Structure and gene expression of avian cyclin D2

Avian cyclin D2 (Cyl D2)-encoding cDNA clones were isolated from a chicken UG9 T-cell lambda gt10 library. Sequence analysis revealed a high degree of sequence conservation with both the mouse and human Cyl D2, and somewhat lower similarity with the mouse and human Cyl D1 and D3. The homology is highest between species in the Cyl-box domain which is well conserved among human, mouse and chicken. A single 6.0-kb CYL2 mRNA is produced in both avian B- and T-cells, as expected.     

Iodine-131-metaiodobenzylguanidine dosimetry in cancer therapy: risk versus benefit

In the treatment of neural crest tumors, such as pheochromocytoma, with[131I]MIBG, bone marrow toxicity limits the amount of administered activity and, thus, a therapeutically useful tumor dose. METHODS: We calculated tumor doses in a series of diagnostic studies with [123I]MIBG using accurate quantification of SPECT and planar scintigraphy. By extrapolating diagnostic results to therapeutic activities of [131I]MIBG, we could compare the results with whole-body doses from a series of therapies. RESULTS: The tumor dose was DT = 2.2 mGy MBq(-1) (median value of 27 measurements, range 0.04 < or = DT < or = 20 mGy MBq(-1) and the whole-body dose in a series of 16 patients undergoing 50 therapies was DWB = 0.12 +/- 0.04 mGy MBq(-1) (mean +/- s.d.). The therapeutic ratio varied between 130 to below 10 in some patients. CONCLUSION: The results were compared with published data. We found clearly skewed distribution of tumor doses, with a majority of tumors receiving only a few mGy per MBq administered activity. In some patients, however, doses did reach 20 mGy MBq(-1).     

Micromechanical digital-to-analog converter for out-of-plane motion

This paper describes a novel micromechanical digital-to-analog converter (MDAC) for out-of-plane motion using electrostatic parallel-plate actuators. The proposed mechanism converts an N-bit digital signal to a mechanical out-of-plane displacement that is proportional to the analog value represented by the N-bit binary word. The mechanism is analogous to that of an electrical binary-weighted-input digital-to-analog converter (DAC). It consists of a movable platform, an array of parallel-plate microactuators each operating in an ON/OFF mode and a set of connection springs that connect the actuators to the platform. The spring constants of the connection springs are weighted so that the stiffness of successive springs is related by a factor of 2. A 4-bit mechanism has been fabricated using the Poly-MUMPS process, achieving a total stroke of 675 nm (full-scale output) and step size (LSB) of 45 nm in a highly repeatable and stable manner. The linearity error (LE) of the device is within /spl plusmn/0.28 LSB, and the differential linearity error (DLE) is within /spl plusmn/0.25 LSB. This mechanism can be configured for many promising applications, particularly in optical devices and systems such as tunable external cavity diode laser, tunable VCSELs, adaptive micromirror array and tunable wavelength filter.     

Effects of vesnarinone, a novel orally active inotropic agent with an immunosuppressive action, on experimental cardiac transplantation in rats

BACKGROUND: Vesnarinone (VES) has been used for treatment of patients with congestive heart failure. In addition to inotropic effects, it seems to have immunosuppressive action. We tested the hypothesis that VES suppresses graft rejection, inotropic dysfunction caused by early rejection, and chronic coronary obstruction in a heterotopic rat cardiac transplantation model. METHODS: (1) To study acute rejection, hearts from Lewis-Brown Norway (LBN) rats were transplanted into Lewis rats, which were treated with or without VES (50 or 100 mg/kg/day orally). (2) In a functional study, LBN hearts with or without VES (100 mg/kg/ day) were isolated and perfused on day 3 after transplantation to assess inotropic response to isoproterenol (3 x 10(-8) M). (3) To study chronic rejection, Lewis hearts were transplanted into Fisher 344 rats, which were treated with or without VES (50 mg/kg/day) for 90 days. Coronary obstructive disease was assessed by morphometric analysis. There were five to six animals in each group. RESULTS: (1) VES (100 mg/kg/day) prolonged LBN heart survival (11.7 +/- 0.7 vs. 9.6 +/- 0.7 days in control; P < 0.05). (2) Left ventricular developed pressure was depressed in transplanted hearts regardless of VES treatment (84 +/- 12, 90 +/- 8 vs. 144 +/- 16 mmHg in untransplanted hearts; P < 0.01). The developed pressure after administration of isoproterenol in VES-treated hearts (184 +/- 20 mmHg) was higher than transplanted hearts without VES (118 +/- 16 mmHg; P < 0.05), and similar to untransplanted hearts (203 +/- 27 mmHg; P = NS). (3) Transplanted hearts treated with or without VES showed similar grades of rejection (2.0 +/- 0.3 vs. 2.6 +/- 0.2; P = NS), intimal area (6,996 +/- 3,186 vs. 13,441 +/- 5,165 microns2; NS), and coronary luminal obstruction (45 +/- 16% vs. 67 +/- 14%; NS). CONCLUSIONS: VES produces mild prolongation in survival of rat heart grafts, but has no significant effect on chronic graft atherosclerosis. VES preserves the positive inotropic effects of isoproterenol that are otherwise deteriorated by early acute rejection.     

2-Aminopurine overrides a late telophase delay created by ectopic expression of the PITSLRE beta 1 protein kinase

Minimal overexpression of the PITSLRE beta 1 protein kinase in CHO cells leads to a marked delay in late mitosis. We have previously shown that this delay is characterized by the presence of substantially increased numbers of tubulin midbodies, inhibition of cytokinesis, and numerous multinucleated and micronucleated cells. Others have shown that the protein kinase inhibitor 2-aminopurine (2-AP) is capable of overriding drug induced cell cycle blocks. In this study we demonstrate that the late mitotic delay and altered cellular morphology caused by ectopic expression of the PITSLRE beta 1 protein kinase can be overcome by 2-aminopurine treatment. Furthermore, 2-aminopurine inhibits PITSLRE beta 1 protein kinase activity in vivo, but does not effect p34cdc2 protein kinase activity in a similar manner.     

Research and the cumulation of knowledge in Physical Therapy

BACKGROUND AND PURPOSE: Published research contributes to the knowledge base that distinguishes one discipline from another. More research is now published in the physical therapy journals, but concerns with the profession's knowledge base continue. SUBJECTS: The study examined citations from 78 clinical articles published and indexed on three thematic areas in Physical Therapy between 1951 and 1990. METHODS: Unique items and multiple-cited items were identified and counted and their sources ascertained. Linkages among multiple-cited items in each thematic area were identified and described. RESULTS: Most cited items were unique and not from the physical therapy literature. Few linkages were identified among the clinical articles. CONCLUSION AND DISCUSSION: The lack of evidence of cumulation or of coherence among the articles examined and the extent of reliance on non-physical therapy sources suggest that concerns with the knowledge base of the profession are well founded.     

Induction of tolerance to an experimental cardiac allograft through intrathymic inoculation of class II major histocompatibility complex disparate antigens

Indefinite donor-specific tolerance to a cardiac allograft can be induced through pretransplantation intrathymic injection of donor spleen cells and a single intraperitoneal injection of antilymphocyte serum. This study was designed to determine whether this phenomenon was reproducible with grafts differing in either class I major histocompatibility complex only or class II MHC only. Donors of cells and hearts in all experiments were RP rats. Class I MHC disparate grafts were performed by placing an RP heart into a Lewis recipient, and class II disparate grafts were performed with RP donors and Wistar Furth recipients. Lewis (n = 10) and Wistar Furth (n = 10) recipients underwent intraperitoneal injection of 1 ml antilympocyte serum and intrathymic injection of 5 x 10(7) RP spleen cells. Three weeks later, heterotopic cardiac transplantation was done with a heart from an RP rat. Control rats had no pretreatment or received antilympocyte serum alone. Without pretreatment, RP hearts survived 7 to 9 days (mean 8 days) in Lewis recipients (n = 5) and 9 to 14 days (mean 12 days) in Wistar Furth recipients (n = 5). Antilymphocyte serum alone produced slight prolongation of graft survival. Lewis rats pretreated with class I disparate RP splenocytes and antilympocyte serum had graft survivals of 8 to 27 days (mean 14 days), not significantly different from the results with antilympocyte serum alone. Class II disparate RP grafts placed in pretreated Wistar Furth rats had significant prolongation of graft survival, with four of five grafts surviving longer than 60 days (p < 0.01 vs antilympocyte serum alone). These results suggest that a disparity at the class II locus of the major histocompatibility complex is critical for the induction of cardiac allograft tolerance after intrathymic inoculation of allogeneic cells.     

The carcinoid endocardial plaque; an ultrastructural study

Ultrastructural studies disclosed that the plaque-like endocardial thickenings in three patients with the carcinoid syndrome were composed of smooth muscle cells embedded in a stroma that was rich in acid mucopolysaccharides, collagen, and microfibrils, but devoid of elastic fibers. The smooth muscle cells contained variable numbers of myofilaments and cisterns of rough surfaced endoplasmic reticulum, and their basement membranes were greatly thickened, reduplicated, and arranged in layers. The endocardial plaques appeared histologically and ultrastructurally similar regardless of their location in the heart. The smooth muscle cells in these plaques appear to have been derived from primitive mesenchymal cells, which normally are present in the subendocardial endothelial space. These observations are interpreted as indicating that the plaques develop as a result of healing of a superficial endocardial injury, which may be initiated by release of bradykinin from hepatic metastases of a carcinoid tumor.