bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential localization and function of antibody-forming cells responsive to inactivated or live-attenuated influenza virus vaccines
Authors: Sealy Robert , Webby Richard J. , Crumpton Jeri C. , Hurwitz Julia L. 
Published: November 2012

AbstractCurrently, there are two different types of licensed influenza virus vaccines available in the USA, the live attenuated cold-adapted vaccine and the inactivated vaccine. Children greater than 2 years of age and adults younger than 50 years (apart from those suffering from immunodeficiencies or lung disease) may choose between the two vaccines. Previous studies have shown that both vaccines elicit significant serum antibody responses. However, comprehensive analyses of antibody-forming cells (AFCs) in the upper respiratory tract (URT), the critical site of pathogen entry, have been lacking. We therefore compared influenza virus-specific antibody and AFC activities in systemic and mucosal tissues following immunizations of cotton rats with inactivated or live-attenuated vaccines, including vaccines from the 2009-10 and 2010-11 seasons. Results demonstrated that inactivated and live-attenuated vaccines induced virus-specific AFCs, but patterns of residence and function were highly disparate. The inactivated vaccine elicited AFCs predominantly in the spleen and bone marrow; IgG was the main isotype. In contrast, the live attenuated vaccine elicited acute and long-sustained AFC responses in the diffuse nasal-associated lymphoid tissue (d-NALT) and lung, with IgA being the predominant isotype. The appearance of these d-NALT URT responses was confirmed by a similar study of the 2009–10 live attenuated vaccine in ferrets. Data emphasize that the inactivated and live-attenuated vaccines that are each capable of protecting humans from influenza virus disease do so by very different modes of immune surveillance.
Long‐term (12‐month) improvement in meibomian gland function and reduced dry eye symptoms with a single thermal pulsation treatment
Authors: Greiner Jack V 
Published: November 2012

AbstractPurposeTo determine the 1‐year post‐treatment dry eye status of subjects with meibomian gland dysfunction and dry eye symptoms after receiving a single LipiFlow Thermal Pulsation System treatment.DesignSingle‐centre, prospective, observational, open‐label, 1‐month‐registered clinical trial with a 1‐year follow‐up examination.ParticipantsPatients with evaporative dry eye disease with meibomian gland dysfunction and dry eye symptoms who had participated in the registered 1‐month clinical trial.MethodsEighteen of 30 subjects initially enrolled were able to return for a 1‐year follow‐up. Both eyes of all patients were treated with a single 12‐min treatment using the LipiFlow Thermal Pulsation System. Meibomian gland function, tear break‐up time and dry eye symptoms were measured. Data are presented for pretreatment (baseline), and 1‐month and 1‐year post‐treatment.Main Outcome MeasuresMeibomian gland secretion scores, and tear break‐up time and dry eye symptoms.ResultsSignificant improvement in meibomian gland secretion scores from baseline measurements (4.0 ± 3.4) to 1‐month post‐treatment (11.3 ± 4.7; P < 0.0005) was maintained at 1‐year (7.3 ± 4.6; P < 0.05). Baseline tear break‐up time (4.9 ± 3.0) was significantly increased at 1‐month (9.5 ± 6.9; P < 0.05); however, this improvement was no longer evident at 1‐year post‐treatment (6.0 ± 4.4). The significant improvement in symptom scores on Ocular Surface Disease Index and Standard Patient Evaluation of Eye Dryness questionnaires observed at 1‐month (P < 0.0005) was maintained at 1‐year (Ocular Surface Disease Index [P < 0.05]; Standard Patient Evaluation of Eye Dryness [P < 0.0005]).ConclusionA single 12‐min treatment with the Lipi Flow Thermal Pulsation System offers an effective treatment for evaporative dry eye and meibomian gland dysfunction resulting in significant and sustained improvement in signs and symptoms for up to 1 year.
A homozygous mutation of voltage‐gated sodium channel βI gene SCN1B in a patient with Dravet syndrome
Authors: Ogiwara Ikuo , Nakayama Tojo , Yamagata Tetsushi , Ohtani Hideyuki , Mazaki Emi , Tsuchiya Shigeru , Inoue Yushi , Yamakawa Kazuhiro 
Published: November 2012

SummaryDravet syndrome is a severe form of epileptic encephalopathy characterized by early onset epileptic seizures followed by ataxia and cognitive decline. Approximately 80% of patients with Dravet syndrome have been associated with heterozygous mutations in SCN1A gene encoding voltage‐gated sodium channel (VGSC) αI subunit, whereas a homozygous mutation (p.Arg125Cys) of SCN1B gene encoding VGSC βI subunit was recently described in a patient with Dravet syndrome. To further examine the involvement of homozygous SCN1B mutations in the etiology of Dravet syndrome, we performed mutational analyses on SCN1B in 286 patients with epileptic disorders, including 67 patients with Dravet syndrome who have been negative for SCN1A and SCN2A mutations. In the cohort, we found one additional homozygous mutation (p.Ile106Phe) in a patient with Dravet syndrome. The identified homozygous SCN1B mutations indicate that SCN1B is an etiologic candidate underlying Dravet syndrome.
Medicine use and medicine-related problems experienced by ethnic minority patients in the United Kingdom: a review
Authors: Alhomoud Faten , Dhillon Soraya , Aslanpour Zoe , Smith Felicity 
Published: November 2012

Abstract

Objective
The aim of this review was to establish type(s) and possible cause(s) of medicine-related problems (MRPs) experienced by ethnic minorities in the UK and to identify recommendations to support these patients in the effective use of medicines.

Methods
A systematic search of studies related to problems with medicine use experienced by ethnic minorities in the UK was performed using the following databases: PubMed, Embase, International Pharmaceutical Abstract and Scopus from 1990 to 2011. A hand search for relevant citations and key journals was also performed.

Key findings
Fifteen studies were found. The MRPs identified across studies included lack of information, problems with not taking medicines as advised, concern of dependency or side effects, lack of regular monitoring and review, risk of adverse drug reactions, adverse events and problems in accessing healthcare services. Many problems are common in other groups, however, studies examining possible explanatory factors discussed how the cultural and religious beliefs, previous experiences, different expectations, language and communication barriers, lack of knowledge of the healthcare services and underestimating patients' desire for information may contribute to the problems. Some of the recommendations were made based on the problems that were found, but these have not been evaluated.

Conclusions
Little evidence is known of what influences MRPs among ethnic minorities, despite the increased diversification of populations in countries throughout the world. To support their entire populations in the use of medicines, we have to ensure that we understand their different perspectives and needs regarding the effective use of medicines.
Role of immediate radical cystectomy in the treatment of patients with residual T1 bladder cancer on restaging transurethral resection
Authors: Sternberg Itay A. , Keren Paz Gal E. , Chen Ling Y. , Herr Harry W. , Dalbagni Guido 
Published: November 2012

What's known on the subject? and What does the study add?
Bladder cancer patients with lamina propria invasion (T1 disease) and residual T1 disease on restaging transurethral resection of bladder tumour (re‐TURBT) are at a very high risk for recurrence and progression. Despite this risk, most patients are treated with a bladder preserving approach and not immediate radical cystectomy (RC).
In this study we have shown that a quarter of patients with T1 bladder cancer and residual T1 on re‐TURBT who are treated with immediate RC are found to have carcinoma invading bladder muscle at RC and 5% have lymph node metastases. We have also found that >30% of patients treated with deferred RC after initial bladder‐preserving therapy harbour carcinoma invading bladder muscle and almost 20% of these patients have lymph node metastases. Thus, immediate RC should be considered in all patients with T1 bladder cancer and residual T1 on re‐TURBT.
Objective
To report the overall survival (OS) and cancer‐specific survival (CSS) of patients with residual T1 bladder cancer on restaging transurethral resection of the bladder tumour (re‐TURBT).
Materials and Methods
We performed a retrospective review of 150 evaluable patients treated for T1 bladder cancer with residual T1 disease found on re‐TURBT between 1990 and 2007.
Patients were treated with immediate radical cystectomy (RC) or a bladder‐preserving approach (deferred or no RC).
A univariate Cox proportional hazards regression model was used to test the association between treatment approach and survival.
Results
Residual T1 bladder cancer was found in 150 evaluable patients, of whom 57 received immediate RC and 93 were treated with a bladder‐preserving approach.
Fourteen out of 57 patients receiving immediate RC and 8/26 patients receiving deferred RC had carcinoma invading bladder muscle in the RC specimen. Three out of 57 and 5/26 patients had lymph node metastases in the RC specimen.
Median follow‐up was 3.74 years.
Thirty‐nine patients died during follow‐up, 16 from bladder cancer. There was no significant association between immediate RC and CSS (hazard ratio [HR] 1.15, 95% confidence interval [CI] 0.43–3.09, P = 0.8) or OS (HR 0.79, 95% CI 0.4–1.53, P = 0.5).
Conclusions
Because of the low number of events we cannot conclude whether RC offers a survival advantage in patients with residual T1 bladder cancer on re‐TURBT.
Since a quarter of patients had carcinoma invading bladder muscle, RC should be considered in these patients.
A larger, preferably randomized, study with longer follow‐up is needed.
Suits you? A qualitative study exploring preferences regarding the tailoring of consumer medicines information
Authors: Dickinson Rebecca , Hamrosi Kim , Knapp Peter , Aslani Parisa , Sowter Julie , Krass Ines , Raynor David K 
Published: November 2012

Abstract

Objectives
To explore participants' opinions and preferences on tailored written medicines information.

Methods
Forty-five participants were recruited to eight focus groups, run concurrently in Australia (23 participants in four groups) and the UK (22 participants in four groups). Participants were provided with exemplar leaflets for a cardiovascular medicine based on the angiotensin-converting enzyme (ACE) inhibitor ramipril, which was tailored for a man aged 55 with hypertension. Reference to other indications of the medicine, children's doses, pregnancy and breast-feeding information were removed. A topic guide directed the discussion and explored preferences and opinions on tailored leaflets. Focus group discussions were recorded, transcribed verbatim and content analysed using adapted cross-case study analysis.

Key findings
Participants welcomed the concept of tailored information, desiring shorter and more relevant information. Information tailored to their condition or disease was most sought-after, followed by tailoring by age or gender. However, some participants voiced concerns about the potential for the wrong information being given to patients who would be unable to recognise that it was incorrect. Other concerns included how tailoring might impact upon the quality of information available and the feasibility of delivery, especially regarding the legal implications (Australia) and the cost (UK). A key finding was the participants' desire for a truly individualised approach to tailoring medicines information, as opposed to the generalised tailored information provided in the study. Participants said they would value having spoken communication with a healthcare professional at the same time as they received tailored leaflets.

Conclusions
Most participants welcomed tailored leaflets but overall valued a more personalised approach than the generalised tailored information we provided. Despite concerns about quality and delivery, many felt tailoring written medicines information could improve the relevance of the information to the individual and potentially encourage them to value it.
DNA damage induces nucleoid compaction via the Mre11‐Rad50 complex in the archaeon Haloferax volcanii
Authors: Delmas Stéphane , Duggin Iain G. , Allers Thorsten 
Published: November 2012

SummaryIn prokaryotes the genome is organized in a dynamic structure called the nucleoid, which is embedded in the cytoplasm. We show here that in the archaeon Haloferax volcanii, compaction and reorganization of the nucleoid is induced by stresses that damage the genome or interfere with its replication. The fraction of cells exhibiting nucleoid compaction was proportional to the dose of the DNA damaging agent, and results obtained in cells defective for nucleotide excision repair suggest that breakage of DNA strands triggers reorganization of the nucleoid. We observed that compaction depends on the Mre11‐Rad50 complex, suggesting a link to DNA double‐strand break repair. However, compaction was observed in a radA mutant, indicating that the role of Mre11‐Rad50 in nucleoid reorganisation is independent of homologous recombination. We therefore propose that nucleoid compaction is part of a DNA damage response that accelerates cell recovery by helping DNA repair proteins to locate their targets, and facilitating the search for intact DNA sequences during homologous recombination.
Immunoglobulin G4‐related lung disease: Clinicoradiological and pathological features
Authors: Matsui Shoko , Hebisawa Akira , Sakai Fumikazu , Yamamoto Horoshi , Terasaki Yasuhiro , Kurihara Yasuyuki , Waseda Yuko , Kawamura Tetsuji , Miyashita Tomoko , Inoue Hiromasa , Hata Norihiko , Masubuchi Hiroaki , Sugino Keishi , Kishi Jun , Kobayashi Hideo , Usui Yutaka , Komazaki Yoshitoshi , Kawabata Yoshinori , Ogura Takashi 
Published: November 2012

AbstractBackground and objectiveImmunoglobulin G4 (IgG4)‐related disease is a multi‐organ disorder that can include the lungs. IgG4‐related lung disease can present in various forms; the clinical, radiological and pathological features of patients with this disease have been assessed.MethodsForty‐eight patients suspected of having IgG4‐related lung disease, with a high serum concentration of IgG4 and abundant IgG4‐positive plasma cell infiltration into the intrathoracic organs, were retrospectively evaluated. Their clinical features, chest imaging findings and pathological findings were examined, with final diagnoses made by an open panel conference.ResultsOf the 48 patients, 18 with extrathoracic manifestations were diagnosed as having IgG4‐related lung disease. Most of these patients were middle‐aged to elderly men. IgG4‐related lung disease was characterized by high serum concentrations of IgG and IgG4, normal white blood cell count and serum C‐reactive protein concentration and a good response to corticosteroids. Common radiological findings included mediastinal lymphadenopathy and thickening of the perilymphatic interstitium, with or without subpleural and/or peribronchovascular consolidation. Pathological examination showed massive lymphoplasmacytic infiltration with fibrosis in and around the lymphatic routes, with distribution well correlated with radiological manifestations.ConclusionsThe findings suggest that the intrathoracic manifestations of IgG4‐related lung disease develop through lymphatic routes of the lungs and show various clinical characteristics. Because some lymphoproliferative disorders show similar findings, the correlation of clinicoradiological and pathological characteristics is crucial for the diagnosis of IgG4‐related lung disease.
Social Competence in Preschool Children: Replication of Results and Clarification of a Hierarchical Measurement Model
Authors: Santos António J. , Peceguina Inês , Daniel João R. , Shin Nana , Vaughn Brian E. 
Published: November 2012

AbstractThis study tested assumptions and conclusions reached in an earlier confirmatory factor analysis (CFA) study of the social competence (SC) construct for preschool children. Two samples (total N = 408; a new Portuguese sample and one from US samples that had participated in the original study) contributed data. Seven SC indicators were tested for mean differences across age, sex, and sample. Significant sex differences were found for peer acceptance (favoring girls) and for initiating affectively neutral interactions (boys had higher rates), and the sex by sample interaction also was significant for initiating interactions (i.e., effect significant only in the Portuguese sample). In CFAs, the hypothesized structure of SC fits the data and was invariant across sample and age within sample in both measurement and structural tests. The model was invariant at the measurement level for sex within sample tests, but not at the structural level. The results replicate and extend understandings of SC reported in the original study.
Effects of glutamine supplementation on muscle function and stress responses in a mouse model of spinal cord injury
Authors: Chamney Carissa , Godar Michelle , Garrigan Ethan , Huey Kimberly A. 
Published: November 2012

New Findings
What is the central question of this study?The beneficial effects of glutamine supplementation are related to heat shock protein induction and reduced inflammation, but its effects on skeletal muscle function, heat shock protein expression and inflammatory factors after spinal cord injury (SCI) are unknown.
What is the main finding and its importance?Using a mouse model of SCI, glutamine supplementation for 7 days following SCI was associated with significant improvements in muscle force, fatigue resistance and maintenance of contractile proteins versus placebo. Lower protein levels of heat shock proteins, interleukin‐6 and tumour necrosis factor‐α after SCI suggest that reduced stress is experienced by skeletal muscles with glutamine. The findings support glutamine as a therapeutic intervention to moderate inflammation and accelerate recovery of muscle function after SCI.
Spinal cord injury (SCI) results in loss of muscle function due to rapid breakdown of contractile proteins. Glutamine supplementation improves clinical outcomes, but its effects on muscle function after SCI are unknown. The benefits of glutamine in non‐skeletal muscle tissues involve elevated heat shock protein (Hsp)70 and Hsp25, but the muscle response may differ because it is the largest contributor to plasma glutamine. We tested the hypothesis that glutamine preserves muscle function after SCI and that this is associated with increased heat shock protein and reduced inflammatory factors, interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNFα). Changes in plantarflexor force, fatigability and total myofibrillar, Hsp70, Hsp25, IL‐6 and TNFα muscle protein levels were measured 7 days after sham or spinal cord transection surgery in mice receiving daily placebo or glutamine. Compared with placebo, after SCI glutamine significantly attenuated the reductions in maximal isometric force (0.22 ± 0.01 versus 0.31 ± 0.03 N, respectively) and fatigue resistance (34 ± 4 versus 59 ± 4% of initial force, respectively). Glutamine significantly ameliorated the loss of myofibrillar protein with spinal cord transection. Spinal cord transection was associated with decreased Hsp70 and Hsp25 with glutamine only (45 ± 3 and 44 ± 5% of placebo, respectively). Glutamine significantly reduced spinal cord transection‐associated increases in IL‐6 and TNFα compared with placebo (38 ± 6 and 37 ± 8% of placebo, respectively). Functionally, early reductions in contractile protein, force and fatigue resistance after SCI were reversed with glutamine. Spinal cord transection‐associated reductions in Hsp70, Hsp25, IL‐6 and TNFα with glutamine versus placebo suggest lower stress in the muscle, possibly related to a reduced need to produce glutamine. These findings support glutamine as a therapeutic intervention to accelerate recovery of muscle function after SCI.
Ca2+‐dependent proteolysis of junctophilin‐1 and junctophilin‐2 in skeletal and cardiac muscle
Authors: Murphy R. M. , Dutka T. L. , Horvath D. , Bell J. R. , Delbridge L. M. , Lamb G. D. 
Published: November 2012

Key points
If skeletal muscle fibres are subjected to excessive activation, or stretched whilst contracting, they subsequently display long‐term reductions in their force response, apparently due in part to structural or molecular changes at the triad junction, where excitation of the surface membrane triggers Ca2+ release from the internal Ca2+ store.
The changes appear to be due to excessive or prolonged increases in intracellular Ca2+ levels, which activate Ca2+‐dependent proteases known as calpains, but their target proteins are currently unknown.
This study shows that excessive muscle stimulation, or directly raising intracellular Ca2+ levels, causes calpain activation in tandem with proteolysis of junctophilin, a key protein thought to hold the triad junction together.
Proteolysis of junctophilin is also seen in muscle of mice with muscular dystrophy and in cardiac muscle following ischaemic damage.
Proteolysis of junctophilin may be a major factor causing muscle weakness and cardiac dysfunction in a range of circumstances.
Abstract  Excessive increases in intracellular [Ca2+] in skeletal muscle fibres cause failure of excitation–contraction coupling by disrupting communication between the dihydropyridine receptors in the transverse tubular system and the Ca2+ release channels (RyRs) in the sarcoplasmic reticulum (SR), but the exact mechanism is unknown. Previous work suggested a possible role of Ca2+‐dependent proteolysis in this uncoupling process but found no proteolysis of the dihydropyridine receptors, RyRs or triadin. Junctophilin‐1 (JP1; ∼90 kDa) stabilizes close apposition of the transverse tubular system and SR membranes in adult skeletal muscle; its C‐terminal end is embedded in the SR and its N‐terminal associates with the transverse tubular system membrane. Exposure of skeletal muscle homogenates to precisely set [Ca2+] revealed that JP1 undergoes Ca2+‐dependent proteolysis over the physiological [Ca2+] range in tandem with autolytic activation of endogenous μ‐calpain. Cleavage of JP1 occurs close to the C‐terminal, yielding a ∼75 kDa diffusible fragment and a fixed ∼15 kDa fragment. Depolarization‐induced force responses in rat skinned fibres were abolished following 1 min exposure to 40 μm Ca2+, with accompanying loss of full‐length JP1. Supraphysiological stimulation of rat skeletal muscle in vitro by repeated tetanic stimulation in 30 mm caffeine also produced marked proteolysis of JP1 (and not RyR1). In dystrophic mdx mice, JP1 proteolysis is seen in limb muscles at 4 and not at 10 weeks of age. Junctophilin‐2 in cardiac and skeletal muscle also undergoes Ca2+‐dependent proteolysis, and junctophilin‐2 levels are reduced following cardiac ischaemia–reperfusion. Junctophilin proteolysis may contribute to skeletal muscle weakness and cardiac dysfunction in a range of circumstances.