Scales for the measurement of attitudes toward blood donation

Attitudes toward blood donation are frequently assumed to vary along a single dimension from unfavorable to favorable. In contrast, theories of attitude structure specify three distinct attitude components: affect, cognition, and behavior. This article describes the development of three new scales for the measurement of affective, cognitive, and behavioral components of attitudes toward blood donation. The scales were developed using the method of equal-appearing intervals and were administered to both donors of blood and nondonors. Correlations among the scales were relatively small and supported the three-component distinction. Affect was more strongly correlated with the number of prior donations than was cognition, which suggested an important role for emotional factors in blood donation. Scores on all three scales showed the attitudes of blood donors to be more favorable than those of nondonors.     

The influence of bright light during the daytime upon circadian rhythm of core temperature and its implications for nocturnal sleep

Abstract The purpose of the present study was to investigate how bright light during the daytime could influence circadian rhythms of core temperature and nocturnal sleep. Seven females (age 20 ± 2 years) served as participants. The participants lived in the experimental unit for 4 days and were exposed to either 6000 lx (bright) or 200 lx (dim) light during the daytime. Rectal temperature (T_re) was measured during the experimental period. Subjective alertness was measured by the Kansei-gakuin Sleeping Scale five times a day. The minimum T_re was significantly lower after bright exposure ( P < 0.05). The T_re fell rapidly after bright exposure before they retired ( P < 0.05) and increased more rapidly during bright light after they woke up ( P < 0.05). The morning wakefulness under bright exposure was more active than under dim exposure ( P < 0.05). The melatonin secretion at wake up during bright exposure was significantly lower than during dim exposure ( P < 0.05). Exposure to bright light during daytime lowered the nocturnal level of T_re, its evening fall was faster and the morning rise quicker. This suggests that indoor light during daytime should be bright enough to promote healthy sleep at night.     

Transforming growth factor beta-1 (TGFB1) and peak bone mass: association between intragenic polymorphisms and quantitative ultrasound of the heel

Background  

Variance of peak bone mass has a substantial genetic component, as has been shown with twin studies examining quantitative measures such as bone mineral density (BMD) and quantitative ultrasound (QUS). Evidence implicating single nucleotide polymorphisms (SNPs) of the transforming growth factor beta-1 (TGFB1) gene is steadily accumulating. However, a comprehensive look at multiple SNPs at this locus for their association with indices of peak bone mass has not been reported.     

糖基化恢复冷藏血小板的存活率

血小板冷藏会使血管假性血友病因子受体复合物(von Willebrand factor receptor complex)聚集成簇。巨噬细胞αMβ2 整合素结合在成簇复合物的GPIbα亚基,导致输注的冷藏血小板被快速清除。因此输注用血小板不能冷藏,但现在的室温保存方式也存在很大缺点。我们已证明αMβ2是一种凝集素,它能识别GPIbα的N-连接葡聚糖上暴露的β-N-乙酰葡萄胺。冷藏血小板的酶促半乳糖苷化阻止了αMβ2的这种识别,延长了有     

Correlation between serum lipoprotein (a) and angiographic coronary artery disease in non-insulin-dependent diabetes mellitus

Abstract. Comlekqi A, Biberoglu S, Kozan 0, Bahqeci 0, Ergene 0, Nazli C, Kinay 0, Guner G (Dokuz Eylul University, Medical School, Inciralti, Izmir, Turkey). Correlation between serum lipoprotein(a) and angio-graphic coronary artery disease in non-insulin-dependent diabetes mellitus. J Intern Med 1997; 242:449-54.
Objectives: To examine the impact of diabetic state on the concentrations of lipoprotein(a) [Lp(a)] in patients with non-insulin-dependent diabetes mellitus (NIDDM) and the correlation between angiographic coronary artery disease (CAD) and serum Lp(a) concentrations in NIDDM.
Design: In this cross-sectional study of 26 patients with NIDDM and 19 nondiabetic sex- and agematched patients who underwent coronary angiography, CAD was assessed visually using coronary artery score (CAS), and plasma Lp(a) was measured by an enzyme-linked immunosorbent assay.
Setting: The study was performed in an internal medicine clinic at a university hospital.
Subjects: Twenty-six age- and sex-matched patients with NIDDM and 19 control patients without diabetes.
Results: There was no significant difference between the Lp(a) concentrations of patientswith NIDDM and nondiabetic subjects (P > 0.05). When patients with NIDDM were stratified by absence or presence of CAD, patients with CAD had higher levels of Lp(a) (P < 0.05). However, there was no significant correlation between the concentrations of Lp(a) and CAS (P > 0.05).
Conclusions: Diabetic state does not have any impact on Lp(a) concentrations. Lp(a) excess seems to be atherogenic in patients with NIDDM as shown in nondiabetic patients in previous studies. Although diabetic patients with CAD have higher Lp(a) concentrations than the diabetic patients without CAD, Lp(a) levels were not correlated with CAS.     

C1q binding to surface-bound IgG is stabilized by C1r2s2 proteases

Complement is an important effector mechanism for antibody-mediated clearance of infections and tumor cells. Upon binding to target cells, the antibody’s constant (Fc) domain recruits complement component C1 to initiate a proteolytic cascade that generates lytic pores and stimulates phagocytosis. The C1 complex (C1qr₂s₂) consists of the large recognition protein C1q and a heterotetramer of proteases C1r and C1s (C1r₂s₂). While interactions between C1 and IgG-Fc are believed to be mediated by the globular heads of C1q, we here find that C1r₂s₂ proteases affect the capacity of C1q to form an avid complex with surface-bound IgG molecules (on various 2,4-dinitrophenol [DNP]-coated surfaces and pathogenic Staphylococcus aureus). The extent to which C1r₂s₂ contributes to C1q–IgG stability strongly differs between human IgG subclasses. Using antibody engineering of monoclonal IgG, we reveal that hexamer-enhancing mutations improve C1q–IgG stability, both in the absence and presence of C1r₂s₂. In addition, hexamer-enhanced IgGs targeting S. aureus mediate improved complement-dependent phagocytosis by human neutrophils. Altogether, these molecular insights into complement binding to surface-bound IgGs could be important for optimal design of antibody therapies.

Antibodies are important mediators of the human complement response, which offers critical protection against microbial infections and damaged host cells (1). In order to initiate a complement response, an antibody molecule first needs to bind antigens on the target cell via its antigen-binding (Fab) domains (2–5). Subsequently, the antibody’s constant (Fc) domain recruits the first complement protein complex, C1, to the cell surface (SI Appendix, Fig. S1A). The large C1 complex (also denoted as C1qr₂s₂, 766 kDa) consists of the recognition protein C1q (410 kDa) and a heterotetramer of serine proteases C1r and C1s (denoted C1r₂s₂, 356 kDa) (SI Appendix, Fig. S1B). While C1q is responsible for antibody recognition, its attached proteases C1r₂s₂ induce the activation of downstream enzymatic complexes (i.e., C3 convertases [C4b2b (6)]) that catalyze the covalent deposition of C3-derived molecules (e.g., C3b and its degradation product iC3b) onto the target cell surface (SI Appendix, Fig. S1A) (7, 8). C3b opsonizes the target cell surface and can induce formation of lytic pores (membrane attack complex [MAC]) in the target cell membrane (9–11). In contrast to human cells and gram-negative bacteria, gram-positive bacteria are not susceptible to the MAC due to their thick cell wall (12). On these bacteria, efficient decoration with C3b and iC3b is essential for triggering effective phagocytic uptake of target cells via complement receptors (CR) expressed on phagocytes of which the integrin CR3 (also denoted CD11b/CD18) is considered most important (13, 14).In recent years, our insights into IgG-dependent complement activation have increased significantly. A combination of structural, biophysical, and functional studies revealed that surface-bound IgG molecules (after Fab-mediated antigen binding) require organization into higher-ordered structures, namely hexamers, to induce complement activation most effectively (15–19). Hexamerized IgGs are being held together by noncovalent Fc–Fc interactions and form an optimal platform for C1q docking (SI Appendix, Fig. S1A). C1q has a “bunch of tulips–” like structure, consisting of six collagen arms that each end in a globular (gC1q) domain (SI Appendix, Fig. S1B) that binds the Fc region of an IgG. As the affinity of C1q for a single IgG is very weak (20, 21), avidity achieved through simultaneous binding of its globular domains to six oligomerized IgG molecules is paramount for a strong response (15, 17–19). Furthermore, it was found that IgG hexamerization could be manipulated by specific point mutations in the Fc–Fc contact region that enhance such oligomerization (15, 18, 22). While these hexamer-enhancing mutations in IgG potentiate the efficacy of MAC-dependent cytotoxicity on tumor cells and gram-negative bacteria (15, 23), their effect on complement-dependent phagocytosis is not known.Because complement is an important effector mechanism to kill bacteria and tumor cells, development of complement-enhancing antibodies represents an attractive strategy for immune therapies (1, 24). Immunotherapy based on human monoclonal antibodies is not yet available for bacterial infections (25–28). Such developments are mainly hampered by the fact that little is known about the basic mechanisms of complement activation on bacterial cells. For instance, we do not understand why certain antibodies induce complement activation on bacteria and others do not. In this study, we set out to investigate how antibacterial IgGs induce an effective complement response. By surprise, we noticed that C1q–IgG stability differs between human IgG subclasses. More detailed molecular investigations revealed that C1r₂s₂ proteases are important for generating stable C1q–IgG complexes on various target surfaces. Furthermore, we demonstrate that C1q–IgG stability is influenced by antibody oligomerization. These molecular insights into C1q binding to surface-bound IgGs may pave the way for optimal design of antibody therapies.     

Cytogenetic studies in patients with secondary leukemia/dysmyelopoietic syndrome after different treatment modalities

Cytogenetic studies of 68 patients who developed secondary leukemia (SL)/dysmyelopoietic syndrome (DMS) after extensive chemotherapy and/or radiation therapy as well as patients who developed SL/DMS without such treatment showed that those patients who received radiation alone or with chemotherapy had more extensive numerical and structural abnormalities than those who received only chemotherapy. In terms of the specific chromosomal abnormalities, there are no differences between the various treatment groups. Hypodiploidy is the most common form of aneuploidy in these patients, with the most common numerical abnormality being the loss of chromosome 7. The most common structural abnormalities involved chromosomes 3 and 5. When compared with patients with de novo leukemia and DMS, the chromosomal abnormalities in these patients are more complex and extensive. Serial studies revealed that cytogenetic abnormalities do not precede the development of hematologic changes by significant time periods.