Search

The past academic gender literature has focused on the underproduction of academic women in research outcomes and related reasons such as prejudice, more frequent career breaks and personality differences between genders. This study examines the top six journals in the world and finds no difference between women and men productivity when the percentage of women participating in the academic work force is factored in. Women have a 30-35% participation rate in academic university positions and represented almost 30% of the authors in the top tiered journals. There are also no significantly statistical differences in Journal Impact Factor ratings between men and women. These findings are consistent across all the major disciplines, science, business and social science. Other trends are noted such as the significantly higher number of authors in science journals and the different trends between US and non-US authors. Science authors quality (as measured by Journal Impact Factor (JIF of 31.9) is significantly higher than non-science authors (JIF 6.5); thus differences in quality are discipline specific not a gender issue. The implications are that academic womens research contribution matches that of a mans productivity.

Clinicians working in community mental health clinics are at high risk for burnout. Burnout is a problem involving emotional exhaustion, depersonalization, and reduced personal accomplishment. Reiki is a holistic biofield energy therapy beneficial for reducing stress. The purpose of this study was to determine if 30 minutes of healing touch could reduce burnout in community mental health clinicians.We utilized a crossover design to explore the efficacy of Reiki versus sham Reiki, a pseudo treatment designed to mimic true Reiki, as a means to reduce symptoms of burnout. Subjects were randomized to whether they started with Reiki or sham. The Maslach Burnout Inventory-Human Services Survey (MBI-HSS) and the Measure Your Medical Outcome Profile Version 2 (MYMOP-2) were used as outcome measures. Multilevel modeling was used to represent the relations among variables.Reiki was statistically significantly better than sham Reiki in reducing burnout among community mental health clinicians (p=0.011). Reiki was significant in reducing depersonalization (p0.001), but only among single people. Reiki reduced the primary symptom on the MYMOP also only among single people (p=0.03).The effects of Reiki were differentiated from sham Reiki. Reiki could be helpful in community mental health settings for the mental health of the practitioners.

The cerebellar cortex contains at least two classes of Purkinje cells, which are organized into alternating arrays of parasagittal bands. The clearest demonstration of this compartmentation is the pattern of expression of a family of polypeptide antigens, the zebrins, which are expressed selectively by Purkinje cell subsets. Furthermore, anterograde tracing experiments show that the zebrin compartments are closely correlated with both afferent and efferent projection maps. The further subdivision of long parasagittal bands into smaller modules may occur through several different mechanisms, including the intrinsic cerebellar lobulation and the selective distribution of afferent terminal fields. However, while the longitudinal subdivisions are straightforwardly shown, the mediolateral boundaries are more subtle. In this report we describe a novel mediolateral and anteroposterior compartmentation boundary in mice, running across lobule VIII, that is revealed by the consequences of the lurcher (Lc/+) allele for zebrin expression. In normal mice zebrin compartmentation develops in several discrete stages: until postnatal day 5 (PD5) there is no zebrin expression; from PD5–PD7 zebrin is found only in the posterior lobe vermis, with immunoreactive Purkinje cells in lobules X, IX, and VIII but not elsewhere; from PD7–PD12 most Purkinje cells in the vermis become zebrin+ from PD12–PD15 immunoreactivity also appears in the hemispheres so that almost all Purkinje cells now are zebrin+ and finally, from PD15–PD25 zebrin is gradually suppressed in those Purkinje cells that are zebrin- in the adult until the mature pattern of parasagittal compartments is revealed. In the Lc/+ mutant the normal developmental progression is interrupted at around PD7. As a result, the pattern of zebrin expression becomes frozen at that stage when immunoreactive Purkinje cells are confined exclusively to the posterior lobe vermis. A reproducible boundary between expressing and nonexpressing zones runs mediolaterally across the dorsal surface of lobule VIII. Apart from zebrin expression itself, there are no obvious structural correlates of this transition. This mediolateral boundary identifies a developmental unit in the posterior lobe vermis of the cerebellum, and provides further evidence that the cerebellum is a highly heterogeneous structure. © 1992 Wiley-Liss, Inc.

The motor neuron degeneration mutation (Mnd) causes a late-onset, progressive degeneration of upper and lower motor neurons in mice. After establishing genetic and environmental conditions that distinguish the phenotypes of Mnd/Mnd from +/Mnd mice, Mnd was mapped to proximal Chr 8, using endogenous retroviruses as markers. The map location was confirmed with additional linked polymorphic markers. The outcross/intercross matings to the strain AKR/J, which were used to follow the segregation of the retroviral markers with respect to Mnd, also revealed the existence of a timing effect. Approximately one-fourth of the affected Mnd/Mnd F2 progeny showed accelerated disease. The Mnd mouse model should allow study of mechanisms affecting onset and progression of specific neuronal degeneration in both animal and human neurological disease.

The hierarchy of the various processes responsible for the development of the complex, elaborated Purkinje cell can be examined by taking advantage of a series of spontaneous mutations that affect cerebellar development in the mouse. This study uses double mutants containing genes for two separate hereditary cerebellar mutations that have been shown to act intrinsically in Purkinje cells in order to investigate the time course and modes of action of these mutations. Lurcher mice show 100% degeneration of Purkinje cells, starting during the second postnatal week, while staggerer mice show reduced numbers of Purkinje cells in a distinctive mediolateral distribution from the time of birth, with the remainder grossly stunted. When these mutations are combined genetically, mice shown by progeny tests to harbor both staggerer and Lurcher genotypes exhibit staggerer-like behavior and overall cerebellar morphology; they also do not lose 100% of their Purkinje cells, as Lurcher mutants would otherwise do. Instead, they show a characteristic staggerer cerebellar pathology. We conclude that the intrinsic action of the staggerer gene in Purkinje cells occurs earlier in development than do effects of the Lurcher gene, and that the action of the staggerer gene prevents Purkinje cells from acquiring the characteristics required for the cytotoxic action of the Lurcher gene.

Compared with other primary photosynthetic products (e.g. sucrose and starch), little is known about sugar alcohol metabolism, its regulation, and the manner in which it is integrated with other pathways. Mannose-6-phosphate reductase (M6PR) is a key enzyme that is involved in mannitol biosynthesis in celery (Apium graveolens L.). The M6PR gene was cloned from a leaf cDNA library, and clonal authenticity was established by assays of M6PR activity, western blots, and comparisons of the deduced amino acid sequence with a celery M6PR tryptic digestion product. Recombinant M6PR, purified from Escherichia coli, had specific activity, molecular mass, and kinetic characteristics indistinguishable from those of authentic celery M6PR. Sequence analyses showed M6PR to be a member of the aldo-keto reductase superfamily, which includes both animal and plant enzymes. The greatest sequence similarity was with aldose-6-phosphate reductase (EC 1.1.1.200), a key enzyme in sorbitol synthesis in Rosaceae. Developmental studies showed M6PR to be limited to green tissues and to be under tight transcriptional regulation during leaf initiation, expansion, and maturation. These data confirmed a close relationship between the development of photosynthetic capacity, mannitol synthesis, and M6PR activity.

To examine the effects of multiple stressors on the onset and specificity of a neurodegenerative disease, we derivedmnd/mndmice expressing a neurofilament-H/lacZ transgene. Themndmutation causes adult-onset motor dysfunction, and produces abnormal ubiquitous accumulation of autofluorescent lipopigment, with retinal degeneration and late-onset motor neuron degeneration. The neurofilament H-β-galactosidase fusion protein causes endogenous neurofilament subunits to precipitate in perikarya, but shows neither significant neuronal degeneration nor behavioral changes until advanced age. Inmnd/mnd-transgenic animals, neurological symptoms, lipopigment accumulation, and motor neuron loss were substantially accelerated. Newly vulnerable populations of neurons also degenerated, including cerebellar Purkinje cells and dorsal roots. This study exemplifies a synergistic interaction between a neuron-specific and a ubiquitous defect, leading to significant neurological consequences. It further indicates that cytoskeletal abnormalities similar to those observed in late-onset human neurodegenerative disorders can interact with other cellular defects and contribute to pathogenesis.

The mnd mouse shows a spontaneous adult-onset hereditary neurological disease, with motor abnormality by 6 months of age, progressing to severe spastic paralysis and premature death. The disease is autosomal recessive, with heterozygote effects seen under stress. It maps to mouse chromosome (chr) 8. Histopathology with Nissl stains documents substantial abnormalities of upper and lower motor neurons, and there is retinal degeneration beginning in the first month, even without light exposure. Increasing levels of autofluorescent lipopigment are found in both neuronal and non-neuronal tissues as the mnd mice age. Recently, NCL-like inclusions and accumulating subunit c have also been described. When mnd is outcrossed to the AKR/J genetic background, ca. 40% of the mnd/mnd F2 progeny show early onset (onset by 4.5-5 months and death by 7 months.) This accelerated timing effect seems to be strain-specific, and unlinked to the mnd gene itself. Our current working hypothesis is that the timing effect is due to 2 or 3 unlinked dominant genes with incomplete penetrance at any single locus. In a combined RFLP/PCR fragment genetic analysis, the strongest deviation from the expected ratio of AKR vs B6 alleles occurs with markers on proximal half of chr 1. Additional loci on chrs 5 and 10 may also be involved. The mechanism of interaction of these modifying genes with the primary mnd gene may offer new therapeutic avenues. 1995 Wiley-Liss, Inc.

It has been suggested that the degeneration of motor neurons in amyotrophic lateral sclerosis is a consequence of excitotoxicity resulting from a loss of synaptosomal glutamate uptake. The role of synaptosomal glutamate uptake in the pathogenesis of motor neuron disease was studied in the Mnd mouse. Glutamate uptake in spinal-cord synaptosomes declined in parallel with the onset of behavioral deficits in Mnd mice but lagged considerably behind the appearance of pathology in motor neurons. Glutamate uptake did not decline significantly in corpus striatum, and GABA uptake did not change significantly in either spinal cord or striatum. The presence of pronounced histopathological changes before the loss of glutamate uptake suggests that the decline of glutamate uptake is a consequence rather than the primary cause of motor neuron disease in the Mnd mouse.

The mouse mutant Motor neuron degeneration (Mnd) displays an adult-onset progressive degeneration of upper and lower motor neurons, with mild symptoms recognizable at 6 months, leading to spastic paralysis and premature death at 10-12 months on the C57B1/6 background. Despite this late onset, abnormally-accumulating autofluorescent material can be seen in both the spinal cord and other regions as early as the first month. This pigmented material is present in both increasing numbers of cells, and in increasing amounts within individual cells, as the animals age. Motor neurons then go on to degenerate, while most other cell types stabilize. The level of pathological involvement, well before the onset of clear clinical symptoms, suggests that the full degenerative process is an extremely gradual and protracted one with some selectivity for motor neurons.