bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bone Stress Injuries Causing Exercise-Induced Knee Pain
Authors: Niva Maria H. , Kiuru Martti J. , Haataja Riina , Pihlajamäki Harri K. 
Published: September 2005

Background No comprehensive studies of bone stress injuries in the knee based on magnetic resonance imaging findings have been published. Purpose Assess the incidence, location, nature, and patterns of bone stress injuries in the knee in military conscripts with exercise-induced knee pain. Study Design Case series; Level of evidence, 4. Methods During a period of 70 months, 1330 patients with exercise-induced knee pain underwent magnetic resonance imaging of the knee. A total of 1577 knees were imaged; the images with bone stress injury findings were retrospectively reevaluated with respect to location and type of injury. The person-based incidence of bone stress injuries in the knee was calculated, based on the number of conscripts within the hospital's catchment area. Results Of the 1330 patients, 88 (7%) met the inclusion criteria, and 141 bone stress injuries were found in the 110 knees imaged. The incidence of bone stress injuries was 103 per 100 000 person-years. Of the patients, 25% had bilateral bone stress injuries; 28% had 2 solitary bone stress injuries in the same knee simultaneously, all situated in the femoral condyle and tibial plateau. The most common anatomical location for a bone stress injury was the medial tibial plateau (31%), which was also the most typical location for a more advanced injury. After the commencement of military service, a bone stress injury in the medial tibial plateau caused knee pain earlier than did a bone stress injury elsewhere in the knee (P=. 014). Conclusion The incidence of bone stress injuries in the knee with exercise-induced knee pain is relatively high in conscripts. Multiple and bilateral injuries can occur. For accurate diagnosis and to ensure appropriate treatment, magnetic resonance imaging is recommended as a routine imaging method when a physical activity can be regularly associated with the onset of symptoms.
Induction of tumor arrest and differentiation with prolonged survival by intermittent hypoxia in a mouse model of acute myeloid leukemia
Authors: Liu Wei , Guo Meng , Xu Ya-Bei , Li Dao , Zhou Zhao-Nian , Wu Ying-Li , Chen Zhu , Kogan Scott C. , Chen Guo-Qiang 
Published: September 2005

AbstractWe showed previously that mild real hypoxia and hypoxia-mimetic agents induced in vitro cell differentiation of acute myeloid leukemia (AML). We here investigate the in vivo effects of intermittent hypoxia on syngenic grafts of leukemic blasts in a PML-RARα transgenic mouse model of AML. For intermittent hypoxia, leukemic mice were housed in a hypoxia chamber equivalent to an altitude of 6000 m for 18 hours every consecutive day. The results show that intermittent hypoxia significantly prolongs the survival of the leukemic mice that received transplants, although it fails to cure the disease. By histologic and cytologic analyses, intermittent hypoxia is shown to inhibit the infiltration of leukemic blasts in peripheral blood, bone marrow, spleen, and liver without apoptosis induction. More intriguingly, intermittent hypoxia also induces leukemic cells to undergo differentiation with progressive increase of hypoxia-inducible factor-1α protein, as evidenced by morphologic criteria of maturating myeloid cells and increased expression of mouse myeloid cell differentiation–related antigens Gr-1 and Mac-1. Taken together, this study represents the first attempt to characterize the in vivo effects of hypoxia on an AML mouse model. Additional investigations may uncover ways to mimic the differentiative effects of hypoxia in a manner that will benefit human patients with AML.
Novel collectin/C1q receptor mediates mast cell activation and innate immunity
Authors: Edelson Brian T. , Stricker Thomas P. , Li Zhengzhi , Dickeson S. Kent , Shepherd Virginia L. , Santoro Samuel A. , Zutter Mary M. 
Published: September 2005

AbstractMast cells play a critical role in innate immunity, allergy, and autoimmune diseases. The receptor/ligand interactions that mediate mast cell activation are poorly defined. The α2β1 integrin, a receptor for collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1 (MMP-1), endorepellin, and several viruses, has been implicated in normal developmental, inflammatory, and oncogenic processes. We recently reported that α2 integrin subunit–deficient mice exhibited markedly diminished neutrophil and IL-6 responses during Listeria monocytogenes–and zymosan-induced peritonitis. Peritoneal mast cells require α2β1 integrin expression for activation in response to pathogens, yet the ligand and molecular mechanisms by which the α2β1 integrin induces activation and cytokine secretion remain unknown. We now report that the α2β1 integrin is a novel receptor for multiple collectins and the C1q complement protein. We demonstrate that the α2β1 integrin provides a costimulatory function required for mast cell activation and cytokine secretion. This finding suggests that the α2β1 integrin is not only important for innate immunity but may serve as a critical target for the regulation of autoimmune/allergic disorders.
The tyrphostin adaphostin interacts synergistically with proteasome inhibitors to induce apoptosis in human leukemia cells through a reactive oxygen species (ROS)-dependent mechanism
Authors: Dasmahapatra Girija , Rahmani Mohamed , Dent Paul , Grant Steven 
Published: September 2005

Abstract
Interactions between the tyrphostin adaphostin and proteasome inhibitors (eg, MG-132 and bortezomib) were examined in multiple human leukemia cell lines and primary acute myeloid leukemia (AML) specimens. Cotreatment of Jurkat cells with marginally toxic concentrations of adaphostin and proteasome inhibitors synergistically potentiated mitochondrial damage (eg, cytochrome c release), caspase activation, and apoptosis. Similar interactions occurred in other human leukemia cell types (eg, U937, HL-60, Raji). These interactions were associated with a marked increase in oxidative damage (eg, ROS generation), down-regulation of the Raf/MEK/ERK pathway, and JNK activation. Adaphostin/MG-132 lethality as well as mitochondrial damage, down-regulation of Raf/MEK/ERK, and activation of JNK were attenuated by the free-radical scavenger NAC, suggesting that oxidative damage plays a functional role in antileukemic effects. Ectopic expression of Raf-1 or constitutively active MEK/ERK or genetic interruption of the JNK pathway significantly diminished adaphostin/MG-132-mediated lethality. Interestingly, enforced Raf or MEK/ERK activation partially diminished adaphostin/MG-132-mediated ROS generation, suggesting the existence of an amplification loop. Finally, the adaphostin/MG-132 regimen displayed similar toxicity toward 5 primary AML samples but not normal hematopoietic progenitors (eg, bone marrow CD34+ cells). Collectively, these findings suggest that potentiating oxidative damage by combining adaphostin with proteasome inhibitors warrants attention as an antileukemic strategy.
Activating Notch1 mutations in mouse models of T-ALL
Authors: O'Neil Jennifer , Calvo Jennifer , McKenna Keith , Krishnamoorthy Veena , Aster Jon C. , Bassing Craig H. , Alt Frederick W. , Kelliher Michelle , Look A. Thomas 
Published: September 2005

AbstractRecent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1. We sought to determine whether these mutations are also acquired in mouse models of T-ALL. We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1. Cell lines derived from these tumors undergo G0/G1 arrest and apoptosis when treated with a γ-secretase inhibitor. In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes. Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations. (Blood. 2006;107:781-785)
Effects of nano particles on antigen-related airway inflammation in mice
Authors: Inoue Ken-ichiro , Takano Hirohisa , Yanagisawa Rie , Sakurai Miho , Ichinose Takamichi , Sadakane Kaori , Yoshikawa Toshikazu 
Published: September 2005

AbstractBackgroundParticulate matter (PM) can exacerbate allergic airway diseases. Although health effects of PM with a diameter of less than 100 nm have been focused, few studies have elucidated the correlation between the sizes of particles and aggravation of allergic diseases. We investigated the effects of nano particles with a diameter of 14 nm or 56 nm on antigen-related airway inflammation.MethodsICR mice were divided into six experimental groups. Vehicle, two sizes of carbon nano particles, ovalbumin (OVA), and OVA + nano particles were administered intratracheally. Cellular profile of bronchoalveolar lavage (BAL) fluid, lung histology, expression of cytokines, chemokines, and 8-hydroxy-2'-deoxyguanosine (8-OHdG), and immunoglobulin production were studied.ResultsNano particles with a diameter of 14 nm or 56 nm aggravated antigen-related airway inflammation characterized by infiltration of eosinophils, neutrophils, and mononuclear cells, and by an increase in the number of goblet cells in the bronchial epithelium. Nano particles with antigen increased protein levels of interleukin (IL)-5, IL-6, and IL-13, eotaxin, macrophage chemoattractant protein (MCP)-1, and regulated on activation and normal T cells expressed and secreted (RANTES) in the lung as compared with antigen alone. The formation of 8-OHdG, a proper marker of oxidative stress, was moderately induced by nano particles or antigen alone, and was markedly enhanced by antigen plus nano particles as compared with nano particles or antigen alone. The aggravation was more prominent with 14 nm of nano particles than with 56 nm of particles in overall trend. Particles with a diameter of 14 nm exhibited adjuvant activity for total IgE and antigen-specific IgG1and IgE.ConclusionNano particles can aggravate antigen-related airway inflammation and immunoglobulin production, which is more prominent with smaller particles. The enhancement may be mediated, at least partly, by the increased local expression of IL-5 and eotaxin, and also by the modulated expression of IL-13, RANTES, MCP-1, and IL-6.
Rapid urban malaria appraisal (RUMA) I: Epidemiology of urban malaria in Ouagadougou
Authors: Wang Shr-Jie , Lengeler Christian , Smith Thomas A , Vounatsou Penelope , Diadie Diallo A , Pritroipa Xavier , Convelbo Natalie , Kientga Mathieu , Tanner Marcel 
Published: September 2005

Abstract

Background
Rapid urbanization in sub-Saharan Africa has a major impact on malaria epidemiology. While much is known about malaria in rural areas in Burkina Faso, the urban situation is less well understood.

Methods
An assessment of urban malaria was carried out in Ouagadougou in November -December, 2002 during which a rapid urban malaria appraisal (RUMA) was applied.

Results
The school parasitaemia prevalence was relatively high (48.3%) at the cold and dry season 2002. Routine malaria statistics indicated that seasonality of malaria transmission was marked. In the health facilities, the number of clinical cases diminished quickly at the start of the cold and dry season and the prevalence of parasitaemia detected in febrile and non-febrile cases was 21.1% and 22.0%, respectively. The health facilities were likely to overestimate the malaria incidence and the age-specific fractions of malaria-attributable fevers were low (0–0.13). Peak prevalence tended to occur in older children (aged 6–15 years). Mapping of Anopheles sp. breeding sites indicated a gradient of endemicity between the urban centre and the periphery of Ouagadougou. A remarkable link was found between urban agriculture activities, seasonal availability of water supply and the occurrence of malaria infections in this semi-arid area. The study also demonstrated that the usage of insecticide-treated nets and the education level of family caretakers played a key role in reducing malaria infection rates.

Conclusion
These findings show that determining local endemicity and the rate of clinical malaria cases are urgently required in order to target control activities and avoid over-treatment with antimalarials. The case management needs to be tailored to the level of the prevailing endemicity.
Neurobrucellosis presenting as an intra-medullary spinal cord abscess
Authors: Vajramani Girish V , Nagmoti Mahantesh B , Patil Chidanand S 
Published: September 2005

Abstract

Background
Of the diverse presentation of neurobrucellosis, intra-medullary spinal cord abscess is extremely rare. Only four other cases have been reported so far. We present a case of spinal cord intra-medullary abscess due to Brucella melitensis.

Case presentation
A forty-year-old female presented with progressive weakness of both lower limb with urinary incontinence of 6 months duration. She was febrile. Neurological examination revealed flaccid areflexic paraplegia with T10 below sensory impairment including perianal region. An intramedullary mass was diagnosed on Magnetic Resonance Image (MRI) scan extending from T12 to L2. At surgery, a large abscess was encountered at the conus medullaris, from which Brucella melitensis was grown on culture. She was started on streptomycin and doxycycline for 1 month, followed by rifampicin and doxycycline for 1 month. At 2-year follow-up, she had recovered only partially and continued to have impaired bladder function.

Conclusion
Neurobrucellosis, if not treated early, can result in severe neurological morbidity and sequale, which may be irreversible. Hence it is important to consider the possibility of neurobrucellosis in endemic region and treat aggressively.
Segregation of a M404V mutation of the p62/sequestosome 1 (p62/SQSTM1) gene with polyostotic Paget's disease of bone in an Italian family
Authors: Falchetti Alberto , Di Stefano Marco , Marini Francesca , Del Monte Francesca , Gozzini Alessia , Masi Laura , Tanini Annalisa , Amedei Antonietta , Carossino Annamaria , Isaia Giancarlo , Brandi Maria Luisa 
Published: September 2005

AbstractMutations of the p62/Sequestosome 1 gene (p62/SQSTM1) account for both sporadic and familial forms of Paget's disease of bone (PDB). We originally described a methionine→valine substitution at codon 404 (M404V) of exon 8, in the ubiquitin protein-binding domain of p62/SQSTM1 gene in an Italian PDB patient. The collection of data from the patient's pedigree provided evidence for a familial form of PDB. Extension of the genetic analysis to other relatives in this family demonstrated segregation of the M404V mutation with the polyostotic PDB phenotype and provided the identification of six asymptomatic gene carriers. DNA for mutational analysis of the exon 8 coding sequence was obtained from 22 subjects, 4 PDB patients and 18 clinically unaffected members. Of the five clinically ascertained affected members of the family, four possessed the M404V mutation and exhibited the polyostotic form of PDB, except one patient with a single X-ray-assessed skeletal localization and one with a polyostotic disease who had died several years before the DNA analysis. By both reconstitution and mutational analysis of the pedigree, six unaffected subjects were shown to bear the M404V mutation, representing potential asymptomatic gene carriers whose circulating levels of alkaline phosphatase were recently assessed as still within the normal range. Taken together, these results support a genotype–phenotype correlation between the M404V mutation in the p62/SQSTM1 gene and a polyostotic form of PDB in this family. The high penetrance of the PDB trait in this family together with the study of the asymptomatic gene carriers will allow us to confirm the proposed genotype–phenotype correlation and to evaluate the potential use of mutational analysis of the p62/SQSTM1 gene in the early detection of relatives at risk for PDB.
Effect of Age and Previous Autologous Transplantation on Nonrelapse Mortality and Survival in Patients Treated With Reduced-Intensity Conditioning and Allografting for Advanced Hematologic Malignancies
Authors: Corradini P. , Zallio F. , Mariotti J. , Farina L. , Bregni M. , Valagussa P. , Ciceri F. , Bacigalupo A. , Dodero A. , Lucesole M. , Patriarca F. , Rambaldi A. , Scimè R. , Locasciulli A. , Bandini G. , Gianni A.M. , Tarella C. , Olivieri A. 
Published: September 2005

Purpose Older age and a previously failed autologous stem-cell transplantation (SCT) are poor prognostic factors for patients receiving myeloablative conditioning and allogeneic SCT. Reduced-intensity conditioning (RIC) regimens achieved a significant reduction of treatment-related mortality, but the influence of previously described risk factors on the outcome of this novel transplantation strategy have not been fully analyzed yet. Patients and Methods One hundred fifty patients with advanced hematologic malignancies received a RIC regimen containing thiotepa (10 mg/kg), fludarabine (60 mg/m2), and cyclophosphamide (60 mg/kg), followed by an allogeneic transplantation from an HLA-identical sibling donor. Patients were divided into two cohorts according to age; 90 patients were younger than 55 years, and 60 patients were 55 years old or older. The other pretransplantation characteristics were fairly balanced. Results Actuarial 5-year nonrelapse mortality (NRM) rate was not statistically different between the groups (13% in the younger group and 19% in the older group). By univariate and multivariate analysis, NRM was significantly higher in older patients who previously experienced failure with an autograft. The occurrence of grade 3 to 4 acute graft-versus-host disease (GVHD) or extensive chronic GVHD was associated with a higher NRM in both age cohorts. Overall survival (OS) was not statistically different between the younger (66%) and older groups (61%). By multivariate analysis, refractory disease was associated with a worse OS irrespective of age group. Conclusion RIC transplantations show a rather low NRM, and age ≥ 55 years per se cannot be considered a risk factor anymore. The timing of transplantation and novel strategies for the prevention of severe GVHD could further improve patient outcome.
Minority Adult Survivors of Childhood Cancer: A Comparison of Long-Term Outcomes, Health Care Utilization, and Health-Related Behaviors From the Childhood Cancer Survivor Study
Authors: Castellino Sharon M. , Casillas Jacqueline , Hudson Melissa M. , Mertens Ann C. , Whitton John , Brooks Sandra L. , Zeltzer Lonnie K. , Ablin Arthur , Castleberry Robert , Hobbie Wendy , Kaste Sue , Robison Leslie L. , Oeffinger Kevin C. 
Published: September 2005

Purpose To determine the influence of race/ethnicity on outcomes in the Childhood Cancer Survivor Study (CCSS). Patients and Methods Of CCSS adult survivors in the United States, 443 (4.9%) were black, 503 (5.6%) were Hispanic and 7,821 (86.6%) were white. Mean age at interview, 26.9 years (range, 18 to 48 years); mean follow-up, 17.2 years (range, 8.7 to 28.4 years). Late mortality, second malignancy (SMN) rates, health care utilization, and health status and behaviors were assessed for blacks and Hispanics and compared with white survivors. Results Late mortality rate (6.5%) and 15-year cumulative incidence of SMN (3.5%) were similar across racial/ethnic groups. Minority survivors were more likely to have lower socioeconomic status (SES); final models were adjusted for income, education, and health insurance. Although overall health status was similar, black survivors were less likely to report adverse mental health (females: odds ratio [OR], 0.6; 95% CI, 0.4 to 0.9; males: OR, 0.5; 95% CI, 0.3 to 0.8). Differences in health care utilization and behaviors noted: Hispanic survivors were more likely to report a cancer center visit (females: OR, 1.5; 95% CI, 1.1 to 2.0; males: OR, 1.7; 95% CI, 1.2 to 2.3); black females were more likely (OR, 1.6; 95% CI, 1.1 to 2.4), and Hispanic females less likely to have a recent Pap smear (OR, 0.7; 95% CI, 0.5 to 1.0); black and Hispanic survivors were less likely to report smoking; black survivors were less likely to report problem drinking. Conclusion Adjusted for SES, adverse outcomes in CCSS were not associated with minority status. Importantly, black survivors reported less risky behaviors and better preventive practices. Hispanic survivors had equitable access to cancer related care.
An investigation of the role of carbonic anhydrase in aquatic and aerial gas transfer in the African lungfishProtopterus dolloi
Authors: Perry1 S. F. , Gilmour K. M. , Swenson E. R. , Vulesevic B. , Chew S. F. , Ip Y. K. 
Published: September 2005

SUMMARYExperiments were performed on bimodally breathing African lungfish Protopterus dolloi to examine the effects of inhibition of extracellular vs total (extracellular and intracellular) carbonic anhydrase (CA) activity on pulmonary and branchial/cutaneous gas transfer. In contrast to previous studies on Protopterus, which showed that the vast majority of CO2 is excreted into the water through the gill and/or skin whereas O2 uptake largely occurs via the lung, P. dolloi appeared to use the lung for the bulk of both O2uptake (91.0±2.9%) and CO2 excretion (76.0±6.6%). In support of the lung as the more important site of CO2 transfer,aerial hypercapnia (PCO2=40 mmHg) caused a significant rise in partial pressure of arterial blood CO2(PaCO2) whereas a similar degree of aquatic hypercapnia was without effect on PaCO2. Intravascular injection of low levels (1.2 mg kg-1) of the slowly permanent CA inhibitor, benzolamide, was without effect on red blood cell CA activity after 30 min, thus confirming its suitability as a short-term selective inhibitor of extracellular CA. Benzolamide treatment did not affect CO2 excretion, blood acid–base status or any other measured variable within the 30 min measurement period. Injection of the permeant CA inhibitor acetazolamide (30 mg kg-1) resulted in the complete inhibition of red cell CA activity within 10 min. However, CO2excretion (measured for 2 h after injection) and arterial blood acid–base status (assessed for 24 h after injection) were unaffected by acetazolamide treatment. Intra-arterial injection of bovine CA (2 mg kg-1) caused a significant increase in overall CO2excretion (from 0.41±0.03 to 0.58±0.03 mmol kg-1h-1) and an increase in air breathing frequency (from 19.0±1.3 to 24.7±1.8 breaths min-1) that was accompanied by a slight, but significant, reduction in PaCO2 (from 21.6±1.6 to 19.6±1.8 mmHg).The findings of this study are significant because they (i) demonstrate that, unlike in other species of African lungfish that have been examined, the gill/skin is not the major route of CO2 excretion in P. dolloi, and (ii) suggest that CO2 excretion in Protopterus may be less reliant on carbonic anhydrase than in most other fish species.