Cause or prevention of breast cancer with estrogens: analysis from tumor biologic data, growth kinetic model and Women's Health Initiative study.

The existing medical literature suggests that estrogens may cause breast cancer but, paradoxically, can also prevent this neoplasm under specific circumstances. Appropriate interpretation of this complex data requires an understanding of emerging concepts of tumor biology. A substantial body of data, including animal models and epidemiologic studies, suggests that estrogens contribute to the development of breast cancer.

Elective intubation.

Endotracheal intubation is a commonly performed operating room (OR) procedure that provides safe delivery of anesthetic gases and airway protection during surgery. The most common intubation technique in the perioperative environment is direct laryngoscopy with orotracheal tube insertion. Infrequently, difficulties that require an alternative intubation technique are encountered due to patient anatomy, equipment limitations, or patient pathophysiology.

Inhibition of deprivation-induced food intake by GABA(A) antagonists: roles of the hypothalamic, endocrine and alimentary mechanisms.

The role of gamma amino butyric acid A receptors/neurons of the hypothalamic, endocrine and alimentary systems in the food intake seen in hunger was studied in 20 h food-deprived rats. Food deprivation decreased blood glucose, serum insulin and produced hyperphagia. The hyperphagia was inhibited by subcutaneous or ventromedial hypothalamic administration of gamma amino butyric acid A antagonists picrotoxin or bicuculline.

Incidence of protein on actin bridges between endothelium and smooth muscle in arterioles demonstrates heterogeneous connexin expression and phosphorylation.

Although much physiology in resistance vessels has been attributed to the cytoplasmic connection between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), little is known of the protein expression between the two cell types. In an attempt to identify the proteins between ECs and VSMCs, mouse cremaster arterioles were stained with phalloidin-Alexa 594 and viewed on a confocal microscope that resolved "actin bridges" within the internal elastic lamina between ECs and VSMCs. To determine the incidence of protein, the pixel intensity from the antibodies on actin bridges were compared with the pixel intensity from antibodies within ECs or VSMCs.

Differential gene expression among the proximal segments of the rat epididymis is lost after efferent duct ligation.

The epididymis has traditionally been divided into the caput, corpus, and cauda regions, which are further organized into intraregional segments. In the rat and mouse, these segments have high degrees of transcriptional differentiation, and what has traditionally been called the initial segment of the rat epididymis actually consists of three transcriptionally different intraregional segments. These segments are regulated by endocrine, lumicrine, and paracrine factors, whose relative importance remains a topic of investigation.

Caspase-9-dependent pathway to murine germ cell apoptosis: mediation by oxidative stress, BAX, and caspase 2.

Ischemia-reperfusion (IR) of the testis results in germ-cell-specific apoptosis (GCA) and a reduction in daily sperm production. This has been correlated with and is dependent upon neutrophil recruitment to the testis. In a rat model of testicular IR, this has also been correlated with an increase in reactive oxygen species (ROS).

Caspase 2 activity contributes to the initial wave of germ cell apoptosis during the first round of spermatogenesis.

Early in postnatal life the first phase of spermatogenesis is accompanied by an initial wave of germ cell apoptosis. This wave of germ cell death is thought to reflect an adjustment of germ cell numbers that can be adequately maintained by Sertoli cells. Caspase 2 is an initiator caspase whose activation has been found to stimulate apoptosis through the mitochondria.

Lidocaine block of neonatal Nav1.3 is differentially modulated by co-expression of beta1 and beta3 subunits.

The effects of lidocaine on neonatal Na(v)1.3 (Na(v)1.3n) expressed alone and in combination with beta1 and beta3 subunits in Xenopus oocytes were examined.

Ischemia-reperfusion of the murine testis stimulates the expression of proinflammatory cytokines and activation of c-jun N-terminal kinase in a pathway to E-selectin expression.

Ischemia-reperfusion (IR) of the testis results in germ cell-specific apoptosis and can lead to aspermatogenesis. Germ cell-specific apoptosis after IR of the testis has been shown to be correlated with and dependent on neutrophil recruitment to the testis after IR. Studies that used E-selectin-deficient mice have demonstrated that E-selectin expression is critical for neutrophil recruitment to subtunical venules in the testis after IR and for the resultant germ cell-specific apoptosis.

5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.

Hox genes determine the formation of segmented structures during development. The epididymis shows a segmented organization in its structure and function beyond embryogenesis. This study examined the adult mouse epididymis and vas deferens for expression of 5' hox genes and a hox-DNA binding cofactor.

Peptide and nonpeptide reactive oxygen scavengers provide partial rescue of the testis after torsion.

Ischemia-reperfusion (IR) of the testis results in germ cell-specific apoptosis, followed by a reduction in testis weight and daily sperm production (DSP). This has been associated with an increase in the adhesion of neutrophils to testicular subtunical venules and an increase in reactive oxygen species (ROS). The present study investigated: 1) the effects of a direct, non-IR-related ROS insult to the testis and 2) the effects of catalase, superoxide dismutase (SOD), and a novel nonpeptide mimic of SOD, M40403, on neutrophil recruitment, ROS production, testis weight, and DSP following IR of the rat testis.

ATM-dependent dissociation of B55 regulatory subunit from nuclear PP2A in response to ionizing radiation.

Ionizing radiation (IR) is known to activate multiple cell cycle checkpoints that are thought to enhance the ability of cells to respond to DNA damage. Protein phosphatase 2A (PP2A) has been implicated in IR-induced activation of checkpoints; therefore, Jurkat cells were exposed to an activating dose of IR or sham treatment as control, and nuclear extracts were analyzed for PP2A by Mono Q anion exchange chromatography and microcystin affinity chromatography. PP2A exists in eukaryotic cells both as a heterodimer consisting of a 65-kDa scaffolding subunit (A) plus a 36-kDa catalytic subunit (C) and as ABC heterotrimers, containing one of a variety of regulatory (B) subunits.

Color Doppler ultrasonography of the superior mesenteric artery for prenatal ultrasonographic diagnosis of a left-sided congenital diaphragmatic hernia.

The incidence of congenital diaphragmatic hernia (CDH) has been estimated as 1 per 2000 to 1 per 4000 births. The etiology of the malformation is unknown, but it has been reported in association with maternal administration of medications such as thalidomide or antiepileptics before closure of the pleuroperitoneal canal at 9 to 10 weeks' gestation as well as having a familial inheritance pattern. Congenital diaphragmatic hernia is associated with other congenital anomalies in 25% to 57% of cases and with chromosomal abnormalities in 10% to 20% of cases.

Histone H1 and H3 dephosphorylation are differentially regulated by radiation-induced signal transduction pathways.

We recently demonstrated that linker histone H1, which is thought to have a fundamental role in higher-order chromatin structure, becomes transiently dephosphorylated after ionizing radiation (IR) in a mutated ataxia telangiectasia (ATM) dependent manner. To establish whether H1 dephosphorylation was a component of a damage-response pathway that included dephosphorylation of other histones, we asked whether H3 was dephosphorylated in response to IR in a manner similar to H1. H1 and H3 are maximally phosphorylated in metaphase and both are dephosphorylated after IR.

Effects of volatile anesthetics on the direct and indirect protein kinase C-mediated enhancement of alpha1E-type Ca(2+) current in Xenopus oocytes.

The effect of the volatile anesthetics (VAs) halothane (0.59 mM) and isoflurane (0.70 mM) on protein kinase C (PKC)-mediated modulation of alpha1E type of high-voltage-gated Ca(2+) channels was examined in Xenopus oocytes coexpressing m1 muscarinic acetylcholine receptors.

Histone H1 dephosphorylation is mediated through a radiation-induced signal transduction pathway dependent on ATM.

Ionizing radiation is known to activate multiple signal transduction pathways, but the targets of these pathways are poorly understood. Phosphorylation of histone H1 is thought to have a role in chromatin condensation/decondensation, and we asked whether ionizing radiation (IR) would alter H1 phosphorylation. Our data demonstrate that low doses of IR result in a dramatic, but transient, dephosphorylation of H1 isoforms.