Retraction: ‘Sunlight exposure is important for preventing hip fractures in patients with Alzheimer's disease,Parkinson's disease,or stroke’ by J. Iwamoto,T. Takeda and H. Matsumoto

The above article from Acta Neurologica Scandinavica, published online on 18 June 2011 in Wiley Online Library ( http://wileyonlinelibrary.com ) and in Volume 125, pp. 279‐284, has been retracted by agreement between the authors, the Journal Editor‐in‐Chief Elinor Ben‐Menachem and John Wiley & Sons Ltd. The Retraction has been agreed due to extensive duplication of previously published material on the part of Dr Sato, who has acknowledged full responsibility. Dr. Iwamoto would like to note the following information related to this retraction:

• Dr. Sato admitted that he was solely involved in the scientific misconducts.
• I did not actually participate in Dr. Sato's studies. I am an honorary author of Sato's Papers.
• When I was preparing the Subject Paper in the year 2012, I clearly was unaware of the fact Dr. Sato was involved in scientific misconducts.

REFERENCES Sato Y, Iwamoto J, Kanoko T, Satoh K. Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in hospitalized, elderly women with Alzheimers disease: a randomized controlled trial. J Bone Miner Res. 2005;20:1327‐1333. Sato Y, Iwamoto J, Honda Y. Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in Parkinson's disease. Parkinsonism Relat Disord. 2011;17:22‐26. Sato Y, Metoki N, Iwamoto J, Satoh K. Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in stroke patients. Neurology. 2003;61:338‐342. Iwamoto J, Takeda T, Matsumoto H. Sunlight exposure is important for preventing hip fractures in patients with Alzheimer's disease, Parkinson's disease, or stroke. Acta Neurol Scand. 2012;125:279‐284.     

Retracted: ‘Increased ICAM,VCAM, and E‐selectin levels in first manic episode’ by Sermin Kesebir, Çetin Turan, Özgür Süner,and Elif Tatlidil Yaylaci

http://onlinelibrary.wiley.com/doi/10.1111/bdi.12269/pdf . The above article from Bipolar Disorders – An International Journal of Psychiatry and Neurosciences, published online on 16 October 2014 in Wiley Online Library ( http://onlinelibrary.wiley.com/doi/10.1111/bdi.12269/abstract ), has been retracted by agreement among the authors, the journal Editors‐in‐Chief, K.N. Roy Chengappa and Samuel Gershon, and John Wiley & Sons, Ltd. The retraction has been agreed due to overlap between this article and the following article published in the Journal of Affective Disorders, ‘Are ICAM, VCAM and E‐selectin levels different in first manic episode and subsequent remission?’ by Çetin Turan, Sermin Kesebir, and Özgür Süner, Volume 163, 2014, pages 76–80. Reference Kesebir S, TuranÇ, Süner Ö, Yaylaci ET. Increased ICAM, VCAM, and E‐selectin levels in first manic episode. Bipolar Disord doi/ 10.1111/bdi.12269 .     

Endothelial nitric oxide synthase Glu298Asp, 4b/a,and −786T>C gene polymorphisms and the risk of ischemic stroke

Saidi S, Mallat SG, Almawi WY, Mahjoub T. Endothelial nitric oxide synthase Glu298Asp, 4b/a, and ?786T>C gene polymorphisms and the risk of ischemic stroke
Acta Neurol Scand: 2010: 121: 114–119.
© 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Background and purpose – Endothelial nitric oxide synthase (eNOS) gene polymorphisms were associated with reduced NO production, and were evaluated as risk factors for ischemic stroke (IS). We investigated the association between eNOS gene ?786T>C (promoter), 27‐bp repeat 4b/4a (intron 4), and Glu298Asp (exon 7) polymorphisms with IS in 329 IS patients and 444 controls. Materials and methods – Glu298Asp and ?786T>C genotyping was done by PCR‐RFLP, 4b/4a was assessed by PCR–ASA. The contribution of eNOS polymorphisms to IS was analyzed by haplotype and multivariate regression analysis. Results – Higher frequency of 298Asp allele was seen in IS patients (P = 1.2 × 10^?10), which remained independently associated with IS on multivariate analysis after controlling for traditional cerebrovascular risk factors. Allele and genotype distribution of 4b/4a and ?786T>C polymorphisms were comparable between patient and controls. Significantly higher prevalence of 298Asp/4b/?786T and 298Asp/4b/?786C haplotypes were seen in IS cases, thus conferring a disease susceptibility nature to these haplotypes. Multivariate regression analysis confirmed the association of 298Asp/4b/?786T and 298Asp/4b/?786C haplotypes, and in addition identified 298Asp/4a/?786T haplotype to be independently associated with IS, after controlling for traditional cerebrovascular risk factors. Conclusions – Genetic variation at the eNOS locus represent genetic risk factor for increased susceptibility to IS.     

Retraction: Effect of Fasudil on remyelination following cuprizone‐induced demyelination.

Retraction: Wang J, Sui R‐X, Miao Q, et al. Effect of Fasudil on remyelination following cuprizone‐induced demyelination. CNS Neuroscience & Therapeutics, 2020;26:76–89. https://doi.org/10.1111/cns.13154 . The above article published online on May 23, 2019, in Wiley Online Library ( wileyonlinelibrary.com ), has been retracted by agreement between the authors, the journal Editor in Chief, Professor Jun Chen, and John Wiley & Sons Ltd. The retraction has been agreed due to major overlap with a previously published article from the same group of authors.     

The cardiorespiratory response and physiological determinants of the assisted 6‐minute handbike cycle test in adult males with muscular dystrophy

Introduction: The assisted 6‐minute cycle test (A6MCT) distance was assessed in adults with muscular dystrophy (MD). Methods: Forty‐eight males, including those with Duchenne MD (DMD), limb‐girdle MD (LGMD), fascioscapulohumeral MD (FSHD), and Becker MD (BMD), as well as a group without MD (CTRL), completed handgrip strength (HGS), lung function [forced expiratory volume in 1 second (FEV₁) and forced vital capacity (FVC)], body fat, and biceps thickness assessments. During the A6MCT, ventilation (VE ), oxygen uptake (VO ₂), carbon dioxide (VCO ₂), and heart rate (HR) were recorded. Results: A6MCT and HGS were lower in MD than CTRL subjects. FEV₁, FVC, and biceps thickness were lower in MD than CTRL; lower in DMD than BMD, LGMD, and FSHD; but were not different between BMD, LGMD, and FSHD. A6MCT correlated with HGS, FEV₁, FVC, body fat, VO ₂, VCO ₂, HR, and VE (r = 0.455–0.708) in pooled BMD, LGMD, and FSHD participants. Discussion: A shorter A6MCT distance in adult males with MD was attributable to HGS and lung function. The A6MCT is appropriate for assessment of physical function in adults with MD. Muscle Nerve 58 : 427–433, 2018     

The value of putaminal diffusion imaging versus 18‐fluorodeoxyglucose positron emission tomography for the differential diagnosis of the Parkinson variant of multiple system atrophy

Differentiating the Parkinson variant of multiple system atrophy (MSA‐P) from idiopathic Parkinson's disease (PD) and other forms of atypical parkinsonism can be difficult because symptoms overlap considerably. 18‐Fluorodeoxyglucose positron emission tomography (FDG‐PET) is a powerful imaging technique that can assist in the diagnosis of MSA‐P via detection of putaminal and cerebellar hypometabolism. Recent studies suggest that diffusion‐weighted imaging (DWI) might be of similar diagnostic value, as it can detect microstructural damage in the putamen by means of an increased mean diffusivity (MD). The aim of this study was a direct comparison of DWI and FDG‐PET by using both methods on the same subject cohort. To this end, combined DWI and FDG‐PET were employed in patients with MSA‐P (n = 11), PD (n = 13), progressive supranuclear palsy (n = 8), and in 6 control subjects. MD values and FDG uptake ratios were derived from volumetric parcellations of the putamen and subjected to further analysis of covariance (ANCOVA) and receiver operating characteristics analyses. MSA‐P was found to be associated with an increased posterior putaminal MD (P < 0.001 in all subgroup comparisons) that correlated strongly with local reductions in FDG uptake (r = ?0.85, P = 0.002). DWI discriminated patients with MSA‐P from other subgroups nearly as accurately as FDG‐PET (area under the curve = 0.89 vs 0.95, P = 0.27 [pooled data]). Our data suggest a close association between the amount of putaminal microstructural damage and a reduced energy metabolism in patients with MSA‐P. The clinical use of DWI for the differential diagnosis of MSA‐P is encouraged. © 2013 International Parkinson and Movement Disorder Society     

Accrued somatic mutations (nucleic acid changes) trigger ALS: 2005–2015 update

Amyotrophic lateral sclerosis (ALS) is a multilevel disease of the motor neuron system. The mechanisms triggering disease onset should be considered separately from those facilitating its spread and motor neuron death. In 2005, I brought together clinical and epidemiological evidence to support the hypothesis that acquired nucleic acid changes may trigger sporadic ALS. Since 2005, the conceptual foundations for this hypothesis have been strengthened. The journal Amyotrophic Lateral Sclerosis was renamed Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration. The focal onset, with simultaneous initial maximal upper and lower motor neuron involvement in the region of onset, and patterns of spread, were characterized further. Clues from the epidemiology of sporadic ALS were affirmed by quantitative analysis, including the increase in disease incidence with age, suggesting accrual of time‐dependent changes, and the confirmation of smoking as an established risk factor. Additional observations support the conclusion that accrued somatic mutations trigger onset of ALS. Muscle Nerve 53 : 842–849, 2016     

Fibrosis inhibition and muscle histopathology improvement in laminin‐α2‐deficient mice

In muscular dystrophies (MD) the loss of muscle and its ability to function are associated with fibrosis. We evaluated the efficacy of halofuginone in reducing fibrosis in the dy^2J/dy^2J mouse model of congenital MD. Mice were injected intraperitoneally with 5 μg of halofuginone 3 times a week for 5 or 15 weeks, starting at the age of 3 weeks. Halofuginone caused a reduction in collagen synthesis in hindlimb muscles. This was associated with reductions in the degenerated area, in cell proliferation, in the number of myofibers with central nuclei, with increased myofiber diameter, and with enhanced motor coordination and balance. Halofuginone caused a reduction in infiltrating fibroblasts that were located close to centrally nucleated myofibers. Our results suggest that halofuginone reduced the deleterious effects of fibrosis, thus improving muscle integrity. Halofuginone meets the criteria for a novel antifibrotic therapy for MD patients. Muscle Nerve, 2010     

Response to Rosburg: A voxel‐based statistical parametric mapping of MMN current densities

The original article to which this Commentary refers was published in the November, 2002 issue of Human Brain Mapping ( Park H‐J, Kwon JS, Youn T, Pae JS, Kim J‐J, Kim M‐S, Ha K‐S. Statistical Parametric Mapping of LORETA Using High‐Density EEG and Individual MRI: Application to Mismatch Negativities in Schizophrenia. Hum Brain Mapp 2002;17:168–178 ). A Commentary appears in the January, 2004 issue ( Rossburg T: Left Parietal Lobe Activation to Auditory Mismatch? Hum. Brain Mapp. 2004;21:46–48 ). © 2003 Wiley‐Liss, Inc.     

Twitch and M‐wave potentiation induced by intermittent maximal voluntary quadriceps contractions: Differences between direct quadriceps and femoral nerve stimulation

Introduction: The aim of this study was to investigate differences in twitch and M‐wave potentiation in the quadriceps femoris when electrical stimulation is applied over the quadriceps muscle belly versus the femoral nerve trunk. Methods: M‐waves and mechanical twitches were evoked using direct quadriceps muscle and femoral nerve stimulation between 48 successive isometric maximal voluntary contractions (MVC) from 10 young, healthy subjects. Potentiation was investigated by analyzing the changes in M‐wave amplitude recorded from the vastus medialis (VM) and vastus lateralis (VL) muscles and in quadriceps peak twitch force. Results: Potentiation of twitch, VM M‐wave, and VL M‐wave were greater for femoral nerve than for direct quadriceps stimulation (P < 0.05). Despite a 50% decrease in MVC force, the amplitude of the M‐waves increased significantly during exercise. Conclusions: In addition to enhanced electrogenic Na⁺‐K⁺ pumping, other factors (such as synchronization in activation of muscle fibers and muscle architectural properties) may significantly influence the magnitude of M‐wave enlargement. Muscle Nerve 48 : 920–929, 2013     

Apolipoprotein E ε4 modulates functional brain connectome in Alzheimer's disease

The apolipoprotein E (APOE) ?4 allele is a well‐established genetic risk factor for Alzheimer's disease (AD). Recent research has demonstrated an APOE ?4‐mediated modulation of intrinsic functional brain networks in cognitively normal individuals. However, it remains largely unknown whether and how APOE ?4 affects the brain's functional network architecture in patients with AD. Using resting‐state functional MRI and graph‐theory approaches, we systematically investigated the topological organization of whole‐brain functional networks in 16 APOE ?4 carriers and 26 matched noncarriers with AD at three levels: global whole‐brain, intermediate module, and regional node/connection. Neuropsychological analysis showed that the APOE ?4 carriers performed worse on delayed memory but better on a late item generation of a verbal fluency task (associated with executive function) than noncarriers. Whole‐brain graph analyses revealed that APOE ?4 significantly disrupted whole‐brain topological organization as characterized by (i) reduced parallel information transformation efficiency; (ii) decreased intramodular connectivity within the posterior default mode network (pDMN) and intermodular connectivity of the pDMN and executive control network (ECN) with other neuroanatomical systems; and (iii) impaired functional hubs and their rich‐club connectivities that primarily involve the pDMN, ECN, and sensorimotor systems. Further simulation analysis indicated that these altered connectivity profiles of the pDMN and ECN largely accounted for the abnormal global network topology. Finally, the changes in network topology exhibited significant correlations with the patients' cognitive performances. Together, our findings suggest that the APOE genotype modulates large‐scale brain networks in AD and shed new light on the gene‐connectome interaction in this disease. Hum Brain Mapp 36:1828–1846, 2015. © 2015 Wiley Periodicals, Inc .     

APOE ɛ4 constrains engagement of encoding‐related compensatory networks in amnestic mild cognitive impairment

People with amnestic mild cognitive impairment (aMCI), compared to healthy older adults (HO), benefit less from semantic congruent cues during episodic encoding. The presence of the apolipoprotein E (APOE) ?4 makes this congruency benefit smaller, but the neural correlates of this deficit are unknown. Here, we estimated the source generators of EEG oscillatory activity associated with successful encoding of face‐location associations preceded by semantically congruent and incongruent cues in HO (N = 26) and aMCI subjects (N = 34), 16 of which were ?4 carriers (?4⁺) and 18 ?4 noncarriers (?4^?). Source estimation was performed in those spectrotemporal windows where the power of low‐alpha, high‐alpha, and beta oscillatory activity differed either between congruent and incongruent faces or between groups. Differences in high‐alpha and beta‐oscillatory dynamics indicated that aMCI ?4⁺ are unable to activate lateral regions of the temporal lobe involved in associative memory and congruency benefit in HO. Interestingly, and regardless of APOE genotype, aMCI activated additional regions relative to HO, through alpha oscillations. However, only activation in a distributed fronto‐temporo‐parietal network in ?4 noncarriers was paralleled by enhanced memory. On the contrary, the redundant prefrontal activation shown by aMCI ?4⁺ did not prevent performance from decreasing. These results indicate that the effect of aMCI‐related degeneracy on functional networks is constrained by the presence of APOE ?4. Whereas individuals with aMCI ?4^? activate attentional, perceptual and semantic compensatory networks, aMCI ?4⁺ show reduced processing efficiency and capacity. © 2015 Wiley Periodicals, Inc.     

Idiopathic generalized epilepsies: a follow‐up study in a single‐center

Kharazmi E, Peltola M, Fallah M, Keränen T, Peltola J. Idiopathic generalized epilepsies: a follow‐up study in a single‐center.
Acta Neurol Scand: 122: 196–201.
© 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective – To characterize adult patients with idiopathic generalized epilepsies (IGEs) with precise evaluation and to assess factors related to refractoriness. Materials and methods – Hospital records of all our patients with IGEs (n = 128) were evaluated in 2005 and followed‐up until 2008. Results – In 2005, 76% of patients were 1‐year seizure‐free. Seizure freedom increased to 82% during the 3‐year follow‐up. Seizure freedom was not significantly associated with age, age at diagnosis, epilepsy duration, exposure to inappropriate initial antiepileptic drug (AED), or delay time between starting initial AED and appropriate AED. Women constituted 78% of patients with merely provoked seizures. In 58% of women with recent seizure, one to two avoidable precipitating factors, such as lack of sleep, alcohol, and forgetting to take AED, were observed. In 2008, all patients with no medication, 91% of monotherapy patients, 60% of patients on two AED, and 14% of patients on three AED were seizure‐free. Conclusions – Most of patients with IGEs can be successfully treated with monotherapy. Refractory seizures in some patients may be because of avoidable factors, especially in young women.     

Microglial TNF‐α mediates enhancement of dopaminergic degeneration by brain angiotensin

In vitro and in vivo models of Parkinson's disease were used to investigate whether TNF‐α plays a major role in the enhancement of the microglial response and dopaminergic degeneration induced by brain angiotensin hyperactivity. Treatment of primary mesencephalic cultures with low doses of the neurotoxin MPP⁺ induced a significant loss of dopaminergic neurons, which was enhanced by cotreatment with angiotensin II and inhibited by TNF‐α inhibitors. Treatment of primary cultures with angiotensin induced a marked increase in levels of TNF‐α, which was inhibited by treatment with angiotensin type‐1‐receptor antagonists, NADPH‐oxidase inhibitors and NFK‐β inhibitors. However, TNF‐α levels were not significantly affected by treatment with angiotensin in the absence of microglia. The microglial origin of the angiotensin‐induced increase in TNF‐α levels was confirmed using dopaminergic (MES 23.5) and microglial (N9) cell lines. Inhibition of the microglial Rho‐kinase activity also blocked the AII‐induced increase in TNF‐α levels. Treatment of the dopaminergic cell line with TNF‐α revealed that NFK‐β activation mediates the deleterious effect of microglial TNF‐α on dopaminergic neurons. Treatment of mice with MPTP also induced significant increases in striatal and nigral TNF‐α levels, which were inhibited by angiotensin type‐1‐receptor antagonists or NFK‐β inhibitors. The present results show that microglial TNF‐α plays a major role in angiotensin‐induced dopaminergic cell death and that the microglial release of TNF‐α is mediated by activation of angiotensin type‐1 receptors, NADPH‐oxidase, Rho‐kinase and NFK‐β. GLIA 2014;62:145–157     

Mutation in the caveolin‐3 gene causes asymmetrical distal myopathy

Mutations in the gene encoding caveolin‐3 (CAV3) can cause a broad spectrum of clinical phenotypes, including limb girdle muscular dystrophy, rippling muscle disease, distal myopathy (MD), idiopathic persistent elevation of serum creatine kinase and cardiomyopathy. MD is a relatively rare subtype of caveolinopathy. Here, we report a sporadic case of a middle‐aged female Chinese patient with MD in which a CAV3 mutation was identical to that previously reported in cases of rippling muscle disease. T1‐weighted enhanced skeletal muscle MRI of the lower limbs showed an abnormal signal in the distal and proximal muscles. A muscle biopsy revealed moderate dystrophic changes, and immunohistochemical staining showed reduced CAV‐3 expression in the plasmalemma. Genetic analysis revealed a heterozygous c.136G > A (p.Ala46Thr) CAV3 mutation that appeared to be de novo because it was absent from the patient's parents. This study suggested that the CAV3 c.136G > A (p.Ala46Thr) mutation can cause MD as well as different phenotypes in different individuals, suggesting that additional unknown loci must affect the disease phenotypes.     

Can’t lead from behind – Happy New Year 2009

Objective: To determine and estimate the efficacy of discharge planning interventions in mental health care from in‐patient to out‐patient treatment on improving patient outcome, ensuring community tenure, and saving costs. Method: A systematic review and meta‐analysis identified studies through an electronic search on the basis of defined inclusion and exclusion criteria and extracted data. Results: Of eleven studies included, six were randomised controlled trials, three were controlled clinical trials, and two were cohort studies. The discharge planning strategies used varied widely, most were limited to preparation of discharge during in‐patient treatment. Pooled risk ratios were 0.66 (95% CI = 0.51 to 0.84; P < 0.001) for hospital readmission rate, and 1.25 (1.07 to 1.47; P < 0.001) for adherence to out‐patient treatment. Effect sizes (Hedge’s g) were ?0.25 (?0.45 to ?0.05; P = 0.02) for mental health outcome, and 0.11(?0.05 to 0.28; NS) for quality of life. Conclusion: Discharge planning interventions are effective in reducing rehospitalisation and in improving adherence to aftercare among people with mental disorders.     

Major Depression in Long‐Term Oxygen Therapy Dependent Chronic Obstructive Pulmonary Disease

PURPOSE

We aimed to investigate the frequency of major depression (MD) in long‐term oxygen therapy (LTOT) dependent chronic obstructive pulmonary disease (COPD) patients and the effect of depression on patients' compliance with the treatment.

DESIGN AND METHODS

Fifty‐four consecutive patients were enrolled in the study and diagnosed as stage 4 COPD according to Global Initiative for Chronic Obstructive Lung Disease guideline. MD was diagnosed with the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition/Clinical Version.

FINDINGS

Thirty‐four (63.0%) patients had MD. MD frequency was significantly higher in patients who were noncompliant with LTOT compared with compliant patients.

PRACTICE IMPLICATIONS

MD is a common psychiatric disorder in COPD patients receiving LTOT.     

Free insulin‐like growth factor (IGF)‐1 and IGF‐binding proteins‐2 and ‐3 in serum and cerebrospinal fluid of amyotrophic lateral sclerosis patients

Background: The insulin‐like growth factor‐1 (IGF‐1) signaling system is regulated by many factors which interact in regulating the bioavailability of IGF‐I. In this context, little information is available on free IGF‐1, the bioactive form of IGF‐1, in amyotrophic lateral sclerosis (ALS). Methods: We investigated the endogenous expression of IGF‐1, and two related binding proteins (IGF‐binding proteins, IGFBP‐2 and BP‐3) in serum and cerebrospinal fluid (CSF) of 54 sporadic ALS (sALS) patients. Twenty‐five healthy individuals and 25 with other neurological diseases (OND) were used as controls. Total and free IGF‐1, and IGFBP‐3 levels were detected by immunoradiometric assay (IRMA); IGFBP‐2 levels were determined by radioimmunoassay (RIA). Results: Total and free IGF‐1, IGFBP‐2 and BP‐3 serum levels were not significantly different between patients and controls, although in sALS patients free IGF‐1 was negatively correlated with ALS‐Functional Rating Scale‐revised (ALS‐FRS‐R) score (r = ?0.4; P = 0.046) and forced vital capacity (FVC) (r = ?0.55; P < 0.04). In CSF, free IGF‐1 was significantly increased in sALS patients compared with OND (P < 0.0001). Conclusions: Though in the serum we did not find significant differences amongst the three groups, IGF‐1 bioavailability, represented by the free IGF‐1 levels, correlated with disease severity. In the CSF, the significant increment of the free fraction of IGF‐1 suggests an up‐regulation of the IGF‐1 system in the intrathecal compartment of sALS patients. Since IGF‐1 is a trophic factor for different tissues, we speculate that high levels of the free IGF‐1 in sALS might reflect a physiological defensive mechanism promoted in response to neural degeneration and/or muscle atrophy.