Biomedical subjects

S A Lazarou

Publications and source records attributed to S A Lazarou.

8 recordsLinked to original sources

PubMed1995

Planning mandibular distraction: preliminary report.

Normal lengths of the vertical ramus, body, and angle of the mandible at different ages are presented. Before mandibular distraction is embarked on, the extent of the deficiency of the mandible is assessed. The length of the vertical ramus and body are measured on cephalometric radiographs or three-dimensional computed tomography (3D CT) scans. Deficiency of the length of the mandible is calculated. The position of the pin placement angle (from the horizontal ramus) is calculated by means of the following formula: 180 degrees minus mandibular angle times vertical ramus deficiency divided by total deficiency. Placing the pins correctly will result in correction of the vertical ramus and body deficiency of the mandible and the excessively obtuse angle of the mandible will become more acute.

Bone Lengthening↗

PubMed1993

The lateral arm flap for elbow coverage.

A technique for coverage of periolecranon (elbow) defects is presented. The technique uses the local tissues of the lateral upper arm as an axial flap and minimizes the donor defect for this type of reconstruction by obviating the need for a skin graft.

Adult↗

PubMed1990

Wound healing and T-lymphocytes.

T-cell depletion leads to impaired wound healing. We studied the effect of combined T-helper and T-suppressor lymphocyte depletion on wound healing and compared it with the effect of all T-cell depletion. Groups of 10 male balb/c mice, 8 weeks old, underwent a 2.5-cm skin incision and subcutaneous implantation of polyvinyl alcohol sponges. Twenty-four hours prior to wounding one group was treated with 3OH12, a rat anti-mouse monoclonal antibody against the Thy-1.2 antigen present on all T-cells (1 mg); another group received 1 mg each of GK1.5 (anti-L3T4, CD4; anti-helper/effector subset) and 2.43 (anti-Lyt 2.1, CD8; anti-suppressor/cytotoxic subset). All monoclonal antibodies are cytotoxic in vivo. Controls received 1 mg of nonspecific rat IgG. Treatments were repeated weekly. Animals were sacrificed at 2 and 4 weeks postwounding. Equal depletion of all T- and Th- and Ts-subsets in peripheral blood and spleens was noted in the two experimental groups at sacrifice. Depleting Thy-1.2 cells (all T-cells) impaired wound healing as assessed by wound breaking strength and collagen synthesis. Combined anti-T-helper/effector and T-suppressor/cytotoxic depletion resulted in improved wound-healing parameters. This suggests that there is a Thy-1.2+, L3T4-, Lyt2- subpopulation of T lymphocytes which normally stimulates wound healing.

Animals↗

PubMed1990

Arginine enhances wound healing and lymphocyte immune responses in humans.

Arginine has been shown to enhance wound healing and T-cell-mediated immune function in rodents. In this study the effect of oral arginine supplementation on human collagen synthesis and T-cell function was studied in 36 healthy, nonsmoking human volunteers. While volunteers were under local anesthesia, a 5 cm segment of expanded polytetrafluoroethylene tubing (1 mm outer diameter, 90 mu pore size) was inserted subcutaneously into the right deltoid region. The volunteers were then randomized into three groups that were given the following substances: (1) daily supplements of 30 gm arginine hydrochloride (24.8 gm free arginine); (2) 30 gm arginine aspartate (17 gm free arginine) daily; or (3) placebo. The supplements were given orally for 2 weeks; dietary intake was not controlled. Mitogenic responses of peripheral blood lymphocytes to phytohemagglutinin and concanavalin A were assayed at the start of study and at 1 and 2 weeks after supplementation. At 2 weeks the catheters were removed, and the amount of hydroxyproline was determined as an index of new collagen synthesis and deposition. Arginine supplementation significantly enhanced the amount of collagen deposited into a standardized wound as assessed by the amount of hydroxyproline present (10.1 +/- 2.32 nmol/cm graft in controls vs 17.57 +/- 2.16 nmol/cm in the arginine aspartate group, [p = 0.028] and vs 23.85 +/- 2.16 nmol/cm in the arginine hydrochloride group [p less than 0.001]). In parallel, arginine supplementation at both doses increased lymphocyte mitogenesis in response to phytohemagglutinin and concanavalin A. The data suggest that arginine may be of clinical benefit in improving wound healing and immune responses.

Adult↗

PubMed1989

The wound is a possible source of posttraumatic immunosuppression.

Wound fluid from 10-day-old healing wounds in rats inhibits lymphocyte immune responses. Since severe injury is frequently complicated by immunosuppression as manifested by sepsis, we hypothesized that the wound may be a source of factors that impair host immune responses. Therefore, we studied the effect of systemic wound fluid administration on the survival of rats subjected to an acute peritonitis model. Male Sprague-Dawley rats, fitted with internal jugular catheters 48 hours previously, underwent cecal ligation and puncture with a 23-gauge needle. Immediately after the operation, rats were treated intravenously every 12 hours with either wound fluid obtained from 10-day-old healing wounds and adjusted to 10 mg of protein per milliliter or rat serum. In vitro testing of the wound fluid showed it to be highly inhibitory of thymic lymphocyte mitogenesis. Rats treated with wound fluid had significantly higher mortality after peritonitis than did control rats. The data show that the wound contains factors that can impair host immune responses to sepsis. This suggests that the wound may be the source of posttraumatic host immunosuppression.

Animals↗

PubMed1987

Vasculitis in primary Sjögren's syndrome. Histologic classification and clinical presentation.

Nine out of 70 patients with primary Sjögren's syndrome had vasculitis of small and/or medium-sized vessels. The small vessel vasculitis was of the hypersensitivity type: leukocytoclastic and lymphocytic. The medium vessel vasculitis was acute necrotizing and simulated polyarteritis nodosa histologically but lacked the characteristic aneurysmal formation. A healing stage of vasculitis, presenting as endarteritis obliterans, was seen in patients with Sjögren's syndrome and a long-standing history of vasculitis. The hypersensitivity vasculitis was localized mainly in the skin and provided mild clinical symptoms. The polyarteritis nodosa-like vasculitis was localized predominantly in internal organs and was associated with life-threatening symptoms. Endarteritis obliterans was mainly seen in acral sites of the extremities and presented with recurrent symptoms of obstruction. One patient died of vasculitis. The remaining patients are alive. The presence of anemia, cryoglobulinemia, and hypocomplementemia suggested an immune-complex origin of the vasculitic process.

Adult↗

PubMed1982

Lactate dehydrogenase isoenzymes in normal and malignant human lymphoid cells.

Intracellular lactate dehydrogenase (LD) isoenzyme patterns were studied in the malignant cells of patients with a variety of lymphoid malignancies. These were compared with intracellular LD isoenzyme patterns of normal lymphoid cells and were also correlated with immunologic cell surface marker characteristics. Results showed that, in general, the malignant B cells of Burkitt's lymphoma and the lymphoblasts of T-cell acute lymphoblastic leukemia had isoenzyme patterns similar to those of normal B and T cells, respectively. The isoenzyme patterns of malignant lymphoid cells from patients with non-T, and non-B acute lymphoblastic leukemia, cutaneous T-cell lymphoma, and chronic lymphocytic leukemia were more heterogeneous. These data, although based on small numbers of patients, are consistent with the hypothesis that LD isoenzymes may reflect differences in the maturational status of cells within a single diagnostic category.

B-Lymphocytes↗

PubMed1981

Isoenzymes of lactate dehydrogenase in human leukemic cells in culture treated with inducers of differentiation.

The human leukemic cell lines HL60 and K562, were induced to differentiate terminally by chemical agents. The isoenzyme patterns of lactate dehydrogenase (LD) in the cells before and after differentiation were determined electrophoretically on agarose gels. In general, treatment of the leukemic cells with inducers of differentiation resulted in a quantitative shift of the isoenzyme pattern towards anodic or cathodic forms. This was correlated with the conversion of the chemically treated cells to morphologically more normal cells, as verified by light microscopy and/or synthesis of hemoglobin. The LD isoenzyme patterns of the chemically differentiated cells were: (a) characteristic for the particular cell type obtained rather than for the nature of the inducer used; and (b) not similar to those of normally differentiated cells of the corresponding lineage, indicating that incomplete differentiation had occurred.

Acetamides↗