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S L Welles

Publications and source records attributed to S L Welles.

25 records · Page 2Linked to original sources

The distribution of T-cell subsets among HTLV-I carriers in Japan.

Data on T-cell subsets from 89 human T-cell lymphotropic virus-I (HTLV-I) carriers and 25 seronegative people were analyzed to identify differences in T-cell subset values among three subgroups: HTLV-I carriers with abnormal lymphocytes (Ably; n = 24), carriers without Ably (n = 65), and HTLV-I seronegatives (n = 25). Estimates of mean values were adjusted for age, sex, smoking, and alcohol drinking, as appropriate. The percentage of CD25+ T cells was elevated in carriers with Ably (mean, 16.7 +/- 1.0) compared with the seronegatives (11.4 +/- 1.4; p = 0.0002); individuals with CD25 T-cell percentages above the median for the seronegatives had a corresponding 5.4-fold risk for being a carrier with Ably. Similarly, the percentage of CD4 T cells was elevated in carriers with Ably. Conversely, the percentage of CD8 T cells was lower among both groups of HTLV-I carriers than in the seronegatives. There was a corresponding significant increase (p = 0.0004) of the CD4/CD8 ratio among carriers with Ably (1.57 +/- 0.12) compared with the seronegatives (1.22 +/- 0.12). Among subjects with CD4/CD8 ratios above the median for the seronegatives, there were 6.8- and 4.5-fold risks for being carriers with or without Ably, respectively. The percentage of CD7 was lower among carriers with Ably (75.6 +/- 1.6) than among seronegatives (78.9 +/- 1.5; p = 0.13). The percentage of beta-interleukin-2-receptor-positive T cells did not vary among the three subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗

Changes in hematologic parameters among Japanese HTLV-I carriers.

Hematologic data from 1,039 persons who participated in the Miyazaki Cohort study on human T-cell lymphotropic virus type-I (HTLV-I) infection were analyzed. Individuals were classified by HTLV-I antibody status and the presence of abnormal lymphocytes (Ably). We identified several differences in selected leukocyte populations: lymphocyte percent was higher among the HTLV-I carriers with Ably (36.5 +/- 2.0%, n = 29) compared with the carriers without Ably (33.1 +/- 0.6%, n = 299) and the seronegatives 36.4 +/- 0.4%, n = 711) (p = 0.04). Conversely, there was a trend of decreasing eosinophil percent among both carrier groups with the lowest percent among carriers with Ably (1.8 +/- 0.5%) compared with the seronegatives (2.8 +/- 0.1%) (p = 0.05). Mean basophil percent was decreased among both carriers groups (p = 0.09). Additionally, red cell count was elevated among the carriers with Ably (461 +/- 7 x 10(4)/mm3) compared with the seronegatives (446 +/- 2 x 10(4)/mm3) (p = 0.03). The HTLV-I carriers with Ably had lower serum albumin (4.39 +/- 0.05 g%) compared with the seronegatives (4.47 +/- 0.01 g%) (p = 0.10). These alterations may be a consequence of HTLV-I infection, with the greatest changes among carriers with Ably, a subset thought to be at risk for developing adult T-cell leukemia.

Alanine Transaminase↗

Vasoactive amines modulate actin cables (stress fibers) and surface area in cultured bovine endothelium.

Cultured bovine aortic endothelial cells were fixed and stained with NBD-phallicidin and quantitated with a digital image analyzer for changes in actin cables and surface area. Serotonin (5-HT), norepinephrine (NE), dopamine and histamine (all at 10(-4)M concentrations) were tested for their ability to induce cytoskeletal changes. Only 5-HT and NE increased actin cables significantly (p less than 0.01), 80.7% and 97.9%, respectively. Dopamine and histamine treated cells showed a 67.4% and 80.8% decrease in actin cables respectively (p less than 0.01). Stimulated increases of actin cables by 5-HT were inhibited by Ketanserin, and propranolol inhibited NE stimulation of actin cables. Treatment of cells with these blockers alone also decreased actin cables below control values (p less than 0.01). Pretreatment of cells with diphenhydramine, but not cimetidine, inhibited histamine-induced decreases in actin cables. Stimulation of surface area by 5-HT and NE was also observed, with 40.8% and 80.7% increases respectively, when compared with controls (p less than 0.01). The increases in actin cables were associated with a lack of ruffled edges that are indicative of motile cells. In contrast, induced decreases in actin cables resulted in cells with ruffled edges. Exogenous 5-HT and NE have been shown to prevent the increased permeability visible as extravasation of red blood cells from postcapillary venules in thrombocytopenic animals. The present data suggest that 5-HT and NE may be involved in maintaining the endothelial barrier function by a receptor-mediated stimulation of actin cables. Also, histamine-induced decreases in actin cables may be correlated with the amine's action in vivo as a mediator of increased inflammatory permeability.

Actins↗

Eicosanoid modulation of stress fibers in cultured bovine aortic endothelial cells.

Leukotrienes (LT) B4, LTD4, and thromboxanes (TX) are cytotoxic, and increase microvascular permeability. Because endothelial stress fibers are theorized to be part of the cytoskeletal mechanism by which microvessels maintain their barrier function, the effect of these eicosanoids on stress fibers in bovine aortic endothelial cells was tested. LTB4, LTD4, and TXB2 each decreased stress fiber numbers by 93%, 62%, and 66%, respectively, when compared to controls (P less than 0.01). In contrast, endothelial cells treated with prostacyclin (PGI2) at 10(-7) M, produced a significant increase (P greater than 0.01) in stress fiber numbers, 211% to that of controls. Azaprostanoic acid (13-APA) and FPL55712, receptor antagonists to TX and slow-reacting substance of anaphylaxis (SRS) receptors, respectively, the cyclooxygenase inhibitor ibuprofen, and the TX synthase inhibitors imidazole and ketoconazole were used to test for possible endothelial cell receptor mediation and de novo prostanoid synthesis associated with inflammatory eicosanoid-induced disassembly of stress fibers. Each pharmacologic agent inhibited the LTD4- and TXB2-induced decreases in stress fibers; LTB4-stimulated stress fiber decreases were inhibited only by pretreatment with TX synthase blockers. These data suggest that increased permeability associated with inflammatory eicosanoid metabolites may have as a common target stress fiber disassembly, and the mechanism may be receptor-mediated. That cyclooxygenase and TX synthase blockers inhibited the eicosanoid action suggests that endogenous TX synthesis may be a step in the mechanism. PGI2 enhancement of the microvascular barrier may be related to the effect of PGI2 on promoting stress fiber assembly. In summary, endothelial cell synthesized autocoids derived from arachidonic acid may help to regulate microvascular permeability by way of their action on stress fiber assembly/disassembly, and unbalanced prostanoid secretion by way of LT stimulation may result in a loss of the microvascular barrier and increased permeability.

Actin Cytoskeleton↗

Vasoactive agonists prevent erythrocyte extravasation in thrombocytopenic hamsters.

The mediating action of selected vasoactive amines and their respective antagonists on vascular fragility, visible as cutaneous petechiae, was assayed with thrombocytopenic (TCP) hamsters. Serotonin (5-HT), norepinephrine (NE), epinephrine, dopamine and isoproterenol administered IP reduced petechiae significantly within 10 min; phenylephrine had no effect. Of the natural amines, 5-HT and NE were most effective in reducing petechial sensitivity to values obtained with untreated, normal animals; hence these two amines only were tested pharmacologically. Pretreatment of TCP animals with Ketanserin or propranolol, administered IP or IV, abolished any petechial inhibitory action of 5-HT and NE respectively; pretreatment with phenoxybenzamine reduced significantly the NE inhibition of petechiae, but to a lesser degree than propranolol. In contrast, atenolol, prazosin and yohimbine had no significant effect. Ketanserin abolished the action of NE, but adrenoceptor blockers had no effect on 5-HT-treated TCP hamsters. The results suggest that 5-HT and NE inhibition of petechiae may be receptor-mediated and that there may be receptor interaction. This was supported by the observation that non-additive subthreshold doses of 5-HT and NE, which individually did not prevent petechial formation in TCP hamsters, when combined totally inhibited petechiae. The theorized importance of endogenous 5-HT and NE to maintain postcapillary venule junctional integrity (site of petechial hemorrhaging) was also demonstrated by treating normal hamsters with drugs known to block or antagonize either 5-HT or NE uptake. In every instance petechial sensitivity rapidly occurred, and the loss of microvascular integrity in Ketanserin-treated hamsters mimicked quantitatively the petechial sensitivity observed with TCP animals.

Animals↗

Undiagnosed adult T-cell leukemia/lymphoma in central Brooklyn, NY.

We present a case, identified by surveillance for adult T-cell leukemia/lymphoma (ATL), who had initial symptoms not specifically related to ATL, and who would not have been identified as having ATL otherwise. A 51-year-old Trinidadian black woman was hospitalized for abdominal pain, nausea, and vomiting. Hematology and clinical chemistry revealed leukocytosis (19,600/mm3), an elevated lymphocyte percent (63%), and hypercalcemia (19.4 mg/dl). The patient was serologically confirmed with HTLV-I-associated ATL. Lymphoma was diagnosed at autopsy. This case is representative of ATL, which along with HTLV-I infection, may be emerging public health problems in urban communities of the northeast and southeast United States.

Blotting, Western↗