Search

Introduction Women constitute approximately 17% of the military. Yet, relatively little is known regarding sleep disorders and comorbid diagnoses effecting this gender. The aim of this study was to determine if there were gender-related differences in symptoms of sleep disorders and sleep-related impairment, comorbid sleep, behavioral medicine, and traumatic brain injury (TBI) diagnoses and polysomnographic (PSG) variables in military personnel with insomnia, OSA, and comorbid insomnia and OSA (COMISA). Methods Participants were 372 military personnel (46.2% females, 53.8% males) with an average age of 37.7±7.46 years and median BMI of 28.4 (5.50) kg/m2. Based on clinical evaluation and video-PSG, participants were diagnosed with insomnia (n = 118, 71.2% female), OSA (n = 118, 28.8% female) and COMISA (n = 136, 39.7% female). Insomnia severity, excessive daytime sleepiness, sleep quality, nightmare disorder, sleep impairment, fatigue, posttraumatic stress disorder (PTSD), anxiety, depression symptoms, and traumatic brain injury (TBI) were evaluated with validated questionnaires. Descriptive statistics, parametric and non-parametric pairwise comparisons and effect-size analyses were used to assess differences between sexes in terms of variables of interest. Results Female service members had significantly greater symptoms of nightmare disorder, PTSD, anxiety, and depression than their male counterparts. There were no significant differences between males and females with insomnia or OSA in sleep-related symptoms, impairment, or PSG based apnea-hypopnea index (AHI). Male service members with COMISA had a significantly greater AHI; females with COMISA had significantly greater symptoms of nightmare disorder, PTSD and anxiety. Conclusion In the largest study to date to clinically evaluate sleep disorders in military personnel, COMISA was the most frequent diagnosis. Surprisingly, there were minimal differences in self-reported symptoms of sleep disorders and PSG characteristics. However, male servicemembers with COMISA have more severe sleep disordered breathing while female servicemembers with COMISA have greater mental health morbidity. Military service may result in distinct sleep disorder phenotype(s). Support (if any) This work was supported by the Defense Health Agency, Defense Medical Research and Development Program, Clinical Research Intramural Initiative for Military Women’s Health (DM170708; Mysliwiec) and the US Air Force (USAF) Air Force Materiel Command (AFMC), Wright Patterson Air Force Base, Ohio (FA8650-18-2-6953; Peterson).

Introduction Chronic pain and post-traumatic stress disorder (PTSD) comorbidity is prevalent among veterans and is associated with increased levels of pain severity and pain-related disability. An improved understanding of the relationship between these co-occurring disorders, in addition to effective integrated treatments, will develop by considering the changes to the PTSD diagnostic criteria in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). The current study examined the relationship between the revised PTSD Checklist for DSM-5 (PCL-5) symptom clusters (i.e., intrusion, avoidance, negative alterations in cognition and mood [NACM], and arousal) and chronic pain measurements (i.e., pain severity, interference, and disability). Materials and Methods Participants included 103 veterans (ages 26-70, mean = 45.33) participating in a randomized clinical trial examining the efficacy of an interdisciplinary pain management program for chronic musculoskeletal pain. The study was approved by a university system Institutional Review Board and affiliated healthcare system. Results The participants with a provisional PTSD diagnosis based on PCL-5 responses (N = 76) had significantly greater pain severity, interference, and disability than the participants without a provisional diagnosis (N = 23). Correlations between symptom clusters and pain measurements were mostly significant and positive with varying strengths. The avoidance symptom cluster, however, had relatively weaker correlations with pain measurements and was not significantly associated with the numeric rating scale of pain severity. Path analyses revealed that, after controlling for avoidance symptoms, significant associations remained between NACM and all the pain measurements. After controlling for NACM symptoms, however, there were no significant associations between avoidance symptoms and pain measurements. Conclusion The current study highlights a need to re-examine the leading theories about the mutual maintenance of these disorders in order to develop effective integrative treatment approaches. PTSD-related avoidance may have a relatively weaker role in co-occurring chronic pain than the other symptom clusters and may have a qualitatively different role than chronic pain–related avoidance. Future research should explore the relationship between the avoidance in PTSD and the avoidance in chronic pain as well as identify which chronic pain measurements are the most useful when examining the relationship between PTSD and chronic pain. The potential impact of trauma-related cognition and mood on chronic pain indicates that this is an important area for intervention and should be considered in the development of integrated treatments for chronic pain and PTSD among veterans.

Introduction An estimated twenty-five percent of American women are at high risk of having obstructive sleep apnea (OSA). However, male sex is the predominantly reported risk factor. Women are less likely to report “classic” symptoms such as snoring that prompt referral for sleep evaluation. This dichotomy potentially represents a disparity in clinical evaluation and treatment of OSA in women. Consumer digital health devices are frequently used to monitor sleep in people with and without sleep disturbances. They are generally highly sensitive yet have lower specificity when compared with formal actigraphy or polysomnography. They may be used in conjunction with physician evaluation to guide decision-making. Report of Cases: A 33 year-old female with a pertinent past medical history of obesity (BMI 37.83 kg/m ), depression, chronic pain, and anxiety was referred to our sleep center with a multi-year history of excessive daytime fatigue and non-restorative sleep that persisted despite healthy habits counseling and unremarkable lab evaluation. She ultimately presented her primary care physician with biometric data collected by her Garmin watch and Oura ring. This data, which included a reported low SpO of 83%, motivated a referral to Sleep Medicine. Her presentation Epworth Sleepiness Scale (ESS) score and Insomnia Severity Index (ISI) were 14 and 17, respectively. Polysomnography revealed an AHI of 32.6/hr, oxygen nadir of 79%, ODI of 28.7/hr, and a 97.2% sleep efficiency. PLMS index was 23.2/hour but did not contribute to sleep fragmentation and there was increased proportion of stage N3 sleep (28.2%). Severe OSA was treated with APAP. The two month follow-up ESS and ISS improved to 9 and 4, respectively. Device data revealed greater than 6 hours of consistent nightly use with a residual AHI of 3.1/hr. She subjectively stated APAP “has been a life changer” personally and professionally, as well as spousal report of resolution of snoring. Her consumer devices similarly reported improved sleep measures. Conclusion Minorities and women may be underserved in evaluation, diagnosis, and treatment of OSA. Portable monitoring using readily available consumer biometric devices may be a viable strategy for patients to further identify high risk features and prompt referral by primary care. Support (If Any) This work was supported by the Defense Health Agency, Defense Medical Research and Development Program, Clinical Research Intramural Initiative for Military Women’s Health (DM170708; Mysliwiec) and the Air Force Research Laboratory, Wright Patterson Air Force Base, Ohio (FA8650-18-2-6953; Peterson).

O presente artigo tem como objetivo analisar a importância da utilização dos recursos hídricos subterrâneos na produção de flores e plantas ornamentais em Holambra-SP. Trata-se de verificar como é realizado o uso da água subterrânea e quais vulnerabilidades territoriais são resultantes. Com apoio de dados do DAEE-SP e de mapeamentos elaborados pelo autor, procura demonstrar a fragilidade do sistema de gestão de recursos hídricos em São Paulo, que aliado à especialização produtiva agrícola provoca situações de estresse hídrico em diversas áreas, tais como o município de Holambra-SP.

Made available in DSpace on 2016-05-17T16:51:50Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-11-23. Added 1 bitstream(s) on 2016-05-17T16:55:45Z : No. of bitstreams: 1 000864131.pdf: 3570347 bytes, checksum: c5b59299bff235b17b9345ce7b0b655e (MD5) O município de Holambra, localizado no estado de São Paulo, configura-se como o principal polo produtor de flores e plantas ornamentais no Brasil. Sua intensa especialização produtiva pode ser percebida a partir do aparato técnico ali instalado, onde imensas estufas e incontáveis equipamentos de irrigação desenham sua paisagem. O cultivo de flores é diferenciado dos demais cultivos agrícolas do Brasil, sua produção é realizada em pequenas propriedades com uso intenso de mão-deobra, mas também requer grande número de insumos e recursos, tais como os recursos hídricos. Diante disso, Holambra apresenta inúmeras captações de água em seu território, o que vem ocasionando reveses na disponibilidade hídrica de suas bacias hidrográficas. Neste cenário, o objetivo proposto por esse trabalho é de analisar a importância do uso dos recursos hídricos na produção de flores e plantas ornamentais em Holambra, procurando identificar as vulnerabilidades socioambientais geradas pelo uso corporativo deste recurso, o qual é indispensável à vida de qualquer indivíduo The city of Holambra, located in São Paulo, is the major producer of flowers and ornamental plants in Brazil. His intense productive specialization can be seen from the technical apparatus installed there, where huge greenhouses and a lot of irrigation equipment draw your landscape. The cultivation of flowers is differentiated from other crops in Brazil, its production takes place on small farms with many workers, but also requires large number of inputs and resources, such as water resources. Therefore, Holambra have many water captation systems at your territory, which has caused setbacks in water availability of their watersheds. In this scenario, the objective proposed for this work is to analyze the importance of using water resources in the production of flowers and ornamental plants in Holambra, trying to identify the social and environmental vulnerabilities generated by the corporate use of this resource, which is indispensable to the life of any individual

Unqualified, the statement that ≈1.3% of the ≈10,000 presently known bird species have become extinct since A.D. 1500 yields an estimate of ≈26 extinctions per million species per year (or 26 E/MSY). This is higher than the benchmark rate of ≈1 E/MSY before human impacts, but is a serious underestimate. First, Polynesian expansion across the Pacific also exterminated many species well before European explorations. Second, three factors increase the rate: ( i ) The number of known extinctions before 1800 is increasing as taxonomists describe new species from skeletal remains. ( ii ) One should calculate extinction rates over the years since taxonomists described the species. Most bird species were described only after 1850. ( iii ) Some species are probably extinct; there is reluctance to declare them so prematurely. Thus corrected, recent extinction rates are ≈100 E/MSY. In the last decades, the rate is

Neurofilaments are synthesised and assembled in neuronal cell bodies, transported along axons and degraded at the synapse. However, in several pathological situations they aggregate in cell bodies or axons. To investigate their turnover when separated from their normal site of degradation, we used a previously described transgenic model characterised by perikaryal retention of neurofilaments, and compared the basic features of both neurofilament synthesis and degradation with that observed in normal mice. Despite the massive perikaryal aggregates, neurofilament transcript levels were found to be unchanged, whereas the total accumulation of neurofilament proteins was markedly reduced. Neurofilaments isolated from transgenic samples are more sensitive to both trypsin and α-chymotrypsin mediated proteolysis. Consistent with their greater in vitro sensitivity, trypsin immunolabeling of cell bodies was stronger in transgenic mice. These results show a novel mechanism to regulate the amount of neurofilaments when they abnormally aggregate.

The Beaver Creek Madison project is the most recent CO2 EOR project in the state of Wyoming. Having pre-project oil production of 43 MMBO, this flood is projected to increase recovery by 11.1 MMBO or 10% of the estimated 109 MMBO OOIP. Early CO2 flood response has yielded production increasing from a pre-flood rate of 280 BOPD to its current rate of 5100 BOPD since July, 2008. Since project initiation, the reservoir has realized 2.6 MMBO of incremental oil. The Madison reservoir, located in the Beaver Creek Field, 14 miles SSE of Riverton, Wyoming, is found at an average depth of 11,235’ placing it among the deepest CO2 EOR projects in the United States. Reservoir temperature is approximately 234° F. in this limestone/dolomite reservoir. The Madison is a highly structured, fault bounded reservoir encompassing just under 1000 acres with an average net pay of 212’, and an oil column thickness of 740’. The CO2 flood is a mixed design peripheral and gravity stable flood incorporating localized continuous gas injection and water alternating gas (WAG) processes which takes advantage of the reservoir's geometry and structural relief. The flood incorporates 32 wells. This report provides a case study for a deep carbonate CO2 flood. It includes the Beaver Creek Madison's geologic and reservoir characterization, flood design, early production performance, and reservoir management. Also included in this presentation is a discussion of the pre-flood evaluation and design which incorporated a 3 phase evaluation process progressing from preliminary scoping and screening to more costly laboratory testing, detailed reservoir modeling and flood design. Early life reservoir management includes some minor, yet functionally significant, changes to the injection pattern and WAG cycles intended to optimize the reservoirs performance compensating for early deviations from the field's anticipated responses.

To investigate the expression of nerve cell-specific transgene products in neural transplants, we implanted into the hippocampus of immunosuppressed adult Sprague - Dawley rats cell suspensions obtained from the septal region of the fetal brain of mice that carry the human neurofilament-light (hNF-L) gene. In grafts examined between 3 weeks and 7 months after transplantation, axons and nerve cell somata immunoreacted to antibodies specific to the human NF-L subunit. Thus, the hNF-L protein appears to be a suitable marker of these grafted neurons. Transgenic mice bearing the hNF-L gene may be a convenient source of donor tissue or be used as hosts for neural transplantation studies. Furthermore, the hNF-L promoter/enhancer elements in this transgene may help direct neuronal expression of heterologous genes that could influence nerve cell responses in either the transplant or host tissues.

Sarcolipin (SLN) inhibits the cardiac sarco(endo)plasmic reticulum Ca 2+ ATPase (SERCA2a) by direct binding and is superinhibitory if it binds through phospholamban (PLN). To determine whether overexpression of SLN in the heart might impair cardiac function, transgenic (TG) mice were generated with cardiac-specific overexpression of NF-SLN (SLN tagged at its N terminus with the FLAG epitope). The level of NF-SLN expression (the NF-SLN/PLN expression ratio) was equivalent to that which induces profound superinhibition when coexpressed with PLN and SERCA2a in HEK-293 cells. In TG hearts, the apparent affinity of SERCA2a for Ca 2+ was decreased compared with non-TG littermate control hearts. Invasive hemodynamic and echocardiographic analyses revealed impaired cardiac contractility and ventricular hypertrophy in TG mice. Basal PLN phosphorylation was reduced. In isolated papillary muscle subjected to isometric tension, peak amplitudes of Ca 2+ transients and peak tensions were reduced, whereas decay times of Ca 2+ transients and relaxation times of tension were increased in TG mice. Isoproterenol largely restored contractility in papillary muscle and stimulated PLN phosphorylation to wild-type levels in intact hearts. No compensatory changes in expression of SERCA2a, PLN, ryanodine receptor, and calsequestrin were observed in TG hearts. Coimmunoprecipitation indicated that overexpressed NF-SLN was bound to both SERCA2a and PLN, forming a ternary complex. These data suggest that NF-SLN overexpression inhibits SERCA2a through stabilization of SERCA2a–PLN interaction in the absence of PLN phosphorylation and through the inhibition of PLN phosphorylation. Inhibition of SERCA2a impairs contractility and calcium cycling, but responsiveness to β-adrenergic agonists may prevent progression to heart failure.

Neurofilament modification and accumulation, occurring in toxicant-induced neuropathies, has been proposed to compromise fast axonal transport and contribute to neurological symptoms or pathology. The current study compares the effects of the neurotoxicants acrylamide (ACR) and 2,5-hexanedione (2,5-HD) on the quantity of fast, bidirectional vesicular traffic within isolated mouse sciatic nerve axons from transgenic mice lacking axonal neurofilaments (Eyer and Peterson, Neuron 12, 1-20, 1994) and nontransgenic littermates possessing neurofilaments. Fast anterograde and retrograde membrane bound organelle (MBO) traffic was quantitated within axons, before and after toxicant exposure, using video-enhanced differential interference contrast (AVEC-DIC) microscopy. Addition of 0.7 mM ACR to the buffer bathing the nerve produced a time-dependent reduction in bidirectional transport with a similar time to onset and magnitude in both transgenic and nontransgenic mice. 2,5-HD (4 mM) exposure reduced bidirectional vesicle traffic by a similar amount in both transgenic and nontransgenic animals. The time to onset of the transport reduction was less and the magnitude of the reduction was greater with 2,5-HD compared to ACR. A single 10-min exposure to ACR or 2,5-HD produced a similar reduction in transport to that produced by prolonged (1 h) exposure. Nonneurotoxic propionamide or 3,4-hexanedione (3,4-HD) produced no changes in bidirectional transport in either transgenic or nontransgenic animals. We conclude that ACR or 2,5-HD produces a rapid, saturable, nonreversible, neurotoxicant-specific reduction in fast bidirectional transport within isolated peripheral nerve axons. These actions are mediated through direct modification of axonal component(s), which are independent of toxicant-induced modifications of, or accumulations of, neurofilaments.

Type 1 diabetes (T1D) is a strongly heritable autoimmune disease due to the destruction of pancreatic β-cells by self-reactive T-cells. The third strongest genetic locus for T1D involves a single-nucleotide polymorphism (SNP) causing an arginine(R) to triptophan(W) substitution at codon 620 (620R>W) in PTPN22, the gene encoding the tyrosine phosphatase LYP, an important negative regulator of T-cell receptor (TCR) activation. However, the cellular effects of the 620R>W risk allele remain controversial, as different studies report either a gain or a loss of function in its ability to inhibit TCR signaling. To study this variant in an animal model, we created a knock-in mouse by introducing the 620R>W substitution in, the murine LYP orthologue, PEP encoded by Ptpn22. The knock-in analyzed on the autoimmune-resistant C57Bl/6 background showed a mild but significant increase in CD4+ helper T-cell activation and proliferation upon weak TCR activation. Conversely, upon strong TCR stimulation, the tendency seemed to be reversed as the 620W allele showed a slightly decreased responsiveness compared to the 620R allele. Phenotypic analysis of other immune cellular compartments, including memory T cells, showed no significant difference between genotypes. There was no evidence of autoimmunity in this genetic background. This dependence of allelic effect on the strength of the TCR signal may reconcile previous observations and indicate a complex role of R620>W in autoimmunity.

The Purkinje cell protein 2 (Pcp-2) is expressed in cerebellar Purkinje cells and retinal bipolar neurons. To illuminate how Pcp-2 expression is restricted to only two neuronal types and to derive tools to express heterologous genes in these neuronal subpopulations, genomic sequences of the mouse Pcp-2 gene have been cloned and flanking sequences have been evaluated as a source of neuron-specific regulatory elements. An upstream region with homology to other genes expressed in neurons was identified and a hybrid gene containing this sequence was constructed by ligating 0.4 kb of upstream and 0.3 kb of downstream Pcp-2-flanking DNA to lacZ. Transgenic mice bearing this construct exhibited beta-galactosidase in a wide array of neuron types, suggesting that this sequence may play an important role in specifying neuronal expression. Addition of a further 3.1 kb of Pcp-2 upstream sequences restricted expression of beta-galactosidase to a small number of neuron types and most notably to Purkinje cells within parasagitally oriented cerebellar compartments. The presence of elements lying within the 3.1-kb upstream region and acting to specifically restrict Pcp-2 expression is therefore suggested. Moreover, as beta-galactosidase was not expressed in the bipolar cells of these transgenic mice, retinal expression of the endogenous Pcp-2 gene must involve elements in addition to those conferring expression within Purkinje cells.

The precise developmental mechanisms leading to myoblast fusion and the subsequent functional relationships that exist amongst the myonuclei contained within each syncytium are for the most part ill-defined. In contrast, extraordinary advances have been achieved in defining the precise molecular deficits causing several inherited diseases of muscle. In such diseases, functional rescue of muscle might be achievable by the introduction of genetically normal myonuclei but this strategy ultimately depends upon the interrelationships that exist between the myonuclei and the syncytial cytoplasm. If the mRNA encoded by each myonucleus was translated into protein molecules that were subsequently restricted to a “nuclear territory”, rescue of such mosaic fibers might depend upon not only the number of transplanted myonuclei but also their intrafiber distribution. Alternatively, if proteins encoded by each myonucleus were distributed uniformly throughout the syncytium, the spatial organization of the transplanted myonuclei could be irrelevant.

In some lines of transgenic mice, the methylation of Mspl sites within or adjacent to the transgene locus is affected by the sex of the parent from which the transgene is inherited. These differences are consistent with a role for DNA methylation in genome imprinting. In a previous report, we noted that in one such line, all offspring of females exhibited hypermethylation of the transgene while only some offspring of males carried a hypometh-ylated transgene. In this report, we provide evidence that this phenomenon is controlled by at least two factors, one of which acts in cis and is dependent on the transgene locus, and one of which acts in trans and is supplied by the maternal genome. We also provide evidence that there are genetic differences between inbred mouse strains in the trans-acting factor.

Homozygous mdg mdg mice die at birth and express a syndrome of abnormalities, the most striking of which is a gross failure of skeletal muscle development. Recently, additional abnormalities in the development of nerve-muscle relationships have been recognized; in particular, on muscle fibers within the diaphragm, motor end plates are inappropriately dispersed and, in all muscles, there is a paucity of the 16 S form of acetylcholinesterase (AChE). These abnormalities could result entirely as secondary consequences of the primary muscle defect or from expression of the mdg defect in additional cell types, e.g., motor neurons. To determine if the muscle genotype alone is responsible for these defects in dysgenic mice, chimeras composed of both dysgenic and normal cells have been investigated. Different glucosephosphate isomerase variants existed in the mdg mdg and normal cells comprising these chimeras and the mutant, normal, or mosaic genotypes of chimera diaphragm and skeletal muscle was estimated by measuring the relative proportions of each isozyme. In two chimeras, the diaphragm innervation pattern was revealed by AChE cytochemistry and in both, discrete regions of abnormally dispersed and normally restricted motor end-plate zones were observed. No correlation between these patterns of innervation and the assessed genotype of the muscle fibers existing in each area was observed. The relative 16 S AChE content in the limbs of four chimeras was found to range from 2.5 to 42.0%. Here also, no correlation between 16 S AChE content and the muscle genotype was observed. The results of these investigations are not consistent with a model of mdg mdg pathogenesis in which only the skeletal muscle is primarily affected; an extramuscular deficiency responsible for at least part of the full mdg mdg syndrome is therefore suggested.

Data derived from both pronuclear transplantation experiments and classical genetic experiments indicate that the maternal and paternal genetic contributions to the mammalian zygote nucleus do not function equivalently during subsequent development1–5. These observations have been interpreted as resulting from differential 'genome imprinting' during male and female gametogenesis2,3. The molecular mechanism responsible for genome imprinting is unknown, but data gathered to date require that the mechanism fulfil at least four criteria: (1) the imprint must be physically linked to the pronucleus2,3; (2) the imprint must persist through DNA replication and cell division6; (3) the mechanism must be capable of affecting gene expression2,7; and (4) the mechanism must be capable of switching the identity of the imprint from one sex to the other in successive generations2,3. One molecular mechanism which could satisfy the first three criteria is differential DNA methylation during gametogenesis itself6,8, or before formation of the zygote nucleus during embry-ogenesis. We present data indicating that the methylation patterns of exogenous DNA sequences in transgenic mice can be changed by switching their gamete of origin in successive generations. These data suggest that DNA methylation can also satisfy the fourth criterion for an imprinting mechanism.

The site of integration of transgenes in the host genome can affect levels of expression1 and occasionally confer ectopic patterns of expression on otherwise tissue-specific genes2. We describe here a line of mice in which an hsp68-lacZ transgene is expressed in unstressed developing neural tissue and where the transgene insertion has caused a mutation of a neural tissue-specific gene, dystonia musculorum (dt). This coincidence suggests that expression of the hsp68-lacZ construct may be controlled directly by cis-acting regulatory sequences that normally control the developmental expression of the dt gene. Such constructs may serve as useful tools for identifying new tissue-specific enhancers and their associated genes3,4.

Publisher Summary This chapter presents a methylation mosaic model for mammalian genome imprinting. This model predicts that the paternally transmitted allele at some loci will be unavailable for appropriate expression, while at other loci the expression of the maternally transmitted allele will be affected. The introduction of new genetic material into the mouse genome by microinjection of DNA has provided a powerful tool with which to investigate gamete-of-origin-dependent DNA methylation. Matings between transgenic and nontransgenic animals yield offspring in which the transgene is inherited from only one parent. Therefore, potential gamete-of-origin-dependent differences in DNA methylation at these loci can be directly assayed in such offspring. If the gamete-of-origin- dependent methylation changes demonstrated for a number of hemizygous transgene loci are directly related to the developmental failure of gynogenotes and androgenotes, several additional observations made in these experiments are unexpected. In the simplest model, the hypomethylation of an allele would result in the expression of that allele, while the hypermethylation of that allele would result in no expression.

To investigate the regulation of neurofilament gene expression, we have generated several lines of transgenic mice carrying multiple copies of a cloned human neurofilament (NF-L) gene. We show that a 21.5-kb DNA fragment including the human NF-L gene contains essential information for correct expression in nervous tissue of transgenic mice. The integrated genes are arranged in multiple tandem arrays, but the extent of transgene expression does not correlate with copy number nor does it influence the expression of the endogenous neurofilament genes. However, the levels of human NF-L protein recovered in neurofilament preparations from brains of transgenic mice correlate directly with the relative abundance of human NF-L mRNA detected in each line. There is an apparent delay in the accumulation of human NF-L protein during development, as determined by immunoblotting with a human-specific monoclonal antibody. Finally, immunohistochemical localization of the human NF-L protein results in the specific staining of neurons and their processes in transgenic mice.

Notes the growing number of mutual self-help groups (MASH) in the United States and outlines five ways in which clergy may be involved in them: (1) as a referral source, (2) as an initiator of such groups, (3) as a provider of meeting space for the groups, (4) as a supporter of religious organizations' self-help efforts, and (5) by initiating self-help groups for clergy themselves. Provides a current list of Self-Help Clearinghouses in the United States.