A Meta-Analysis of Video Modeling Interventions to Enhance Job Skills of Autistic Adolescents and Adults.

Background: Autistic transition-aged youth and young adults face many societal barriers to competitive integrated employment (CIE). Existing evidence-based practices (EBPs) for autistic individuals, such as video modeling (VM), may be a viable on-the-job training method to enhance employment experiences and outcomes for this population.

Methods: The purpose of this meta-analysis was to synthesize VM studies to teach job skills for autistic individuals.

A Review of Developing Communication Skills for Students with Intellectual and Developmental Disabilities on College Campuses.

In the current investigation, we reviewed the literature on communication interventions for individuals with intellectual and developmental disabilities (IDD) on college campuses. Eight studies met our inclusion criteria. Data were extracted related to participant demographics (e.

Structure and signaling at hydroid polyp-stolon junctions, revisited.

The gastrovascular system of colonial hydroids is central to homeostasis, yet its functional biology remains poorly understood. A probe (2',7'-dichlorodihydrofluorescein diacetate) for reactive oxygen species (ROS) identified fluorescent objects at polyp-stolon junctions that emit high levels of ROS. A nuclear probe (Hoechst 33342) does not co-localize with these objects, while a mitochondrial probe (rhodamine 123) does.

Within-colony migration of symbionts during bleaching of octocorals.

Octocorals compose a major part of cnidarian diversity. As with other symbiont-containing cnidarians, octocorals are susceptible to a stress response and subsequent "bleaching," which typically involves the loss of photosynthetic dinoflagellate symbionts. Studies of bleaching often focus on hexacorals, including sea anemones and scleractinians.

Causes and consequences of stolon regression in a colonial hydroid.

A cnidarian colony can be idealized as a group of feeding polyps connected by tube-like stolons. Morphological variation ranges from runner-like forms with sparse polyp and stolon development to sheet-like forms with dense polyp and stolon development. These forms have typically been considered in a foraging context, consistent with a focus on rates of polyp development relative to stolon elongation.

Circulation of fluids in the gastrovascular system of a stoloniferan octocoral.

Cilia-based transport systems characterize sponges and placozoans. Cilia are employed in cnidarian gastrovascular systems as well, but typically function in concert with muscular contractions. Previous reports suggest that anthozoans may be an exception to this pattern, utilizing only cilia in their gastrovascular systems.

Physiological characterization of stolon regression in a colonial hydroid.

As with many colonial animals, hydractiniid hydroids display a range of morphological variation. Sheet-like forms exhibit feeding polyps close together with short connecting stolons, whereas runner-like forms have more distant polyps and longer connecting stolons. These morphological patterns are thought to derive from rates of stolon growth and polyp formation.

Ameliorative effects of exposing DBA/2J mice to an augmented acoustic environment on histological changes in the cochlea and anteroventral cochlear nucleus.

DBA/2J (D2) mice, which exhibit very early progressive sensorineural hearing loss, were treated nightly with an augmented acoustic environment (AAE) initiated before the onset of hearing, and consisting of repetitive bursts of a 70-dB sound pressure level (SPL), 4-25 kHz noise band. At 55 days of age, AAE-treated mice exhibited less elevation of auditory brainstem response thresholds, fewer missing hair cells, and greatly reduced loss of anteroventral cochlear nucleus (AVCN) volume and neuron number compared to untreated control mice. It was hypothesized that the central neuroprotective effect was associated with increased afferent input to AVCN neurons evoked by the AAE as well as a healthier cochlea.

Effects of prolonged exposure to an augmented acoustic environment on the auditory system of middle-aged C57BL/6J mice: cochlear and central histology and sex differences.

Genetic progressive sensorineural hearing loss in mice of the C57BL/6J (B6) inbred strain begins at high frequencies during young adulthood and is severe by 12 months (middle age). Nightly treatment with an augmented acoustic environment (AAE)--12-hour periods of exposure to repetitive noise bursts of moderate intensity, begun at age 25 days--resulted in less severe hearing loss compared with control mice. Cochlear histopathological correlates of AAE treatment, assessed at 12-14 months of age, included lessened severity of progressive loss of outer hair cells in both sexes as well as small savings of spiral ganglion cells in females and inner hair cells in males.

DNA double strand breaks occur independent of AID in hypermutating Ig genes.

Somatic hypermutation (SHM) and class switch recombination (CSR) take place in B cells of the germinal center (GC) and are associated with DNA double-strand breaks (DNA-DSBs). Transcription favors the generation of DNA-DSBs in the V-regions and switch regions of Ig genes. Both SHM and CSR are controlled by the Activation Induced Cytidine Deaminase (AID), an enzyme exclusively expressed in B cells of the GC.

Somatic hypermutation does not require Rad54 and Rad54B-mediated homologous recombination.

Secondary diversification of immunoglobulin (Ig) genes occurs through somatic hypermutation (SHM) in B cells of the germinal center (GC). The GC reaction is associated with a high frequency of DNA double-strand breaks (DSB) in the hypermutation domain of Ig genes. Homologous recombination (HR) is a prominent DSB repair pathway.

DNA double-strand breaks: prior to but not sufficient in targeting hypermutation.

The activation-induced cytidine deaminase (AID) is required for somatic hypermutation (SHM) and class-switch recombination (CSR) of immunoglobulin (Ig) genes, both of which are associated with DNA double-strand breaks (DSBs). As AID is capable of deaminating deoxy-cytidine (dC) to deoxy-uracil (dU), it might induce nicks (single strand DNA breaks) and also DNA DSBs via a U-DNA glycosylase-mediated base excision repair pathway ('DNA-substrate model'). Alternatively, AID functions like its closest homologue Apobec1 as a catalytic subunit of a RNA editing holoenzyme ('RNA-substrate model').

The total number of neurons and calcium binding protein positive neurons during aging in the cochlear nucleus of CBA/CaJ mice: a quantitative study.

The quantitative stereological method, the optical fractionator, was used for determining the total number of neurons and the total number of neurons immunostained with parvalbumin, calbindin-D28k (calbindin), and calretinin in the dorsal and posteroventral cochlear nucleus (DCN and PVCN) in CBA/CaJ (CBA) mice during aging (1-39 months old). CBA mice have only a modest sensorineural pathology late in life. An age-related decrease of the total number of neurons was demonstrated in the DCN (r=-0.

Towards an understanding of somatic hypermutation.

How germinal center (GC) B cells diversify their rearranged immunoglobulin genes by somatic hypermutation is unknown. However, the GC-specific activation-induced cytidine deaminase has been identified as a key factor controlling two central GC-specific events: somatic hypermutation and class-switch recombination of immunoglobulin genes. This factor may function as a catalytic subunit of an RNA-editing complex or, more directly, on DNA as a deoxy-cytidine deaminase in the hypermutation domain and class-switch region.

Indirect and direct evidence for DNA double-strand breaks in hypermutating immunoglobulin genes.

The generation of a diverse antigen receptor repertoire is fundamental for the functionality of the adaptive immune system. While the V(D)J recombination process that generates the primary antigen receptor repertoire is understood in great detail, it is still unclear by which mechanism immunoglobulin (Ig) genes are further diversified by somatic hypermutation. Using mouse strains that carry a non-functional, pre-defined V(H)D(H)J(H) gene segment in their IgH locus we demonstrate DNA double-strand breaks (DSBs) in and around V(H)D(H)J(H) in B cells undergoing somatic hypermutation.

DNA double-strand breaks in immunoglobulin genes undergoing somatic hypermutation.

How rearranged immunoglobulin (Ig) genes are further diversified by somatic hypermutation is unknown. Using VDJ passenger Ig heavy chain (IgH) knockin mouse strains, we now demonstrate a high frequency of DNA double-strand breaks (DSBs) in the targeted VDJ passenger gene of germinal center (GC) B cells. These DSBs parallel the distribution of mutations in the targeted hypermutation domain and are found preferentially at RGYW motifs, the intrinsic hot spots of somatic hypermutation.

Purkinje cell degeneration and control mice: responses of single units in the dorsal cochlear nucleus and the acoustic startle response.

The cartwheel cell is the most numerous inhibitory interneuron of the dorsal cochlear nucleus (DCN). It is expected to be an important determinant of DCN function. To assess the contribution of the cartwheel cell, we examined the discharge characteristics of DCN neurons and behavioral measures in the Purkinje cell degeneration (pcd) mice, which lack cartwheel cells, and compared them to those of the control mice.

A radiation hybrid map of the zebrafish genome.

Recent large-scale mutagenesis screens have made the zebrafish the first vertebrate organism to allow a forward genetic approach to the discovery of developmental control genes. Mutations can be cloned positionally, or placed on a simple sequence length polymorphism (SSLP) map to match them with mapped candidate genes and expressed sequence tags (ESTs). To facilitate the mapping of candidate genes and to increase the density of markers available for positional cloning, we have created a radiation hybrid (RH) map of the zebrafish genome.

Glycine immunoreactivity and receptor binding in the cochlear nucleus of C57BL/6J and CBA/CaJ mice: effects of cochlear impairment and aging.

Glycinergic neurons in the cochlear nucleus (CN) of C57BL/6J (C57) and CBA/CaJ (CBA) mice were studied by using immunocytochemical and receptor-binding techniques. Adult C57 mice exhibit progressive cochlear pathology as they age, whereas aging CBA mice retain good hearing. In the CN of old C57 mice (18 months) with severe hearing loss, the number of glycine-immunoreactive neurons decreased significantly.

Morphological changes in the anteroventral cochlear nucleus that accompany sensorineural hearing loss in DBA/2J and C57BL/6J mice.

Morphological measurements were made on histological sections of the anteroventral cochlear nucleus (AVCN) in mice of the DBA/2J and C57BL/6J strains to determine the effects of sensorineural cochlear pathology on the number, packing density, and size of neurons and on AVCN volume. Both strains possess alleles that cause progressive cochlear pathology initially affecting the organ of Corti: in DBA mice, hearing loss is evident at 4 weeks of age and progresses rapidly; in C57 mice, hearing loss begins after 2 months of age and progresses more slowly. In both strains AVCN volume decreased, some loss of neurons occurred, and these changes paralleled the progression of peripheral hearing loss.

Morphology of the cochlear nucleus in CBA/J mice with chronic, severe sensorineural cochlear pathology induced during adulthood.

The effects of chronic cochlear impairment on morphological features of the adult cochlear nucleus (CN) were assessed in CBA/J mice in which severe sensorineural damage had been induced by exposure to intense noise. Sections from various CN subdivisions, stained for Nissl substance and fibers, were quantitatively evaluated in four groups of noise-exposed mice that differed with regard to the age at noise exposure (2, 6, or 11 months), age at the time the CN was evaluated (6, 11, or 24 months), and the duration (chronicity) of sensorineural impairment (4, 5, 13, or 18 months). Like-aged, non-exposed CBA mice were used as controls, so the effects of peripheral damage and aging could be compared.

Morphology of the inferior colliculus in C57BL/6J and CBA/J mice across the life span.

Basic anatomical features were evaluated in the inferior colliculus (IC) of C57BL/6J and CBA/J mice across the adult life span (1.5 to 30 months of age). C57BL/6J mice exhibit progressive age-related cochlear pathology and become severely hearing-impaired during the second year of life; CBA/J mice exhibit little hearing loss as they age.

Morphology of the dorsal cochlear nucleus in C57BL/6J and CBA/J mice across the life span.

The morphology of the dorsal cochlear nucleus (DCN) was evaluated across the life span in inbred C57BL/6J (C57) and CBA/J (CBA) mice using 5 age groups (young adult to very old). C57 mice exhibit progressive cochlear sensorineural pathology and hearing loss during middle age; CBA mice have only modest sensorineural pathology late in life. DCN layers I, II, and III were evaluated histologically with serial sections stained for Nissl and fibers.

Morphology of the octopus cell area of the cochlear nucleus in young and aging C57BL/6J and CBA/J mice.

The influence of aging and age-related cochlear impairment on the ventral cochlear nucleus was evaluated by measuring morphological properties of the octopus cell area (OCA) in five age groups of inbred C57BL/6J and CBA/J mice (young adult to very old). The former strain demonstrates progressive cochlear sensorineural pathology and hearing loss during middle age; the latter has only modest sensorineural pathology late in life. Histological sections of the OCA were evaluated with serial sections and several strains for neurons, glia, and fibers, and Golgi impregnations were also used.