Examining the associations between self-care practices and psychological distress among nursing students during the COVID-19 pandemic.

There is limited research regarding the impact of self-care practices on psychological distress, specifically on nursing students during a pandemic, such as COVID-19 (Corona Virus Disease- 2019). A 10-minute electronic survey was sent to nursing students at a large academic-medical center, and data from 285 student respondents were analyzed to assess psychological status, attitudes and behaviors in regards to the COVID-19 pandemic. Significant differences were found when comparing self-care practice scores by school grade for total scores (F = 4.48 [df = 4,250], p = .002), emotional subscale (F = 4.78 [df = 4,250], p = .001), and relationship subscale (F = 3.44 [df = 4,250], p = .009). While there were no significant differences in psychological distress by school grade, graduate students had the lowest self-care practice score compared to all the other grades. Finally, the subscale and total self-care practice scores were significantly and negatively associated with psychological distress. These findings suggest that utilization of self-care practices is associated with lower psychological distress, and should therefore be promoted among nursing student populations and integrated into curricula. Future studies should assess specific needs geared towards populations that may have poor self-care practices, such as graduate students, and understand ways to improve sleep quality to mitigate rates of psychological distress during a pandemic.

An integrated neurocognitive and social-cognitive treatment for youth at clinical high risk for psychosis: Cognition for Learning and for Understanding Everyday Social Situations (CLUES).

BACKGROUND: Cognitive deficits, a core feature contributing to disability in schizophrenia, are present in milder form in individuals at clinical high risk (CHR) for psychosis. This study investigated the feasibility of Cognition for Learning and Understanding Everyday Social Situations (CLUES), an integrated neurocognitive and social cognitive treatment for youth at CHR. METHOD: This was an open, pilot feasibility trial. Seventeen individuals meeting CHR criteria were assessed prior to and following participation in CLUES for changes in symptoms, social and role functioning, and cognition. Participant attitudes towards CLUES were also examined. RESULTS: Participants significantly improved in social functioning [t(16) = -4.20, p = .001, d = 1.02], and trended for improvement in reaction time [t(15) = 2.09, p = .054, d = 0.52] from baseline to end of treatment. No other measures significantly changed. No participants transitioned to full psychosis during the treatment and follow up period. Participants reported they generally liked CLUES and found it helpful. CONCLUSION: While limited by the small sample size and the open label design, our preliminary results indicate that CLUES is feasible and shows promise in improving social functioning. However, further investigation is warranted in order to determine its efficacy. Future directions should include conducting a randomized controlled trial in order to compare the efficacy of CLUES to another intervention.

A Comparison of Vocational Engagement Among Young People with Psychosis, Depression and Borderline Personality Pathology.

Poor vocational engagement is well documented among young people experiencing first-episode psychosis (FEP). The aim of the present study was to establish and compare rates of vocational engagement across young people with first-episode psychosis, depression, and borderline personality pathology. A file audit was used to collect vocational data of young people aged 15-25 entering tertiary mental health treatment in 2011. Rates of vocational engagement were similar across groups, indicating that like those with FEP, young people with depression and borderline personality pathology experience impaired vocational engagement and are in need of targeted vocational interventions. Post hoc analysis indicated that that the depression group had significantly more people who were partially vocationally engaged compared with the psychosis group, suggesting that vocational interventions might need to be targeted differently across different diagnostic groups. Future research should explore risk factors for vocational disengagement across diagnostic groups in order to inform intervention development.

Duration of untreated psychosis and neurocognitive functioning in first-episode psychosis: a systematic review and meta-analysis.

BACKGROUND: Previous reviews suggest there is minimal evidence for an association between duration of untreated psychosis (DUP) and neurocognition. This is based on tallied findings of studies with small samples and neurocognition viewed as a single construct. We aimed to conduct a systematic review and meta-analysis examining the association between DUP and individual neurocognitive domains and tests in first-episode psychosis (FEP). METHOD: MOOSE and PRISMA guidelines were followed. Forty-three studies involving 4647 FEP patients were included. For studies providing correlations between DUP and neurocognition, 12 separate meta-analyses were performed based on neurocognitive domains/indices. The influence of demographic/clinical variables was tested using weighted linear meta-regression analyses. RESULTS: The relationship between DUP and most neurocognitive domains/indices was not significant. Longer DUP was associated with a larger cognitive deterioration index, i.e. current minus premorbid intellectual functioning (N = 4; mean ES -0.213, 95% confidence interval (CI) (-0.344 to -0.074), p = 0.003). Findings were homogeneous, with no evidence of publication bias or significant influence from moderators. For studies providing mean and standard deviations for neurocognitive measures and DUP, 20 meta-regressions were performed on individual neurocognitive tests. One significant finding emerged showing that longer DUP was associated with fewer Wisconsin Card Sorting Test-perseverative errors (mean ES -0.031, 95% CI (-0.048 to -0.013), p < 0.001). Exploratory meta-regressions in studies with mean DUP <360 days showed longer DUP was significantly associated with poorer performance on Trail Making Test A and B and higher Full-Scale IQ. CONCLUSION: There may not be a generalised association between DUP and neurocognition, however, specific cognitive functions may be associated with longer DUP or delayed help-seeking.

Community based organizations addressing South Asian American health.

Addressing the health needs of all Americans is central to the public health agenda in the US. Although some progress has been made in documenting health disparities among South Asians living in the US, more attention is needed to fully understand how communities are addressing the health needs of this community. Community Based Organizations (CBOs) play a vital role in strengthening and empowering communities through outreach and health education. Through research conducted via a web survey and key informant interviews, this study provides a context for understanding how CBOs in the US have begun to address the health of South Asian Americans. Additionally, recommendations are identified that may help improve the health outcomes of this population.

The maturation of form and motion perception in school age children.

The purpose of the current study was to investigate the maturation of form and motion perception, specifically the component visual abilities involved in the identification of motion-defined form, in children ranging in age from 3 to 12 years. Experiment 1 compared the maturation of motion-defined and texture-defined shape identification. Minimum speed thresholds on the motion-defined shape task decreased until age 7 years. Orientation difference thresholds on the texture-defined shape task decreased until age 11 years. Experiment 2 compared the maturation of global motion and global texture direction discrimination. Coherence thresholds on both tasks were similar in children of all ages and adults. Experiment 3 compared the maturation of direction discrimination on motion coherence and motion displacement tasks. Maximum displacement thresholds (Dmax) increased until age 7 years. The results are discussed with respect to the maturation of M/dorsal and P/ventral visual pathways.

Blood borne macrophages are essential for the triggering of muscle regeneration following muscle transplant.

The transplantation of satellite cells may constitute a strategy for rebuilding muscle fibres in inherited myopathies. However, its development requires a great understanding of the role of environmental signals in the regenerative process. It is therefore essential to identify the key events triggering and controlling this process in vivo. We investigated whether macrophages play a key role in the course of the regenerative process using skeletal muscle transplants from transgenic pHuDes-nls-LacZ mice. Before grafting, transplants were conditioned with macrophage inflammatory protein 1-beta (MIP 1-beta; stimulating the macrophages infiltration or vascular endothelial growth factor (VEGF) stimulating angiogenesis). Treatment of transplants with MIP 1-beta and VEGF both accelerated and augmented monocyte-macrophage infiltration and satellite cell differentiation and/or proliferation, as compared to controls. In addition, VEGF treatment enhanced the number of newly formed myotubes. When a complete depletion of host monocyte-macrophages was experimentally induced, no regeneration occurred in transplants. Our data suggest that the presence of blood borne macrophages is required for triggering the earliest events of skeletal muscle regeneration. The understanding of macrophage behaviour after muscle injury should allow us to develop future strategies of satellite cell transplantation as a treatment for muscular dystrophies.

Computerised dystrophic muscle simulator: prospecting potential therapeutic strategies for muscle dystrophies using a virtual experimental model.

Inherited muscle diseases are often characterised by widespread muscle damage in the body, limiting the clinical relevance of cell or gene therapy based upon direct injections into muscles. Recent studies have shown, however, that cells originating from the bone marrow are able to target necrosis-regeneration sites as they occur and, in addition, may also participate in the muscle regeneration after undergoing myogenic differentiation. Here, we present a computerised dystrophic muscle simulator that allows the prospecting of different scenarios of both disease evolution and appropriate employment of blood-borne cells as therapeutic shuttles. It provides the option of examining their use either to transfer a healthy gene into the tissue or to impart substances designed to boost its regeneration. One of the major advantages of this tool is that it offers the opportunity of visualising and composing therapeutic strategies in virtual paradigms in which severe clinical situations, not necessarily available in animal models, can be created. The dystrophic muscle simulator is freely accessible via the Genethon web site (www.genethon.fr), and in the online version via http:@www.wiley.co.uk/genmed.

Cell engineering for muscle gene therapy: Extemporaneous production of retroviral vector packaging macrophages using defective herpes simplex virus type 1 vectors harbouring gag, pol, env genes.

Gene therapy as a treatment for neuromuscular diseases is an ever-developing concept based on the use of DNA as the therapeutic agent. In the search for appropriate strategies a bottleneck exists, however, concerning the targeting of vectors carrying the therapeutic gene, to all pathologic sites. These diseases are often characterised by multiple widespread lesions spread over a large area, rendering administration by local injection into tissues, clinically irrelevant. With this in mind, we have proposed that circulating cells (monocytes/macrophages), which home naturally to inflammatory lesions, characteristic of degenerating muscle, could be used as shuttles able to track down every damaged site, and deliver there a corrective gene. Our aim is to mobilise a corrective gene from these infiltrating monocyte-macrophages, into muscle cells, a process of in situ cell to cell gene transfer which could be accomplished using a retroviral vector, since the regeneration process involves the proliferation of muscle precursors before they fuse to form replacement fibres. For this, monocyte-macrophages must be engineered into 'packaging cells' containing both the replication deficient retrovirus carrying the gene of interest and an helper genome (gag-pol-env) needed for its assembly and secretion. Here, we have transduced a monocyte cell line using a defective murine Moloney leukemia retrovirus carrying the LacZ reporter gene. This provided us with a platform to investigate the possibility of gag-pol-env vector driven packaging of the defective retrovirus by macrophages. We show that an herpes simplex virus type I amplicon harbouring the Moloney gag, pol, env sequences is able to rescue the defective retrovirus vector from macrophages, allowing gene transfer into muscle precursor cells. After fusion, these cells gave rise to genetically modified myotubes in vitro.

Selective potentiation of gynecologic cancer cell growth in vitro by electromagnetic fields.

OBJECTIVE: Epidemiological data suggest that exposure to electromagnetic fields (EMF) may increase the risk of various cancers. We evaluated EMF effects on the in vitro growth response of human cell lines isolated from various reproductive tract tissues. We also assessed the effects of EMF on cisplatin- or paclitaxel-induced cytotoxicity. METHODS: Endometrial, ovarian, and prostate cancer cell lines as well as immortalized endometrial stromal cells and immortalized ovarian epithelial cells were exposed continually to EMF. Proliferation was assessed by the metabolic activity assay, MTT, direct cell counting, and anchorage-independent colony formation in soft agar. Cytotoxicity induced by cisplatin or paclitaxel was assessed using the MTT assay. RESULTS: Continuous exposure to EMF at field strengths of 2 G enhanced proliferation of two human prostate and three endometrial, but only one ovarian, cancer cell lines. EMF enhanced metabolic activity of cancer cells within 96 h and increased absolute cell number (anchorage-dependent proliferation) and colony-forming efficiency (anchorage-independent proliferation) over sham-treated controls. EMF had no effect on cytotoxicity induced by the chemotherapeutic agents Taxol or cisplatin. CONCLUSIONS: Continuous exposure to EMF can enhance growth rates of transformed cells for some human epithelial cancers. Cancer cells from the steroid sex hormone regulated tissues of endometrium and prostate appeared to be more responsive to EMF than cells from ovarian cancers.

Adenovirus-mediated gene transfer to the brain: methodological assessment.

The purpose of this short review is to analyse major advantages and limitations of the adenovirus (Ad), specifically with relevance to its use as a vector for gene transfer to the brain. The characteristics of Ad transduction include: the relative absence of cell type specificity; the limited spatial spread of the virus; and the long-term expression of the transgene. In the central nervous system, in contrast to that which occurs in other organs, Ad transduction in the adult does not systematically provoke cell death. Nevertheless, a proportion of the transduced cells do die, and this represents a conspicuous problem. Mechanisms leading to cell death in the brain may include immune rejection and inflammation-related toxicity, although this would not explain all of the results, and direct toxicity related to either inappropriate preparation or the transduction itself. Taking into account uncertainties concerning the innocuousness of Ad transduction, it may seem unwise to envisage Ad gene therapy for diseases that are not life-threatening and/or benefit from adequate drug or surgical treatments (e.g. Parkinson's disease or epilepsy). Ad vectors may not be easily used either in diseases displaying major immune dysfunction (e.g. multiple sclerosis). In contrast, malignant brain tumors and numerous neurodegenerative diseases (such as Huntington's, Alzheimer's diseases or amyotrophic lateral sclerosis) are directly life-threatening and deprived of any adequate treatment. They may be appropriate targets for Ad-mediated gene therapy, once both the vector and the gene of interest have been defined and optimized.

Involvement of the dihydropyridine receptor and internal Ca2+ stores in myoblast fusion.

The process of myoblast fusion during skeletal myogenesis is calcium regulated. Both dihydropyridine receptor and ryanodine receptor are already present on muscle precursors, at the prefusional stage, before they are required for excitation-contraction coupling. Previous pharmacological studies have shown the need for a special pool of Ca2+ associated with the membrane for the fusion process to occur. We hypothesized that this pool of Ca2+ is mobilized via a machinery similar to that involved in excitation-contraction coupling. The process of fusion in rat L6 muscle precursors was either totally or partially abolished in the presence of the L-type calcium channel inhibitors SR33557 and nifedipine (half inhibition towards 2 microM), respectively. The inhibition was reversible and dose-dependent. Drugs able to deplete internal calcium stores (caffeine, ryanodine, and thapsigargin) were also tested on the fusion. Both caffeine and thapsigargin drastically inhibited fusion whereas ryanodine had no effect. This suggests that fusion may be controlled by internal pools of Ca2+ but that its regulation may be insensitive to ryanodine. We presumed that an early form of the ryanodine receptor may exist, with different pharmacological properties than the adult forms. Indeed, Western blot analysis of pre- and postfusional L6 cells demonstrated the presence, at the prefusional stage, of a transient form of the ryanodine receptor protein with an apparent molecular weight slightly different from those of the classical skeletal and cardiac forms. Taken together, these results support the hypothesis that the fusion process is driven by a mechanism involving both the dihydropyridine receptor (alpha1 subunit of the L-type Ca2+ channel) and the internal stores of Ca2+. The machinery underlying this mechanism might consist of slightly different forms of the classic molecules that in adult muscle ensure excitation-contraction coupling. It remains to be seen, however, whether the mobilization of the internal pool of Ca2+ is triggered by the type of mechanism already described in skeletal muscle.

Targeting widespread sites of damage in dystrophic muscle: engrafted macrophages as potential shuttles.

Inherited muscle diseases are characterized by widespread muscle damage in the body. This limits the clinical relevance of cell or gene therapy based upon direct injections into muscles. One way to circumvent this obstacle would be to use circulating cells, capable of homing naturally to the sites of lesion, to deliver therapeutic substances. Certain muscular dystrophies present successive cycles of degeneration-regeneration. These sporadic necrotic lesions trigger local inflammations with subsequent infiltration of blood-borne mononuclear cells. We have, therefore, tested the possibility that homing monocytes and macrophages could be appropriate shuttles for delivering a therapeutic agent to disseminated pathogenic sites, their targeting being triggered by the pathogeny itself. First, fluorescently labeled immortalized monocytes were intravenously injected into mice which had previously undergone freeze-damaging of individual muscles. In agreement with our hypothesis, intense labelling was observed in the muscle, specifically in damaged regions. Second, the technique was adapted to meet the needs of chronic diseases with characteristic continuous, widespread degeneration of muscle fibers, by creating a reservoir of genetically engineered monocytes, via bone marrow transplantation. Mdx mice received bone marrow from transgenic mice expressing the lacZ reporter gene, under the control of the vimentin promoter, which is active in monocytes and macrophages. Histological and molecular analyses demonstrated the homing of engineered macrophages at the sites of muscle damage, for periods as long as 2 months. Bone marrow progenitor cells, appropriately engineered to elicit the synthesis, in macrophages, of therapeutically relevant substances, may be of clinical value in various pathologies involving an inflammatory phase.

Characterization of the low-molecular-mass proteins of virulent Treponema pallidum.

We previously demonstrated that Treponema pallidum cells incubated in vitro in the presence of heat-inactivated normal rabbit serum (HINRS) synthesize, in very small quantities, several pathogen-specific, low-molecular-mass proteins that appear to be localized extracellularly. In this study, we have taken advantage of our ability to metabolically radiolabel T. pallidum cells to high specific activity to further characterize these antigens. We found that the low-molecular-mass proteins are not related to the 15- and 17-kDa detergent-phase proteins (J. D. Radolf, N. R. Chamberlain, A. Clausell, and M. V. Norgard, Infect. Immun. 56:490-498, 1988). The low-molecular-mass proteins did not incorporate 3H-labeled fatty acids and were not precipitated by rabbit immunoglobulin G (IgG) antibodies directed against glutathione S-transferase fusions to the nonlipidated 15- and 17-kDa proteins. We prepared polyclonal antisera to the low-molecular-mass proteins by immunizing two rabbits with the concentrated supernatant of T. pallidum cells. IgG antibodies present in the sera of both rabbits precipitated a 21.5-kDa protein from solubilized extracts of T. pallidum supernatant and cells. IgG antibodies in the serum of the second rabbit precipitated an additional 15.5-kDa low-molecular-mass protein only from solubilized extracts of supernatant. While investigating the effect of eliminating HINRS from the extraction medium, we observed that the low-molecular-mass proteins remained associated with treponemal cells that were incubated in the absence of HINRS. These proteins could be eluted from the cells by the addition of HINRS or rabbit serum albumin, suggesting that they are located on or near the treponemal cell surface. The 15.5- and 21.5-kDa low-molecular-mass proteins were not washed off treponemal cells with buffer containing 1 M KCl. Experiments employing selective solubilization of the T. pallidum outer membrane with 0.1% Triton X-114 and proteinase K accessibility indicated that the 15.5-kDa protein, but not the 21.5-kDa protein, is cell surface exposed.

Distribution and expression of two interactive extracellular matrix proteins, cytotactin and cytotactin-binding proteoglycan, during development of Xenopus laevis. I. Embryonic development.

An immunohistochemical study of the localization of cytotactin and cytotactin-binding (CTB) proteoglycan throughout embryonic development of the anuran Xenopus laevis reveals that both appear in a restricted pattern related to specific morphogenetic events. CTB proteoglycan expression is first detected during gastrulation at the blastopore lip. Later, it is seen in the archenteron roof around groups of cells forming the notochord, somites and neural plate. Cytotactin first appears after neurulation, and is restricted to the intersomitic regions. Both molecules appear along the migratory pathways of neural crest cells in the trunk and tail. Later, cytotactin is present at sites where neural crest cells differentiate, around the aorta and in the smooth muscle coat of the gut; CTB proteoglycan is absent from these sites. In the head, cytotactin is initially restricted to the regions between cranial somites, while CTB proteoglycan is distributed throughout the cranial mesenchyme. The expression of both molecules is later associated with key events in chondrogenesis during the development of the skull. After chondrogenesis, CTB proteoglycan is distributed throughout the cartilage matrix, while cytotactin is restricted to a thin perichondrial deposit. Both molecules are expressed in developing brain. These findings are compared to studies of the chick embryo and although distinct anatomical differences exist between frog and chick, the expression of these molecules is associated with similar developmental processes in both species. These include mesoderm segmentation, neural crest cell migration and differentiation, cartilage development, and central nervous system histogenesis.

Distribution and expression of two interactive extracellular matrix proteins, cytotactin and cytotactin-binding proteoglycan, during development of Xenopus laevis. II. Metamorphosis.

During metamorphosis of Xenopus laevis the extracellular matrix (ECM) proteins cytotactin and cytotactin-binding (CTB) proteoglycan and the cell adhesion molecules N-CAM and Ng-CAM, appear in highly restricted patterns determined by immunofluorescence histology. During limb development, cytotactin appears from the earliest stages in a meshwork of ECM fibrils associated with migrating mesenchymal cells forming the limb bud. Cytotactin also appears in the ECM between the apical limb ectoderm and mesenchyme. Later, both cytotactin and CTB proteoglycan appear co-localized within the central (prechondrogenic) limb mesenchyme. During chondrogenesis in these areas, cytotactin becomes restricted to perichondrium, while CTB proteoglycan is expressed throughout the cartilage matrix. The premyogenic mesenchyme surrounding the chondrogenic areas expressed N-CAM. Later, N-CAM is concentrated at the myogenic foci where cytotactin appears at sites of nerve/muscle contact and in tendons. Expression of these molecules in the blastemas of regenerating limbs was also studied, and during development of the central nervous system, stomach, and small intestine. Analysis of the expression patterns of cytotactin and CTB proteoglycan throughout development and metamorphosis reveals several consistent themes. The expression of these molecules is highly dynamic, often transient, and associated with key morphogenetic events. Cytotactin appears at multiple sites where cells undergo a transition from an undifferentiated, migratory phenotype to a differentiated phenotype. One or both molecules appear at several sites of border formation between disparate cell collectives, and CTB proteoglycan expression is associated with chondrogenesis.

Automatic measurements of fetal long bones. A feasibility study.

We investigated whether it would be possible for a computer to propose values for measurements commonly obtained (femur and humerus) during obstetrical sonography. In this preliminary study, the images were scanned and analyzed off-line using morphological operators. The procedure described allowed us to measure the long bones and has a very high coefficient of correlation with measurements obtained by humans. Ideally, the whole procedure could probably be part of the computer instructions that are built into the machine.

Heat shock response of spirochetes.

We examined the heat shock response of the pathogenic spirochetes Treponema pallidum, Borrelia burgdorferi, and Leptospira interrogans and certain saprophytic spirochetes. Cellular proteins synthesized after shifts to higher temperatures were [35S]methionine labeled and analyzed by gel electrophoresis and fluorography. Only T. pallidum failed to exhibit an obvious heat shock response. GroEL and DnaK homologs were identified in the various species, although these proteins were not thermoinducible in T. pallidum or Treponema denticola. DNA hybridization studies indicate that spirochetal groEL and dnaK genes are highly conserved.

Cloning of the recA gene from a free-living leptospire and distribution of RecA-like protein among spirochetes.

A recombinant plasmid carrying the recA gene of Leptospira biflexa serovar patoc was isolated from a cosmid library of genomic DNA by complementation of an Escherichia coli recA mutation. The cloned serovar patoc recA gene efficiently restored resistance to UV radiation and methyl methanesulfonate. Recombination proficiency was also restored, as measured by the formation of Lac+ recombinants from duplicated mutant lacZ genes. Additionally, the cloned recA gene increased the spontaneous and mitomycin C-induced production of lambda phage in lysogens of an E. coli recA mutant. The product of the cloned recA gene was identified in maxicells as a polypeptide with an Mr of 43,000. Antibodies prepared against the E. coli RecA protein cross-reacted with the serovar patoc RecA protein, indicating structural conservation. Southern hybridization data showed that the serovar patoc recA gene has diverged from the recA gene of L. interrogans, Leptonema illini, and E. coli. With the exception of the RecA protein of L. interrogans serovar hardjo, the RecA protein of the Leptospira serovars and L. illini were synthesized at elevated levels following treatment of cells with nalidixic acid. The level of detectable RecA correlated with previous studies demonstrating that free-living cells of L. biflexa serovars and L. illini were considerably more resistant to DNA-damaging agents than were those of parasitic L. interrogans serovars. RecA protein was not detected in cells of virulent Treponema pallidum or Borrelia burgdorferi.