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Investigation on metal ion (Cd2+and Pb2+) retention within the embryonic shell of Tachypleus gigas embryos was investigated. Inductively coupled plasma optical emission spectrometry was used for metal observations whereas developmental abnormalities were observed using a scanning electron microscope and histology via Harrison-Eosin staining. Metal ions penetrate and regulate between the extra- and embryonic shell environments to cause delayed embryogenesis only in early embryonic stages (Stages-E and DE). Ionic regulation was studied and findings showed that the embryonic shell (ES) was capable of selecting required ions whereas the extra-embryonic shell (EES) having higher retention potential. Throughout the 34 d of exposure, Se2+was accumulated in the yolk mass (YM). Ionic regulation of embryos was influenced by stocking density and concentration of metabolites. Bioaccumulation factor revealed accumulation potential as EES > ES > YM and thus EES is suitable for biological membrane development. The mechanism of ionic regulation in the ES membrane can be used as a model to design a biological membrane capable of removing metals from polluted waters.

Irritability and aggression are among the most common reasons that children are referred to outpatient mental health services and represent symptoms of several child psychiatric disorders. Over the past 40 years, several types of psychosocial interventions have been developed to treat these problems. This review examines well-established interventions for childhood irritability and aggression as well as newer interventions with a growing evidence base.

This study examined the cross-sectional relationships between neighborhood social composition and gentrification, and acculturation stressors.

ABSTRACTThe increasing prevalence of extremely low frequency electromagnetic fields (ELF-EMFs) exposure has raised considerable public concern regarding the potential hazardous effects of ELF-EMFs on male reproductive function. Increasing evidence indicates that miRNAs are necessary for spermatogenesis and male fertility. However, the regulation of miRNA expression and the roles of miRNAs in response to ELF-EMFs remain unclear. In our study, mouse spermatocyte-derived GC-2 cells were intermittently exposed to a 50 Hz ELF-EMF for 72 h (5 min on/10 min off) at magnetic field intensities of 1 mT, 2 mT and 3 mT. MiR-26b-5p was differentially expressed in response to different magnetic field intensities of ELF-EMFs. The host gene CTDSP1 showed an unmethylation status in GC-2 cells at different magnetic field intensities of ELF-EMF exposure. MiR-26b-5p had no significant, obvious influence on the cell viability, apoptosis or cell cycle of GC-2 cells. However, the overexpression of miR-26b-5p significantly decreased the percentage of G0/G1 phase cells and slightly increased the percentage of S phase cells compared to the sham group that was exposed to a 50 Hz ELF-EMF. Computational algorithms identified Cyclin D2 (CCND2) as a direct target of miR-26b-5p. MiR-26b-5p and a 50 Hz ELF-EMF altered the expression of CCND2 at both the mRNA and protein levels. Overexpressed miR-26b-5p in GC-2 cells can change the mRNA expression of CCND2 following 50 Hz ELF-EMF at 3 mT. These findings demonstrate that miR-26b-5p could serve as a potential biomarker following 50 Hz ELF-EMF exposure, and miR-26b-5p-CCND2-mediated cell cycle regulation might play a pivotal role in the biological effects of ELF-EMFs.

Copper bis(4‐ethyl‐3‐thiosemicarbazonato) acenaphthenequinone (1) and copper bis(4‐methyl‐3‐thiosemicarbazonato) acenaphthenequinone (2) are synthesized and characterized in solution, in the solid state, and radiolabeled. Serum‐protein binding radioassays show good stability in solution and about 25 % binding to protein over 1 h, which is comparable with the hypoxia selective tracer [64Cu(ATSM)]. Cyclic voltammetry shows fast and reversible reduction at redox potentials similar to the values known for hypoxia‐selective copper compounds. However, despite this, complex 1does not show any hypoxic‐selective uptake in HeLa cells over 1‐h standard assays. Possible reasons for this are studied by using the intrinsic fluorescence of the CuIIcomplexes to determine the cellular distributions and uptake mechanism by confocal microscopy. The complexes are found to bind to the external cell membrane and disperse evenly in the cytoplasm only after a very slow cell internalization (>1 h). No significant changes in distribution are observed by fluorescence imaging under hypoxic conditions. The rate of localization in the cytoplasm contrasts with their ZnIIanalogues, which are known to have fast cell uptake (up to 20 min) and a clear localization in lysosomes and mitochondria. The cytotoxicity mechanism of 1over 24 h against a number of adherent cell lines is seen to be by membrane disruption and is of a comparable magnitude to that of [Cu(ATSM)], as demonstrated by methyl tetrazolium (MTT) and lactate dehydrogenase (LDH) assays.

QA3 is a derivative of the substituted 1,3-dimethyl-1H-quinoxalin-2-ones, which are compounds that may selectively antagonize P-glycoprotein (P-gp) in multidrug resistance (MDR) cancer cells. Our previous work identified QA3 as a candidate compound for reversing MDR in cancer cells. In the present study, we found that QA3 significantly decreases the intracellular level of ATP, stimulates ATPase activity in membrane microsomes and decreases protein kinase C (PKC) activity. These results indicated that QA3 inhibits P-gp activity by blocking ATP hydrolysis and ATP regeneration. Furthermore, QA3 triggered and increased adriamycin-induced K562/A02 cell apoptosis as evidenced by Annexin V-FITC plus PI staining. Western blot analysis showed that the levels of cleaved caspase-9 and cleaved caspase-3 proteins increased, and similarly, the levels of procaspase-9 and procaspase-3 decreased after QA3 treatment. Consequently, poly ADP-ribose polymerase (PARP) activity increased as evidenced by the presence of the PARP cleavage product in K562/A02 cells. QA3 also enhanced the potency of adriamycin against K562/A02 cells as demonstrated by increased apoptosis and activation of caspase-9,-3 and PARP. These data support the observation that P-gp activity is inhibited after QA3 treatment. Moreover, these results indicate that QA3 is a novel MDR reversal agent with potent inhibitory action against P-gp MDR cancer cells.

The serine/threonine kinase Pak1 is a target of the RhoGTPases Rac and Cdc42 and an important regulator of cell morphology and migration. Recent work from several laboratories has indicated that Pak1 controls microtubule dynamics as well as the organisation of F-actin microfilaments. Pak1 is phosphorylated on T212 by the p35/Cdk5 or cyclin B1/Cdc2 kinase in postmitotic neurones and mitotic cells, respectively. To understand its function during development, we have carried out a detailed temporal and spatial analysis of Pak1 expression and phosphorylation on T212. In the embryonic forebrain, Pak1 and Pak1T212(PO4) were seen to accumulate in the corpus callosum, intermediate zone, lateral olfactory tracts, and anterior commissures. Epithelial cells of the mouse embryo lung, kidney, intestine, and skin also exhibited high levels of Pak1 and Pak1T212(PO4), suggesting a previously unsuspected role in epithelial differentiation. Pak1T212(PO4) was undetectable in all adult tissues. Together, these data indicate a specific, developmentally regulated role of the Pak1 kinase. Developmental Dynamics 228:121–127, 2003. © 2003 Wiley-Liss, Inc.

Iron has outstanding biological importance as it is required for a wide variety of essential cellular processes and, as such, is a vital nutrient. The element holds this central position by virtue of its facile redox chemistry and the high affinity of both redox states (iron II and iron III) for oxygen. These same properties also render iron toxic when its redox-active chelatable ‘labile’ form exceeds the normal binding capacity of the cell. Indeed, in contrast to iron bound to proteins, the intracellular labile iron (LI) can be potentially toxic especially in the presence of reactive oxygen species (ROS), as it can lead to catalytic formation of oxygen-derived free radicals such as hydroxyl radical that ultimately overwhelm the cellular antioxidant defense mechanisms and lead to cell damage. While intracellular iron homeostasis and body iron balance are tightly regulated to minimise the presence of potentially toxic LI, under conditions of oxidative stress and certain pathologies, iron homeostasis is severely altered. This alteration manifests itself in several ways, one of which is an increase in the intracellular level of potentially harmful LI. For example acute exposure of skin cells to ultraviolet A (UVA, 320–400 nm), the oxidising component of sunlight provokes an immediate increase in the available pool of intracellular LI that appears to play a key role in the increased susceptibility of skin cells to UVA-mediated oxidative membrane damage and necrotic cell death. The main purpose of this overview is to bring together some of the new findings related to intracellular LI distribution and trafficking under physiological and patho-physiological conditions as well as to discuss mechanisms and consequences of oxidant-induced alterations in the intracellular pool of LI, as exemplified by UVA radiation.