Chromosome-specific aneusomy in carcinoma of the breast

Fluorescence in situ hybridization was performed on touch preparations from 55 primary infiltrating ductal carcinomas of the breast to determine numeric chromosome abnormalities. The frequency of aneusomy, measured by both nondisomy and chromosomal gain, was determined for chromosomes X, 4, 6-12, 17, and 18 with the use of chromosome-specific, alpha-satellite DNA probes. The presence of chromosome-specific numeric abnormalities was correlated with established clinicopathological parameters, including tumor size, lymph node involvement, tumor grade, estrogen receptor level, and menopause status. In addition, a case-control study was performed to explore a possible association between chromosome-specific aneusomy and recurrence in lymph-node-negative patients. Although chromosomes 8 and 6 were most frequently aneusomic, numeric abnormalities of chromosomes 4 and 11 were most strongly associated with established prognostic factors. For chromosomes 4 and 11, strong associations were found with tumor involvement of lymph nodes and increased tumor size, along with a weaker association with tumor grade. In addition, numeric abnormalities of the following chromosomes were associated with the corresponding prognostic factors: chromosomes X, 7, and 12 with lymph node status; chromosomes 10, 17, and 6 with tumor size; and chromosomes 7, 12, 17, and X with tumor grade. No correlations were observed with estrogen receptor level or menopause status. In the case-control study performed on isolated nuclei of paraffin-embedded tissue from lymph node-negative breast cancer patients (19 cases and 19 controls), the gain of chromosome 4 was correlated with disease progression. These findings suggest that chromosome-specific aneusomy is associated with certain established prognostic factors and may be associated with disease progression.     

Effects of ethanol administration on components of the ubiquitin proteolytic pathway in rat liver

Hepatic protein accumulation during ethanol administration may result partly from an ethanol-elicited decline in hepatic protein degradation, which we have previously shown. We conducted the current studies to examine the effects of ethanol administration on the levels of hepatic ubiquitin, an 8.5-kd protein which is an important mediator of extralysosomal protein catabolism. Rats were pair-fed liquid diets containing either ethanol (36% of calories) or isocaloric maltose-dextrin for 1 to 5 weeks. Ubiquitin was immunochemically quantified by competitive enzyme-linked immunosorbent assay (ELISA) in crude cytosol fractions from whole liver and in 12,000g supernatants of hepatocyte lysates. Ubiquitin levels in hepatic cytosol fractions of ethanol-fed rats exceeded those of controls by about 30%. Isolated hepatocytes from ethanol-fed animals also showed a 40% to 75% elevation of ubiquitin above that in cells of pair-fed controls and this difference exceeded the relative rise in hepatocellular protein. In hepatocyte lysates subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting, we detected monomeric ubiquitin and higher molecular mass ubiquitin-protein conjugates. However, the immunoblot analyses revealed no quantitative changes in the level of either free or conjugated ubiquitin. The ubiquitin conjugating activity of crude and diethyl aminoethyl-fractionated liver cytosols of ethanol-fed rats had equal capacities to those from controls in catalyzing the formation of ubiquitin-protein conjugates. Our findings indicate that chronic ethanol consumption increased the level of immunoreactive ubiquitin in rat liver. This may have resulted from enhanced ubiquitin production because of an ethanol-elicited stress response and/or decreased catabolism of ubiquitin and its conjugates. Our findings also provide no indication that the ethanol-elicited reduction in hepatic proteolysis is because of a ubiquitin-mediated mechanisms.     

Longitudinal sliding of the median nerve during movements of the upper limb

Repeated transfusion of small increments of blood are frequently required for the sick and premature newborn infant to correct endogenous hypovolemia and/or to replace blood obtained for laboratory monitoring purposes. Previously fresh group and type specific whole blood was used. To eliminate waste of fresh whole blood, maintain fresh red blood cell properties, eliminate the hazards of transfusing plasma and to provide a more efficient system, a pediatric frozen red cell pack (PFRCP) has been developed. Units of group O rr red blood cells are glycerolized using a high glycerol method. The glycerolized red blood cells are separated into three equal aliquots and frozen. When needed, the PFRCP are deglycerolized by a modified procedure using the IBM Cell Processor. During a six month period, 71 infants were given 153 separate transfusions of deglycerolized red blood cells using 102 PFRCP prepared from 34 units of red blood cells. Red blood cell recovery, hematocrit, white blood cell removal, residual glycerol, total protein, and supernatant hemoglobin levels were measured. Clinical response was followed and found to be excellent.     

A histochemical investigation of catecholamines in spinal cord injury

The catecholamine hypothesis of progressive spinal cord necrosis following mechanical trauma was investigated with the histofluorometric method. Forty-four adult mongrel dog were examined as control, L1 crush-injured, and crush-injured with prior T1 total transection groups. In crush injured dogs, catecholamines were present in a 1 cm length of white matter at the crush site, with the greatest accumulation in the deep lateral and ventral funiculi. Gray matter fluorescence was not enhanced. Prior transection did not abolish the intense accumulation of catecholamines at the site of the cord injury. We propose that the catecholamines accumulating at the cord injured site are not central in origin, but represent an uptake mechanism into white matter as a reflection of cord microperfusion.     

The Imbrication Model for the integration of social services in a community

An innovative model for organising social services in a community, the Imbrication Model, is contrasted with two traditional models, the Entrepreneurial and the Umbrella Agency. The structural characteristics and dynamics of the three models are illustrated with actual case histories. Imbrication Model calls for the interlocking of personnel from several agencies, with the purpose of redirecting the dysfunctional interagency rivalry prevalent in the traditional models. Imbrications at all organisational levels--Board of Directors, Administrators and Staff--facilitate adoption of the superordinate goal of providing clients with the best services available, regardless of which particular agency delivers the service. Few observers of the current social service scene would challenge the statement that needs for service are unlimited and resources limited. In the USA the imbalance between needs and resources persists despite a decade of massive governmental programmes intended to alleviate social ills. Recent substantial cutbacks in federal funds, moreover are not likely to improve the situation. The resource shortage involves more than a limitation of funds. Deliverers of service and competent programme administrators are also on critically short supply. These shortages are more often than not exacerbated by a chronic spirit of competition among agencies and programmes at the local level. Three organizational models for the delivery and administration of social services, two conventional and one of more recent date, are examined in this article. The innovative model, which has been named the Imbrication Model, explicitly calls for redirecting interagency rivalry and competition. Its ambitious goal is to integrate the efforts of those attempting to meet a community's social service needs.