bluuebunny/crossref_metadata_2025_split huggingface dataset:
Disparities of Care for African-Americans and Caucasians with Community-Acquired Pneumonia: A Retrospective Cohort Study
Authors: Frei Christopher R , Mortensen Eric M , Copeland Laurel A , Attridge Russell T , Pugh Mary Jo V , Restrepo Marcos I , Anzueto Antonio , Nakashima Brandy , Fine Michael J 
Published: June 2010

Abstract

Background
African-Americans admitted to U.S. hospitals with community-acquired pneumonia (CAP) are more likely than Caucasians to experience prolonged hospital length of stay (LOS), possibly due to either differential treatment decisions or patient characteristics.

Methods
We assessed associations between race and outcomes (Intensive Care Unit [ICU] variables, LOS, 30-day mortality) for African-American or Caucasian patients over 65 years hospitalized in the Veterans Health Administration (VHA) with CAP (2002-2007). Patients admitted to the ICU were analyzed separately from those not admitted to the ICU. VHA patients who died within 30 days of discharge were excluded from all LOS analyses. We used chi-square and Fisher's exact statistics to compare dichotomous variables, the Wilcoxon Rank Sum test to compare age by race, and Cox Proportional Hazards Regression to analyze hospital LOS. We used separate generalized linear mixed-effect models, with admitting hospital as a random effect, to examine associations between patient race and the receipt of guideline-concordant antibiotics, ICU admission, use of mechanical ventilation, use of vasopressors, LOS, and 30-day mortality. We defined statistical significance as a two-tailed p ≤ 0.0001.

Results
Of 40,878 patients, African-Americans (n = 4,936) were less likely to be married and more likely to have a substance use disorder, neoplastic disease, renal disease, or diabetes compared to Caucasians. African-Americans and Caucasians were equally likely to receive guideline-concordant antibiotics (92% versus 93%, adjusted OR = 0.99; 95% CI = 0.81 to 1.20) and experienced similar 30-day mortality when treated in medical wards (adjusted OR = 0.98; 95% CI = 0.87 to 1.10). African-Americans had a shorter adjusted hospital LOS (adjusted HR = 0.95; 95% CI = 0.92 to 0.98). When admitted to the ICU, African Americans were as likely as Caucasians to receive guideline-concordant antibiotics (76% versus 78%, adjusted OR = 0.99; 95% CI = 0.81 to 1.20), but experienced lower 30-day mortality (adjusted OR = 0.82; 95% CI = 0.68 to 0.99) and shorter hospital LOS (adjusted HR = 0.84; 95% CI = 0.76 to 0.93).

Conclusions
Elderly African-American CAP patients experienced a survival advantage (i.e., lower 30-day mortality) in the ICU compared to Caucasians and shorter hospital LOS in both medical wards and ICUs, after adjusting for numerous baseline differences in patient characteristics. There were no racial differences in receipt of guideline-concordant antibiotic therapies.
Lack of effects of typical and atypical antipsychotics in DARPP-32 and NCS-1 levels in PC12 cells overexpressing NCS-1
Authors: Souza Bruno R , Torres Karen CL , Miranda Débora M , Motta Bernardo S , Scotti-Muzzi Estêvão , Guimarães Melissa M , Carneiro Daniel S , Rosa Daniela VF , Souza Renan P , Reis Helton J , Jeromin Andreas , Romano-Silva Marco A 
Published: June 2010

Abstract

Background
Schizophrenia is the major psychiatry disorder, which the exact cause remains unknown. However, it is well known that dopamine-mediated neurotransmission imbalance is associated with this pathology and the main target of antipsychotics is the dopamine receptor D2. Recently, it was described alteration in levels of two dopamine signaling related proteins in schizophrenic prefrontal cortex (PFC): Neuronal Calcium Sensor-1 (NCS-1) and DARPP-32. NCS-1, which is upregulated in PFC of schizophrenics, inhibits D2 internalization. DARPP-32, which is decreased in PFC of schizophrenics, is a key downstream effector in transducing dopamine signaling. We previously demonstrated that antipsychotics do not change levels of both proteins in rat's brain. However, since NCS-1 and DARPP-32 levels are not altered in wild type rats, we treated wild type PC12 cells (PC12 WT) and PC12 cells stably overexpressing NCS-1 (PC12 Clone) with antipsychotics to investigate if NCS-1 upregulation modulates DARPP-32 expression in response to antipsychotics treatment.

Results
We chronically treated both PC12 WT and PC12 Clone cells with typical (Haloperidol) or atypical (Clozapine and Risperidone) antipsychotics for 14 days. Using western blot technique we observed that there is no change in NCS-1 and DARPP-32 protein levels in both PC12 WT and PC12 Clone cells after typical and atypical antipsychotic treatments.

Conclusions
Because we observed no alteration in NCS-1 and DARPP-32 levels in both PC12 WT and Clone cells treated with typical or atypical antipsychotics, we suggest that the alteration in levels of both proteins in schizophrenic's PFC is related to psychopathology but not with antipsychotic treatment.
Organic farmers use of wild food plants and fungi in a hilly area in Styria (Austria)
Authors: Schunko Christoph , Vogl Christian R 
Published: June 2010

Abstract
Background
Changing lifestyles have recently caused a severe reduction of the gathering of wild food plants. Knowledge about wild food plants and the local environment becomes lost when plants are no longer gathered. In Central Europe popular scientific publications have tried to counter this trend. However, detailed and systematic scientific investigations in distinct regions are needed to understand and preserve wild food uses. This study aims to contribute to these investigations.

Methods
Research was conducted in the hill country east of Graz, Styria, in Austria. Fifteen farmers, most using organic methods, were interviewed in two distinct field research periods between July and November 2008. Data gathering was realized through freelisting and subsequent semi-structured interviews. The culinary use value (CUV) was developed to quantify the culinary importance of plant species. Hierarchical cluster analysis was performed on gathering and use variables to identify culture-specific logical entities of plants. The study presented was conducted within the framework of the master's thesis about wild plant gathering of the first author. Solely data on gathered wild food species is presented here.

Results
Thirty-nine wild food plant and mushroom species were identified as being gathered, whereas 11 species were mentioned by at least 40 percent of the respondents. Fruits and mushrooms are listed frequently, while wild leafy vegetables are gathered rarely. Wild foods are mainly eaten boiled, fried or raw. Three main clusters of wild gathered food species were identified: leaves (used in salads and soups), mushrooms (used in diverse ways) and fruits (eaten raw, with milk (products) or as a jam).

Conclusions
Knowledge about gathering and use of some wild food species is common among farmers in the hill country east of Graz. However, most uses are known by few farmers only. The CUV facilitates the evaluation of the culinary importance of species and makes comparisons between regions and over time possible. The classification following gathering and use variables can be used to better understand how people classify the elements of their environment. The findings of this study add to discussions about food heritage, popularized by organizations like Slow Food, and bear significant potential for organic farmers.
Neutrophil mediated smooth muscle cell loss precedes allograft vasculopathy
Authors: King Chelsey L , Devitt Jennifer J , Lee Timothy DG , Hancock Friesen Camille L 
Published: June 2010

Abstract

Background
Cardiac allograft vasculopathy (AV) is a pathological process of vascular remodeling leading to late graft loss following cardiac transplantation. While there is consensus that AV is alloimmune mediated, and evidence that the most important alloimmune target is medial smooth muscle cells (SMC), the role of the innate immune response in the initiation of this disease is still being elucidated. As ischemia reperfusion (IR) injury plays a pivotal role in the initiation of AV, we hypothesize that IR enhances the early innate response to cardiac allografts.

Methods
Aortic transplants were performed between fully disparate mouse strains (C3H/HeJ and C57BL/6), in the presence of therapeutic levels of Cyclosporine A, as a model for cardiac AV. Neutrophils were depleted from some recipients using anti-PMN serum. Grafts were harvested at 1,2,3,5d and 1,2wk post-transplant. Ultrastructural integrity was examined by transmission electron microscopy. SMC and neutrophils were quantified from histological sections in a blinded manner.

Results
Grafts exposed to cold ischemia, but not transplanted, showed no medial SMC loss and normal ultrastructural integrity. In comparison, allografts harvested 1d post-transplant exhibited > 90% loss of SMC (p < 0.0001). SMC partially recovered by 5d but a second loss of SMC was observed at 1wk. SMC loss at 1d and 1wk post-transplant correlated with neutrophil influx. SMC loss was significantly reduced in neutrophil depleted recipients (p < 0.01).

Conclusions
These novel data show that there is extensive damage to medial SMC at 1d post-transplant. By depleting neutrophils from recipients it was demonstrated that a portion of the SMC loss was mediated by neutrophils. These results provide evidence that IR activation of early innate events contributes to the etiology of AV.
Churg-Strauss syndrome following cessation of allergic desensitization vaccination: a case report
Authors: Masjedi Mohammad Reza , Tafti Saeid Fallah , Cheraghvandi Ali , Fayazi Nader , Talischi Firouzeh , Mokri Bahareh 
Published: June 2010

Abstract

Introduction
Churg-Strauss syndrome is a vasculitis of medium to small sized vessels. Diagnosis is mainly clinical with findings of asthma, eosinophilia, rhinosinusitis and signs of vasculitis in major organs.

Case presentation
We present a case of a 19-year-old Persian male who developed signs and symptoms of this syndrome related to hyposensitization treatments for allergy control.

Conclusions
No unifying etiology for the disease can be presented as it is found associated with environmental factors, medications, infections and is even considered a variant of asthma with predisposition to vasculitic involvement. Therefore, it is important to recognize this disease and be aware of underdiagnosis because of emphasis on pathologic evidence. Here, we present a case of allergic desensitization causing Churg-Strauss syndrome in the absence of other known factors.
Clinical significance of the expression of connexin26 in colorectal cancer
Authors: Nomura Shinya , Maeda Kiyoshi , Noda Eiji , Inoue Toru , Fukunaga Shinya , Nagahara Hisashi , Hirakawa Kosei 
Published: June 2010

AbstractBackgroundConnexin26 (Cx26) is one of the connexins (Cxs) family members which form gap junction channels. Cx26 is considered to be a tumor suppressor gene. However, recent studies revealed that over expression of Cx26 is associated with a poor prognosis in several human cancers. This study investigated the correlation between Cx26 expression and the clinicopathological features and P53 expression in colorectal cancer.MethodsOne hundred and fifty-three patients who underwent a curative resection were studied. Tissue samples were investigated by immunohistochemical staining using antibodies for Cx26 and P53. Moreover, apoptotic cells were detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining.ResultsCx26 expression was found in 83 cases (54.2%) and P53 expression in 71 cases (46.4%). A correlation was observed between the Cx26 expression and recurrence, histology, and p53 expression (P < 0.05). Cx26 positive tumors had significantly longer survival than Cx26 negative tumors (P < 0.05). A multivariate Cox analysis demonstrated that Cx26 expression was an independent prognostic factor (P < 0.05). However, no significant correlation was observed between Cx26 and AI.ConclusionThis study suggests that Cx26 expression is an independent prognostic factor in patients that undergo a curative resection of colorectal cancer.
MYEOV (myeloma overexpressed gene) drives colon cancer cell migration and is regulated by PGE2
Authors: Lawlor Garrett , Doran Peter P , MacMathuna Padraic , Murray David W 
Published: June 2010

Abstract

Introduction
We have previously reported that Myeov (MYEloma OVerexpressed gene) expression is enhanced in colorectal cancer (CRC) and that it promotes CRC cell proliferation and invasion. The role of Myeov in CRC migration is unclear. ProstaglandinE2 (PGE 2) is a known factor in promoting CRC carcinogenesis. The role of PGE 2 in modulating Myeov expression has also not been defined.

Aim
To assess the role of Myeov expression in CRC cell migration and to evaluate the role of PGE 2 in Myeov bioactivity.

Methods
siRNA mediated Myeov knockdown was achieved in T84 CRC cells. Knockdown was assessed using quantitative real time PCR. The effect of knockdown on CRC cell migration was assessed using a scratch wound healing assay. Separately, T84 cells were treated with PGE 2 (0.00025 μ M, 0.1 μ M and 1 μ M) from 30 min to 3 hours and the effect on Myeov gene expression was assessed using real time PCR.

Results
Myeov knockdown resulted in a significant reduction in CRC cell migration, observable as early as 12 hours (P < 0.05) with a 39% reduction compared to control at 36 hours (p < 0.01). Myeov expression was enhanced after treatment with PGE 2, with the greatest effect seen at 60 mins for all 3 PGE 2 doses. This response was dose dependent with a 290%, 550% & 1,000% increase in Myeov expression for 0.00025 μ M, 0.1 μ M and 1 μ M PGE 2 respectively.

Conclusion
In addition to promoting CRC proliferation and invasion, our findings indicate that Myeov stimulates CRC cell migration, and its expression may be PGE 2 dependant.
The role of chemotherapeutic drugs in the evaluation of breast tumour response to chemotherapy using serial FDG-PET
Authors: Schneider-Kolsky Michal E , Hart Stewart , Fox Jane , Midolo Peter , Stuckey John , Hofman Michael , Ganju Vinod 
Published: June 2010

Abstract
Introduction
The aims of this study were to investigate whether drug sequence (docetaxel followed by anthracyclines or the drugs in reverse order) affects changes in the maximal standard uptake volume (SUVmax) on [18F]flourodeoxyglucose positron emission tomography (FDG-PET) during neoadjuvant chemotherapy in women with locally advanced breast cancer.

Methods
Women were randomly assigned to receive either drug sequence, and FDG-PET scans were taken at baseline, after four cycles and after eight cycles of chemotherapy. Tumour response to chemotherapy was evaluated based on histology from a surgical specimen collected upon completion of chemotherapy.

Results
Sixty women were enrolled into the study. Thirty-one received docetaxel followed by anthracyclines (Arm A) and 29 received drugs in the reverse order (Arm B). Most women (83%) had ductal carcinoma and 10 women (17%) had lobular or lobular/ductal carcinoma. All but one tumour were downstaged during therapy. Overall, there was no significant difference in response between the two drug regimens. However, women in Arm B who achieved complete pathological response had mean FDG-PET SUVmax reduction of 87.7% after four cycles, in contrast to those who had no or minor pathological response. These women recorded mean SUVmax reductions of only 27% (P < 0.01). Women in Arm A showed no significant difference in SUVmax response according to pathological response. Sensitivity, specificity, accuracy and positive and negative predictive values were highest in women in Arm B.

Conclusions
Our results show that SUVmax uptake by breast tumours during chemotherapy can be dependent on the drugs used. Care must be taken when interpreting FDG-PET in settings where patients receive varied drug protocols.
Cooperative signaling between Wnt1 and integrin-linked kinase induces accelerated breast tumor development
Authors: Oloumi Arusha , Maidan Mykola , Lock Frances E , Tearle Howard , McKinney Steven , Muller William J , Aparicio Samuel AJR , Dedhar Shoukat 
Published: June 2010

Abstract
Introduction
Breast cancer is genetically and clinically a heterogeneous disease. However, the exact contribution of different cell types and oncogenic mutations to this heterogeneity are not well understood. Recently, we discovered an interaction between Wnt and integrin-linked kinase (ILK) within the signaling cascade that regulates cell growth and survival. Interestingly, mammary-specific expression of either one of these proteins has been shown to promote mammary tumorigenesis. In light of our recent findings and to investigate the potential interaction between Wnt and ILK proteins during mammary tumor formation and progression, we established a transgenic mouse model that expresses both Wnt and ILK in mammary epithelial cells.

Methods
A novel transgenic mouse model with mammary-specific expression of both Wnt1 and ILK was generated by crossing the two previously characterized mouse models, MMTV-Wnt1 and MMTV-ILK. The resulting MMTV-Wnt/ILK mice were closely monitored for tumor development and growth, as well as for the tumor onset. The molecular phenotypes of both tumors and premalignant mammary glands were investigated by using biochemical and global gene-expression analysis approaches.

Results
A significant acceleration in mammary tumor incidence and growth was observed in the MMTV-Wnt/ILK mice. Pre-neoplastic mammary glands also display lobuloalveolar hyperplasia and an increase in ductal epithelium proliferation. Apart from elevated expression of Wnt/ILK targets, such as β-catenin and cyclin D1, gene-expression profiling identified the surprising activation of the FOXA1 transcription factor. Upregulation of FOXA1, which is also known as the molecular marker of differentiated mammary luminal cells, was consistent with the expansion of the enriched luminal progenitor population or CD29loCD24hiCD61+ cells in MMTV-Wnt/ILK tumors.

Conclusions
These results show cooperation between Wnt1 and ILK transgenes during mammary carcinogenesis, leading to changes in a transcriptional network, which could dictate a specific breast cancer phenotype with enhanced growth dynamics. The MMTV-Wnt/ILK can be used as a model to identify further the genes downstream of the estrogen receptor-β/FOXA1 and to investigate the mechanisms targeting the expansion of the luminal progenitor cells leading to hyperplasia and tumorigenesis.
Proteomic and transcriptomic profiling reveals a link between the PI3K pathway and lower estrogen-receptor (ER) levels and activity in ER+ breast cancer
Authors: Creighton Chad J , Fu Xiaoyong , Hennessy Bryan T , Casa Angelo J , Zhang Yiqun , Gonzalez-Angulo Ana Maria , Lluch Ana , Gray Joe W , Brown Powell H , Hilsenbeck Susan G , Osborne C Kent , Mills Gordon B , Lee Adrian V , Schiff Rachel 
Published: June 2010

Abstract
Introduction
Accumulating evidence suggests that both levels and activity of the estrogen receptor (ER) and the progesterone receptor (PR) are dramatically influenced by growth-factor receptor (GFR) signaling pathways, and that this crosstalk is a major determinant of both breast cancer progression and response to therapy. The phosphatidylinositol 3-kinase (PI3K) pathway, a key mediator of GFR signaling, is one of the most altered pathways in breast cancer. We thus examined whether deregulated PI3K signaling in luminal ER+ breast tumors is associated with ER level and activity and intrinsic molecular subtype.

Methods
We defined two independent molecular signatures of the PI3K pathway: a proteomic (reverse-phase proteomic array) PI3K signature, based on protein measurement for PI3K signaling intermediates, and a PI3K transcriptional (mRNA) signature based on the set of genes either induced or repressed by PI3K inhibitors. By using these signatures, we scored each ER+ breast tumor represented in multiple independent expression-profiling datasets (four mRNA, n = 915; one protein, n = 429) for activation of the PI3K pathway. Effects of PI3K inhibitor BEZ-235 on ER expression and activity levels and cell growth were tested by quantitative real-time PCR and cell proliferation assays.

Results
Within ER+ tumors, ER levels were negatively correlated with the PI3K activation scores, both at the proteomic and transcriptional levels, in all datasets examined. PI3K signature scores were also higher in ER+ tumors and cell lines of the more aggressive luminal B molecular subtype versus those of the less aggressive luminal A subtype. Notably, BEZ-235 treatment in four different ER+ cell lines increased expression of ER and ER target genes including PR, and treatment with IGF-I (which signals via PI3K) decreased expression of ER and target genes, thus further establishing an inverse functional relation between ER and PI3K. BEZ-235 had an additional effect on tamoxifen in inhibiting the growth of a number of ER+ cell lines.

Conclusions
Our data suggest that luminal B tumors have hyperactive GFR/PI3K signaling associated with lower ER levels, which has been correlated with resistance to endocrine therapy. Targeting PI3K in these tumors might reverse loss of ER expression and signaling and restore hormonal sensitivity.
Echocardiography: a help in the weaning process
Authors: Caille Vincent , Amiel Jean-Bernard , Charron Cyril , Belliard Guillaume , Vieillard-Baron Antoine , Vignon Philippe 
Published: June 2010

Abstract
Introduction
To evaluate the ability of transthoracic echocardiography (TTE) to detect the effects of spontaneous breathing trial (SBT) on central hemodynamics and to identify indices predictive of cardiac-related weaning failure.

Methods
TTE was performed just before and at the end of a 30-min SBT in 117 patients fulfilling weaning criteria. Maximal velocities of mitral E and A waves, deceleration time of E wave (DTE), maximal velocity of E' wave (tissue Doppler at the lateral mitral annulus), and left ventricular (LV) stroke volume were measured. Values of TTE parameters were compared between baseline (pressure support ventilation) and SBT in all patients and according to LV ejection fraction (EF): >50% (n = 58), 35% to 50% (n = 30), and <35% (n = 29). Baseline TTE indices were also compared between patients who were weaned (n = 94) and those who failed (n = 23).

Results
Weaning failure was of cardiac origin in 20/23 patients (87%). SBT resulted in a significant increase in cardiac output and E/A, and a shortened DTE. At baseline, DTE was significantly shorter in patients with LVEF <35% when compared to other subgroups (median [25th-75th percentiles]: 119 ms [90-153]; vs. 187 ms [144-224] vs. 174 ms [152-193]; P < 0.01) and E/E' was greater (7.9 [5.4-9.1] vs. 6.0 [5.3-9.0] vs. 5.2 [4.7-6.0]; P < 0.01). When compared to patients who were successfully weaned, those patients who failed exhibited at baseline a significantly lower LVEF (36% [27-55] vs. 51% [43-55]: P = 0.04) and higher E/E' (7.0 [5.0-9.2] vs. 5.6 [5.2-6.3]: P = 0.04).

Conclusions
TTE detects SBT-induced changes in central hemodynamics. When performed by an experienced operator prior to SBT, TTE helps in identifying patients at high risk of cardiac-related weaning failure when documenting a depressed LVEF, shortened DTE and increased E/E'. Further studies are needed to evaluate the impact of this screening strategy on the weaning process and patient outcome.