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Generative Artificial Intelligence technologies can potentially transform education, benefiting teachers and students. This study evaluated various GAIs, including ChatGPT 3.5, ChatGPT 4.0, Google Bard, Bing Chat, Adobe Firefly, Leonardo.AI, and DALL-E, focusing on textual and imagery content. Utilizing initial, intermediate, and advanced prompts, we aim to simulate GAI responses tailored to users with varying levels of knowledge. We aim to investigate the possibilities of integrating content from Chemistry Teaching. The systems presented responses appropriate to the scientific consensus for textual generation, but they revealed alternative chemical content conceptions. In terms of the interpretation of chemical system representations, only ChatGPT 4.0 accurately identified the content in all of the images. In terms of image production, even with more advanced prompts and subprompts, Generative Artificial Intelligence still presents difficulties in content production. The use of prompts involving the Python language promoted an improvement in the images produced. In general, we can consider content production as support for chemistry teaching, but only with more advanced prompts do the answers tend to present fewer errors. The importance of previously understanding chemistry concepts and systems’ functioning is noted.

Objective:The objective of the scoping review will be to understand and describe risk factors associated with surgical site infection (SSI) in an orthopaedic surgery population in Sub-Saharan Africa and South Africa. This paper describes the protocol that will be used for the scoping review.Method:A comprehensive literature search will be conducted using MEDLINE (PubMed), CINAHL (EBSCO), Embase and Cochrane Libraries to identify articles meeting the inclusion criteria, including both published and grey literature, in order to provide a broad overview of the reported risk factors associated with patients who have undergone an orthopaedic surgery with an outcome of SSI within 90 days of a procedure. Additional studies will be sourced by exploring the reference list of included eligible studies. By using a combination of the Population, Exposure, Outcome framework, terms and synonyms related to each category, in different variations, along with Boolean operators (AND, OR, NOT) in the search strategy, identified comprehensive and relevant literature for the scoping review.Results:It is anticipated the results will provide a baseline of risk factors that will inform the development of a risk assessment tool for clinical use.Conclusion:This protocol will inform the development of a scoping review to describe factors associated with SSIs following orthopaedic surgery in Sub-Saharan Africa and South Africa.

ABSTRACTIndigenous plant naming systems and systematic botanical nomenclature involve different methodologies that result in different knowledge systems. Botanical nomenclature provides a single, universal name for a plant based on its taxonomic and evolutionary relationships. Indigenous classifications allow ready identification of plants for particular communities sharing a common language and cultural milieu to which the names are specific. The two systems are independent, but they can profit from mutual comparison, and each should be respected and valued for its distinctive role. A recent proposal argues that indigenous vernacular plant names, being older than those given in colonial circumstances, should have priority over existing botanical names. This suggestion, along with the call for greater use of indigenous languages in specific epithets, is here discussed in relation to the New Zealand flora. We conclude that the proposal would require extensive, complex changes to the International Code of Nomenclature, result in nomenclatural instability, and subject indigenous names to the rules of botanical nomenclature while severing them from their local cultural contexts. We suggest the proposal undermines indigenous naming systems, threatens the integrity of indigenous languages, and would disrupt botanical nomenclature for little benefit.

Usher syndrome (USH) is the most common form of deaf-blindness, with an estimated prevalence of 4.4 to 16.6 per 100,000 people worldwide. The most common form of USH is type IIA (USH2A), which is caused by homozygous or compound heterozygous mutations in the USH2Agene and accounts for around half of all USH cases. USH2A patients show moderate to severe hearing loss from birth, with diagnosis of retinitis pigmentosa in the second decade of life and variable vestibular involvement. Although hearing aids or cochlear implants can provide some mitigation of hearing deficits, there are currently no treatments aimed at preventing or restoring vision loss in USH2A patients. In this review, we first provide an overview of the molecular biology of the USH2Agene and its protein isoforms, which include a transmembrane protein (TM usherin) and an extracellular protein (EC usherin). The role of these proteins in the inner ear and retina and their impact on the pathogenesis of USH2A is discussed. We review animal cell-derived and patient cell-derived models currently used in USH2A research and conclude with an overview of potential treatment strategies currently in preclinical development and clinical trials.

ABSTRACTIt is argued that the greater use of te reo Māori and ta re Moriori languages for naming new taxa in the flora of Aotearoa / New Zealand supports the aspirations of Māori and Te Tiriti o Waitangi. However, using these indigenous languages in botanical nomenclature is more complex than a simplistic ‘more is better’, and we identify a number of issues requiring consideration. We appraise Waitangi Tribunal claim Wai 262 and Te Tiriti o Waitangi, collaboration at the interface of mātauranga Māori and research science, debate whether iwi are active collaborators or informants, and, crucially, defend the credibility and utility of te reo Māori / ta re Moriori and botanical nomenclatural systems. We conclude that (1) formal botanical nomenclature and (2) te reo and ta re vernacular plant names are independent, complementary, and mutually supportive classifications, each with different purposes and denoting two functional knowledge systems. Our recommendation when naming new taxa is to derive names from botanical Latin terminology. To provide clarity for the application of indigenous languages in naming Aotearoa / New Zealand vascular plants and bryophytes, an assessment of the rules and recommendations in the International Code of Nomenclature(ICN) is presented, including the use of geographical, personal and plant vernacular names as epithets, diacritical signs, hyphens, combinations of different languages, and epithet authorship. For those considering using te reo or ta re names for a new taxon, we present guidelines that address dialogue between scientists and iwi, key aspects of the ICN to consider, and suggestions for maintaining the scientific credibility of nomenclatural practices. A knowledge gap is identified for ethnobotanical folk taxonomy research into vernacular te reo and ta re names, and to document and promote this mātauranga we recommend Māori-led research into etymology, hierarchical structure, cultural relationships, whakapapa, and relationships to botanical names.

Background: Exon skipping strategies in Duchenne muscular dystrophy (DMD) have largely been directed toward altering splicing of exons flanking out-of-frame deletions, with the goal of restoring an open mRNA reading frame that leads to production of an internally deleted but partially functional dystrophin protein.Objective: We sought to apply exon skipping to duplication mutations, assuming that the inherently limited efficiency of antisense oligonucleotide-induced exon skipping would more frequently skip a single copy of a duplicated exon, rather than both and result in significant amounts of wild-type DMDmRNA.Methods: We tested this hypothesis in fibroblast cell lines derived from patients with a variety of single or multiple exon duplications that have been modified to allow transdifferentiation into a myogenic lineage.Results: Using a variety of 2’O-methyl antisense oligonucleotides, significant skipping was induced for each duplication leading to a wild-type transcript as a major mRNA product.Conclusions: This study provides another proof of concept for the feasibility of therapeutic skipping in patients carrying exon duplications in order to express wild-type, full-length mRNA, although careful evaluation of the skipping efficiency should be performed as some exons are easier to skip than others. Such a personalized strategy is expected to be highly beneficial for this subset of DMD patients, compared to inducing expression of an internally-deleted dystrophin.

Exon skipping strategies in Duchenne muscular dystrophy (DMD) have largely been directed toward altering splicing of exons flanking out-of-frame deletions, with the goal of restoring an open mRNA reading frame that leads to production of an internally deleted but partially functional dystrophin protein. We sought to apply exon skipping to duplication mutations, assuming that the inherently limited efficiency of antisense oligonucleotide-induced exon skipping would more frequently skip a single copy of a duplicated exon, rather than both and result in significant amounts of wild-type DMDmRNA. We tested this hypothesis in fibroblast cell lines derived from patients with a variety of single or multiple exon duplications that have been modified to allow transdifferentiation into a myogenic lineage. Using a variety of 2’O-methyl antisense oligonucleotides, significant skipping was induced for each duplication leading to a wild-type transcript as a major mRNA product. This study provides another proof of concept for the feasibility of therapeutic skipping in patients carrying exon duplications in order to express wild-type, full-length mRNA, although careful evaluation of the skipping efficiency should be performed as some exons are easier to skip than others. Such a personalized strategy is expected to be highly beneficial for this subset of DMD patients, compared to inducing expression of an internally-deleted dystrophin.

A major obstacle for effective utilization of therapeutic oligonucleotides such as siRNA, antisense, antimiRs etc. is to deliver them specifically to the target tissues. Toward this goal, nucleic acid aptamers are re-emerging as a prominent class of biomolecules capable of delivering target specific therapy and therapeutic monitoring by various molecular imaging modalities. This class of short oligonucleotide ligands with high affinity and specificity are selected from a large nucleic acid pool against a molecular target of choice. Poor cellular uptake of therapeutic oligonucleotides impedes gene-targeting efficacy in vitroand in vivo. In contrast, aptamer-oligonucleotide chimeras have shown the capacity to deliver siRNA, antimiRs, small molecule drugs etc. toward various targets and showed very promising results in various studies on different diseases models. However, to further improve the bio-stability of such chimeric conjugates, it is important to introduce chemically-modified nucleic acid analogs. In this review, we highlight the applications of nucleic acid aptamers for target specific delivery of therapeutic oligonucleotides.

Rare disease registries have now been recognized as a global priority for progress both in monitoring and documenting the natural course, and preventing and treating rare diseases. However, a disease registry is only one element of rare disease translational research. Here, we outline what we believe are ten key components in comprehensive rare disease translational research and describe critical relationships between them. These components are: (i) client–practitioner partnerships; (ii) disease registries; (iii) biobanks; (iv) genomics and other -omicsplatforms; (v) community-based and population-wide studies; (vi) bioinformatics and high performance computing; (vii) interactions with pharma to facilitate drug discovery; (viii) personalized treatments based on genotype-phenotype correlations; (ix) eHealth and a whole of life record; and (x) regulatory frameworks, particularly with regard to specimen and data sharing, and the return of results. Each component has its own inherent complexity, but if effectively integrated they will provide a comprehensive approach to the future management of rare diseases, and aid health care providers in delivering services to individuals affected with rare diseases. We demonstrate that navigation through the roadmap can provide relevant health stakeholders with a blueprint to understand the challenges and barriers which need to be overcome within and across the constituent components. The rare disease roadmap will assist decision-making at all health stakeholder levels and enable the seamless integration of new knowledge, standard operating procedures and the implementation of best practice.

Duchenne muscular dystrophy (DMD) is a devastating muscle-wasting disease caused by mutations in the dystrophin gene. Utrophin is a homologue of dystrophin that can compensate for its absence when overexpressed in DMD animal models. Utrophin upregulation is therefore a promising therapeutic approach for DMD. Utrophin is regulated at both transcriptional and posttranscriptional levels. Transcriptional regulation has been studied extensively, and assays have been described for the identification of utrophin promoter-targeting molecules. However, despite the profound impact that posttranscriptional regulation has on utrophin expression, screening assays have not yet been described that could be used to discover pharmaceuticals targeting this key phase of regulation. We describe the development and validation of a muscle cell line–based assay in which a stably expressed luciferase coding sequence is flanked by the utrophin 5′- and 3′-untranslated regions (UTRs). The assay was validated using the posttranscriptional regulation of utrophin by miR-206. The assay has a Z′ of 0.7, indicating robust performance in high-throughput format. This assay can be used to study utrophin regulatory mechanisms or to screen chemical libraries for compounds that upregulate utrophin posttranscriptionally via its UTRs. Compounds identified via this assay, used alone or in a synergistic combination with utrophin promoter-targeting molecules, would be predicted to have therapeutic potential for DMD.

This review discusses gene therapy as a new treatment paradigm where genetic material is introduced into cells for therapeutic benefit. The genetic material is the ‘drug’. It can have a transient or ongoing effect depending on whether or not the introduced genetic material becomes part of the host cell DNA. Different delivery and gene technologies are chosen by investigators to maximise gene delivery to, and expression within, the target cells appropriate for the disease indication. The presence and expression of the introduced genetic material is monitored by molecular means so that treatment efficacy can be assessed via changes in surrogate and/or actual markers of disease. Of interest to the pathologist will be the approaches being developed for the disease indications highlighted and the monitoring of treatment efficacy.

We report clinical safety and biochemical efficacy from a dose-ranging study of intravenously administered AVI-4658 phosphorodiamidate morpholino oligomer (PMO) in patients with Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) arises from protein-truncating mutations in the large dystrophin gene that preclude synthesis of a functional protein that primarily stabilizes muscle fibre membranes. The absence of dystrophin leads to this most common and serious form of childhood muscle-wasting. Since the identification of the dystrophin gene in 1987, cell and gene repair or replacement therapies have been evaluated for DMD treatment and one genetic intervention, exon skipping, is now in clinical trials. Antisense oligomers have been designed to redirect dystrophin splicing patterns so that targeted exons may be removed from a defective dystrophin pre-mRNA to either restore the reading frame of a deletion, or excise an in-frame exon corrupted by a nonsense mutation or microinsertion/ deletion. This review discusses the evolution of oligomer induced exon skipping, including in vitro applications, evaluation of different oligomer chemistries, the treatment of animal models and alternative exon skipping strategies involving viral expression cassettes and ex vivo manipulation of stem cells. The discussion culminates with the current clinical trials and the great challenges that lie ahead. The major obstacle to the implementation of personalised genetic treatments to address the many different mutations that can lead to DMD, are considered to be establishing effective treatments for the different patients and their mutations. Furthermore, the view of regulatory authorities in assessing preclinical data on potentially scores of different but class-specific compounds will be of paramount importance in expediting the clinical application of exon skipping therapy for this serious and relentlessly progressive muscle wasting disease.

As social geographers of health, we wish to review the field of geography and intoxicants. By intoxicants, we mean substances that have psychoactive, consciousness‐altering effects. This article defines the geography of intoxicants, and provides a selective review of geographically inclined research that has focused on (i) the consumption of intoxicants, especially its regulation within public spaces, (ii) intoxicants and public health, especially concerns over the spread of communicable diseases associated with drug use, and (iii) social geography issues such as the life experiences of addiction and users, and how treatment (and prevention) and place intersect. Part of our goal in this article is to bridge the gap between the more political and medical foci with more social and health perspectives that have thus far remained understated.

We conducted a genome-wide scan using variance components linkage analysis to localize quantitative-trait loci (QTLs) influencing triglyceride (TG), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol, and total cholesterol (TC) levels in 3,071 subjects from 459 families with atherogenic dyslipidemia. The most significant evidence for linkage to TG levels was found in a subset of Turkish families at 11q22 [logarithm of the odds ratio (LOD) = 3.34] and at 17q12 (LOD = 3.44). We performed sequential oligogenic linkage analysis to examine whether multiple QTLs jointly influence TG levels in the Turkish families. These analyses revealed loci at 20q13 that showed strong epistatic effects with 11q22 (conditional LOD = 3.15) and at 7q36 that showed strong epistatic effects with 17q12 (conditional LOD = 3.21). We also found linkage on the 8p21 region for TG in the entire group of families (LOD = 3.08). For HDL-C levels, evidence of linkage was identified on chromosome 15 in the Turkish families (LOD = 3.05) and on chromosome 5 in the entire group of families (LOD = 2.83). Linkage to QTLs for TC was found at 8p23 in the entire group of families (LOD = 4.05) and at 5q13 in a subset of Turkish and Mediterranean families (LOD = 3.72). These QTLs provide important clues for the further investigation of genes responsible for these complex lipid phenotypes. These data also indicate that a large proportion of the variance of TG levels in the Turkish population is explained by the interaction of multiple genetic loci.

In this study we demonstrate the potential for combining biocompatible polymers with genetically engineered cells to elicit axon regrowth across tissue defects in the injured CNS. Eighteen- to 21-day-old rats received implants of poly N-(2-hydroxypropyl)-methacrylamide (HPMA) hydrogels containing RGD peptide sequences that had been infiltrated with control (untransfected) fibroblasts (n = 8), fibroblasts engineered to express brain-derived neurotrophic factor (BDNF) (n = 5), ciliary neurotrophic factor (CNTF) (n = 5), or a mixture of BDNF and CNTF expressing fibroblasts (n = 11). Fibroblasts were prelabeled with Hoechst 33342. Cell/polymer constructs were inserted into cavities made in the left optic tract, between thalamus and superior colliculus. After 4–8 weeks, retinal projections were analyzed by injecting right eyes with cholera toxin (B-subunit). Rats were perfused 24 h later and sections were immunoreacted to visualize retinal axons, other axons (RT97 antibody), host astrocytes and macrophages, donor fibroblasts, and extracellular matrix molecules. The volume fraction (VF) of each gel that was occupied by RT97+ axons was quantified. RT-PCR confirmed expression of the transgenes prior to, and 5 weeks after, transplantation. Compared to control rats (mean VF = 0.02 ± 0.01% SEM) there was increased ingrowth of RT97+ axons into implants in CNTF (mean VF = 0.33 ± 0.19%) and BDNF (mean VF = 0.62 ±0.19%) groups. Axon growth into hydrogels in the mixed BDNF/CNTF group (mean VF = 3.58 ± 0.92%) was significantly greater (P < 0.05) than in the BDNF or CNTF fibroblast groups. Retinal axons exhibited a complex branching pattern within gels containing BDNF or BDNF/CNTF fibroblasts; however, they regrew the greatest distances within implants containing both BDNF and CNTF expressing cells.

A taxonomic treatment is provided for the Sophora microphylla complex in New Zealand. Sophora microphyllu sens. str. is endemic to New Zealand, and includes those plants with a distinct divaricating and/or strongly flexuose juvenile Phase, orange-brown to Yellow-brown Juvenile stems, and distant leaflets. S. chathamica is reinstated at species rank, S.fulvida is a new combination provided for the taxon previously known as S. microphylla Var. fulvida, and S. godleyi and S. molloyi are described as new species. S. chathamica, S. fulvida, S. godleyi and S. molloyi lack a divaricating and/or strongly flexuose juvenile phase and are each distinguished by a number of leaf characters. S. fulvida and S. godleyi have distinctive leaf hairs. S. chathamica is a predominantly coastal species in Northland, Auckland, Waikato, Wellington, and the Chatham Islands, S.fulvida occurs in Northland and North Auckland on volcanic rock outcrops S. godleyi Occurs on calcareous mudstone and sandstone in eastem Taranaki King country, Wanganui and Manawatu, and S. molloyi is restricted to extremely dry and exposed bluffs and rock outcrops of southern North Island headlands, Kapiti Island, and several islands in Cook Strait.Cluster analyses of 11 leaf and 4 growth habit characters provide additional support for the revised classification, and variation in 7 leaf characters is evaluated with box plots. A key is provided to Sophora in New Zealand, hybridism is discussed, an assessment of each species' conservation status is made, and biogeography is reconsidered in view of the new taxonomic treatment.

Statistics for the composition of the New Zealand seed plant flora are presented. The information provided is based on the number of wild speties listed in the New Zealand Plant Names Database Landcare Research' New Zealand' The statistics include the number of wild species, genera, and families; the number of species in the largest genera and families; and species numbers according to biostatus categories.

Gene therapy for inherited muscle disease is an active area of research and development. Initial emphasis has been on gene replacement but alternative approaches are increasingly being considered in order to overcome difficulties, such as the immune rejection of transduced cells, the need for appropriate and tissue-specific control of expression, and the requirement for systemic spread in some conditions. However, the most significant obstacles to the clinical success of gene therapy are still the lack of efficiency and accuracy of gene medicine delivery.

Objective:To determine the relationship between the apolipoprotein E e4allele and autopsy‐verified Alzheimer's disease (AD) in an Australian population. Design:Retrospective case‐control study. Setting:Royal Perth Hospital, Perth, Western Australia (a tertiary referral hospital). Subjects:50 subjects with “definite” AD (according to the histological and clinical criteria of the Consortium to Establish a Registry for Alzheimer's Disease [CERAO]) and 30 control subjects who had died from a non‐neurological disease were randomly selected from the hospital's neuropathology register. Outcome measures:Histological grading of brain sections stained with the modified Bielschowsky stain according to the criteria of CERAO; number (burden) of neuritic plaques; apolipoprotein E genotype (APOE). Results:Frequency of the e4allele was significantly higher in the AD group (37%) than in the control group (2%) (x2 = 25.8; P✠0.00001). In the AD group, 50% of subjects were heterozygous for the e4allele and 12% were homozygous, while in the control group one subject was heterozygous for the allele and none were homozygous. No association was seen between the e4allele and neuritic plaque burden in the hippocampus, entorhinal cortex, middle frontal gyrus or inferior parietal lobul in subjects with AD. Conclusions:Our findings confirm an association between the e4allele and autopsy‐verified AD. The e4allele may be an important risk factor for susceptibility to AD in the general Australian population. 20 Nov 1995 20 Feb 1996

Golden retriever muscular dystrophy (GRMD), the canine model of Duchenne muscular dystrophy (DMD), is caused by a splice site mutation in the dystrophin gene. This mutation predicts a premature termination codon in exon 8 and a peptide that is 5% the size of normal dystrophin. Western blot analysis of skeletal muscle from GRMD dogs reveals a slightly truncated 390‐kD protein that is approximately 91% the size of normal dystrophin. This 390‐kD dystrophin suggests that GRMD dogs, like some DMD patients, employ a mechanism to overcome their predicted frameshift. Reverse‐transcriptase polymerase chain reaction on GRMD muscle has revealed two in‐frame dystrophin transcripts which lack either exons 3–9 or exons 5–12. Both transcripts could be translated into a dystrophin protein of approximately 390 kD. An understanding of how truncated dystrophin is produced in GRMD may allow this mechanism to be manipulated toward a potential therapy for DMD. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:991–998, 1998.

The mdx mouse, an animal model used to study Duchenne muscular dystrophy, has a nonsense mutation in exon 23 of the dystrophin gene which should result in a truncated protein that cannot be correctly localized at the sarcolemma of the muscle fibers. Immunohistochemical staining with antidystrophin antibodies has shown that while most of the muscle tissue is dystrophin‐negative, a small percentage of muscle fibers is clearly dystrophin‐positive and has somehow bypassed the primary nonsense mutation. A sensitive nested polymerase chain reaction‐based examination of dystrophin gene transcripts around the mdx mutation has revealed several alternatively processed transcripts. Four mRNA species skipped the mutation in exon 23, were in‐frame, and could be translated into a shorter but still functional dystrophin protein. Specific tests for these transcripts demonstrated these were also present in normal mouse muscle tissue. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 728–734, 1997.

Golden retriever muscular dystrophy (GRMD), the canine model of Duchenne muscular dystrophy (DMD), is caused by a splice site mutation in the dystrophin gene. This mutation predicts a premature termination codon in exon 8 and a peptide that is 5% the size of normal dystrophin. Western blot analysis of skeletal muscle from GRMD dogs reveals a slightly truncated 390-kD protein that is approximately 91% the size of normal dystrophin. This 390-kD dystrophin suggests that GRMD dogs, like some DMD patients, employ a mechanism to overcome their predicted frameshift. Reverse-transcriptase polymerase chain reaction on GRMD muscle has revealed two in-frame dystrophin transcripts which lack either exons 3–9 or exons 5–12. Both transcripts could be translated into a dystrophin protein of approximately 390 kD. An understanding of how truncated dystrophin is produced in GRMD may allow this mechanism to be manipulated toward a potential therapy for DMD. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:991–998, 1998.

Nemaline myopathies are diseases characterized by the presence in muscle fibres of pathognomonic rod bodies. These are composed largely of α–actinin and actin. We have identified a missense mutation in the α–tropomyosin gene, TPM3, which segregates completely with the disease in a family whose autosomal dominant nemaline myopathy we had previously localized to chromosome 1p13–q25. The mutation substitutes an arginine residue for a highly conserved methionine in a putative actin–binding site near the N terminus of the α–tropomyosin. The mutation may strengthen tropomyosin – actin binding, leading to rod body formation, by adding a further basic residue to the postulated actin–binding motif.

A PCR product was generated from embryonic chicken spinal cord cDNA using primers designed to conserved regions of the human and bovine amino and carboxyl-terminal coding sequences of the Cu, Zn superoxide dismutase (SOD1, EC 1.15.1.1) gene. DNA sequencing confirmed this product to be the chicken homologue of the SOD1 gene. This sequence was compared to SOD1 from bovine, human and Xenopus laevis. Important structural features of SOD1 are shown to be conserved in the chicken gene.

The mdx mouse, an animal model used to study Duchenne muscular dystrophy, has a nonsense mutation in exon 23 of the dystrophin gene which should result in a truncated protein that cannot be correctly localized at the sarcolemma of the muscle fibers. Immunohistochemical staining with antidystrophin antibodies has shown that while most of the muscle tissue is dystrophin-negative, a small percentage of muscle fibers is clearly dystrophin-positive and has somehow bypassed the primary nonsense mutation. A sensitive nested polymerase chain reaction-based examination of dystrophin gene transcripts around the mdx mutation has revealed several alternatively processed transcripts. Four mRNA species skipped the mutation in exon 23, were in-frame, and could be translated into a shorter but still functional dystrophin protein. Specific tests for these transcripts demonstrated these were also present in normal mouse muscle tissue. © 1997 John Wiley & Sons, Inc. Muscle Nerve, 20, 728–734, 1997.

A DNA amplification assay using the polymerase chain reaction technique designed for the rapid identification of Mycobacterium bovis organisms was used to test 211 human mycobacterial isolates and 177 clinical specimens previously submitted for routine mycobacterial culture. The procedures described could be used by routine or specialist laboratories for identification of M. tuberculosis complex organisms in 4 h and/or as a rapid screening method for the direct detection of M. tuberculosis complex organisms in specimens.

Antisense oligomer manipulation of pre-mRNA splicing can be used to remove exons carrying premature stop codons or to restore the reading frame around frame-shifting mutations. Phase 1 clinical trials have demonstrated that antisense oligomer-mediated splicing manipulation can restore dystro-phin expression in muscle in a subset of Duchenne muscular dystrophy (DMD) patients. The complexities of dystrophin gene expression and widespread distribution of the protein have presented major challenges to gene and cell therapies for DMD. However, the size of the dystrophin gene, and the fact that not all of the 79 exons are necessary to encode a protein with at least partial function, make DMD amenable to splice switching intervention.

In this paper, we examine a labor struggle between predominantly Latino service workers and the University of Southern California, the largest private employer in the City of Los Angeles. This struggle is part of a broader revival of the American labor movement, as some unions return to mass action and community-labor alliances. The re-emergence of labor as a social movement allows us to ask new questions about power and resistance. In particular, we maintain that a full understanding of the political potential of social movements requires recognition of their inherently spatial nature. Drawing on the recent spatial turn in social theory, we argue that social movement scholarship can benefit from attention to space as an active dimension of movement organizing. In an ethnography of the USC case, we show how a coalition of workers, students and community members used tactics of spatial transgression on, around, and beyond campus. At the same time, coalition members linked the labor conflict to social and spatial inequalities between the university and surrounding neighborhoods, and to citywide movements for living wages and job security. Through these actions, the coalition undermined a commonsense understanding of USC as a benevolent employer and good neighbor, and challenged the university's move to gain flexibility through sub-contracting. While we are constrained in our ability to generalize from the USC case, our analysis suggests that further attention to the spatiality of such struggles can enrich social movements scholarship.