La belle Lucie: waltz

(Published By H. J. Peters & Co.

Computerized measurement of iron in liver biopsies: A comparison with biochemical iron measurement

The measurement of stainable hepatic iron using a microcomputer image analysis system was compared with standard biochemical measurements of liver iron content in 103 liver biopsy specimens–29 of idiopathic hemochromatosis, 51 of alcoholic liver disease and 23 of various nonalcoholic liver diseases. Sections were stained using Perls' method for iron; the mean area staining positively for iron was measured and expressed as a percentage of the area of biopsy measured. Biochemical (biochemical hepatic iron [μmol/gm dry wt]/age) and morphometrical (morphometrical hepatic iron [%]/age × 100) hepatic iron indices were calculated. Patients in the idiopathic hemochromatosis group had significantly higher biochemical hepatic iron concentrations (p < 0.001) compared with the alcoholic liver disease and nonalcoholic liver disease groups: 284 (range = 119 to 631), 21 (range = 2 to 65) and 15 (range = 3 to 31) μmol/gm dry wt, respectively. The biochemical hepatic iron index was also significantly higher (p < 0.001) in the hemochromatosis group compared with the alcoholic liver disease and nonalcoholic liver disease groups: 5.8 (range = 2.1 to 13.7), 0.4 (range = 0 to 1.6) and 0.4 (range = 0 to 1.1), respectively. Computerized measurements were significantly higher in the hemochromatosis group (p < 0.001) compared with the alcoholic liver disease and nonalcoholic liver disease groups: 9.72% (range = 1.50% to 29.26%), 0.13% (range = 0% to 1.20%) and 0.03% (range = 0% to 0.40%), respectively. The morphometrical hepatic iron index was also significantly higher (p < 0.001) in the hemochromatosis group compared with the alcoholic liver disease and nonalcoholic liver disease groups: 19.32 (range = 2.60 to 75.10), 0.21 (range = 0 to 1.90) and 0.09 (range = 0 to 1.10), respectively. There was no overlap between the hemochromatosis and the alcoholic liver disease and nonalcoholic liver disease groups. Significant linear relationships were demonstrated between morphometrical and biochemical measurements of hepatic iron (p < 0.001) and morphometrical and biochemical hepatic iron indices (p < 0.001). We conclude that computerized measurements of stainable hepatic iron show a significant linear relationship with biochemical iron measurements. Also, the morphometrical hepatic iron index, like the biochemical hepatic iron index, may help differentiate idiopathic hemochromatosis from other disorders with increased hepatic iron levles

The Mount Wilson Observatory S-index of the Sun

Abstract The most commonly used index of stellar magnetic activity is the instrumental flux scale of singly ionized calcium $H$ &amp; $K$ line core emission, $S$, developed by the Mount Wilson Observatory (MWO) HK Project, or the derivative index ${R}_{\mathrm{HK}}^{\prime }$. Accurately placing the Sun on the $S$ scale is important for comparing solar activity to that of the Sun-like stars. We present previously unpublished measurements of the reflected sunlight from the Moon using the second-generation MWO HK photometer during solar cycle 23 and determine cycle minimum ${S}_{23,\min }=0.1634\pm 0.0008$, amplitude ${\rm{\Delta }}{S}_{23}=0.0143\pm 0.0012$, and mean $\langle {S}_{23}\rangle =0.1701\pm 0.0005$. By establishing a proxy relationship with the closely related National Solar Observatory Sacramento Peak calcium $K$ emission index, itself well correlated with the Kodaikanal Observatory plage index, we extend the MWO $S$ time series to cover cycles 15–24 and find on average $\langle {S}_{\min }\rangle =0.1621\pm 0.0008$, $\langle {\rm{\Delta }}{S}_{\mathrm{cyc}}\rangle =0.0145\pm 0.0012$, $\langle {S}_{\mathrm{cyc}}\rangle =0.1694\pm 0.0005$. Our measurements represent an improvement over previous estimates that relied on stellar measurements or solar proxies with non-overlapping time series. We find good agreement from these results with measurements by the Solar-Stellar Spectrograph at Lowell Observatory, an independently calibrated instrument, which gives us additional confidence that we have accurately placed the Sun on the $S$-index flux scale

Efficient transplacental IgG transfer in women infected with Zika virus during pregnancy.

Zika virus (ZIKV) is a newly-identified infectious cause of congenital disease. Transplacental transfer of maternal IgG to the fetus plays an important role in preventing many neonatal infections. However, antibody transfer may also have negative consequences, such as mediating enhancement of flavivirus infections in early life, or trafficking of virus immune complexes to the fetal compartment. ZIKV infection produces placental pathology which could lead to impaired IgG transfer efficiency as occurs in other maternal infections, such as HIV-1 and malaria. In this study, we asked whether ZIKV infection during pregnancy impairs transplacental transfer of IgG. We enrolled pregnant women with fever or rash in a prospective cohort in Vitoria, Brazil during the recent ZIKV epidemic. ZIKV and dengue virus (DENV)-specific IgG, ZIKV and DENV neutralizing antibodies, and routine vaccine antigen-specific IgG were measured in maternal samples collected around delivery and 20 paired cord blood samples. We concluded that 8 of these mothers were infected with ZIKV during pregnancy and 12 were ZIKV-uninfected. The magnitude of flavivirus-specific IgG, neutralizing antibody, and vaccine-elicited IgG were highly correlated between maternal plasma and infant cord blood in both ZIKV-infected and -uninfected mother-infant pairs. Moreover, there was no difference in the magnitude of plasma flavivirus-specific IgG levels between mothers and infants regardless of ZIKV infection status. Our data suggests that maternal ZIKV infection during pregnancy does not impair the efficiency of placental transfer of flavivirus-specific, functional, and vaccine-elicited IgG. These findings have implications for the neonatal outomes of maternal ZIKV infection and optimal administration of antibody-based ZIKV vaccines and therapeutics

Maternal CD4+ T cells protect against severe congenital cytomegalovirus disease in a novel nonhuman primate model of placental cytomegalovirus transmission

Elucidation of maternal immune correlates of protection against congenital cytomegalovirus (CMV) is necessary to inform future vaccine design. Here, we present a novel rhesus macaque model of placental rhesus CMV (rhCMV) transmission and use it to dissect determinants of protection against congenital transmission following primary maternal rhCMV infection. In this model, asymptomatic intrauterine infection was observed following i.v. rhCMV inoculation during the early second trimester in two of three rhCMV-seronegative pregnant females. In contrast, fetal loss or infant CMV-associated sequelae occurred in four rhCMV-seronegative pregnant macaques that were CD4(+) T-cell depleted at the time of inoculation. Animals that received the CD4(+) T-cell-depleting antibody also exhibited higher plasma and amniotic fluid viral loads, dampened virus-specific CD8(+) T-cell responses, and delayed production of autologous neutralizing antibodies compared with immunocompetent monkeys. Thus, maternal CD4(+) T-cell immunity during primary rhCMV infection is important for controlling maternal viremia and inducing protective immune responses that prevent severe CMV-associated fetal disease