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Biomedical subjects

D Green

Publications and source records attributed to D Green.

At least 343 records · Page 19Linked to original sources
PubMed1983

Cervical carcinoma: a drug-responsive tumor--experience with combined cisplatin, vinblastine, and bleomycin therapy.

Thirty-five patients with advanced cervical cancer were treated with a combination chemotherapy regimen comprising cisplatin, vinblastine, and bleomycin (PVB). Sixty-six percent of 33 evaluable patients showed objective tumor response and complete remissions were seen in six (18%) patients. The median duration of tumor response in patients with recurrent cervical cancer was 24 weeks (range 8 to 104 weeks). Multivariate analysis of pretreatment variables including prior radiotherapy did not identify patients with a higher response probability. Nausea and vomiting were usual side effects of chemotherapy and there was one definite treatment-related death. Cervical cancer is responsive to cisplatin based combination chemotherapy. The role of chemotherapy in conjunction with radiotherapy or surgery in the treatment of locally advanced cervical cancer remains to be defined.

Adult↗
PubMed1983

Linkage analysis in von Willebrand disease.

We studied a 3-generation kindred to determine whether the gene responsible for one form of von Willebrand disease (vWD) is linked to 1) the HLA locus, or 2) a polymorphic locus for a serum enzyme or red cell antigen. HLA haplotypes were determined in 12 affected family members, in 10 cases by direct analysis and in 2 cases by deduction. Seven of 12 affected individuals were A2, B7, as compared to 0 of 9 unaffected. However, the maximum lod score was only 0.41 at a recombination frequency of 0.2. Of the 17 serum red cell and plasma protein markers studied, 5 (Kell, ADA, AK1, BF, GC) did not segregate, and 12 (ABO, Rh, JK, Fy, P, PGM1, ACP1, ESD, GLO1, MN, HP, GPT) gave lod scores less than + 1.0. We conclude that there is no strong evidence for linkage between the locus for vWD and any of the markers studied.

Blood Proteins↗
PubMed1983

Bowel complications in the management of ovarian cancer.

In a consecutive series of 163 patients referred with malignant ovarian tumours there were 24 (14.7%) who developed major bowel complications; 21 patients were operated upon for bowel obstruction and had a mean survival time of 8.1 months; 8 of the 24 patients are alive with cancer and 4 are alive without evidence of residual tumour. It is concluded that laparotomy is indicated when bowel complications occur in patients with ovarian carcinoma.

Female↗
PubMed1983

Relation between antithrombin III and clinical and serological parameters in systemic lupus erythematosus.

The increased frequency of thromboembolic events in patients with systemic lupus erythematosus (SLE) has been attributed to reduced or dysfunctional antithrombin III (At-III). We analysed At-III values, measured by three different assay techniques, in SLE patients, patients with rheumatoid arthritis, and normal and hospitalised controls. In addition, attempts were made to correlate At-III activities of SLE patients with specific clinical and serological parameters such as disease activity, renal involvement, previous thrombosis, degree of proteinuria, and serum complement concentrations. Our results failed to show a significantly reduced At-III in SLE with any method. At-III titres did not correlate with disease activity, concentrations of serum complement or albumin (both only minimally reduced in most patients), or a previous history of thrombosis. At-III deficiency does not appear to be an inherent feature of SLE, and reduced activities should only be anticipated when there are specific aetiological factors present, such as massive proteinuria, extensive hepatic disease, or active thrombosis.

Adult↗
PubMed1983

Fibrinolytic activity after administration of diflunisal and aspirin. A double-blind, randomized, placebo-controlled clinical trial.

A double-blind, randomized, placebo-controlled clinical trial was conducted to determine whether fibrinolysis was increased by the chronic administration of aspirin or diflunisal. Healthy male and female volunteers were randomized to receive either aspirin (1,300 mg every 12 h; 10 subjects), diflunisal (1,000 mg initially, then 500 mg every 12 h; 10 subjects), or placebo (10 subjects) for 8 days. Fibrinolytic activity was examined with the clot lysis assay, using native whole blood, platelet-rich plasma, and platelet-poor plasma, and with the kaolin-activated euglobulin lysis test. In addition, measurements were made of fibrinogen, fibrin/fibrinogen degradation products, plasminogen, and the thrombin time. Clot lysis was greater in whole blood and platelet-rich plasma than in platelet-poor plasma, and increased lysis was observed in specimens obtained in the afternoon as compared to those obtained in the morning. Fibrinolytic activity in the afternoon samples was significantly enhanced by both aspirin and diflunisal at the start of the trial (p less than 0.05), but by the afternoon of day 8, only aspirin showed some enhancement. Fibrinolytic activity, as measured by the euglobulin lysis time, actually declined in all study groups during the course of drug administration. No significant changes were recorded in any of the other assayed hemostatic parameters. We conclude that aspirin and diflunisal exert a modest, nonsustained enhancing effect on fibrinolysis in normal subjects.

Adult↗
PubMed1983

Preliminary report on a crosswalk from DSM-III to ICD-9-CM.

The wide use of DSM-III by clinicians and researchers in the United States has led to difficulties in reporting to federal agencies, which adhere to a policy supporting the use of ICD-9-CM. To rectify this situation, three federal agencies collaborated to design a translation, or "crosswalk," from DSM-III to ICD-9-CM. The authors discuss some of the differences between the two systems, describe the development of the crosswalk, and make suggestions concerning future nosological and statistical systems.

Centers for Medicare and Medicaid Services, U.S.↗
PubMed1983

Pattern of uptake of americium-241 by the rat skeleton and its subsequent redistribution and retention: implications for human dosimetry and toxicology.

The distribution and retention of intravenously injected 241Am in the skeleton of the female rat has been investigated using autoradiographic and radiochemical techniques. The studies were designed to assess the dosimetric and toxicologic implications of an 241Am intake by man. They showed that in the rat approximately one third of the intravenously injected 241Am was deposited in the skeleton where it appeared to be retained with a long biological half-time. The studies also showed: 1 241Am is initially deposited onto all types of bone surface including endosteal surfaces, periosteal surfaces and those of the vascular canals within cortical bone, but seems to be preferentially deposited onto those that are resorbing, 2 Bone accretion results in the burial of surface deposits of 241Am, 3 Bone resorption causes the removal of 241Am from surfaces, 4 Resorbed 241Am is retained by phagocytic cells (probably macrophages) in the bone marrow, 5 The transfer of 241Am from the phagocytic cells in the marrow to adjacent bone surfaces seems to occur, (local recycling). 6 The possibility that some of the 241Am removed from the bone surfaces enters the blood and is redeposited in bone, (systemic recycling) cannot be dismissed. These results show that 241Am deposition and redistribution in bone shares many characteristics with other 'bone surface-seeking radionuclides' typified by 239Pu. Consequently, it is suggested that a similar model to that used to calculate annual limits of intake for 239Pu in man would be suitable for the calculation of corresponding values for the 241Am isotopes.

Americium↗
PubMed1983

Autoradiographic studies of the distribution of radium-226 in rat bone: their implications for human radiation dosimetry and toxicity.

A solution containing 226Ra chloride was injected into young female rats via the saphenous vein. Subsequently, the distribution and retention of the 226Ra in the skeleton was studied. The results show that: 226Ra is initially deposited in the rat femur as a volume deposit and is fairly evenly distributed throughout the bone matrix. Much of the 226Ra initially deposited in the skeleton is lost within a few days of its administration. During the first week 226Ra gradually accumulates at sites of bone deposition including accreting surfaces. Subsequent bone growth results in the burial of contaminated bone surfaces and Following bone resorption some of the 226Ra released from individual bones is recycled systemically so that all skeletal components tend towards a uniform 226Ra concentration per unit of bone mineral. Of the two models conventionally used for radiation dosimetry purposes, the results reported here for rats suggest that though neither is ideal, the volume distribution model is preferable to the surface model at all times after the uptake of radium by the skeleton.

Animals↗
PubMed1983

Oculocutaneous albinism, platelet storage pool disease, and progressive lupus nephritis.

Systemic lupus erythematosus (SLE) was seen in a patient with oculocutaneous albinism and platelet storage pool disease (Hermansky Pudlak syndrome). Although the patient had severely compromised platelet function, lupus nephritis developed nonetheless, which progressed to end-stage renal disease. The role of platelets in the pathogenesis of the nephritic process is discussed, and it is concluded that release of platelet granular constituents, particularly serotonin, is not required for the microvascular damage of SLE.

Acute Kidney Injury↗
PubMed1983

The inactivation of hemostatic factors by hematin.

Prolonged clotting times and reduced levels of clotting factors have been reported in hematin-treated patients. This effect persists for up to 5 hr after hematin infusion, associated with plasma levels ranging from 0.01 to 0.04 mg/ml. Therefore we performed in vitro studies to investigate the effects of hematin on fibrinogen, thrombin, factor VIII:C, and plasmin. Hematin in a final concentration of 0.01 mg/ml inhibited the clotting of bovine fibrinogen (1.3 to 2.6 mg/ml) by bovine thrombin (0.12 U/ml) and inhibited the hydrolysis of a synthetic substrate by human thrombin. However, if the hematin was first mixed with albumin (25 mg/ml), fourfold higher concentrations were required to prolong the thrombin clotting time. Hematin, 0.035 mg/ml, reduced VIII:C activity from 0.88 to 0.40 U/ml as measured by two-stage assay. Hematin (0.05 mg/ml) also inhibited the activation of VIII:C by thrombin (0.04 U/ml): baseline activity, 0.84 U/ml; thrombin-activated, 2.94 U/ml; with hematin added, 1.33 U/ml. Hematin also inhibited clot lysis. The inclusion of hematin (0.03 mg/ml) in the diluting buffer reduced the lysis of whole blood clots from 86% +/- 5 to 23% +/- 5 (p less than 0.001, mean +/- S.D. of four determinations) and decreased the lysis of 125I-fibrin clots induced by plasmin (0.02 CTA U/ml) from 100% to 27%. In concentrations as low as 0.09 microgram/ml, hematin inhibited the hydrolysis of a synthetic substrate by plasmin. Hematin was mixed with fibrinogen, albumin, or thrombin, and the mixtures applied to Sephadex G-200 columns. Adherence of the hematin to Sephadex was prevented by either prerinsing the column with albumin or using borate buffer at pH 9.2. Hematin co-eluted with each protein applied to the column and, in the case of fibrinogen, altered its electrophoretic mobility and markedly prolonged the thrombin clotting time of the eluted fibrinogen. We conclude that hematin binds to a variety of hemostatic proteins, inhibiting their biologic activity.

Animals↗
PubMed1983

Hematin: unique effects of hemostasis.

Hematin is clinically useful in the treatment of acute intermittent porphyria. Recently, hematin-induced coagulopathy has been reported, and a patient we treated bled during hematin therapy. On 3 separate occasions, infusions of hematin (4 mg/kg) induced thrombocytopenia, prolongation of the prothrombin time, partial thromboplastin time. Reptilase time, and apparent decreases in fibrinogen and increases in fibrin(ogen) degradation products (FDP). However, fibrinogen assayed by heat precipitation was unchanged, the protamine paracoagulation test was negative, there was no red blood cell fragmentation, and plasminogen and antithrombin III remained normal, excluding the presence of disseminated intravascular coagulation. Furthermore, premedication with heparin, 5000 U i.v., failed to prevent the lengthening of the Reptilase time and exacerbated the thrombocytopenia. In vitro studies revealed that hematin, 0.1 mg/ml, aggregated platelets and induced the release of 14C-serotonin and adenosine triphosphate (ATP). Hematin also aggregated washed or gel-filtered platelets but had no effect on formalin-fixed platelets. Aggregation was inhibited by aspirin (0.12 mg/ml), adenosine triphosphate, and apyrase, suggesting that hematin aggregated platelets by inducing adenosine diphosphate (ADP) release. Hematin (0.07 mg/ml) progressively inactivated thrombin and 0.1 mg/ml prolonged the Reptilase time. Thus, hematin is unique in that it both induces platelet aggregation and inhibits coagulation.

Adult↗
PubMed1982

THe beta-Blocker Heart Attack Trial: studies of platelets and factor VIII.

Serial studies of platelets and factor VIII were performed in 16 patients enrolled in the Beta Blocker Heart Attack Trial. Eight patients received placebo, and eight were treated with propranolol, in doses ranging from 40 to 320 mg per day for periods of from 6 to 31 months. No differences in platelet-collagen affinity, factor VIII coagulant activity, factor VIII related antigen, or ristocetin cofactor activity were observed between treated and untreated patients. However, circulating platelet aggregates, which were initially increased in both groups, significantly declined in those receiving propranolol (p less than 0.05). This indicates that customarily used doses of propranolol affect platelet reactivity in vivo.

Adenosine Diphosphate↗
PubMed1982

Correlation of nitrosourea murine bone marrow toxicity with deoxyribonucleic acid alkylation and chromatin binding sites.

All of the clinically available nitrosourea antitumor agents produce serious treatment-limiting bone marrow toxicity. A reduction in this toxicity can be achieved by attaching the chloroethylnitrosourea cytotoxic group to C2 (chlorozotocin) or C1 (1-(2-chloroethyl)-3-(beta-D-glucopyranosyl)-1-nitrosourea, GANU) of glucose. Both glucose analogs are less myelotoxic in mice than 1-(2-chloroethyl)-3-cyclohepyl-1-nitrosourea (CCNU) or 1-(4-amino-2-methylpyrimidin-5-yl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU), while retaining comparable antitumor activity against the murine L1210 leukemia. To define the nuclear mechanisms for this reduced myelotoxicity, alkylation of L1210 and murine bone marrow DNA was quantitated. With the use of the endonuclease micrococcal nuclease and DNase I, the sites of alkylation within the chromatin substructure were determined. Experiments were performed on L1210 leukemia or bone marrow cells that had been incubated in vitro for 2 hr with 0.1 mM [14C]chloroethyl drug. The quantitative alkylation of DNA by GANU was 1.3-fold greater in L1210, as compared to bone marrow, cells. This ratio of DNA alkylation is comparable to the 1.3 ratio we previously reported for chlorozotocin [L. C. Panasci, D. Green and P. S. Schein, J. clin. Invest. 64, 1103 (1979)]. In contrast, the ratio of alkylation (L1210:bone marrow DNA) for the myelotoxic ACNU was 0.66, similar to 0.59 for CCNU. Nuclease digestion experiments demonstrated that chlorozotocin and GANU preferentially alkylated internucleosomal linker regions of bone marrow chromatin, while nucleosome core particles were the preferred targets of CCNU and ACNU. The reduced myelotoxicity of chlorozotocin and GANU may be correlated with the advantageous ratio of L1210:bone marrow DNA alkylation and preferential alkylation of internucleosomal regions of bone marrow chromatin.

Alkylation↗
PubMed1982

Reduced resorption of cortical bone in mice with induced osteopetrosis.

Two groups of syngeneic radiation chimaeras were established, the reconstitution being with spleen from osteopetrotic mice on the one hand and normal bone marrow on the other. Induced osteopetrosis in the former was evident radiologically not only as metaphyseal opacity but as unduly dense cortices compared with the latter, particularly terminally after 16-18 months. The radiological impressions were confirmed by measurement of cortical thickness in both longitudinal and transverse sections of undecalcified femoral shafts. Measurements were made with a Quantimet-720 System-30 Image Analyser. Terminally the differences were highly significant. One concludes that defective osteoclasts of osteopetrotic mice derived from haematopoietic stem cells fail to resorb not only primitive woven bone but also cortical laminar bone.

Animals↗
PubMed1982

The use of a monoclonal i-j-specific antibody to distinguish cells in the feedback suppression circuit from those in the contrasuppressor circuit.

A monoclonal anti-I-Jb serum designated D-7 reacts in high titer with three different T-cell subsets and one cell-free product involved in generating contrasuppressive activity, but has no activity against I-J T-cell subsets (or their cell-free mediators) involved in feedback suppression. These results give evidence for heterogeneity in the I-J subregion. They also indicate that the serological markers on I-J+ cells may define the functional activity of the regulatory circuits they belong to. Clearly, they do not separate the role that the cells play within a particular immunoregulatory circuit, i.e., inducer, transducer, or effector cells.

Animals↗