villarón, and T. S. Zimmerman. "VON WILLEBRAND'S DISEASE TYPE IIB ASSOCIATED TO A COMPLEX THROMBOCYTOPENIC THROMBOCYTOPATHY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644642.

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A family bleeding disorder characterized by a new association between Type IIB von Willebrand's disease (vWD) and a complex platelet disfunction, with an intermittent thrombocytopenia is described in two patients from the same generation. The mother and a maternal aunt died having severe bleeding diathesis. The platelet abnormalities included: borderline or slightly low platelet count but moderate thrombocytopenia coincedent with the acute bleeding episodes, giant platelet site with a very heterogeneous distribution width, large number of vesicles in platelets by electron-microscopy recalling the "Swiss-Cheese" platelets, abnormal platelet aggregation induced by ADP, collagen, epinephrin and slightly, by thrombin, defective release of 14C-Serotonin, von Willebrand factor (vWF) and platelet factor 4 induced by thrombin or ADP. DDAVP was given to both patient and a partial and transitory correction of bleeding time, thrombocytopenia, presence of platelet aggregates on smear besides a brief appearence of larger multimers of vWF and an increase in all Factor VIII/von Willebrand Factor (FVIII/vWF) properties were seen. Binding of labeled vWF using radiolabelled monoclonal anti-vWF antibody showed an enhanced binding of the patients' vWF, induced by ristocetin, to either normal or patients' platelets. In contrast, the binding of labeled purified normal vWF induced by thrombin to patients' platelets was decreased as compared with the correspondent control. Thus, both patients have platelet disfunctions characteristic for more than one specific platelet disorder. Several associations between platelet and FVIII/vWF abnormalities have been described. This is the first family presenting association of Type IIB vWD and a complex thrombocytopathy. The inherited or acquired (induced by the abnormal IIB vWF platelet interaction) nature of the abnormality is discussed.
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Ware, J. A., B. A. Clark, M. Smith, and E. W. Salzman. "ABNORMALITIES OF CYTOPLASMIC [Ca++] IN PLATELETS FROM UREMIC PATIENTS STUDIED WITH AEQU0RIN AND INDO-1." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644748.

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Uremic patients have a hemorrhagic tendency, often with prolonged bleeding times and abnormalities of platelet function in vitro. Whether these defects result from plasma factors, abnormalities in platelet surface receptors, or intracellular mediators is unknown. Accordingly, blood was obtained from 16 patients with severe uremia (BUN &gt;90), and platelets were washed, loaded with aequorin or indo-1, gel-filtered, and resuspended in either plasma or buffer. Of the 16 patients, 4 had template bleeding times greater than 12 minutes, but platelet aggregation in plasma was not consistently impaired. However, the rise in cytoplasmic [Ca++] in response to the Ca++-ionophore A23187 or ADP in aequorin-loaded platelets from the 4 patients with long bleeding times was much lower than in uremic patients with normal bleejljLng times or in normal volunteers. The reduced [Ca++] response was associated with decreased aggregation of gel-filtered platelets in buffer. Prolonged bleeding time was less consistently correlated with decreased responses to epinephrine or arachidonate. Suspending washed aequorin-loaded uremic platelets in normal plasma for 10-20 min did not reverse the decreased agonist-induced rise in [Ca++]; platelets from a normal donor resuspended in uremic pla^iya responded normally. The agonist-induced rise in [Ca++] shown by indo-1 was not abnormal in patients with prolonged bleeding times; however, uremic patients generally had higher indo-l-indicated basal platelet cytoplasmic [Ca++] than normal. We conclude that the hemorrhagic tendency in some patients with uremia (|s associated with abnormal intracellular platelet [Ca++] regulation marked by elevated resting [Ca++] and a decreased rise in cytoplasmic [Ca++] in response to certain agonists; this latter abnormality appears to be correlated with prolonged bleeding times.
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Reports on the topic "Abnormalies"

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Cohen, Mitchell. Mechanisms of Coagulation Abnormalities and Trauma. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada581645.

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Cohen, Mitchell J., and Jean F. Pittet. Mechanisms of Coagulation Abnormalities and Trauma. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada602708.

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Cohen, Mitchell J., and Jean F. Pittet. Mechanisms of Coagulation Abnormalities and Trauma. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada625634.

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Rosenfeld, Michael G. Molecular Mechanisms of Glial Abnormalities in Neurofibromatosis. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada361589.

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Andrew Coleman, Andrew Coleman. Do turtle shell abnormalities indicate poor health? Experiment, 2014. http://dx.doi.org/10.18258/2742.

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Finsterer, Josef. Cardiac and extra-cardiac abnormalities associated with noncompaction. Science Repository OÜ, 2019. http://dx.doi.org/10.31487/j.rgm.2019.01.002.

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Libertin, C. R., S. Gavinski, and G. E. Woloschak. Evidence of T-cell abnormalities in immunodeficient wasted mice. Office of Scientific and Technical Information (OSTI), 1991. http://dx.doi.org/10.2172/10173435.

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Hall, Timothy J. Real-Time Palpation Imaging for Improved Detection and Discrimination of Breast Abnormalities. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada398298.

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Juergens, Timothy M., Giulio Tononi, and Ruth Benca. Homeostatic and Circadian Abnormalities in Sleep and Arousal in Gulf War Syndrome. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada567969.

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Juergens, Timothy M., Giulio Tononi, and Ruth Benca. Homeostatic and Circadian Abnormalities in Sleep and Arousal in Gulf War Syndrome. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada596544.

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