Enteric Pathogens in Monkeys

From 1964 to 1967, 6,646 monkeys, representing 10 primate species, were examined for Shigella and Salmonella infections upon arrival at the National Center for Primate Biology. Of these animals, 12% were infected with Shigella, and 75% of the Shigella isolates were S. flexneri 4. The incidence of Salmonella infections decreased from 12 to 3% during the period of study. Epidemiological studies of animals in the colony for 90 days or more indicated no seasonal variation in the occurrence of Shigella and Salmonella. Many of the isolates from incoming monkeys as well as from laboratory-conditioned animals were resistant to chloramphenicol, dihydrostreptomycin, and tetracycline. The possible operation of drug-resistance factors in these infections is discussed.     

SUMOylation stabilizes sister kinetochore biorientation to allow timely anaphase

During mitosis, sister chromatids attach to microtubules from opposite poles, called biorientation. Sister chromatid cohesion resists microtubule forces, generating tension, which provides the signal that biorientation has occurred. How tension silences the surveillance pathways that prevent cell cycle progression and correct erroneous kinetochore–microtubule attachments remains unclear. Here we show that SUMOylation dampens error correction to allow stable sister kinetochore biorientation and timely anaphase onset. The Siz1/Siz2 SUMO ligases modify the pericentromere-localized shugoshin (Sgo1) protein before its tension-dependent release from chromatin. Sgo1 SUMOylation reduces its binding to protein phosphatase 2A (PP2A), and weakening of this interaction is important for stable biorientation. Unstable biorientation in SUMO-deficient cells is associated with persistence of the chromosome passenger complex (CPC) at centromeres, and SUMOylation of CPC subunit Bir1 also contributes to timely anaphase onset. We propose that SUMOylation acts in a combinatorial manner to facilitate dismantling of the error correction machinery within pericentromeres and thereby sharpen the metaphase–anaphase transition.     

Glucose dysregulation in obese children: predictive, risk, and potential protective factors

Objective: The aim of our study was to determine the prevalence of impaired glucose tolerance (IGT) and type 2 diabetes (DM2) in obese children and adolescents of Greek origin and compare our data with pertinent literature findings in an attempt to uncover predictive, risk, and preventive factors. Research Methods and Procedures: A total of 117 obese children and adolescents 12.1 ± 2.7 years old underwent a 2‐hour oral glucose tolerance test (OGTT). Insulin resistance (IR) and β‐cell function were estimated using the homeostasis model assessment (HOMA)‐IR and the insulinogenic index, respectively. Results: A total of 17 patients (14.5%) had IGT, and none had DM2. The overall prevalence rates of both IGT and DM2 in our subjects were lower than those reported in a recent multiethnic U.S. study. Nevertheless, the difference between our IGT data and those of the U.S. study was due mostly to the prepubertal subjects (9% vs. 25.4%), whereas no difference was observed in the pubertal population (18% vs. 21%). Fasting glucose, insulin, and HOMA‐IR values were not predictive of IGT. The absolute value of insulin at 2 hours of the OGTT combined with the time‐integrated glycemia (AUCG) can strongly predict IGT, whereas higher area under the curve for insulin (AUCI) values were found to be protective. Discussion: In ethnic groups less prone to diabetes development, IGT or DM2 in obese subjects is more likely to develop at puberty than at the prepubertal stage. It is advisable that physicians caring for obese adolescents perform an OGTT for early detection of IGT because HOMA‐IR values, although higher in IGT subjects and indicative of IR, cannot predict IGT.     

Disturbances in Maternal Steroidogenesis and Appearance of Intrauterine Growth Retardation at High-Altitude Environments Are Established from Early Pregnancy. Effects of Treatment with Antioxidant Vitamins

Pregnancies at high-altitudes are influenced by hypoxia and oxidative stress and frequently affected by IUGR. However, a common thought is that early pregnant women visiting altitude have no major complications for gestation development, since IUGR is developed during the second half of pregnancy. Thus, using a well-characterized sheep-model, we aimed to determine whether long- and/or short-term exposure to high-altitude may affect maternal steroidogenesis and therefore embryo-fetal growth from conception. The second aim was to differentiate the relative role of hypoxia and oxidative stress by assessing the effects of supplementation with antioxidant agents during this early-pregnancy stage, which were previously found to be useful to prevent IUGR. The results indicate that both long- and short-term exposure to high-altitude causes disturbances in maternal ovarian steroidogenesis and negatively affects embryo-fetal growth already during the very early stages of gestation, with the consequences being even worsened in newcomers to high-altitude. The supply of antioxidant during this period only showed discrete effects for preventing IUGR. In conclusion, the present study gives a warning for clinicians about the risks for early-pregnant women when visiting high-altitude regions and suggests the need for further studies on the effects of the length of exposure and on the interaction of the exposure with the pregnancy stage.     

Endocrine changes during pregnancy, parturition and post-partum in guanacos (Lama guanicoe)

Plasma concentrations of progesterone (P4), estradiol-17β (E2), estrone (E1) and estrone sulfate (E1S) were measured during gestation in eight guanacos kept in captivity. Gestational length was 346.1 ± 9.8 days. P4 plasma concentrations increased after ovulation and remained elevated until parturition. However, during the last 4 weeks of gestation, a gradual decrease from 4.17 × 1.17^±1 nmol/L to 2.02 × 1.95^±1 nmol/L on day 5 before parturition was observed, followed by a more abrupt final decline to baseline concentrations which were reached on the day after parturition. Mean E2 plasma concentrations started to increase during the eighth month of gestation, and were significantly elevated up to maximum concentrations of 484.7 × 1.21^±1 pmol/L during the last 2 months of pregnancy. Concentrations returned to baseline during the last 2 days of gestation. An increase of E1S concentrations (p < 0.01) was observed in the eleventh month of gestation. Mean E1S concentrations remained rather constant during the last 3 weeks of gestation between 4 to 8 nmol/L until parturition, when a steep precipitous decline was observed. E1 concentrations were slightly elevated during the last 4 weeks of gestation, however, maximum concentrations did not exceed 1.5 nmol/L. The results show distinct species specific features of gestational steroid hormone profiles in the guanaco in comparison to domestic South American camelids, such as a more pronounced gradual prepartal decrease of P4 concentrations prior to the final decline to baseline, and clearly lesser E1S concentrations during the last 4 weeks of gestation, which lack a continuous prepartal increase.     

Xanthomonas T3S Effector XopN Suppresses PAMP-Triggered Immunity and Interacts with a Tomato Atypical Receptor-Like Kinase and TFT1

XopN is a virulence factor from Xanthomonas campestris pathovar vesicatoria (Xcv) that is translocated into tomato (Solanum lycopersicum) leaf cells by the pathogen''s type III secretion system. Xcv ΔxopN mutants are impaired in growth and have reduced ability to elicit disease symptoms in susceptible tomato leaves. We show that XopN action in planta reduced pathogen-associated molecular pattern (PAMP)-induced gene expression and callose deposition in host tissue, indicating that XopN suppresses PAMP-triggered immune responses during Xcv infection. XopN is predicted to have irregular, α-helical repeats, suggesting multiple protein–protein interactions in planta. Consistent with this prediction, XopN interacted with the cytosolic domain of a Tomato Atypical Receptor-Like Kinase1 (TARK1) and four Tomato Fourteen-Three-Three isoforms (TFT1, TFT3, TFT5, and TFT6) in yeast. XopN/TARK1 and XopN/TFT1 interactions were confirmed in planta by bimolecular fluorescence complementation and pull-down analysis. Xcv ΔxopN virulence defects were partially suppressed in transgenic tomato leaves with reduced TARK1 mRNA levels, indicating that TARK1 plays an important role in the outcome of Xcv–tomato interactions. These data provide the basis for a model in which XopN binds to TARK1 to interfere with TARK1-dependent signaling events triggered in response to Xcv infection.