bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased plasma dipeptidyl peptidase-4 activities are associated with high prevalence of diabetic nephropathy in Chinese patients with newly diagnosed type 2 diabetes: A cross-sectional study
Authors: Zheng Tianpeng , Liu Yihong , Qin Shenghua , Liu Hongbo , Zhang Xiaoxi , Zhao Hailu 
Published: January 2016

Objective: To investigate the association between plasma Dipeptidyl peptidase-4 (DPP4) activities and diabetic nephropathy in type 2 diabetes. Research design and methods: A total of 1193 newly diagnosed type 2 diabetic subjects were studied. Plasma DPP4 activity, mannose 6-phosphate receptor, inflammatory markers and oxidative stress parameters were measured in all participants. Diabetic nephropathy was defined as the presence of albuminuria or an estimated glomerular filtration rate < 60 mL/min/1.73 m2. Results: Participants in the highest quartile of DPP4 activity had higher HbA1c, homeostatic model assessment of insulin resistance, nitrotyrosine, 8-iso-PGF2a, interleukin-6, high-sensitivity C-reactive protein, mannose 6-phosphate receptor, urinary albumin-to-creatinine ratio and lower estimated glomerular filtration rate compared with participants in the lowest quartile (all p < 0.001). DPP4 activities were associated positively with HbA1c, homeostatic model assessment of insulin resistance, nitrotyrosine, 8-iso-PGF2a, interleukin-6, high-sensitivity C-reactive protein, mannose 6-phosphate receptor, urinary albumin-to-creatinine ratio and negatively with estimated glomerular filtration rate (all p < 0.001). In the highest DPP4 quartile, diabetic nephropathy risk was significantly higher (odds ratio: 3.77; 95% confidence interval: 2.34–6.07) than in the lowest quartile after adjustment for potential confounders. This association remained strong (2.85; 1.74–4.68) after further controlling for HbA1c, homeostatic model assessment of insulin resistance, nitrotyrosine and high-sensitivity C-reactive protein. Conclusion: This study shows that increased DPP4 activities are strongly and independently associated with diabetic nephropathy in type 2 diabetes. The associations between DPP4 and diabetic nephropathy, although strong, do not imply causality. There are however plausible mechanisms which could explain such a link.
Promoter polymorphism at the tumour necrosis factor/lymphotoxin-alpha locus is associated with type of diabetes but not with susceptibility to sight-threatening diabetic retinopathy
Authors: Kaidonis Georgia , Craig Jamie E , Gillies Mark C , Abhary Sotoodeh , Essex Rohan W , Chang John H , Pal Bishwanath , Pefkianaki Maria , Daniell Mark , Lake Stewart , Petrovsky Nikolai , Burdon Kathryn P 
Published: January 2016

Aim: To investigate, in a large cohort of 2494 individuals with diabetes mellitus, whether functional single nucleotide polymorphisms in the promoter region of tumour necrosis factor ( TNF) and lymphotoxin-alpha ( LTA) genes are associated with type of diabetes or presence of diabetic retinopathy. Methods: A total of 334 type 1 diabetes and 999 type 2 diabetes participants with sight-threatening diabetic retinopathy, and 260 type 1 diabetes and 901 type 2 diabetes participants with no diabetic retinopathy or minimal non-proliferative diabetic retinopathy, were genotyped for two single nucleotide polymorphisms (rs1800629 and rs361525). Results: The A allele of rs1800629 was associated with type 1 diabetes ( p < 0.001; odds ratio = 0.62). After adjustment for age, sex, diabetes duration, HbA1c, hypertension and nephropathy, no significant association was found between rs1800629 or rs361525 and sight-threatening diabetic retinopathy. Conclusion: An association between the A allele of rs1800629 and type of diabetes was found. No association was found between two promoter variants of TNF and LTA, and diabetic retinopathy in a large cohort of Caucasian patients with type 1 diabetes and type 2 diabetes.
Spinal arteriovenous fistulae in patients with hereditary hemorrhagic telangiectasia: A case report and systematic review of the literature
Authors: Brinjikji Waleed , Nasr Deena M , Cloft Harry J , Iyer Vivek N , Lanzino Giuseppe 
Published: January 2016

Background Although rare, spinal arteriovenous malformations (AVMs) are thought to be more prevalent in the hereditary Hereditary Hemorrhagic Telangiectasia (HHT) population. Methods We report a case of a spinal AVM in a 37-year-old female with HHT treated with endovascular embolization. In addition, we report findings from a systematic review of the literature on the clinical characteristics, angioarchitecture, and clinical outcomes of HHT patients with spinal AVMs. Results The patient is a 37 year-old female with definite HHT who presented with a one-year history of progressive gait difficulty. The spinal fistula was incidentally detected on chest computed tomography (CT). Spinal angiography demonstrated a large perimedullary arteriovenous fistula was supplied by a posterolateral spinal artery. The fistula was treated with detachable coils. The patient made a complete neurological recovery. Our systematic review yielded 25 additional cases of spinal AVMs in HHT patients. All fistulae were perimedullary (100.0%). Treatments were described in 24 of the 26 lesions. Endovascular-only treatment was performed in 16 cases (66.6%) and surgical-only treatment was performed in five cases (20.8%). Complete or near-complete occlusion rates were 86.7% (13/15) for endovascular treated cases, 100.0% (4/4) for surgery and 66.6% (2/3) for combined treatments. Overall, 80.0% of patients (16/20) reported improvement in function following treatment, 100.0% (5/5) in the surgery group and 84.6% (11/13) reported improvement in the endovascular group. Conclusions Spinal fistulae in HHT patients are usually type IV perimedullary fistulae. Both endovascular and surgical treatments appeared to be effective in treating these lesions. However, it is clear that endovascular therapy has become the preferred treatment modality.
Injury Profile in Swedish Elite Floorball
Authors: Tranaeus Ulrika , Götesson Eva , Werner Suzanne 
Published: January 2016

Background: Floorball is an indoor team sport with growing popularity worldwide characterized by rapid accelerations, decelerations, and cutting and pivoting movements. While injuries are common, there are few high-quality epidemiological investigations of floorball injuries. Therefore, the aim of this study was to determine the incidence and severity of injuries in male and female elite-level floorball players in Sweden. Hypothesis: The incidence of injuries has not decreased; female players are more vulnerable to injury than male players. Study Design: Prospective cohort study. Level of Evidence: Level 3. Methods: Twelve floorball teams (6 male, 6 female) in the Swedish premiere leagues were followed for 1 year (preseason, game season, and the entire year). The team medical staff reported injury incidence, location, type (traumatic or overuse), and severity. Differences between male and female players were analyzed using the Mann-Whitney U test. Results: The injury incidence was greater in female players during preseason (22.9 vs 7.4, P = 0.01), game season (39.5 vs 28.3, P = 0.002), as well as the whole year combined (33.9 vs 20.8, P = 0.02). The thigh was the most common injury location in male players and the ankle in female players. Overuse injuries were more common among men and were primarily back problems. Traumatic injuries were more common in women—mainly knee and ankle injuries. Most injuries were of mild severity. A greater number of anterior cruciate ligament injuries occurred in women (n = 11) than in men (n = 2). Conclusion: The injury incidence was significantly greater in female floorball players throughout the entire floorball year. Male players sustained mostly overuse injuries while female players suffered traumatic injuries. The majority of injuries in floorball were mild, irrespective of player sex. Clinical Relevance: Knowledge of the incidence and severity of floorball injuries is an essential step in the sequence of injury prevention. Future research should focus on identifying injury mechanisms and risk factors for these injuries to develop injury prevention strategies.
Whose Land Is It Anyway? Property, Law and Rights in the Land Acquisition Question in India
Authors: De Gitika 
Published: January 2016

The question of land acquisition in India hinges on the nature of land as property, the nature of collective land rights, the nature of individual property rights on land and the nature of the state as expropriator for specific collectivities or benefactor for public good. Defining public use or common good has historically been one of the more protracted contestations between the state and individual/communal ownership of land. Rule-making for acquisition of land and appropriate compensation marks a second contestation, between ‘law’ and ‘justice’, as evidenced both in the colonial law of 1894, and subsequent amendments and legal enactments after independence. Focusing on two of the most crucial aspects of land acquisition law—ownership and consent, and compensation against acquisition—this article explores how the idea of public good for common purpose has been historically constituted within legislative and juridical frameworks, and how the notion of compensation is closely connected to the contested definition of public good and the definition of ‘community rights’. In probing these issues, I seek to arrive at an understanding of the implications of reciprocal rights and obligations that mutually constitute society and state in India.
MicroRNA-224 sustains Wnt/β-catenin signaling and promotes aggressive phenotype of colorectal cancer
Authors: Li Tingting , Lai Qiuhua , Wang Shuyang , Cai Juanjuan , Xiao Zhiyuan , Deng Danling , He Liuqing , Jiao Hongli , Ye Yaping , Liang Li , Ding Yanqing , Liao Wenting 
Published: January 2016

Abstract
Background
Growing evidence suggests that Wnt/β-catenin pathway plays an important role in CRC development, progression and metastasis. Aberrant miR-224 expression has been reported in CRC. However, the mechanism of miR-224 promotes both proliferation and metastatic ability largely remains unclear.

Methods
Real-time PCR was used to quantify miR-224 expression. Luciferase reporter assays were conducted to confirm the activity of Wnt/β-catenin pathway and target gene associations, and immunofluorescence staining assay was performed to observe the nuclear translocation of β-catenin. Bioinformatics analysis combined with in vivo and vitro functional assays showed the potential target genes, GSK3β and SFRP2, of miR-224. Specimens from forty patients with CRC were analyzed for the expression of miR-224 and the relationship with GSK3β/SFRP2 by real-time PCR and western blot.

Results
Bioinformatics and cell luciferase function studies verified the direct regulation of miR-224 on the 3’-UTR of the GSK3β and SFRP2 genes, which leads to the activation of Wnt/β-catenin signaling and the nuclear translocation of β-catenin. In addition, knockdown of miR-224 significantly recovered the expression of GSK3β and SFRP2 and attenuated Wnt/β-catenin-mediated cell metastasis and proliferation. The ectopic upregulation of miR-224 dramatically inhibited the expression of GSK3β/SFRP2 and enhanced CRC proliferation and invasion.

Conclusion
Our research showed mechanistic links between miR-224 and Wnt/β-catenin in the pathogenesis of CRC through modulation of GSK3β and SFRP2.
The reproducibility of acquiring three dimensional gait and plantar pressure data using established protocols in participants with and without type 2 diabetes and foot ulcers
Authors: Fernando Malindu , Crowther Robert G , Cunningham Margaret , Lazzarini Peter A , Sangla Kunwarjit S , Buttner Petra , Golledge Jonathan 
Published: January 2016

AbstractBackgroundSeveral prospective studies have suggested that gait and plantar pressure abnormalities secondary to diabetic peripheral neuropathy contributes to foot ulceration. There are many different methods by which gait and plantar pressures are assessed and currently there is no agreed standardised approach. This study aimed to describe the methods and reproducibility of three‐dimensional gait and plantar pressure assessments in a small subset of participants using pre‐existing protocols.MethodsFourteen participants were conveniently sampled prior to a planned longitudinal study; four patients with diabetes and plantar foot ulcers, five patients with diabetes but no foot ulcers and five healthy controls. The repeatability of measuring key biomechanical data was assessed including the identification of 16 key anatomical landmarks, the measurement of seven leg dimensions, the processing of 22 three‐dimensional gait parameters and the analysis of four different plantar pressures measures at 20 foot regions.ResultsThe mean inter‐observer differences were within the pre‐defined acceptable level (<7 mm) for 100 % (16 of 16) of key anatomical landmarks measured for gait analysis. The intra‐observer assessment concordance correlation coefficients were > 0.9 for 100 % (7 of 7) of leg dimensions. The coefficients of variations (CVs) were within the pre‐defined acceptable level (<10 %) for 100 % (22 of 22) of gait parameters. The CVs were within the pre‐defined acceptable level (<30 %) for 95 % (19 of 20) of the contact area measures, 85 % (17 of 20) of mean plantar pressures, 70 % (14 of 20) of pressure time integrals and 55 % (11 of 20) of maximum sensor plantar pressure measures.ConclusionOverall, the findings of this study suggest that important gait and plantar pressure measurements can be reliably acquired. Nearly all measures contributing to three‐dimensional gait parameter assessments were within predefined acceptable limits. Most plantar pressure measurements were also within predefined acceptable limits; however, reproducibility was not as good for assessment of the maximum sensor pressure. To our knowledge, this is the first study to investigate the reproducibility of several biomechanical methods in a heterogeneous cohort.
Muscle mass, strength and functional outcomes in critically ill patients after cardiothoracic surgery: does neuromuscular electrical stimulation help? The Catastim 2 randomized controlled trial
Authors: Fischer Arabella , Spiegl Matthias , Altmann Klaus , Winkler Andreas , Salamon Anna , Themessl-Huber Michael , Mouhieddine Mohamed , Strasser Eva Maria , Schiferer Arno , Paternostro-Sluga Tatjana , Hiesmayr Michael 
Published: January 2016

AbstractBackgroundThe effects of neuromuscular electrical stimulation (NMES) in critically ill patients after cardiothoracic surgery are unknown. The objectives were to investigate whether NMES prevents loss of muscle layer thickness (MLT) and strength and to observe the time variation of MLT and strength from preoperative day to hospital discharge.MethodsIn this randomized controlled trial, 54 critically ill patients were randomized into four strata based on the SAPS II score. Patients were blinded to the intervention. In the intervention group, quadriceps muscles were electrically stimulated bilaterally from the first postoperative day until ICU discharge for a maximum of 14 days. In the control group, the electrodes were applied, but no electricity was delivered. The primary outcomes were MLT measured by ultrasonography and muscle strength evaluated with the Medical Research Council (MRC) scale. The secondary functional outcomes were average mobility level, FIM score, Timed Up and Go Test and SF-12 health survey. Additional variables of interest were grip strength and the relation between fluid balance and MLT. Linear mixed models were used to assess the effect of NMES on MLT, MRC score and grip strength.ResultsNMES had no significant effect on MLT. Patients in the NMES group regained muscle strength 4.5 times faster than patients in the control group. During the first three postoperative days, there was a positive correlation between change in MLT and cumulative fluid balance (r = 0.43,P = 0.01). At hospital discharge, all patients regained preoperative levels of muscle strength, but not of MLT. Patients did not regain their preoperative levels of average mobility (P = 0.04) and FIM score (P = 0.02) at hospital discharge, independent of group allocation.ConclusionsNMES had no effect on MLT, but was associated with a higher rate in regaining muscle strength during the ICU stay. Regression of intramuscular edema during the ICU stay interfered with measurement of changes in MLT. At hospital discharge patients had regained preoperative levels of muscle strength, but still showed residual functional disability and decreased MLT compared to pre-ICU levels in both groups.Trial registrationClinicaltrials.gov identifierNCT02391103. Registered on 7 March 2015.
Ligand-dependent serum response factor activation by the human CC chemokine receptors CCR2a and CCR2b is mediated by G proteins of the Gq family
Authors: Vatter Petra , Schuhholz Julia , Koenig Carolin , Pfreimer Mariana , Moepps Barbara 
Published: January 2016

Abstract
Expression of the human CCR2 receptors, CCR2a and CCR2b, in mammalian cells results in ligand-dependent changes in the activity of multiple cellular signal transduction pathways, mediated in most cases by pertussis toxin-sensitive heterotrimeric G proteins of the Gi/o subfamily. In addition, CCR2a and CCR2b receptors have been shown to couple to Gq family members, triggering the canonical activation of phospholipase Cβ isoenzymes. Activation of pertussis toxin-insensitive Gq proteins by cell-surface receptors is not only coupled to activation of phospholipase isoenzymes but also to Rho guanine nucleotide exchange factors, which in turn mediate activation of the Rho GTPases. Activated Rho GTPases regulate numerous cellular functions, including the organization of the actin cytoskeleton and gene transcription, such as the transcription factor serum response factor. These findings prompted us to investigate whether CCR2a and/or CCR2b stimulate serum response factor activity. The results presented herein demonstrate that stimulation of human CCR2a- or CCR2b-expressing COS-7 cells caused a vigorous induction of serum response factor activity. This effect was specifically mediated by Gq and/or G14, as well as Rho A and/or a closely related Rho GTPase. Furthermore, the stimulatory effect of CCR2a and CCR2b and Gαq was sensitive to coexpression of the Gαq-interacting leukemia-associated Rho guanine nucleotide exchange factor. The findings of the work indicate a role for Gαq and/or Gα14 and in CCR2a/CCR2b-stimulated Rho A GTPase-mediated serum response factor activation and introduce a noncanonical pathway activated by CCR2 receptors by coupling to Gq proteins.
Estradiol Restrains Prepubertal Gonadotropin Secretion in Female Mice via Activation of ERα in Kisspeptin Neurons
Authors: Dubois Sharon L. , Wolfe Andrew , Radovick Sally , Boehm Ulrich , Levine Jon E. 
Published: January 2016

Abstract
Elimination of estrogen receptorα (ERα) from kisspeptin (Kiss1) neurons results in premature LH release and pubertal onset, implicating these receptors in 17β-estradiol (E2)-mediated negative feedback regulation of GnRH release during the prepubertal period. Here, we tested the dependency of prepubertal negative feedback on ERα in Kiss1 neurons. Prepubertal (postnatal d 14) and peripubertal (postnatal d 34) wild-type (WT) and Kiss1 cell-specific ERα knockout (KERαKO) female mice were sham operated or ovariectomized and treated with either vehicle- or E2-containing capsules. Plasma and tissues were collected 2 days after surgery for analysis. Ovariectomy increased LH and FSH levels, and E2 treatments completely prevented these increases in WT mice of both ages. However, in prepubertal KERαKO mice, basal LH levels were elevated vs WT, and both LH and FSH levels were not further increased by ovariectomy or affected by E2 treatment. Similarly, Kiss1 mRNA levels in the medial basal hypothalamus, which includes the arcuate nucleus, were suppressed with E2 treatment in ovariectomized prepubertal WT mice but remained unaffected by any treatment in KERαKO mice. In peripubertal KERαKO mice, basal LH and FSH levels were not elevated vs WT and were unaffected by ovariectomy or E2. In contrast to our previous findings in adult animals, these results demonstrate that suppression of gonadotropins and Kiss1 mRNA by E2 in prepubertal animals depends upon ERα activation in Kiss1 neurons. Our observations are consistent with the hypothesis that these receptors play a critical role in restraining GnRH release before the onset and completion of puberty.
Common arterial trunk and in Lrp2 knock out mice indicate a crucial role of LRP2 in cardiac development
Authors: Baardman Maria E. , Zwier Mathijs V. , Wisse Lambertus J. , Gittenberger- de Groot Adriana C. , Kerstjens-Frederikse Wilhelmina S. , Hofstra Robert M. W. , Jurdzinski Angelika , Hierck Beerend P. , Jongbloed Monique R. M. , Berger Rolf M. F. , Plösch Torsten , DeRuiter Marco C. 
Published: January 2016

Background Lipoprotein-related receptor protein 2 (LRP2) is important for the embryonic neural crest and brain development in both mice and humans. Although a role in cardiovascular development can be expected, the hearts of Lrp2 knock out (ko) mice have not yet been investigated.Methods We studied the cardiovascular development of Lrp2 ko mice between embryonic day E10.5 and E15.5, applying morphometry and immunohistochemistry, using antibodies against Tfap2α (neural crest cells), Nkx2.5 (second heart field), WT1 (epicardium derived cells), tropomyosin (myocardium) and LRP2.Results The Lrp2 ko mice display a range of severe cardiovascular abnormalities including aortic arch anomalies, common arterial trunk with coronary anomalies, ventricular septal defects, overriding tricuspid valve and marked thinning of the ventricular myocardium. Both the neural crest cells and second heart field, which are essential for the lengthening and growth of the right ventricular outflow tract, are abnormally positioned in the Lrp2 ko. This explains the absence of the aorto-pulmonary septum leading to common arterial trunk and ventricular septal defects. Severe blebbing of the epicardial cells covering the ventricles is seen. Epithelial-mesenchymal transition does occur, however, there are less WT1 positive epicardium derived cells in the ventricular wall as compared to normal coinciding with the myocardial thinning and deep intertrabecular spaces.Conclusions LRP2 plays a crucial role in cardiovascular development in mice. This corroborates findings of cardiac anomalies in humans with LRP2 mutations. Future studies should reveal the underlying signaling mechanisms in which LRP2 is involved during cardiogenesis.