A Study of Needs Assessment Methods Used for Program Development in Adult Education

The Problem. The problem of this study was to evaluate methods employed in identifying needs for program development in adult education among selected public community colleges in the United States. (Abstract shortened.

Sex Difference in Calbindin Cell Number in the Mouse Preoptic Area: Effects of Neonatal Estradiol and Bax Gene Deletion

The sexually dimorphic nucleus of the preoptic area (SDN-POA) was first discovered in rats and is one of the most famous and best studied sex differences in the field of neuroscience. Though well documented in rats (larger in males than females), this sex difference was only recently able to be observed in mice due to the discovery of the protein calbindin-D28k as a marker. Recent studies have shown a larger, more distinct calbindin-immunoreactive (ir) cell cluster in male mice compared to females. However, the exact location of the cluster and whether the sex difference is one of total cell number or cell distribution remains unclear. In this study, we use defined contours to demonstrate that male mice have more calbindin-ir cells than females both in the central cell cluster and areas surrounding the cluster. We also report a full masculinization of these characteristics in females given a single injection of estradiol benzoate (EB) on the day of birth. The potential role of cell death in the development of this sex difference was tested using mice with a deletion of the bax gene, which codes for a pro death factor required for the establishment of other sex differences in the mouse brain. We demonstrate that bax knockout (KO) mice have more cells in the POA region in general, but eliminating cell death does not affect the development of the sex difference in calbindin-ir cell number, nor does it affect calbindin-ir cell spread. Taken together, this suggests that cell death is not a significant underlying mechanism in the establishment of the sex difference in the calbindin-ir cell cluster in the mouse POA

Risks of alcohol-attributable hospitalisation and death in Australia over time: Evidence of divergence by region, age and sex.

BackgroundPast reports on trends of alcohol consumption and related harm have generally been descriptive in nature and have not provided evidence of whether changes over time are significant.AimsWe investigated whether: (i) the risk of alcohol-attributable hospitalisation and death between 1994 and 2005 for three different age groups changed significantly across all Australian jurisdictions; and (ii) the relative rates of hospitalisation for males and females changed over time.MethodEstimates of alcohol-attributable hospitalisations and deaths were calculated using the aetiologic fraction method. Hospitalisations and deaths were grouped by age: 15-29 years, 30-44 years and 45+ years. Risk estimates and risk differences were analysed using Poisson regression.ResultsRisk of alcohol-attributable hospital separations increased nationally and across most jurisdictions throughout the study period. Male and female rates converged over time. Alcohol-attributable deaths decreased nationally across the three age groups and across several jurisdictions beginning in the mid-1990s.ConclusionNationally, alcohol-attributable deaths declined while hospitalisations rose. However, states with higher population density tended to drive national rates, with considerable variation by jurisdiction. The conditions which dominated hospitalisations (e.g. alcohol dependence, falls) differed substantially from those underlying alcohol-attributable deaths (e.g. alcoholic liver cirrhosis, road crashes). Jurisdictional variation in death and hospitalisations rates as well as changes over time may be partly due to differences in: regulation of alcohol supply; patterns and levels of alcohol consumption; the nature and effectiveness of law enforcement; demographic characteristics of general and sub-populations; and medical health services and screening for chronic conditions

Effects of blocking developmental cell death on sexually dimorphic calbindin cell groups in the preoptic area and bed nucleus of the stria terminalis

Background: Calbindin-D28 has been used as a marker for the sexually dimorphic nucleus of the preoptic area (SDN-POA). Males have a distinct cluster of calbindin-immunoreactive (ir) cells in the medial preoptic area (CALB-SDN) that is reduced or absent in females. However, it is not clear whether the sex difference is due to the absolute number of calbindin-ir cells or to cell position (that is, spread), and the cellular mechanisms underlying the sex difference are not known. We examined the number of cells in the CALB-SDN and surrounding regions of C57Bl/6 mice and used mice lacking the pro-death gene, Bax, to test the hypothesis that observed sex differences are due to cell death. Methods: Experiment 1 compared the number of cells in the CALB-SDN and surrounding regions in adult males, females, and females injected with estradiol benzoate on the day of birth. In experiment 2, cell number in the CALB-SDN and adjacent regions were compared in wild-type and Bax knockout mice of both sexes. In addition, calbindin-ir cells were quantified within the principal nucleus of the bed nucleus of the stria terminalis (BNSTp), a nearby region that is larger in males due to Bax-dependent cell death. Results: Males had more cells in the CALB-SDN as well as in surrounding regions than did females, and estradiol treatment of females at birth masculinized both measures. Bax deletion had no effect on cell number in the CALB-SDN or surrounding regions but increased calbindin-ir cell number in the BNSTp. Conclusions: The sex difference in the CALB-SDN of mice results from an estrogen-dependent difference in cell number with no evidence found for greater spread of cells in females. Blocking Bax-dependent cell death does not prevent sex differences in calbindin-ir cell number in the BNST or CALB-SDN but increases calbindin-ir cell number in the BNSTp of both sexes

Ultrasonic Synthetic-Aperture Holographic Imaging†

Ultrasonic reflection imaging has become an important tool in NDE [1,2,3]. The lateral resolution of such images is limited by the aperture size of the transducer, while the depth resolution is limited by the pulse length. In addition, for a given aperture diameter, the lateral resolution degrades with depth as given by the Rayleigh criterion. In this paper we discuss a method to increase the effective aperture through aperture synthesis. Waveform data, collected from a scanned transducer focused near the surface of the sample, is coherently processed to yield a synthesized aperture which can be focused to any depth with constant resolution. The synthetic aperture method allows efficient volume inspection by trading off scan time with processing time, the latter of which is constantly decreasing with increasing computing power

Quantitative proteomic analysis of the effect of 24(S),25-epoxycholesterol on SN4741 neuron cells.

Oxysterols are oxygenated derivatives of cholesterol or its precursors. One oxysterol, 24(S),25-epoxycholesterol (24(S),25-EC), which results from a shunt in the cholesterol synthesis pathway has been found at higher than expected levels in embryonic murine brain. Interestingly, the receptor that 24(5),25-EC is a ligand for, Liver X Receptor (LXR), has been implicated in neurogenesis in the ventral mid brain region of embryonic brain; an area with a high density of dopaminergic neurons. The mechanism by which LXR induces this effect is unclear. Therefore, proteomic and phosphoproteomic studies were performed using a stable isotope labelled in amino acid in cell culture (SILAC) approach in order to quantify changes in the proteome between different treatment groups in a mouse substantia nigra dopaminergic cell line (SN4741) SN4741 cells were cultured in SILAC media containing differentially isotope labelled arginine and lysine. For protein expression studies SN4741 cells were treated in serum free media with vehicle, 10muM 24(S),25-EC, or 1muM GW3965, a synthetic ligand of LXR, for 24 hours. For analysis of changes in the phosphoproteome SN4741 cells were treated in serum free media with vehicle, 10muM 24(5),25-EC, or 30muM 25- hydroxycholesterol for 6 hours. Cells were lysed and protein combined in a 1:1 ratio before trypsin digestion and peptide separation via strong cation exchange chromatography. Phosphopeptides were enriched using immobilised metal affinity chromatography (IMAC). Resulting fractions were analysed, using a data dependent LC-MS/MS method. Data was quantified using MaxQuant software in conjunction with Mascot using an IPl mouse database. In protein expression analysis known oxysterol regulated genes, via SREBP or LXR, were differentially expressed. Oxysterol treatment induced global changes in proteins involved in lipid (cholesterol, fatty acid, phospholipid, triglyceride) synthesis. LXR? protein expression increased after GW3965 and 24(5),25-EC treatment, though no change was seen on LXRp mRNA, implying that ligand binding protects LXR? from degradation. 24(S),25-EC induced changes in expression and localisation of the membrane protein caveolin-1. Also, phosphoethanolamine cytidylyltransferase and collagen type IV alpha-3-binding protein, 2 proteins involved in phospholipid synthesis, had an altered expression after 24(S),25-EC treatment suggesting a role for oxysterols in membrane homeostasis. A cytokine, macrophage colony stimulating factor, which is required for normal neuronal development and macrophage differentiation had an LXR independent increased expression after 24(S),25-EC treatment. Quantitative RT-PCR data demonstrated that proteomic changes were due to both transcriptional and post-transcriptional effects of oxysterol. In addition, studies examining changes in the mouse phosphoproteome identified a number of novel phosphorylation sites

Historical Study of the Oklahoma Agricultural Experiment Station

Higher Educatio