A description of a male-focused breastfeeding promotion corporate lactation program.

The role of the father has been identified as one of the strongest influences on the initiation and duration of breastfeeding by mothers in the United States. This report describes a corporate lactation program that focuses on promoting breastfeeding through male employees. Since 1990, a full-time on-site lactation program has been offered to male employees at the Los Angeles Department of Water and Power, a public utility company. The male program participants are from diverse backgrounds. Participation in the Fathering Program has grown since 1990 based on word of mouth, fathers' interest in the benefits of breastfeeding for the infant, and the female partners' interest in getting a free pump rental. This report illustrates the viability of a breastfeeding support program that targets male employees and that is offered in a corporate setting.     

Training parents as behavior therapists for their autistic children

This review examines the use of behavioral procedures with autistic children. There is a focus on the role of parents as teachers, particularly in the acquisition of language. The use of parents as teachers is placed in an historical context and procedures for teaching speech are described in some detail. There is consideration of the importance of language environment for facilitating speech. Finally, the authors examine the clinical usues that arise in parent training.     

Fas (CD95) participates in peripheral T cell deletion and associated apoptosis in vivo

Following exposure to some types of antigen (superantlgens),responsive T cells expand and then decline in numbers, a phenomenonthat has been called ‘peripheral deletion’. Thisprocess may play a role in limiting autoimmune reactions andin the maintenance of immune homeostasis. Here we describe experimentson peripheral deletion in mice carrying the Ipr/lpr defect,which has been shown to be due to defective production of theCD95/Fas molecule. Young Ipr/lpr mice with no apparent Immunologlcabnormalities display a defect in bacterial superantlgen-inducedperipheral deletion. Apoptotic death of the expanded T cellpopulation associated with such peripheral deletion in normalanimals is dramatically reduced in the mutant mice. Further,the levels of Fas on responding cells in normal mice Increasesand decreases together with increases and decreases in cellnumbers, suggesting that cells with the highest levels of Fasare preferentially deleted. These observations are consistentwith the known ability of CD95 to transduce a signal leadingto apoptosis, and they implicate this signal transduction pathwayIn peripheral deletion. In contrast, bacterial superantigen-induceddeletion of thymocytes appears to be fully functional in thesemice, and thus Fas/APO-1 does not appear to be required forthis process. Further, antibody ligatlon of the TCR on activatedT cells from normal or young Ipr/lpr mice can induce apoptosisand therefore under some circumstances this phenomenon is notdependent upon CD95/Fas. Thus, to avoid autoreactivity and ensureimmune homeostasis, several different apoptotic mechanisms existIn peripheral T lymphocytes, only some of which involve Fas.Defects in one or more of these mechanisms may have profounddeleterious consequences.     

Mechanism of hERG K+ channel blockade by the fluoroquinolone antibiotic moxifloxacin

The fluoroquinolone antibiotic moxifloxacin has been associated with the acquired long QT syndrome and is used as a positive control in the evaluation of the QT-interval prolonging potential of new drugs. In common with other QT-prolonging agents, moxifloxacin is known to inhibit the hERG potassium K+ channel, but at present there is little mechanistic information available on this action. This study was conducted in order to characterise the inhibition of hERG current (I(hERG)) by moxifloxacin, and to determine the role in drug binding of the S6 aromatic amino-acid residues Tyr652 and Phe656. hERG currents were studied using whole-cell patch clamp (at room temperature and at 35-37 degrees C) in an HEK293 cell line stably expressing hERG channels. Moxifloxacin reversibly inhibited currents in a dose-dependent manner. We investigated the effects of different voltage commands to elicit hERG currents on moxifloxacin potency. Using a 'step-ramp' protocol, the IC50 was 65 microM at room temperature and 29 microM at 35 degrees C. When a ventricular action potential waveform was used to elicit currents, the IC50 was 114 microM. Block of hERG by moxifloxacin was found to be voltage-dependent, occurred rapidly and was independent of stimulation frequency. Mutagenesis of the S6 helix residue Phe656 to Ala failed to eliminate or reduce the moxifloxacin-mediated block whereas mutation of Tyr652 to Ala reduced moxifloxacin block by approximately 66%. Our data demonstrate that moxifloxacin blocks the hERG channel with a preference for the activated channel state. The Tyr652 but not Phe656 S6 residue is involved in moxifloxacin block of hERG, concordant with an interaction in the channel inner cavity.