A portable,adjustable finger printing stand

A lightweight finger printing stand is described which can be adjusted to the proper printing height. Based upon experience printing over 1,100 subjects, 12 advantages of using the stand are suggested.     

Cortical activity in vertebrate eggs. I: The activation waves

We present a physical model for the propagation of chemical and mechanical waves on the surface of vertebrate eggs. As a first step we analyzed the propagation of the calcium wave observed to sweep over the surface of the Medaka egg (Gilkey et al., 1978). It has been assumed that this wave is driven by a mechanism of calcium-stimulated-calcium-release. By formulating this hypothesis mathematically we can use the observed wavefront data to obtain a map of cortical reactivity. This map indicates a gradient of reactivity along the egg: highest in the animal hemisphere and tapering off towards the vegetal hemisphere. The cortex of Xenopus eggs is also capable of propagating a calcium wave (Busa & Nuccitelli, 1985). At about the same time a wave of expansion followed by a wave of contraction sweeps across the egg surface (Takeichi et al., 1984). We have proposed a mechanism for this wave pair based on the physical chemistry of actomyosin gels. The calcium wave activates solation factors which sever some of the actin chains which leads to an osmotic swelling of the gel. Calcium also activates the contractile machinery of the actomyosin system which causes the gel to contract. The contraction lags the swelling because of the nature of the kinetics: solation and swelling is a more rapid process than contraction. By writing the equations for gel expansion and contraction we can mimic the mechanical and chemical wave propagation by a computer simulation. If the model is correct this provides a method for using the waves as a diagnostic of the mechanochemical properties of the egg cortex.     

Correlations of blood selenium with hematological parameters in West German Adults

The serum selenium and the whole blood selenium of 72 healthy persons (47 women, 25 men) was determined. There exist sex specific differences of the whole blood selenium between men (98±19 μg Se/L) and women (89±17 μg Se/L). The serum selenium did not show sex specific differences, but sex specific differences are found if the total amount of extracellular selenium is calculated by correction of the serum selenium with the hematocrit. Women have more extracellular selenium/L whole blood (40±8 μg Se) than men (36±7 μg Se). Men have more intraerythrocyte selenium (cellular selenium=67±14 μg Se) in one L whole blood than women (52±17 μg Se). There exist also sex specific differences if the cellular selenium is calculated/g hemoglobin (men .44 μg Se/g Hb, women .37 μg Se/Hb) or per erythrocyte (men 136.1×10^?19 g Se/Ery, women 113.9×10^?19 g Se/Ery). In the cellular compartment of one L whole blood on the average 1.56 times more selenium is present than in the extracellular compartment. Most of the intraerythrocyte selenium is hemoglobin bound (84%) and utmost 16% glutathione peroxidase associated. An erythrocyte contains about 3500 mol glutathione peroxidase, or, for every 80000 mol hemoglobin one mol glutathione peroxidase. A standard man needs about 2.5 μg selenium/d for the synthesis of the hemoglobin and the erythrocyte. The hematological parameters hemoglobin and the erythrocyte number are correlated with the cellular selenium and the ratio cellular selenium/extracellular selenium. Positive significant correlations are found that are best if a parabolic model is used to interpret the shape of the curves. From the shape of the best correlation lines it can be concluded that selenium may be beneficial for hemoglobin synthesis and erythropoesis. The extracellular selenium may have influence on the volume of the erythrocyte by protecting the outer erythrocyte membrane from lipid peroxidation. A method is reported based on the carbon furnace atomic absorption spectroscopy, which is able to determine without wet digestion selenium in whole blood.     

Macrophage activation to kill Leishmania tropica: kinetics of macrophage response to lymphokines that induce antimicrobial activities against amastigotes

Lymphokine (LK) treatment of resident peritoneal macrophages from C3H/HeN mice induced two antimicrobial activities against Leishmania tropica: increased resistance of activated macrophages to infection with amastigotes and intracellular destruction of those parasites that entered activated cells. The onset and duration of these two antimicrobial activities were quite different. Resistance to infection was observed as early as 4 hr after the addition of LK, became maximal at 8 hr, and persisted in a subpopulation of treated cells for as long as 72 hr. In contrast, intracellular killing occurred with as little as 4 hr of LK treatment after infection, and maximal killing was observed in cultures exposed to LK 24 hr. Intracellular killing capacity of lymphokine-treated cells was progressively lost in macrophages treated longer than 12 hr before exposure to parasites. This decay in ability to destroy intracellular L. tropica was also seen in macrophages cultured longer than 12 hr before LK treatment, and may reflect loss of macrophage responsiveness to LK with increasing time in vitro. Thus, treatment of macrophages with lymphokines induced both a stable change in cell-parasite interactions, resistance to infection, and a short-lived capacity to destroy intracellular amastigotes.     

Entrainment and phase shifting of the circadian rhythm of cell division by light in cultures of the achlorophyllous ZC mutant ofEuglena gracilis

The photosynthesis-deficient ZC mutant ofEuglena gracilis Klebs (strain Z) was cultured at 16°C on an aerated, magnetically stirred, mineral medium containing 0.1% ethanol (pH 7.0). Cell division could be entrained by a 12: 12 light: dark cycle (LD: 12, 12) or even by a one-pulse skeleton photoperiod (LD: 1,23) The rhythm free-ran in DD for at least 8 days with a circadian period (=25.5 h) in populations that had been previously entrained by LD. The freerunning rhythm could be phase-shifted by a single 1-h light pulse (3000 lx). The strong (Type 0) phase-response curve derived from the resetting effects of such signals given at different circadian times was similar to that for the photosynthetic wild-type strain. These results demonstrate that the presence of a functional chloroplast compartment is not necessary for the circadian clock to function inEuglena and suggest that phase resetting of the circadian clock by light occurs via a similar pathway in both photosynthetic and non-photosynthetic cell types.     

The renal excretion of selenium.

The excretion of selenium in urine was determined in West German healthy volunteers. Women excrete 17.7 +/- 4.2 micrograms Se/d and men 19.0 +/- 9.0 micrograms Se/d. The daily selenium excretion per gram creatinine is 13.5 +/- 3.8 micrograms Se/g crea for women and 9.8 +/- 3.3 micrograms Se/g crea for men. The clearance of selenium from the plasma is calculated with 0.18 mL/min. The selenium excretion per day is positively correlated with the 24 h excretion of urea and creatinine. The correlation of the selenium excretion with the urea excretion is most probably owing to the fact that the selenium intake of West Germans is linked primarily to foods with high protein contents. That the selenium excretion is directly correlated with the creatinine excretion is an indicator that the muscle, which accounts for nearly 50% of the whole body selenium in West German adults, influences the selenium excretion in urine. The positive correlation of the selenium excretion with the potassium excretion also indicates that the muscle mass contributes significantly to the selenium excretion in urine. Another indicator that the selenium excretion is influenced by the muscle is that after intensive muscular activity (running), selenium excretion is enhanced. The 24 h selenium excretion is dependent on the glomerular filtration rate of the kidney characterized by the creatinine clearance. This result is important, because if the selenium excretion is used as parameter for the selenium status of humans, the kidney function should be known. This is a limitation for the use of the urinary selenium excretion as parameter for the selenium status. This is especially important for patients whose glomerular filtration rate is low. The 24 h selenium excretion is further influenced by the 24 h urine volume. Selenium losses via urine may be concomitant with protein losses in urine.     

Lipoprotein-associated paf (LA-paf) was found in washed human platelets and monocyte/macrophage-like U937 cells

Beyond cholesterol, inflammatory ether phospholipids such as platelet-activating factor (paf) may play a role in atherogenesis. (1) We detected a paf-like compound (‘LA-paf’) associated with human serum lipoproteins, mainly in LDL but not with the lipoprotein-poor fraction. (2) LA-paf was also found in washed human platelets, from where it was partially released during platelet aggregation in response to paf (50 nM) or thrombin (1 U). In addition, resident monocyte/macrophage-like U937 cells carried huge amounts of LA-paf (41 ng per 10⁷ cells) and metabolized added [³H]paf to a labelled compound co-eluting with the retention time of LA-paf in standard HPLC. (3) Functionally, LA-paf had a comparable potency to synthetic paf, because LA-paf aggregated washed aspirin-treated platelets in a concentration-dependent manner. The specific paf receptor antagonist WEB2086 inhibited the platelet aggregation induced by three distinct LA-paf preparations as compared with synthetic paf with similar inhibitory concentrations (IC₅₀: 35.6 ± 12.8, 24.0 ± 4.0, 38.0 ± 15.8 nM for LA-paf, and 43.6 ± 6.5 nM for synthetic paf), indicating that LA-paf interacted with paf receptors. (4) However, LA-paf had a distinct retention time using high-pressure liquid chromatography (HPLC) as compared with synthetic paf. LA-paf eluted at 9–15 min and synthetic paf at 21–24 min. In addition, total and non-specific [³H]paf binding to intact washed human platelets was affected differently by the two unlabelled agonists: while LA-paf increased total and non-specific (but not specific) binding in a significant manner (P < 0.002 and P < 0.007) as LDL did (P < 0.006 and P < 0.03), synthetic paf decreased total binding (P < 0.03). Similarly, low-density lipoproteins (LDL) increased significantly the total [³H]paf binding. In contrast, paf did not affect specific [¹²⁵I]LDL binding to human fibroblasts. Our results show the presence of LA-paf in lipoproteins,