bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cross‐sectional survey of diabetic neuropathy in Kanagawa and clinical significance of a touch test using tissue paper
Authors: Jin Yasuyuki , Kanamori Akira , Ito Shogo , Matoba Kiyokazu , Miyakawa Masaaki , Kaneshige Hideaki , Obana Mitsuo , Takai Masahiko , Takeda Hiroshi , Machimura Hideo , Minami Nobuaki , Kawata Takahiro , Honda Shin , Aoyagi Sachio , Amemiya Hikaru , Sasai Nobuo , Nakayama Michio , Naka Yoshikazu , Terauchi Yasuo , Matsuba Ikuro 
Published: November 2011

AbstractAims/Introduction:  The prevalence of diabetes mellitus is increasing rapidly in Japan, and diabetic neuropathy is a major factor decreasing diabetic patients’ quality of life, as well as a risk factor for sudden death. The present study aimed to determine the prevalence of diabetic neuropathy and raise awareness about it among patients and their physicians.Materials and Methods:  Diabetic outpatients (N = 5077) at 249 medical institutions within Kanagawa Prefecture, Japan, were surveyed by questionnaire and underwent foot examinations. The questionnaire included 10 questions about sensory abnormalities of both feet, muscle cramps and autonomic symptoms. Foot examinations included testing for vibratory perception of the medial malleolus, Achilles tendon reflexes and touch sensation of the bottom of the great toe using tissue paper.Results:  Of the 5077 patients surveyed, 70.4% reported symptoms. Overall, 75.4% of the patients underwent vibratory perception testing, of whom 44.9% had abnormal thresholds (≤10 s). On the tissue paper touch test, performed in 94.6% of patients, 11.9% had no touch sensation. Of the 2803 type 2 diabetic patients with known background factors who underwent foot examinations, 49.4% had diabetic neuropathy. There was a high prevalence of diabetic neuropathy (36.1%) in patients with <5‐year history. Of the patients with no touch sensation on the tissue paper test, 81.3% had diabetic neuropathy.Conclusions:  The present study identified the prevalence of diabetic neuropathy in Kanagawa Prefecture. The tissue paper test is a simple and excellent method of evaluating decreased superficial sensation that can help evaluate the severity of diabetic neuropathy. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00174.x, 2011)
Nictitating membrane resection in the horse: A comparison of long‐term outcomes using local vs. general anaesthesia
Authors: LABELLE A. L. , METZLER A. G. , WILKIE D. A. 
Published: November 2011

SummaryReasons for performing study:Neoplasia, for which surgical excision is a frequent treatment, is the most common disease of the equine nictitating membrane. There is little long‐term follow‐up information available to the practitioner regarding the long‐term effects of nictitating membrane excision on ocular health. No information is available to compare recurrence of primary neoplasia of the nictitating membrane after excision with local or general anaesthesia.Objectives:To evaluate the long‐term complications of nictitating membrane resection in horses; recurrence of neoplasia of the nictitating membrane when nictitating membrane resection is performed under local vs. general anaesthesia and if the method of anaesthesia used to permit resection of the affected membrane influences the recurrence of neoplasia of the nictitating membrane after complete nictitating membrane resection.Methods:Records of 26 horses receiving resection of the nictitating membrane for primary neoplasia of the nictitating membrane 1999–2009 were reviewed. Clinical examination findings, surgical procedure, anaesthesia type, histopathological findings and details of adjunctive treatment were recorded. Owners were contacted via telephone regarding post operative outcomes. Data were analysed using a Fisher's exact test (P<0.05).Results:The most common long‐term complication of nictitating membrane excision was mild ocular discharge. Squamous cell carcinoma was the most frequent histopathological diagnosis. Recurrence of neoplasia was uncommon (2/26 horses). No significant difference in the number of horses experiencing recurrence of neoplasia was detected between groups receiving general anaesthesia vs. those receiving local anaesthesia.Conclusions:Resection of the nictitating membrane in horses following local anaesthesia is not associated with increased risk of recurrence of neoplasia compared with excision under general anaesthesia. Resection of the nictitating membrane is not associated with any long‐term ocular side effects and can be an effective modality for cure of primary neoplasia of the nictitating membrane in selected cases.
Assembly of Xylanases into Designer Cellulosomes Promotes Efficient Hydrolysis of the Xylan Component of a Natural Recalcitrant Cellulosic Substrate
Authors: Moraïs Sarah , Barak Yoav , Hadar Yitzhak , Wilson David B. , Shoham Yuval , Lamed Raphael , Bayer Edward A. 
Published: November 2011

ABSTRACT

In nature, the complex composition and structure of the plant cell wall pose a barrier to enzymatic degradation. Nevertheless, some anaerobic bacteria have evolved for this purpose an intriguing, highly efficient multienzyme complex, the cellulosome, which contains numerous cellulases and hemicellulases. The rod-like cellulose component of the plant cell wall is embedded in a colloidal blend of hemicelluloses, a major component of which is xylan. In order to enhance enzymatic degradation of the xylan component of a natural complex substrate (wheat straw) and to study the synergistic action among different xylanases, we have employed a variation of the designer cellulosome approach by fabricating a tetravalent complex that includes the three endoxylanases of
Thermobifida fusca
(Xyn10A, Xyn10B, and Xyn11A) and an Xyl43A β-xylosidase from the same bacterium. Here, we describe the conversion of Xyn10A and Xyl43A to the cellulosomal mode. The incorporation of the Xyl43A enzyme together with the three endoxylanases into a common designer cellulosome served to enhance the level of reducing sugars produced during wheat straw degradation. The enhanced synergistic action of the four xylanases reflected their immediate juxtaposition in the complex, and these tetravalent xylanolytic designer cellulosomes succeeded in degrading significant (~25%) levels of the total xylan component of the wheat straw substrate. The results suggest that the incorporation of xylanases into cellulosome complexes is advantageous for efficient decomposition of recalcitrant cellulosic substrates—a distinction previously reserved for cellulose-degrading enzymes.

IMPORTANCE
Xylanases are important enzymes for our society, due to their variety of industrial applications. Together with cellulases and other glycoside hydrolases, xylanases may also provide cost-effective conversion of plant-derived cellulosic biomass into soluble sugars en route to biofuels as an alternative to fossil fuels. Xylanases are commonly found in multienzyme cellulosome complexes, produced by anaerobic bacteria, which are considered to be among the most efficient systems for degradation of cellulosic biomass. Using a designer cellulosome approach, we have incorporated the entire xylanolytic system of the bacterium
Thermobifida fusca
into defined artificial cellulosome complexes. The combined action of these designer cellulosomes versus that of the wild-type free xylanase system was then compared. Our data demonstrated that xylanolytic designer cellulosomes displayed enhanced synergistic activities on a natural recalcitrant wheat straw substrate and could thus serve in the development of advanced systems for improved degradation of lignocellulosic material.
Mechanisms of injuries in World Cup Snowboard Cross: a systematic video analysis of 19 cases
Authors: Bakken Arnhild , Bere Tone , Bahr Roald , Kristianslund Eirik , Nordsletten Lars 
Published: November 2011

BackgroundSnowboard cross (SBX) became an official Olympic sport in 2006. This discipline includes manoeuvring several obstacles while competing in heats. It is common for the riders to collide, making this sport both exciting and at risk of injuries. Although a recent study from the 2010 Olympic Games has shown that the injury risk was high, little is known about the injury mechanisms.ObjectiveTo qualitatively describe the injury situation and mechanism of injuries in World Cup Snowboard Cross.Study designDescriptive video analysis.MethodsNineteen video recordings of SBX injuries reported through the International Ski Federation Injury Surveillance System for four World Cup seasons (2006 to 2010) were obtained. Five experts in the field of sports medicine, snowboard and biomechanics performed analyses of each case to describe the injury mechanism in detail (riding situation and rider behaviour).ResultsInjuries occurred at jumping (n=13), bank turning (n=5) or rollers (n=1). The primary cause of the injuries was a technical error at take-off resulting in a too high jump and subsequent flat-landing. The rider was then unable to recover leading to fall at the time of injury. Injuries at bank turn was characterised by a pattern where the rider in a balanced position lost control due to unintentional contact with another rider.ConclusionJumping appeared to be the most challenging obstacle in SBX, where a technical error at take-off was the primary cause of the injuries. The second most common inciting event was unintentional board contact between riders at bank turning.
Association of the von Hippel–Lindau Protein with AUF1 and Posttranscriptional Regulation of VEGFA mRNA
Authors: Xin Hong , Brown Julie A. , Gong Changning , Fan Hao , Brewer Gary , Gnarra James R. 
Published: November 2011

Abstract
The von Hippel–Lindau (VHL) tumor suppressor gene product is the recognition component of an E3 ubiquitin ligase and is inactivated in patients with VHL disease and in most sporadic clear-cell renal cell carcinomas (RCC). pVHL controls oxygen-responsive gene expression at the transcriptional and posttranscriptional levels. The VEGFA mRNA contains AU-rich elements (ARE) in the 3′–untranslated region, and mRNA stability or decay is determined through ARE-associated RNA-binding factors. We show here that levels of the ARE-binding factor, AUF1, are regulated by pVHL and by hypoxia. pVHL and AUF1 stably associate with each other in cells and AUF1 is a ubiquitylation target of pVHL. AUF1 and another RNA-binding protein, HuR, bind to VEGFA ARE RNA. Ribonucleoprotein (RNP) immunoprecipitations showed that pVHL associates indirectly with VEGFA mRNA through AUF1 and/or HuR, and this complex is associated with VEGFA mRNA decay under normoxic conditions. Under hypoxic conditions pVHL is downregulated, whereas AUF1 and HuR binding to VEGF mRNA is maintained, and this complex is associated with stabilized mRNA. These studies suggest that AUF1 and HuR bind to VEGFA ARE RNA under both normoxic and hypoxic conditions, and that a pVHL–RNP complex determines VEGFA mRNA decay. These studies further implicate the ubiquitin–proteasome system in ARE-mediated RNA degradation. Mol Cancer Res; 10(1); 108–20. ©2011 AACR.
N-nitroso-tris-chloroethylurea Induces Premalignant Squamous Dysplasia in Mice
Authors: Hudish Tyler M. , Opincariu Laura I. , Mozer Anthony B. , Johnson Micah S. , Cleaver Timothy G. , Malkoski Stephen P. , Merrick Daniel T. , Keith Robert L. 
Published: November 2011

Abstract
Squamous cell carcinoma (SCC) and premalignant endobronchial lesions have been difficult to study in murine models. In this study, we evaluate the topical N-nitroso-tris-chloroethylurea (NTCU) murine SCC model, determine the extent to which resulting premalignant airway dysplasia develops, discuss clinicopathologic grading criteria in lesion progression, and confirm that immunohistochemical (IHC) staining patterns are consistent with those observed in human endobronchial dysplasia and SCC. Male and female FVB mice were treated biweekly with topical NTCU (4, 8, or 40 mmol/L) or vehicle for 32 weeks. Following sacrifice, squamous cell lesions were enumerated and categorized into the following groups: flat atypia, low-grade dysplasia, high-grade dysplasia, and invasive SCC. The 40 mmol/L NTCU concentration produced the entire spectrum of premalignant dysplasias and squamous cell carcinomas, but was associated with poor survival. Concentrations of 4 and 8 mmol/L NTCU were better tolerated and produced only significant levels of flat atypia. Squamous origin of the range of observed lesions was confirmed with IHC staining for cytokeratin 5/6, p63, thyroid transcription factor-1 (TTF-1), and Napsin-A. This study shows that topical application of high-dose NTCU produces endobronchial premalignant lesions with classic squamous characteristics and should allow for improved preclinical evaluation of potential chemopreventive agents. Cancer Prev Res; 5(2); 283–9. ©2011 AACR.
Glycogen Synthase Kinase-3α Limits Ischemic Injury, Cardiac Rupture, Post–Myocardial Infarction Remodeling and Death
Authors: Lal Hind , Zhou Jibin , Ahmad Firdos , Zaka Raihana , Vagnozzi Ronald J. , DeCaul Morgan , Woodgett James , Gao Erhe , Force Thomas 
Published: November 2011

Background—
The molecular pathways that regulate the extent of ischemic injury and post–myocardial infarction (MI) remodeling are not well understood. We recently demonstrated that glycogen synthase kinase-3α (GSK-3α) is critical to the heart's response to pressure overload. However, the role, if any, of GSK-3α in regulating ischemic injury and its consequences is not known.

Methods and Results—

MI was induced in wild-type (WT) versus GSK-3α
(−/−)
(KO) littermates by left anterior descending coronary artery ligation. Pre-MI, WT, and KO hearts had comparable chamber dimensions and ventricular function, but as early as 1 week post-MI, KO mice had significantly more left ventricular dilatation and dysfunction than WT mice. KO mice also had increased mortality during the first 10 days post-MI (43% versus 22%;
P
=0.04), and postmortem examination confirmed cardiac rupture as the cause of most of the deaths. In the mice that survived the first 10 days, left ventricular dilatation and dysfunction remained worse in the KO mice throughout the study (8 weeks). Hypertrophy, fibrosis, and heart failure were all increased in the KO mice. Given the early deaths due to rupture and the significant reduction in left ventricular function evident as early as 1 week post-MI, we examined infarct size following a 48-hour coronary artery ligation and found it to be increased in the KO mice. This was accompanied by increased apoptosis in the border zone of the MI. This increased susceptibility to ischemic injury–induced apoptosis was also seen in cardiomyocytes isolated from the KO mice that were exposed to hypoxia. Finally, Bax translocation to the mitochondria and cytochrome C release into the cytosol were increased in the KO mice.

Conclusion—
GSK-3α confers resistance to ischemic injury, at least in part, via limiting apoptosis. Loss of GSK-3α promotes ischemic injury, increases risk of cardiac rupture, accentuates post-MI remodeling and left ventricular dysfunction, and increases the progression to heart failure. These findings are in striking contrast to multiple previous reports in which deletion or inhibition of GSK-3β is protective.
Biomechanical Evaluation of a Novel Reverse Coracoacromial Ligament Reconstruction for Acromioclavicular Joint Separation
Authors: Shu Beatrice , Johnston Tyler , Lindsey Derek P. , McAdams Timothy R. 
Published: November 2011

Background: Enhancing anterior-posterior (AP) stability in acromioclavicular (AC) reconstruction may be advantageous. Purpose: To compare the initial stability of AC reconstructions with and without augmentation by either (1) a novel “reverse” coracoacromial (CA) ligament transfer or (2) an intramedullary AC tendon graft. Hypothesis: Reverse CA transfer will improve AP stability compared with isolated coracoclavicular (CC) reconstruction. Study Design: Controlled laboratory study. Methods: Six matched pairs of cadaveric shoulders underwent distal clavicle resection and CC reconstruction. Displacement (mm) was measured during cyclic loading along AP (±25 N) and superior-inferior (SI; 10-N compression, 70-N tension) axes. Pairs were randomized to receive each augmentation and the same loading protocol applied. Results: Reverse CA transfer (3.71 ± 1.3 mm, standard error of the mean [SEM]; P = .03) and intramedullary graft (3.41 ± 1.1 mm; P = .03) decreased AP translation compared with CC reconstruction alone. The SI displacement did not differ. Equivalence tests suggest no difference between augmentations in AP or SI restraint. Conclusion: Addition of either reverse CA transfer or intramedullary graft demonstrates improved AP restraint and provides similar SI stability compared with isolated CC reconstruction. Clinical Relevance: Reverse CA ligament transfer may be a reasonable alternative to a free tendon graft to augment AP restraint in AC reconstruction.
A Theoretical Framework for Understanding Neuromuscular Response to Lower Extremity Joint Injury
Authors: Pietrosimone Brian G. , McLeod Michelle M. , Lepley Adam S. 
Published: November 2011

Background: Neuromuscular alterations are common following lower extremity joint injury and often lead to decreased function and disability. These neuromuscular alterations manifest in inhibition or abnormal facilitation of the uninjured musculature surrounding an injured joint. Unfortunately, these neural alterations are poorly understood, which may affect clinical recognition and treatment of these injuries. Understanding how these neural alterations affect physical function may be important for proper clinical management of lower extremity joint injuries. Methods: Pertinent articles focusing on neuromuscular consequences and treatment of knee and ankle injuries were collected from peer-reviewed sources available on the Web of Science and Medline databases from 1975 through 2010. A theoretical model to illustrate potential relationships between neural alterations and clinical impairments was constructed from the current literature. Results: Lower extremity joint injury affects upstream cortical and spinal reflexive excitability pathways as well as downstream muscle function and overall physical performance. Treatment targeting the central nervous system provides an alternate means of treating joint injury that may be effective for patients with neuromuscular alterations. Conclusions: Disability is common following joint injury. There is mounting evidence that alterations in the central nervous system may relate to clinical changes in biomechanics that may predispose patients to further injury, and novel clinical interventions that target neural alterations may improve therapeutic outcomes.
Surface IgM stimulation induces MEK1/2-dependent MYC expression in chronic lymphocytic leukemia cells
Authors: Krysov Sergey , Dias Samantha , Paterson Alex , Mockridge C. Ian , Potter Kathleen N. , Smith Kelly-Ann , Ashton-Key Margaret , Stevenson Freda K. , Packham Graham 
Published: November 2011

Abstract
Although long considered as a disease of failed apoptosis, it is now clear that chronic lymphocytic leukemia (CLL) cells undergo extensive cell division in vivo, especially in progressive disease. Signaling via the B-cell receptor is thought to activate proliferation and survival pathways in CLL cells and also has been linked to poor outcome. Here, we have analyzed the expression of the proto-oncoprotein MYC, an essential positive regulator of the cell cycle, after stimulation of surface IgM (sIgM). MYC expression was rapidly increased after sIgM stimulation in a subset of CLL samples. The ability of sIgM stimulation to increase MYC expression was correlated with sIgM-induced intracellular calcium fluxes. MYC induction was partially dependent on the MEK/ERK signaling pathway, and MYC and phosphorylated ERK1/2 were both expressed within proliferation centers in vivo. Although stimulation of sIgD also resulted in ERK1/2 phosphorylation, responses were relatively short lived compared with sIgM and were associated with significantly reduced MYC induction, suggesting that the kinetics of ERK1/2 activation is a critical determinant of MYC induction. Our results suggest that ERK1/2-dependent induction of MYC is likely to play an important role in antigen-induced CLL cell proliferation.
Genome-wide analysis of gene expression during Xenopus tropicalis tadpole tail regeneration
Authors: Love Nick R , Chen Yaoyao , Bonev Boyan , Gilchrist Michael J , Fairclough Lynne , Lea Robert , Mohun Timothy J , Paredes Roberto , Zeef Leo AH , Amaya Enrique 
Published: November 2011

Abstract

Background
The molecular mechanisms governing vertebrate appendage regeneration remain poorly understood. Uncovering these mechanisms may lead to novel therapies aimed at alleviating human disfigurement and visible loss of function following injury. Here, we explore tadpole tail regeneration in Xenopus tropicalis, a diploid frog with a sequenced genome.

Results
We found that, like the traditionally used Xenopus laevis, the Xenopus tropicalis tadpole has the capacity to regenerate its tail following amputation, including its spinal cord, muscle, and major blood vessels. We examined gene expression using the Xenopus tropicalis Affymetrix genome array during three phases of regeneration, uncovering more than 1,000 genes that are significantly modulated during tail regeneration. Target validation, using RT-qPCR followed by gene ontology (GO) analysis, revealed a dynamic regulation of genes involved in the inflammatory response, intracellular metabolism, and energy regulation. Meta-analyses of the array data and validation by RT-qPCR and in situ hybridization uncovered a subset of genes upregulated during the early and intermediate phases of regeneration that are involved in the generation of NADP/H, suggesting that these pathways may be important for proper tail regeneration.

Conclusions
The Xenopus tropicalis tadpole is a powerful model to elucidate the genetic mechanisms of vertebrate appendage regeneration. We have produced a novel and substantial microarray data set examining gene expression during vertebrate appendage regeneration.