bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electromyographic Analysis of the Triceps Surae Muscle Complex During Achilles Tendon Rehabilitation Program Exercises
Authors: Mullaney Michael , Tyler Timothy F. , McHugh Malachy , Orishimo Karl , Kremenic Ian , Caggiano Jessica , Ramsey Abi 
Published: September 2011

Background: Specific guidelines for therapeutic exercises following an Achilles tendon repair are lacking. Hypothesis: A hierarchical progression of triceps surae exercises can be determined on the basis of electromyographic (EMG) activity. Study Design: Randomized laboratory trial. Methods: Bipolar surface electrodes were applied over the medial and lateral heads of the gastrocnemius as well as the soleus on 20 healthy lower extremities (10 participants, 27 ± 5 years old). Muscle activity was recorded during 8 therapeutic exercises commonly used following an Achilles repair. Maximal voluntary isometric contractions (MVICs) were also performed on an isokinetic device. The effect of exercise on EMG activity (% MVIC) was assessed using repeated measures analysis of variance with Bonferroni corrections for planned pairwise comparisons. Results: Seated toe raises (11% MVIC) had the least amount of activity compared with all other exercises ( P < 0.01), followed by single-leg balance on wobble board (25% MVIC), prone ankle pumps (38% MVIC), supine plantarflexion with red elastic resistance (45% MVIC), normal gait (47% MVIC), lateral step-ups (60% MVIC), single-leg heel raises (112% MVIC), and single-leg jumping (129% MVIC). Conclusion: There is an increasing progression of EMG activity for exercises that target the triceps surae muscle complex during common exercises prescribed in an Achilles tendon rehabilitation program. Seated toe raises offer relatively low EMG activity and can be utilized as an early rehabilitative exercise. In contrast, the single-leg heel raise and single-leg jumping should be utilized only during later-stage rehabilitation. Clinical Relevance: EMG activity in the triceps surae is variable with common rehab exercises.
Joint Line Fullness and Meniscal Pathology
Authors: Couture Jean-Francois , Al-Juhani Wazzan , Forsythe Michael E. , Lenczner Eric , Marien Robert , Burman Mark 
Published: September 2011

Background: Meniscal tears have been associated with meniscal cysts and fullness of the knee joint line on physical examination. Hypothesis: Joint line fullness is an accurate, sensitive, and specific test to detect meniscal tears. Study Design: Prospective cohort study. Methods: One hundred consecutive patients undergoing knee arthroscopy were included. All had physical examinations documenting the presence of joint line fullness, joint line tenderness, and the McMurray sign. Arthroscopy was the gold standard for tears. Accuracy, sensitivity, and specificity were calculated and correlated with type of tear. Sixty-one patients had a magnetic resonance imaging preoperatively (the gold standard for determining the presence of a cyst). Results: Meniscal tears were found in 67 patients at arthroscopy. The accuracy, sensitivity, and specificity of joint line fullness were, respectively, 73%, 70%, and 82% in detecting meniscal tears; 68%, 87%, and 30% for joint line tenderness; and 47%, 32%, and 78% for the McMurray sign. The highest positive predictive value for detecting a tear was 88% for joint line fullness, compared with 77% for joint line tenderness and 76% for the McMurray sign. However, joint line fullness did not correlate well with the presence of a cyst, with a low positive predictive value (29%). Of those patients with joint line fullness on physical examination, 89% had a horizontal cleavage component of their tear at arthroscopy. Conclusion: Joint line fullness is an accurate, sensitive, and specific test to detect meniscal tears. Clinical Relevance: The findings support the routine use of joint line fullness during physical examination along with other common tests to improve the accuracy of clinically diagnosing meniscal tears.
PTEN deficiency in mast cells causes a mastocytosis-like proliferative disease that heightens allergic responses and vascular permeability
Authors: Furumoto Yasuko , Charles Nicolas , Olivera Ana , Leung Wai Hang , Dillahunt Sandra , Sargent Jennifer L. , Tinsley Kevin , Odom Sandra , Scott Eric , Wilson Todd M. , Ghoreschi Kamran , Kneilling Manfred , Chen Mei , Lee David M. , Bolland Silvia , Rivera Juan 
Published: September 2011

AbstractKit regulation of mast cell proliferation and differentiation has been intimately linked to the activation of phosphatidylinositol 3-OH kinase (PI3K). The activating D816V mutation of Kit, seen in the majority of mastocytosis patients, causes a robust activation of PI3K signals. However, whether increased PI3K signaling in mast cells is a key element for their in vivo hyperplasia remains unknown. Here we report that dysregulation of PI3K signaling in mice by deletion of the phosphatase and tensin homolog (Pten) gene (which regulates the levels of the PI3K product, phosphatidylinositol 3,4,5-trisphosphate) caused mast cell hyperplasia and increased numbers in various organs. Selective deletion of Pten in the mast cell compartment revealed that the hyperplasia was intrinsic to the mast cell. Enhanced STAT5 phosphorylation and increased expression of survival factors, such as Bcl-XL, were observed in PTEN-deficient mast cells, and these were further enhanced by stem cell factor stimulation. Mice carrying PTEN-deficient mast cells also showed increased hypersensitivity as well as increased vascular permeability. Thus, Pten deletion in the mast cell compartment results in a mast cell proliferative phenotype in mice, demonstrating that dysregulation of PI3K signals is vital to the observed mast cell hyperplasia.
CD5 costimulation induces stable Th17 development by promoting IL-23R expression and sustained STAT3 activation
Authors: de Wit Jelle , Souwer Yuri , van Beelen Astrid J. , de Groot Rosa , Muller Femke J. M. , Klaasse Bos Hanny , Jorritsma Tineke , Kapsenberg Martien L. , de Jong Esther C. , van Ham S. Marieke 
Published: September 2011

AbstractIL-17–producing CD4+ T helper (Th17) cells are important for immunity against extracellular pathogens and in autoimmune diseases. The factors that drive Th17 development in human remain a matter of debate. Here we show that, compared with classic CD28 costimulation, alternative costimulation via the CD5 or CD6 lymphocyte receptors forms a superior pathway for human Th17-priming. In the presence of the Th17-promoting cytokines IL-1β, IL-6, IL-23, and transforming growth factor-β (TGF-β), CD5 costimulation induces more Th17 cells that produce higher amounts of IL-17, which is preceded by prolonged activation of signal transducer and activator of transcription 3 (STAT3), a key regulator in Th17 differentiation, and enhanced levels of the IL-17–associated transcription factor retinoid-related orphan receptor-γt (ROR-γt). Strikingly, these Th17-promoting signals critically depend on CD5-induced elevation of IL-23 receptor (IL-23R) expression. The present data favor the novel concept that alternative costimulation via CD5, rather than classic costimulation via CD28, primes naive T cells for stable Th17 development through promoting the expression of IL-23R.
HIV envelope-mediated, CCR5/α4β7-dependent killing of CD4-negative γδ T cells which are lost during progression to AIDS
Authors: Li Haishan , Pauza C. David 
Published: September 2011

AbstractHIV infects and replicates in CD4+ T cells but effects on host immunity and disease also involve depletion, hyper-activation, and modification of CD4-negative cell populations. In particular, the depletion of CD4-negative γδ T cells is common to all HIV+ individuals. We found that soluble or cell-associated envelope glycoproteins from CCR5-tropic strains of HIV could bind, activates the p38-caspase pathway, and induce the death of γδ cells. Envelope binding requires integrin α4β7 and chemokine receptor CCR5 which are at high levels and form a complex on the γδ T cell membrane. This receptor complex facilitated V3 loop binding to CCR5 in the absence of CD4-induced conformational changes. Cell death was increased by antigen stimulation after exposure to envelope glycoprotein. Direct signaling by envelope glycoprotein killed CD4-negative γδ T cells and reproduced a defect observed in all patients with HIV disease.
A polymorphism in the leptin gene promoter is associated with anemia in patients with HIV disease
Authors: Vanasse Gary J. , Jeong Jee-Yeong , Tate Janet , Bathulapalli Harini , Anderson Damon , Steen Hanno , Fleming Mark , Mattocks Kristin , Telenti Amalio , Fellay Jacques , Justice Amy C. , Berliner Nancy 
Published: September 2011

AbstractTo study factors associated with anemia and its effect on survival in HIV-infected persons treated with modern combined antiretroviral therapy (cART), we characterized the prevalence of anemia in the Veterans Aging Cohort Study (VACS) and used a candidate gene approach to identify proinflammatory gene single nucleotide polymorphisms (SNPs) associated with anemia in HIV disease. The study comprised 1597 HIV+ and 865 HIV− VACS subjects with DNA, blood, and annotated clinical data available for analysis. Anemia was defined according to World Health Organization criteria (hemoglobin < 13 g/dL and < 12 g/dL in men and women, respectively). The prevalence of anemia in HIV+ and HIV− subjects was 23.1% and 12.9%, respectively. Independent of HIV status, anemia was present in 23.4% and 8% in blacks and whites, respectively. Analysis of our candidate genes revealed that the leptin −2548 G/A SNP was associated with anemia in HIV+, but not HIV−, patients, with the AA and AG genotypes significantly predicting anemia (P < .003 and P < .039, respectively, logistic regression). This association was replicated in an independent cohort of HIV+ women. Our study provides novel insight into the association between genetic variability in the leptin gene and anemia in HIV+ individuals.
Allogeneic stem cell transplantation for patients harboring T315I BCR-ABL mutated leukemias
Authors: Nicolini Franck Emmanuel , Basak Grzegorz W. , Soverini Simona , Martinelli Giovanni , Mauro Michael J. , Müller Martin C. , Hochhaus Andreas , Chuah Charles , Dufva Inge H. , Rege-Cambrin Giovanna , Saglio Giuseppe , Michallet Mauricette , Labussière Hélène , Morisset Stéphane , Hayette Sandrine , Etienne Gabriel , Olavarria Eduardo , Zhou Wei , Peter Senaka , Apperley Jane F. , Cortes Jorge 
Published: September 2011

Abstract
T315I+ Philadelphia chromosome–positive leukemias are inherently resistant to all licensed tyrosine kinase inhibitors, and therapeutic options remain limited. We report the outcome of allogeneic stem cell transplantation in 64 patients with documented BCR-ABLT315I mutations. Median follow-up was 52 months from mutation detection and 26 months from transplantation. At transplantation, 51.5% of patients with chronic myeloid leukemia were in the chronic phase and 4.5% were in advanced phases. Median overall survival after transplantation was 10.3 months (range 5.7 months to not reached [ie, still alive]) for those with chronic myeloid leukemia in the blast phase and 7.4 months (range 1.4 months to not reached [ie, still alive]) for those with Philadelphia chromosome–positive acute lymphoblastic leukemia but has not yet been reached for those in the chronic and accelerated phases of chronic myeloid leukemia. The occurrence of chronic GVHD had a positive impact on overall survival (P = .047). Transplant-related mortality rates were low. Multivariate analysis identified only blast phase at transplantation (hazard ratio 3.68, P = .0011) and unrelated stem cell donor (hazard ratio 2.98, P = .011) as unfavorable factors. We conclude that allogeneic stem cell transplantation represents a valuable therapeutic tool for eligible patients with BCR-ABLT315I mutation, a tool that may or may not be replaced by third-generation tyrosine kinase inhibitors.
Symmetric strong vector quasiequilibrium problems in Hausdorff locally convex spaces
Authors: Chen Bin , Huang Nan-jing , Cho Yeol Je 
Published: September 2011

Abstract
In this article, a new symmetric strong vector quasiequilibrium problem in real locally convex Hausdorff topological vector spaces is introduced and studied. An existence theorem of solutions for the symmetric strong vector quasiequilibrium problem by using Kakutani-Fan-Glicksberg fixed point theorem is obtained. Moreover, the closedness of the solution set for this problem is derived. The results presented in this article improve and extend some known results according to Long et al. [Math. Comput. Model. 47, 445-451 (2008)], Somyot and Kanokwan [Fixed Point Theory Appl. doi:10.1155/2011/475121], and Wang et al. [Bull. Malays. Math. Sci. Soc. http://www.emis.de/journals/BMMSS/pdf/acceptedpapers/2009-11-022_R1.pdf].

2000 MSC: 49J40; 90C29.
Coma in fatal adult human malaria is not caused by cerebral oedema
Authors: Medana Isabelle M , Day Nicholas PJ , Sachanonta Navakanit , Mai Nguyen TH , Dondorp Arjen M , Pongponratn Emsri , Hien Tran T , White Nicholas J , Turner Gareth DH 
Published: September 2011

Abstract

Background
The role of brain oedema in the pathophysiology of cerebral malaria is controversial. Coma associated with severe Plasmodium falciparum malaria is multifactorial, but associated with histological evidence of parasitized erythrocyte sequestration and resultant microvascular congestion in cerebral vessels. To determine whether these changes cause breakdown of the blood-brain barrier and resultant perivascular or parenchymal cerebral oedema, histology, immunohistochemistry and image analysis were used to define the prevalence of histological patterns of oedema and the expression of specific molecular pathways involved in water balance in the brain in adults with fatal falciparum malaria.

Methods
The brains of 20 adult Vietnamese patients who died of severe malaria were examined for evidence of disrupted vascular integrity. Immunohistochemistry and image analysis was performed on brainstem sections for activation of the vascular endothelial growth factor (VEGF) receptor 2 and expression of the aquaporin 4 (AQP4) water channel protein. Fibrinogen immunostaining was assessed as evidence of blood-brain barrier leakage and perivascular oedema formation. Correlations were performed with clinical, biochemical and neuropathological parameters of severe malaria infection.

Results
The presence of oedema, plasma protein leakage and evidence of VEGF signalling were heterogeneous in fatal falciparum malaria and did not correlate with pre-mortem coma. Differences in vascular integrity were observed between brain regions with the greatest prevalence of disruption in the brainstem, compared to the cortex or midbrain. There was a statistically non-significant trend towards higher AQP4 staining in the brainstem of cases that presented with coma (P = .02).

Conclusions
Histological evidence of cerebral oedema or immunohistochemical evidence of localised loss of vascular integrity did not correlate with the occurrence of pre-mortem coma in adults with fatal falciparum malaria. Enhanced expression of AQP4 water channels in the brainstem may, therefore, reflect a mix of both neuropathological or attempted neuroprotective responses to oedema formation.
Hop-distance relationship analysis with quasi-UDG model for node localization in wireless sensor networks
Authors: Gao Deyun , Chen Ping , Foh Chuan Heng , Niu Yanchao 
Published: September 2011

Abstract
In wireless sensor networks (WSNs), location information plays an important role in many fundamental services which includes geographic routing, target tracking, location-based coverage, topology control, and others. One promising approach in sensor network localization is the determination of location based on hop counts. A critical priori of this approach that directly influences the accuracy of location estimation is the hop-distance relationship. However, most of the related works on the hop-distance relationship assume the unit-disk graph (UDG) model that is unrealistic in a practical scenario. In this paper, we formulate the hop-distance relationship for quasi-UDG model in WSNs where sensor nodes are randomly and independently deployed in a circular region based on a Poisson point process. Different from the UDG model, quasi-UDG model has the non-uniformity property for connectivity. We derive an approximated recursive expression for the probability of the hop count with a given geographic distance. The border effect and dependence problem are also taken into consideration. Furthermore, we give the expressions describing the distribution of distance with known hop counts for inner nodes and those suffered from the border effect where we discover the insignificance of the border effect. The analytical results are validated by simulations showing the accuracy of the employed approximation. Besides, we demonstrate the localization application of the formulated relationship and show the accuracy improvement in the WSN localization.
Mammary gland specific expression of Brk/PTK6 promotes delayed involution and tumor formation associated with activation of p38 MAPK
Authors: Lofgren Kristopher A , Ostrander Julie H , Housa Daniel , Hubbard Gregory K , Locatelli Alessia , Bliss Robin L , Schwertfeger Kathryn L , Lange Carol A 
Published: September 2011

Abstract
Introduction
Protein tyrosine kinases (PTKs) are frequently overexpressed and/or activated in human malignancies, and regulate cancer cell proliferation, cellular survival, and migration. As such, they have become promising molecular targets for new therapies. The non-receptor PTK termed breast tumor kinase (Brk/PTK6) is overexpressed in approximately 86% of human breast tumors. The role of Brk in breast pathology is unclear.

Methods
We expressed a WAP-driven Brk/PTK6 transgene in FVB/n mice, and analyzed mammary glands from wild-type (wt) and transgenic mice after forced weaning. Western blotting and immunohistochemistry (IHC) studies were conducted to visualize markers of mammary gland involution, cell proliferation and apoptosis, as well as Brk, STAT3, and activated p38 mitogen-activated protein kinase (MAPK) in mammary tissues and tumors from WAP-Brk mice. Human (HMEC) or mouse (HC11) mammary epithelial cells were stably or transiently transfected with Brk cDNA to assay p38 MAPK signaling and cell survival in suspension or in response to chemotherapeutic agents.

Results
Brk-transgenic dams exhibited delayed mammary gland involution and aged mice developed infrequent tumors with reduced latency relative to wt mice. Consistent with delayed involution, mammary glands of transgenic animals displayed decreased STAT3 phosphorylation, a marker of early-stage involution. Notably, p38 MAPK, a pro-survival signaling mediator downstream of Brk, was activated in mammary glands of Brk transgenic relative to wt mice. Brk-dependent signaling to p38 MAPK was recapitulated by Brk overexpression in the HC11 murine mammary epithelial cell (MEC) line and human MEC, while Brk knock-down in breast cancer cells blocked EGF-stimulated p38 signaling. Additionally, human or mouse MECs expressing Brk exhibited increased anchorage-independent survival and resistance to doxorubicin. Finally, breast tumor biopsies were subjected to IHC analysis for co-expression of Brk and phospho-p38 MAPK; ductal and lobular carcinomas expressing Brk were significantly more likely to express elevated phospho-p38 MAPK.

Conclusions
These studies illustrate that forced expression of Brk/PTK6 in non-transformed mammary epithelial cells mediates p38 MAPK phosphorylation and promotes increased cellular survival, delayed involution, and latent tumor formation. Brk expression in human breast tumors may contribute to progression by inducing p38-driven pro-survival signaling pathways.
Impact of quetiapine on resolution of individual delirium symptoms in critically ill patients with delirium: a post-hoc analysis of a double-blind, randomized, placebo-controlled study
Authors: Devlin John W , Skrobik Yoanna , Riker Richard R , Hinderleider Eric , Roberts Russel J , Fong Jeffrey J , Ruthazer Robin , Hill Nicholas S , Garpestad Erik 
Published: September 2011

Abstract
Introduction
We hypothesized that delirium symptoms may respond differently to antipsychotic therapy. The purpose of this paper was to retrospectively compare duration and time to first resolution of individual delirium symptoms from the database of a randomized, double-blind, placebo-controlled study comparing quetiapine (Q) or placebo (P), both with haloperidol rescue, for critically ill patients with delirium.

Methods
Data for 10 delirium symptoms from the eight-domain, intensive care delirium screening checklist (ICDSC) previously collected every 12 hours were extracted for 29 study patients. Data between the Q and P groups were compared using a cut-off P- value of ≤0.10 for this exploratory study.

Results
Baseline ICDSC scores (5 (4 to 7) (Q) vs 5 (4 to 6)) (median, interquartile range (IQR)) and % of patients with each ICDSC symptom were similar in the two groups (all P > 0.10). Among patients with the delirium symptom at baseline, use of Q may lead to a shorter time (days) to first resolution of symptom fluctuation (4 (Q) vs. 14, P = 0.004), inattention (3 vs. 8, P = .10) and disorientation (2 vs. 10, P = 0.10) but a longer time to first resolution of agitation (3 vs. 1, P = 0.04) and hyperactivity (5 vs. 1, P = 0.07). Among all patients, Q-treated patients tended to spend a smaller percent of time with inattention (47 (0 to 67) vs. 78 (43 to 100), P = 0.025), hallucinations (0 (0 to 17) vs. 28 (0 to 43), P = 0.10) and symptom fluctuation (47 (19 to 67) vs. 89 (33 to 00), P = 0.04] and there was a trend for Q-treated patients to spend a greater percent of time at an appropriate level of consciousness (26% (13 to 63%) vs. 14% (0 to 33%), P = 0.17].

Conclusions
Our exploratory analysis suggests that quetiapine may resolve several intensive care unit (ICU) delirium symptoms faster than the placebo. Individual symptom resolution appears to differ in association with the pharmacologic intervention (that is, P vs Q, both with as needed haloperidol). Future studies evaluating antipsychotics in ICU patients with delirium should measure duration and resolution of individual delirium symptoms and their relation to long-term outcomes.
An investigation of side-effects and efficacy of foam-based sclerotherapy with carbon dioxide or room air in the treatment of reticular leg veins: a pilot study
Authors: Peterson J D , Goldman M P 
Published: September 2011

Objectives In sclerotherapy, carbon dioxide (CO2) or room air can be employed by phlebologists for foam creation. We compared room air (RA) and carbon dioxide in treating reticular leg veins with foam sclerotherapy. Methods Twenty patients were randomly treated with RA- or CO2-created sodium tetradecyl sulphate (STS) foam. Concentration and volume of STS, side-effects and efficacy were determined. Results There was no difference in the efficacy, local side-effects or distant side-effects between RA and CO2 foam in the treatment of reticular leg veins. The total volume of foam sclerosant required for treatment was greater with CO2 compared with RA ( P value = 0.01). Conclusion No differences were found in efficacy or side-effects between RA- and CO2-foam sclerotherapy for reticular leg veins. CO2 foam's shorter half-life was hypothesized to be responsible for larger total volumes of CO2 foam sclerosant.