Ocena związku poziomu wiremii HCMV u matki z przebiegiem ciąży i stanem urodzeniowym noworodków

Congenital cytomegaly is caused by intrauterine mother-to-fetus HCMV transmission and constitutes the most common vertical infection. Objectives: The aim of the study was to analyze the viremia level in maternal blood and its influence on the course and duration of pregnancy, as well as newborn condition. Material and methods: The material included blood samples collected from 117 pregnant women with serological features of HCMV infection and from 29 neonates hospitalized at DFMMG in Lodz between 1999 and 2009. The presence of HCMV DNA in the maternal and fetal blood was tested using real-time PCR. Results: Prevalence of maternal viremia was observed to increase the risk of viremia in neonates, as compared to children born to mothers with no viremia. However, lack of HCMV DNA in maternal blood does not exclude fetal infection in utero. Newborn condition assessed by Apgar scores was significantly lower in the group of infants born to mothers with serological features of acute cytomegaly (pWrodzona cytomegalia wywołana transmisją wirusa cytomegalii (HCMV) od matki do płodu, jest najczęstszym zakażeniem wertykalnym. Cel pracy: Celem pracy była ocena poziomu wiremii u kobiet ciężarnych i jej wpływu na przebieg i czas trwania ciąży oraz stan urodzeniowy noworodków. Materiał i metody: Materiałem do badań była krew pobrana od 117 ciężarnych z serologicznymi cechami zakażenia HCMV oraz 29 noworodków hospitalizowanych w Klinice Medycyny Matczyno-Płodowej i Ginekologii Instytutu Centrum Zdrowia Matki Polki w latach 1999-2009. Liczba kopii DNA HCMV we krwi matek i dzieci oznaczana była metodą PCR w czasie rzeczywistym (real-time PCR). Wyniki: Stwierdzono, że występowanie wiremii HCMV u matki zwiększa ryzyko występowania wiremii u noworodków w porównaniu z ryzykiem u dzieci matek bez wiremii, jednakże brak DNA HCMV we krwi matki nie wyklucza zakażenia płodu in utero. Stan urodzeniowy noworodków oceniany w skali Apgar był istotnie niższy w grupie noworodków urodzonych przez matki z serologicznymi cechami ostrej cytomegalii (

Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging

Reactive oxygen species (ROS) are highly reactive molecules, mainly generated inside mitochondria that can oxidize DNA, proteins, and lipids. At physiological levels, ROS function as “redox messengers” in intracellular signalling and regulation, whereas excess ROS induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of ROS in activation of autophagy and their importance in the regulation of aging. This review will focus on mitochondria as producers and targets of ROS and will summarize different proteins that modulate the redox state of the cell. Moreover, the involvement of ROS and mitochondria in different molecular pathways controlling lifespan will be reported, pointing out the role of ROS as a “balance of power,” directing the cell towards life or death

p66Shc Aging Protein in Control of Fibroblasts Cell Fate

Reactive oxygen species (ROS) are wieldy accepted as one of the main factors of the aging process. These highly reactive compounds modify nucleic acids, proteins and lipids and affect the functionality of mitochondria in the first case and ultimately of the cell. Any agent or genetic modification that affects ROS production and detoxification can be expected to influence longevity. On the other hand, genetic manipulations leading to increased longevity can be expected to involve cellular changes that affect ROS metabolism. The 66-kDa isoform of the growth factor adaptor Shc (p66Shc) has been recognized as a relevant factor to the oxygen radical theory of aging. The most recent data indicate that p66Shc protein regulates life span in mammals and its phosphorylation on serine 36 is important for the initiation of cell death upon oxidative stress. Moreover, there is strong evidence that apart from aging, p66Shc may be implicated in many oxidative stress-associated pathologies, such as diabetes, mitochondrial and neurodegenerative disorders and tumorigenesis. This article summarizes recent knowledge about the role of p66Shc in aging and senescence and how this protein can influence ROS production and detoxification, focusing on studies performed on skin and skin fibroblasts

Relation Between Mitochondrial Membrane Potential and ROS Formation

Mitochondria are considered the main source of reactive oxygen species (ROS) in the cell. For this reason they have been recognized as a source of various pathological conditions as well as aging. Chronic increase in the rate of ROS production is responsible for the accumulation of ROS-associated damages in DNA, proteins, and lipids and may result in progressive cell dysfunctions and, in a consequence, apoptosis, increasing the overall probability of an organism's pathological conditions. The superoxide anion is the main undesired by-product of mitochondrial oxidative phosphorylation. Its production is triggered by a leak of electrons from the mitochondrial respiratory chain and the reaction of these electrons with O-2. Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix, as well as superoxide dismutase (Cu/ ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, converts superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H2O.In the chapter we describe a relation between mitochondrial membrane potential and the rate of ROS formation. We present different methods applicable for isolated mitochondria or intact cells. We also present experiments demonstrating that a magnitude and a direction (increase or decrease) of a change in mitochondrial ROS production depend on the metabolic state of this organelle

Low-Noise SOI Hall Devices

Hall sensors are used in a very wide range of applications. A very demanding one is electrical current measurement for metering purposes. In addition to high precision and stability, a sufficiently low noise level is required. Cost reduction through sensor integration with low-voltage/low-power electronics is also desirable. The purpose of this work is to investigate the possible use of SOI (Silicon On Insulator) technology for this integration. We have fabricated SOI Hall devices exploring a wide range of silicon layer thickness and doping level. We show that noise is influenced by the presence of LOCOS and p-n depletion zones near the edges of the active zones of the devices. A proper choice of SOI technological parameters and process flow leads to up to 18 dB reduction in Hall sensor noise level. This result can be extended to many categories of devices fabricated using SOI technology

Differences in the metabolic rates of exploited and unexploited fish populations: a signature of recreational fisheries induced evolution?

Non-random mortality associated with commercial and recreational fisheries have the potential to cause evolutionary changes in fish populations. Inland recreational fisheries offer unique opportunities for the study of fisheries induced evolution due to the ability to replicate study systems, limited gene flow among populations, and the existence of unexploited reference populations. Experimental research has demonstrated that angling vulnerability is heritable in Largemouth Bass Micropterus salmoides, and is correlated with elevated resting metabolic rates (RMR) and higher fitness. However, whether such differences are present in wild populations is unclear. This study sought to quantify differences in RMR among replicated exploited and unexploited populations of Largemouth Bass. We collected age-0 Largemouth Bass from two Connecticut drinking water reservoirs unexploited by anglers for almost a century, and two exploited lakes, then transported and reared them in the same pond. Field RMR of individuals from each population was quantified using intermittent-flow respirometry. Individuals from unexploited reservoirs had a significantly higher mean RMR (6%) than individuals from exploited populations. These findings are consistent with expectations derived from artificial selection by angling on Largemouth Bass, suggesting that recreational angling may act as an evolutionary force influencing the metabolic rates of fishes in the wild. Reduced RMR as a result of fisheries induced evolution may have ecosystem level effects on energy demand, and be common in exploited recreational populations globally

p53 at the endoplasmic reticulum regulates apoptosis in a Ca2+-dependent manner

The tumor suppressor p53 is a key protein in preventing cell transformation and tumor progression. Activated by a variety of stimuli, p53 regulates cell-cycle arrest and apoptosis. Along with its well-documented transcriptional control over cell-death programs within the nucleus, p53 exerts crucial although still poorly understood functions in the cytoplasm, directly modulating the apoptotic response at the mitochondrial level. Calcium (Ca(2+)) transfer between the endoplasmic reticulum (ER) and mitochondria represents a critical signal in the induction of apoptosis. However, the mechanism controlling this flux in response to stress stimuli remains largely unknown. Here we show that, in the cytoplasm, WT p53 localizes at the ER and at specialized contact domains between the ER and mitochondria (mitochondria-associated membranes). We demonstrate that, upon stress stimuli, WT p53 accumulates at these sites and modulates Ca(2+) homeostasis. Mechanistically, upon activation, WT p53 directly binds to the sarco/ER Ca(2+)-ATPase (SERCA) pump at the ER, changing its oxidative state and thus leading to an increased Ca(2+) load, followed by an enhanced transfer to mitochondria. The consequent mitochondrial Ca(2+) overload causes in turn alterations in the morphology of this organelle and induction of apoptosis. Pharmacological inactivation of WT p53 or naturally occurring p53 missense mutants inhibits SERCA pump activity at the ER, leading to a reduction of the Ca(2+) signaling from the ER to mitochondria. These findings define a critical nonnuclear function of p53 in regulating Ca(2+) signal-dependent apoptosis

Low-noise SOI Hall devices

Hall sensors are used in a very wide range of applications. A very demanding one is electrical current measurement for metering purposes. In addition to high precision and stability, a sufficiently low noise level is required. Cost reduction through sensor integration with low-voltage/low-power electronics is also desirable. The purpose of this work is to investigate the possible use of SOI (Silicon On Insulator) technology for this integration. We have fabricated SOI Hall devices exploring a wide range of silicon layer thickness and doping level. We show that noise is influenced by the presence of LOCOS and p-n depletion zones near the edges of the active zones of the devices. A proper choice of SOI technological parameters and process flow leads to up to 18 dB reduction in Hall sensor noise level. This result can be extended to many categories of devices fabricated using SOI technology