Help Seeking for Mental Health Problems in Mental Health Counselors: Prevalence, Barriers, and Predictors

This study surveyed a sample of 255 mental health counselors in the United States and used descriptive statistics, chi-square tests, one-way ANOVA, and logistic regression analysis to investigate the prevalence of mental health problems and help seeking, the perceived barriers to, and predictors of help seeking for mental health problems among mental health counselors. In this sample, 62.6% (n = 159) reported they had experienced a mental health problem during the time since licensure. Of those, 13.2% (n = 21) reported they had not received treatment. “Handling the problem on my own” was the most cited barrier to help seeking, followed by “not being able to afford the financial costs,” “difficulty taking time off, and “having had bad experiences with mental health care.” The study also found that increased help-seeking self- stigma predicted decreased intention to seek help from a mental health professional, while experience of role model disclosure of positive experiences with mental health treatment predicted increased intention to seek help. A limitation of this study was the use of availability sampling which resulted in a non-representative sample, skewed toward white, non-Hispanic, females. Important areas for future research include studies with larger more representative samples, studies of interventions to encourage help seeking in mental health counselors, studies of other potential predictors of help seeking, and studies to develop instruments for use specifically with mental health counselors. The study findings underscore the importance of more open dialogue about these issues within the counseling profession to support and encourage help seeking in mental health counselors and find ways to ensure that mental health counselors have the information and resources they need to access quality mental health care

Monoclonal Antibody Identification of Subpopulations of Cerebral Cortical Neurons Affected in Alzheimer disease

Neuronal degeneration is one of the hallmarks of Alzheimer disease (AD). Given the paucity of molecular markers available for the identification of neuronal subtypes, the specificity of neuronal loss within the cerebral cortex has been difficult to evaluate. With a panel of four monoclonal antibodies (mAbs) applied to central nervous system tissues from AD patients, we have immunocytochemically identified a population of vulnerable cortical neurons; a subpopulation of pyramidal neurons is recognized by mAbs 3F12 and 44.1 in the hippocampus and neocortex, and clusters of multipolar neurons in the entorhinal cortex reactive with mAb 44.1 show selective degeneration. Closely adjacent stellate-like neurons in these regions, identified by mAb 6A2, show striking preservation in AD. The neurons recognized by mAbs 3F12 and 44.1, to the best of our knowledge, do not comprise a single known neurotransmitter system. mAb 3A4 identifies a phosphorylated antigen that is undetectable in normal brain but accumulates early in the course of AD in somas of vulnerable neurons. Antigen 3A4 is distinct from material reactive with thioflavin S or antibody generated against paired helical filaments. Initially, antigen 3A4 is localized to neurons in the entorhinal cortex and subiculum, later in the association neocortex, and, ultimately in cases of long duration, in primary sensory cortical regions. mAb 3F12 recognizes multiple bands on immunoblots of homogenates of normal and Ad cortical tissues, whereas mAb 3A4 does not bind to immunoblots containing neurofilament proteins or brain homogenates from AD patients. Ultrastructurally, antigen 3A4 is localized to paired-helical filaments. Using these mAbs, further molecular characterization of the affected cortical neurons is now possible

p493F12 kinase: A novel MAP kinase expressed in a subset of neurons in the human nervous system

AbstractMonoclonal antibody 31712 identifies a cytoplasmic antigen of 49 kDa in human hippocampus and neocortex. The distribution of 31712 immunoreactive neurons closely matches that of Alzheimer's disease (AD) targeted neurons in these areas. In some hippocampal neurons of AD patients, this antigen colocalizes with ALZ-50, indicating the presence of AD pathology in these neurons. Molecular characterization of the 3F12 cDNA revealed it to be a member of the MAP kinase family, showing 43% amino acid sequence identity to human extracellular related kinase 2 (p42mapk). We have confirmed that p493F12 kinase autophosphorylates both threonine and tyrosine residues, as expected for a MAP kinase. The p49 mRNA is expressed exclusively in the nervous system. In the brain, the distribution of these neurons closely corresponds to 31712 antigenbearing neurons. The p493F12 gene maps to the human chromosome 21q21 region, a region that may be important in the pathogenesis of AD and Down's syndrome

A New Metric for Quantifying Burn Severity: The Relativized Burn Ratio

Satellite-inferred burn severity data have become increasingly popular over the last decade for management and research purposes. These data typically quantify spectral change between pre-and post-fire satellite images (usually Landsat). There is an active debate regarding which of the two main equations, the delta normalized burn ratio (dNBR) and its relativized form (RdNBR), is most suitable for quantifying burn severity; each has its critics. In this study, we propose and evaluate a new Landsat-based burn severity metric, the relativized burn ratio (RBR), that provides an alternative to dNBR and RdNBR. For 18 fires in the western US, we compared the performance of RBR to both dNBR and RdNBR by evaluating the agreement of these metrics with field-based burn severity measurements. Specifically, we evaluated (1) the correspondence between each metric and a continuous measure of burn severity (the composite burn index) and (2) the overall accuracy of each metric when classifying into discrete burn severity classes (i.e., unchanged, low, moderate, and high). Results indicate that RBR corresponds better to field-based measurements (average R2 among 18 fires = 0.786) than both dNBR (R2 = 0.761) and RdNBR (R2 = 0.766). Furthermore, the overall classification accuracy achieved with RBR (average among 18 fires = 70.5%) was higher than both dNBR (68.4%) and RdNBR (69.2%). Consequently, we recommend RBR as a robust alternative to both dNBR and RdNBR for measuring and classifying burn severity

Myoclonic Epilepsy and Ragged Red Fibers (MERRF) Syndrome: Selective Vulnerability of CNS Neurons Does Not Correlate with the Level of Mitochondrial tRNA^(lys) Mutation in Individual Neuronal Isolates

Selective vulnerability of subpopulations of neurons is a striking feature of neurodegeneration. Mitochondrially transmitted diseases are no exception. In this study CNS tissues from a patient with myoclonus epilepsy and ragged red fibers (MERRF) syndrome, which results from an A to G transition of nucleotide (nt) 8344 in the mitochondrial tRNA^(Lys) gene, were examined for the proportion of mutant mtDNA. Either individual neuronal somas or the adjacent neuropil and glia were microdissected from cryostat tissue sections of histologically severely affected brain regions, including dentate nuclei, Purkinje cells, and inferior olivary nuclei, and from a presumably less affected neuronal subpopulation, the anterior horn cells of the spinal cord. Mutant and normal mtDNA were quantified after PCR amplification with a mismatched primer and restriction enzyme digestion. Neurons and the surrounding neuropil and glia from all CNS regions that were analyzed exhibited high proportions of mutant mtDNA, ranging from 97.6 ± 0.7% in Purkinje cells to 80.6 ± 2.8% in the anterior horn cells. Within each neuronal group that was analyzed, neuronal soma values were similar to those in the surrounding neuropil and glia or in the regional tissue homogenate. Surprisingly, as compared with controls, neuronal loss ranged from 7% of the Purkinje cells to 46% of the neurons of the dentate nucleus in MERRF cerebellum. Thus, factors other than the high proportion of mutant mtDNA, in particular nuclear-controlled neuronal differences among various regions of the CNS, seem to contribute to the mitochondrial dysfunction and ultimate cell death

Myoclonic Epilepsy and Ragged Red Fibers (MERRF) Syndrome: Selective Vulnerability of CNS Neurons Does Not Correlate with the Level of Mitochondrial tRNA^(lys) Mutation in Individual Neuronal Isolates

Selective vulnerability of subpopulations of neurons is a striking feature of neurodegeneration. Mitochondrially transmitted diseases are no exception. In this study CNS tissues from a patient with myoclonus epilepsy and ragged red fibers (MERRF) syndrome, which results from an A to G transition of nucleotide (nt) 8344 in the mitochondrial tRNA^(Lys) gene, were examined for the proportion of mutant mtDNA. Either individual neuronal somas or the adjacent neuropil and glia were microdissected from cryostat tissue sections of histologically severely affected brain regions, including dentate nuclei, Purkinje cells, and inferior olivary nuclei, and from a presumably less affected neuronal subpopulation, the anterior horn cells of the spinal cord. Mutant and normal mtDNA were quantified after PCR amplification with a mismatched primer and restriction enzyme digestion. Neurons and the surrounding neuropil and glia from all CNS regions that were analyzed exhibited high proportions of mutant mtDNA, ranging from 97.6 ± 0.7% in Purkinje cells to 80.6 ± 2.8% in the anterior horn cells. Within each neuronal group that was analyzed, neuronal soma values were similar to those in the surrounding neuropil and glia or in the regional tissue homogenate. Surprisingly, as compared with controls, neuronal loss ranged from 7% of the Purkinje cells to 46% of the neurons of the dentate nucleus in MERRF cerebellum. Thus, factors other than the high proportion of mutant mtDNA, in particular nuclear-controlled neuronal differences among various regions of the CNS, seem to contribute to the mitochondrial dysfunction and ultimate cell death

Molecular Dynamics Study of the Opening Mechanism for DNA Polymerase I

During DNA replication, DNA polymerases follow an induced fit mechanism in order to rapidly distinguish between correct and incorrect dNTP substrates. The dynamics of this process are crucial to the overall effectiveness of catalysis. Although Xray crystal structures of DNA polymerase I with substrate dNTPs have revealed key structural states along the catalytic pathway, solution fluorescence studies indicate that those key states are populated in the absence of substrate. Herein, we report the first atomistic simulations showing the conformational changes between the closed, open, and ajar conformations of DNA polymerase I in the binary (enzyme:DNA) state to better understand its dynamics. We have applied long time-scale, unbiased molecular dynamics to investigate the opening process of the fingers domain in the absence of substrate for B. stearothermophilis DNA polymerase in silico. These simulations are biologically and/or physiologically relevant as they shed light on the transitions between states in this important enzyme. All closed and ajar simulations successfully transitioned into the fully open conformation, which is known to be the dominant binary enzyme-DNA conformation from solution and crystallographic studies. Furthermore, we have detailed the key stages in the opening process starting from the open and ajar crystal structures, including the observation of a previously unknown key intermediate structure. Four backbone dihedrals were identified as important during the opening process, and their movements provide insight into the recognition of dNTP substrate molecules by the polymerase binary state. In addition to revealing the opening mechanism, this study also demonstrates our ability to study biological events of DNA polymerase using current computational methods without biasing the dynamics

3D-XY critical fluctuations of the thermal expansivity in detwinned YBa2Cu3O7-d single crystals near optimal doping

The strong coupling of superconductivity to the orthorhombic distortion in YBa2Cu3O7-d makes possible an analysis of the superconducting fluctuations without the necessity of subtracting any background. The present high-resolution capacitance dilatometry data unambiguously demonstrate the existence of critical, instead of Gaussian, fluctuations over a wide temperature region (+/- 10 K) around Tc. The values of the amplitude ratio A+/A-=0.9-1.1 and the leading scaling exponent |alpha|<0.018, determined via a least-squares fit of the data, are consistent with the 3D-XY universality class. Small deviations from pure 3D-XY behavior are discussed.Comment: 11 pages including three figure