Genetic Mapping of , a New Lethal Allele of .

The mutation was generated in a Flp/FRT EMS screen for conditional mutations that cause growth and developmental defects in a genetic background that blocks apoptosis. The mutations were conditional, based on the allele being present on the starting chromosome, and blocking canonical apoptosis in a homozygous state. The mosaic eyes exhibit defects in eye development including patches of rough eye and irregular surface structure.

Bringing the Vascular Lab Inside the Procedure Room.

The advantages of the vascular lab (VL) are a specialized knowledgeable team and a dedicated equipment which is transferrable to the procedure room to facilitate the procedure and gather information about the procedure endpoints. In this article, Registered Vascular Technologists (RVT) from various institutions discuss the basic and the complex ways the VL can be used inside a procedure room. The advantages of the vascular lab (VL) are a specialized knowledgeable team and dedicated equipment which is transferrable to the procedure room to facilitate the procedure and gather information about procedure endpoints.

Percutaneous Deep Venous Arterialization: Treatment of Patients with End-Stage Plantar Disease.

Background: Percutaneous deep venous arterialization (pDVA) is a minimally invasive technique connecting the tibial arteries below the knee to the tibial venous system into plantar venous circulation to deliver oxygenated blood to otherwise nonperfused foot. This study demonstrated outcomes of pDVA with commercially available equipment and described single-center experience on pDVA for critical limb-threatening ischemia patients with small artery diseases and end-stage plantar disease (ESPD) who were deemed no-option cases.

Methods: A single-center retrospective review was performed on patients who underwent pDVA.

Pharmacokinetics of Lidocaine and Its Metabolites Following Vaginal Administration of Lidocaine Gel to Healthy Female Subjects.

Lidocaine vaginal bioadhesive gel is being developed as a local anesthetic for use in minimally invasive outpatient gynecological procedures and was investigated in single-dose and multiple-dose studies in healthy young adult women. Lidocaine doses of 2.5%, 5%, and 10% (w/w) were administered, and parent drug and metabolites monoethylglycinexylidide and glycinexylidide were measured in plasma.

Pharmacokinetic Compatibility Study of Lidocaine with EXPAREL in Yucatan Miniature Pigs.

We explored the potential for EXPAREL to interact with lidocaine. Sixty (60) male Yucatan Swine were randomized into 20 groups (N = 3/group). EXPAREL (2 or 4 mg/kg) and/or lidocaine HCl solution 1% or 2% (with epinephrine 1 : 200,000) were injected subcutaneously along a 5 cm virtual incision line.

HLA-DQ6 and ingestion of contaminated water: possible gene-environment interaction in an outbreak of Leptospirosis.

Leptospirosis is a zoonosis that can cause severe multisystem disease. While host gene-environment interactions likely modify infectious disease susceptibility, including for leptopsirosis, this has not been documented. In a 1998 leptospirosis outbreak investigation among triathletes in a lake swim, swallowing lake-water was a disease risk-factor.

Uncoupling of 5-HT1A receptors in the brain by estrogens: regional variations in antagonism by ICI 182,780.

Previously we have shown that 17beta-estradiol (in vivo and in vitro) rapidly decreases the function of serotonin(1A) (5-HT(1A)) receptors, allowing us to hypothesize that 17beta-estradiol accomplished this via activation of a membrane estrogen receptor. Hippocampus and frontal cortex obtained from ovariectomized rats were incubated with 17beta-estradiol or bovine serum albumin (BSA)-estradiol in the presence or absence of the estrogen receptor (ER) antagonist ICI 182,780. Membranes were prepared to measure R(+)8-OH-DPAT-stimulated [(35)S]GTPgammaS binding (a measure of 5-HT(1A) receptor coupling and function).

Rapid uncoupling of serotonin-1A receptors in rat hippocampus by 17beta-estradiol in vitro requires protein kinases A and C.

17beta-Estradiol decreases R(+)8-OH-DPAT-stimulated [(35)S]GTPgammaS binding [an index of serotonin-1A (5-HT(1A)) receptor coupling] through the activation of estrogen receptors. We hypothesize that this occurs as a result of activation of protein kinase A (PKA) and/or protein kinase C (PKC) and phosphorylation of 5-HT(1A) receptors. Hippocampus from ovariectomized rats was incubated with 17beta-estradiol in HEPES buffer (37 degrees C).

Estrogen receptor-mediated neuroprotection from oxidative stress requires activation of the mitogen-activated protein kinase pathway.

It is well documented that estrogen mediates responses by both genomic and nongenomic mechanisms, both of which are important for cell survival. Because direct evidence showing that the estrogen receptors (ERs) alpha and/or beta can activate rapid signaling that may mediate neuroprotection is lacking, the hippocampal-derived cell line, HT22, was stably transfected with ERalpha (HTERalpha), ERbeta (HTERbeta), or a mutated form of ERalpha (HTERalphaHE27), which lacks the ability to mediate ER element-mediated transcription. Treatment of HT22, HTERalpha, HTERbeta, and HTERalphaHE27 cells with glutamate (5 mM) resulted in a significant decrease in cell viability.

Estrogen-mediated neuroprotection against beta-amyloid toxicity requires expression of estrogen receptor alpha or beta and activation of the MAPK pathway.

It is well documented that estrogen can activate rapid signaling pathways in a variety of cell types. These non-classical effects of estrogen have been reported to be important for cell survival after exposure to a variety of neurotoxic insults. Since direct evidence of the ability of the estrogen receptors (ERs) alpha and/or beta to mediate such responses is lacking, the hippocampal-derived cell line HT22 was stably transfected with either ERalpha (HTERalpha) or ERbeta (HTERbeta).

Acute and chronic estrogen supplementation decreases uterine sympathetic innervation in ovariectomized adult virgin rats.

Uterine innervation undergoes substantial reorganization associated with changes in reproductive status. Nerves innervating the uterus are decreased in pregnancy and puberty, and even the normal rodent estrous cycle is characterized by fluctuations in numbers of myometrial nerve fibers. During the follicular (proestrus/estrous) phase of the estrous cycle, intact nerves are rapidly depleted and then return over the next 2-3 days in the luteal (metestrus/diestrus) phase.

Estrogens act in rat hippocampus and frontal cortex to produce rapid, receptor-mediated decreases in serotonin 5-HT(1A) receptor function.

Previously our laboratory has shown that 17beta-estradiol in vivo rapidly decreases R(+)-8-OH-DPAT-stimulated [(35)S]GTPgammaS binding (a measure of the initial biochemical event in the intracellular signaling pathway associated with 5-HT(1A) receptors) in the hippocampus, frontal cortex and amygdala. Studies were designed to determine if 17beta-estradiol also acts in vitro on estrogen receptors in the hippocampus and frontal cortex to decrease 5-HT(1A) receptor function. Hippocampus and frontal cortex were dissected from ovariectomized rats and incubated for up to 3 h with various estrogens and antiestrogens; membrane homogenates were prepared for R(+)-8-OH-DPAT-stimulated [(35)S]GTPgammaS binding assays.

Acute and long-term effects of 17beta-estradiol on G(i/o) coupled neurotransmitter receptor function in the female rat brain as assessed by agonist-stimulated [35S]GTPgammaS binding.

Estrogens exert effects on mood, mental state, memory and other central nervous system (CNS) functions by modulating neurotransmitter receptor systems in the brain. Studies were designed to investigate the effect of 17beta-estradiol (E(2)) on agonist-stimulated [35S]GTPgammaS binding in membranes to assess the first step in the intracellular signal transduction cascade in a functional assay following: (1) an acute, one-time bolus subcutaneous injection, or (2) 14-day continuous exposure by a slow-release pellet implanted subcutaneously. In rats treated with E(2) acutely, the maximal response produced by activation of serotonin(1A) (5-HT(1A)) receptors was decreased approximately 25% in the hippocampus, cortex, and amygdala.

Serotonin 5-HT(1B/1D) agonist-stimulated [(35)S]GTPgammaS binding in rat and guinea pig striatal membranes.

Serotonin (5-hydroxytryptamine; 5-HT) receptor ligands were used to assess agonist-stimulated [(35)S]GTPgammaS binding in rat and guinea pig striatal membranes. The assay contained 45-60 microgram protein, 300 microM GDP and 0.1 nM [(35)S]GTPgammaS, incubated at 37 degrees C for 20 min.

Removal of femoral sheaths by registered nurses: issues and outcomes.

The results of this evaluation indicate that specially trained critical care nurses can remove femoral sheaths with an acceptable margin of safety. As a result, these nurses can provide quality, cost-effective care to angioplasty patients. However, before this procedure is included as part of the RN's responsibility, written protocols are needed to identify appropriate patients, proper removal technique, and specific actions to take if complications occur.