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Light chain receptors on human circulating lymphocytes of thirty-three normal individuals were visualized by the immunocyto-adhesion reaction in which human (anuclear) erythrocytes coated with κ chains and chicken (nucleated) erythrocytes coated with λ chains (or vice versa) were used, 4.4 (±2.3)% of the lymphocytes had κ and 4.15 (±2.4)% had λ receptors, when the lymphocytes were sensitized with antisera to either κ and λ chains. When both antisera were used simultaneously only 5.3 (±3)% were found to have receptors and the majority of cells carried both κ and λ receptors. These findings suggest that in these cells the genes for the constant regions of both light chains are active. [ABSTRACT FROM AUTHOR]

From its small-scale, community-based roots, hospice care in America has evolved into a competitive, highly-regulated industry. Hospice nurses today often find themselves challenged by increased patient caseloads, faster-paced work environments, and ever-growing documentation demands. This article addresses these issues through the lived experience of the author, a registered nurse who has worked "at the bedside" with terminally ill patients for over two decades. It also touches upon some of the additional challenges associated with delivering hospice care "after hours," and in non-traditional settings such as nursing facilities and acute-care hospitals. The author concludes that it is still possible to successfully navigate the complexities of end-of-life care in the 21(st) century without losing one's "hospice heart.", (© 2011 Wiley Periodicals, Inc.)

Verapamil has been shown to overcome acquired drug resistance to vincristine in P388 leukemia both in vitro and in vivo. To study the selectivity of this action, the effect of addition of verapamil on the cytotoxicity of vincristine was studied using lymphocytes from eight patients with chronic lymphocytic leukemia (CLL), lymphoblasts from a T-acute lymphoblastic leukemia (T-ALL) cell line (GM 3639), and peripheral blood lymphocytes (PBL) from eight normal healthy volunteers. Using the differential staining cytotoxicity (DiSC) assay, we demonstrated that verapamil at 1 microM concentration potentiated the in-vitro cytotoxicity of vincristine on CLL and GM 3639 cells in concentrations of 0.04-0.25 micrograms/l. There was however, no enhancement of cytotoxicity noted against the control PBL. The data demonstrate that verapamil preferentially enhances the in-vitro cytotoxicity of vincristine on CLL and GM 3639 cells but no enhancement of cytotoxicity is seen against PBL.

The effect of different levels of Zn intake on survival was studied in 6 groups of 4-week-old BALB/c mice inoculated with MOPC 104E tumor cells. The first 3 groups received either a Zn-deficient (0.5 microgram Zn/g), a Zn-supplemented (1 mg Zn/g), or a control diet (37.5 micrograms Zn/g) starting 11 days after tumor inoculation (T11). The remaining 3 groups received the same diets starting the day the tumor was implanted (T0). The mean survival of rats beginning the Zn-deficient diet at T11 was significantly increased compared with that of the control group. However, when the same diet was begun at T0, the mean survival of the Zn-deficient group was significantly reduced; for this group the results probably related to the combined adverse effects from prolonged Zn deficiency and to those effects of the tumor itself. Similarly, excess Zn intake significantly prolonged the mean survival when given at T11. However, excess Zn intake at T0 produced no significant effect on survival, probably because of the elevation of plasma Zn level following oral Zn intake that occurred before the establishment of the tumor or possibly because of the inability of the small intestine to absorb excess Zn at T11 when the tumor was fully developed.

The structure and replication of human leukocyte mitochondrial DNA (mtDNA) was investigated in healthy young adult males (23--37 years old), middle-aged males (42--52 years old) with secondary polycythemia, and elderly males (80--89 years old) who exhibited different degrees of age-related disease syndromes. The distribution of the various cell types within the white cell population was within normal limits in all samples. Total mtDNA was isolated in ethidium bromide--CsCl gradients and examined by electron microscopy after spreading by the aqueous and formamide techniques. The individual frequencies of catenated forms ranged from 2 to 6% but showed relatively little change (declining slightly) with age. The individual frequencies of circular dimers varied from 0 to 0.1% in the young adult and polycythemic groups and in 10 out of 12 elderly individuals. One elderly individual had a circular dimer frequency of 0.3% (including a circular molecular of tetramer size) and another had 4.5%. This finding suggest that agerelated cellular pathology may exist in the blood-forming system in some cases. The mode of replication of leukocyte mtDNA agrees well with that described for mouse L cells. There was no evidence of aberrant mtDNA replication as a result of aging.

These studies examined the fate of Factor XIII (fibrin-stabilizing factor) in mice with plasmacytoma (MOPC-300, MOPC-384, MOPC-467, and J-558). Plasma Factor XIII levels in these mice decreased progressively with tumor expansion. No plasma inhibitors of Factor XIII activity could be detected. Factor XIII was found on plasmacytoma cell membranes and in the cytoplasm of the malignant cells by immunofluorescence. The inverse relationship between tumor load and plasma Factor XIII levels suggested that the fibrin-stabilizing factor was absorbed by the malignant cells.

Abnormal cellular interactions between T and B lymphocytes were identified in patients with CLL and AT. The system employed utilized the detection of a newly recognized lymphokine, NIF-T. This mediator is produced by T lymphocytes as a result of the interaction between T and B cells. Our studies demonstrated impaired T cell function but normal B cell activity in patients with AT with respect to mitogenic stimulation and MLC reactivity. In contrast, patients with B cell CLL had normal T cell function. The leukemic B cells from these patients, however, failed to collaborate with normal T cells in response to mitogens, and they did not participate in MLC reactions. In contrast, lymphocytes from patients with HCL functioned normally with respect to NIF-T production.

A lectinlike activity was discovered in serum from 25 patients with CF, 70 obligate heterozygotes (parents), and 18 of 27 siblings (67%) of 675 controls, 4.2% were found to have a positive test for the CF-lectin, approximating the 5% estimated prevalence of CF heterozygotes. The CF-lectin can be detected by dextran-enhanced agglutination of mouse RBCs and confirmed by agglutination inhibition with D-fructose. This simple and inexpensive assay has been found useful to detect carriers of the CF gene, but variability of commercial dextran and some unusual characteristics of the lectin itself have interfered with the successful completion of blind studies. All sugar moieties present in mucus inhibit the agglutination of mouse RBCs by CF serum, implying that the CF-lectin can bind the glycoproteins of mucus. The factor may play a role in the pathogenesis of Cf by stimulating mucus secretion and reacting with mucous glycoproteins to cause their precipitation. Most antibiotics remove or inhibit the CF-lectin activity, suggesting a therapeutic effect of antibiotics unrelated to their antibacterial action. This discovery of a lectinlike factor in the blood of patients with CF and their parents opens a new area for investigation of this devastating disease.

An agglutination inhibition technic using CrCl3-treated erythrocytes for the quantification of circulating fibrin degradation products in patients with thromboembolic and fibrinolytic states is described.