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Biomedical subjects

K Beaman

Publications and source records attributed to K Beaman.

10 recordsLinked to original sources
PubMed2002

Coagulation changes in individuals with sickle cell trait.

Sickle cell disorders, such as Hb SS and Hb SC, are associated with a hypercoagulable state that may contribute to the vaso-occlusive episodes observed in the disorders. To what extent increased coagulation activity occurs in individuals with sickle cell trait has had limited study. Because such information may help clarify clinical and pathologic findings that may occur in these individuals and may be useful in clarifying the hypercoagulable state in sickle cell disease, we have examined individuals with Hb AS to determine the extent that increased coagulation activity does occur. We measured d-dimers, thrombin-antithrombin (TAT) complexes, prothrombin fragment 1.2 (F1.2), absolute blood monocyte levels, proteins C and S, and isotypes of antiphospholipid antibodies in individuals with Hb AS and in matched controls (Hb AA). Results showed that d-dimers, TAT, and F1.2 were increased significantly above normal levels. Absolute blood monocyte levels were increased. The d-dimers, TAT, F1.2, and monocyte counts showed significant increasing trends through groups of increasing severity (Hb AA, Hb AS, Hb SC, and Hb SS). Our study shows that individuals with Hb AS have increased coagulation activity, with d-dimers, TAT, and F1.2 being consistent indicators. The measures of coagulation activity in Hb AS are lower than in patients with Hb SC and Hb SS disease. These results extend our previous observation that the degree of coagulation activation parallels the degree of disease severity among sickle cell genotypes. The findings suggest that monocytosis, with the possible expression of monocyte-derived tissue factor, and the associated hypercoagulable state are driven by disease severity.

Adult↗
PubMed2000

Immune modulation following aerobic exercise in children with cystic fibrosis.

Previous studies have demonstrated altered immune response following exercise in healthy adults and children. As data are lacking in children with cystic fibrosis, we evaluated the immune response following acute exercise and hypothesized that acute increases in cellular changes would be seen but would be blunted in subjects with CF. Leukocytes, lymphocytes, and their subsets as well as natural killer cell number and activity were determined before, immediately after, and one hour post exhaustive exercise in 15 children with cystic fibrosis (8-21 yrs, FEV1 69.5+/-18.0%, colonized with P aeruginosa) and 15 healthy controls (8-18 yrs, FEV1 107.5+/-10.7%). At baseline the cystic fibrosis group had greater leukocytes (9.25+/-2.83 vs. 5.17+/-0.96 x 10(9) cells/liter). Immediately post exercise, the cystic fibrosis group demonstrated increases in cell counts for leukocytes (32.4%), lymphocytes (61.8%), granulocytes (36.4%), monocytes (76.2%), and natural killer cells (315%). Similar percentage increases were seen in cell counts for the controls (leukocytes: 39.5%, lymphocytes: 78.5%, granulocytes: 32.0%, monocytes: 75.9%, and NK cells: 442%). Natural killer cell activity also increased by 57.9% in the group with cystic fibrosis and by 43.6% in the healthy controls. Except for elevated leukocyte and granulocyte counts, values returned to baseline at one hour post-exercise. In conclusion, the cellular immune response to acute exercise in children with mild to moderate cystic fibrosis appears normal.

Adolescent↗
PubMed1999

Antiphospholipid antibodies, proteins C and S, and coagulation changes in sickle cell disease.

The significance, interactions, and sources of coagulation abnormalities and their relationship to clinical severity and painful episodes in sickle cell disease are not clear. To evaluate this, we have examined various measures of coagulation in 37 patients with sickle cell disease (20 patients with HbSS disease and 17 patients with HbSC disease). Measurements have included isotypes of antiphospholipid antibodies (IgG, IgM, IgA) to specific phospholipids; proteins C (activity, total antigen) and S (activity, total and free antigen); measures of coagulation activation (prothrombin fragment 1.2, thrombin-antithrombin, fibrinopeptide A, d-dimers); indicators of clinical severity; and studies obtained during steady states and painful episodes. Results in HbSS disease showed that antiphospholipid antibodies were increased, with IgG phosphatidylserine showing the highest and most frequently increased levels (37% of patients). Protein C (activity) and protein S (activity, total, free antigen) were decreased (P<.01), and all measures of coagulation activation were increased (P<.001). In HbSC disease, antiphospholipid antibodies were normal, protein C (activity) and protein S (free antigen) were decreased (P<.001), and all measures of coagulation activation were increased (P<.02). A strong correlation was observed in HbSS disease between IgG-PS and d-dimers. Moderate correlations occurred between protein C activity and thrombin-antithrombin and fibrinopeptide A, between protein S activity and prothrombin fragment 1.2 and d-dimers, and between protein C and protein S activity. In HbSC disease, moderate and fewer correlations occurred. Significant differences between HbSS disease and HbSC disease were observed in aPLs, proteins C and S, and measures of coagulation activation. Measurements during steady states and during painful episodes were not significantly different. We conclude that the antiphospholipid antibody IgG-PS may contribute to coagulation activation in HbSS disease and that IgG-PS, protein C, and protein S relate to each other and jointly to measures of coagulation activation. The increased level of IgG-PS in HbSS disease most likely reflects exposure of the procoagulant phosphatidylserine on the surfaces of red cell-shed vesicles and sickle red cells, which would further affect coagulation activation. The significant differences in coagulation measures between HbSS disease and HbSC disease are consistent with differences in clinical severity between the diseases. The development of painful episodes does not appear to be related to the coagulation changes.

Adult↗
PubMed1996

TJ6: the pregnancy-associated cytokine.

These studies have demonstrated that TJ6m protein can be measured in women prior to a spontaneous abortion based on expression of TJ6 on CD56-positive NK cells. This suggested to us a possible regulator function for TJ6 during pregnancy. We have shown that in T cells only crosslinking of the T-cell receptor can upregulate TJ6 expression and the other activators, such as mitogens, do not. A clear discrepancy in the pattern of expression of TJ6 on CD56 and CD19-positive cells was noted between successful and unsuccessful pregnancies. A successful pregnancy is denoted by TJ6 expression on B cells, whereas in a potential spontaneous abortion there is TJ6 expression on both NK and B cells.

Animals↗
PubMed1996

Transforming growth factor-beta 2-related-decidual suppressor factor is not related to TJ6 protein.

Transforming growth factor (TGF)-beta 2-related-decidual suppressor factor (DSF) and TJ6 protein are both immunosuppressive molecules present in murine and human pregnancy. Treatment of mice with either anti-TJ6 or anti-TGF-beta 2 neutralizing antibodies results in increased fetal loss. Western blots of supernatants from pregnant mouse decidua probed with anti-TJ6 (soluble form) showed a doublet at a similar molecular size as when the blot was probed with anti-TGF-beta 2 antibody. The problem is to determine whether TJ6 and DSF are the same protein. In order to determine if TJ6 and DSF are the same or different proteins, we used affinity column purified TGF-beta 2-DSF and stained Western blots with anti-TJ6. The TGF-beta 2-monoclonal antibody affinity column-purified DSF that stained with anti TGF-beta 2 was not reactive with anti-TJ6 antibody. TJ6 has only a 30% gene sequence homology and a 13% amino acid homology to TGF-beta 2. TJ6 and TGF-beta 2-related DSF appear to be different immunosuppressive proteins in decidua.

Animals↗
PubMed1993

Antiphospholipid antibodies in sickle cell disease.

Antiphospholipid antibody formation can be induced in mice by phospholipid in a hexagonal II phase but not by phospholipid in a bilayer phase. Since sickle red cell membranes have increased hexagonal II phase content, we have measured serum antiphospholipid antibody levels in 25 patients with sickle cell disease to determine whether anti-phospholipid antibody may similarly be induced in these patients. Seventeen of the 25 patients (68%) had increased levels of antiphospholipid antibodies. Eleven patients (65%) had IgG and six each (35%) had IgM and IgA isotypes. Antiphosphatidylethanolamine, antiphosphatidylserine, antiphosphatidylinositol, and antiphosphatidic acid were the most frequently increased antibodies. The finding of increased antiphospholipid antibodies in these patients is compatible with the concept that antiphospholipid antibody formation is associated with structural changes in the red cell membrane and that such structural changes occur in the red cells of patients with sickle cell disease.

Antibodies, Antiphospholipid↗
PubMed1993

MHC class II compatibility in aborted fetuses and term infants of couples with recurrent spontaneous abortion.

Maternal-fetal histocompatibility for alleles at HLA class II loci, HLA-DQA1 and HLA-DQB1, was examined in 40 abortuses and 31 liveborn children of 68 couples with a history of idiopathic recurrent spontaneous abortion (RSAB) who underwent leukocyte immunization prior to the index pregnancy. Significantly more couples with RSAB shared two HLA-DQA1 alleles as compared with fertile control couples (0.18 vs. 0.03, respectively; P = 0.031). There were no differences in HLA sharing between couples with RSAB who experienced a repeat abortion in the index pregnancy as compared with couples with RSAB who were delivered of a liveborn child. Non-significant deficits of abortuses who were compatible for alleles at the HLA-DQA1 (6 observed vs. 8.5 expected; P = 0.225) and the HLA-DQB1 (7 observed vs. 9.2 expected; P = 0.254) loci were observed. A significant deficit of HLA-DQA1 compatible liveborn children was observed (1 observed vs. 5.5 expected; P = 0.0069). The overall deficit of HLA-DQA1 compatible fetuses (7 observed vs. 14.0 expected; P = 0.0018) after approximately 8 weeks gestation suggests that HLA-DQA1 compatible fetuses may be aborted early in pregnancy, prior to the time when fetal tissue can be recovered for genetic studies.

Abortion, Habitual↗
PubMed1991

Mr X-A case of amnesia.

A case of psychogenic amnesia in a 58-year-old man supports the view that complete loss of personal identity can follow a traumatic experience. He regained his memory by being helped to develop an affective link with the painful event.

Adaptation, Psychological↗