bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distortion correction for diffusion‐weighted MRI tractography and fMRI in the temporal lobes
Authors: Embleton Karl V. , Haroon Hamied A. , Morris David M. , Ralph Matthew A. Lambon , Parker Geoff J.M. 
Published: February 2010

AbstractSingle shot echo‐planar imaging (EPI) sequences are currently the most commonly used sequences for diffusion‐weighted imaging (DWI) and functional magnetic resonance imaging (fMRI) as they allow relatively high signal to noise with rapid acquisition time. A major drawback of EPI is the substantial geometric distortion and signal loss that can occur due to magnetic field inhomogeneities close to air‐tissue boundaries. If DWI‐based tractography and fMRI are to be applied to these regions, then the distortions must be accurately corrected to achieve meaningful results. We describe robust acquisition and processing methods for correcting such distortions in spin echo (SE) EPI using a variant of the reversed direction k space traversal method with a number of novel additions. We demonstrate that dual direction k space traversal with maintained diffusion‐encoding gradient strength and direction results in correction of the great majority of eddy current‐associated distortions in DWI, in addition to those created by variations in magnetic susceptibility. We also provide examples to demonstrate that the presence of severe distortions cannot be ignored if meaningful tractography results are desired. The distortion correction routine was applied to SE‐EPI fMRI acquisitions and allowed detection of activation in the temporal lobe that had been previously found using PET but not conventional fMRI. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
Cortical gamma‐oscillations modulated by auditory–motor tasks‐intracranial recording in patients with epilepsy
Authors: Nagasawa Tetsuro , Rothermel Robert , Juhász Csaba , Fukuda Miho , Nishida Masaaki , Akiyama Tomoyuki , Sood Sandeep , Asano Eishi 
Published: February 2010

AbstractHuman activities often involve hand‐motor responses following external auditory–verbal commands. It has been believed that hand movements are predominantly driven by the contralateral primary sensorimotor cortex, whereas auditory–verbal information is processed in both superior temporal gyri. It remains unknown whether cortical activation in the superior temporal gyrus during an auditory–motor task is affected by laterality of hand‐motor responses. Here, event‐related γ‐oscillations were intracranially recorded as quantitative measures of cortical activation; we determined how cortical structures were activated by auditory‐cued movement using each hand in 15 patients with focal epilepsy. Auditory–verbal stimuli elicited augmentation of γ‐oscillations in a posterior portion of the superior temporal gyrus, whereas hand‐motor responses elicited γ‐augmentation in the pre‐ and postcentral gyri. The magnitudes of such γ‐augmentation in the superior temporal, precentral, and postcentral gyri were significantly larger when the hand contralateral to the recorded hemisphere was required to be used for motor responses, compared with when the ipsilateral hand was. The superior temporal gyrus in each hemisphere might play a greater pivotal role when the contralateral hand needs to be used for motor responses, compared with when the ipsilateral hand does. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
A case‐control study of ocular surface squamous neoplasia (OSSN) in Uganda
Authors: Waddell Keith , Kwehangana James , Johnston William T. , Lucas Sebastian , Newton Robert 
Published: February 2010

AbstractHIV increases the risk of OSSN. Here we investigate other factors in a case‐control study from Uganda with 318 cases (48 CIN I, 66 CIN II, 81 CIN III and 123 with invasive disease) and 762 controls. Initial analyses were stratified by HIV serostatus (204 cases and 202 controls were HIV seropositive), but since findings were similar in infected and uninfected people, the combined results are presented here. The risk of OSSN increased with increasing time spent in direct sunlight (ptrend = 0.003, adjusted for age, sex, residential district and HIV serostatus): compared to those who reported spending up to 1 hr a day in direct sunlight, the risk was 1.7 (95% Confidence Interval [CI] 1.2–2.4) in those reporting 2–4‐hr exposure and 1.8 (95% CI 1.1–3.1) in those reporting 5+ hr. The risk was also increased among people reporting a previous injury to the affected eye (OR 2.4, 95% CI 1.2–4.5). Pinguecula in the nasal quadrant of the unaffected eye were evident on clinical examination for 98% of cases (293/300) and for 91% of the same quadrant in the right eye (246/271) of controls (OR = 6.4, 95% CI 2.5–16.1). We confirm associations with exposure to solar ultraviolet radiation and with the presence of pinguecula and report a role for previous ocular trauma in the aetiology of OSSN. We did not identify any additional factors that point to an underlying infectious cause, although this is an area of on‐going research.
Expression of laminin γ2 chain monomer enhances invasive growth of human carcinoma cells in vivo
Authors: Tsubota Yoshiaki , Ogawa Takashi , Oyanagi Jun , Nagashima Yoji , Miyazaki Kaoru 
Published: February 2010

AbstractLaminin γ2 chain is a subunit of the heterotrimeric basement membrane protein laminin‐332 (α3β3γ2). The γ2 chain is highly expressed by human cancers at the invasion fronts and this expression correlates with poor prognosis of the cancers. Our previous study showed that the γ2 chain is expressed as a monomer form in invading carcinoma cells. However, the role of the γ2 protein in tumor invasion remains unknown. Here, we demonstrate that the monomeric γ2 chain promotes invasive growth of human cancer cells in vivo. First, we analyzed regulatory factors for the γ2 chain expression using 2 gastric carcinoma cell lines. It was found that tumor necrosis factor‐α, by itself or in a combination with transforming growth factor‐β1, strongly induced the secretion of the monomeric γ2 chain. In addition, epidermal growth factor families appeared to function as the γ2 chain inducers in human cancers. Next, we established T‐24 bladder carcinoma cell lines expressing the full‐length or the short arm of the laminin γ2 chain. When these cell lines were i.p. injected into nude mice, they produced larger tumors in the abdominal cavity and showed much stronger invasive growth onto the diaphragms than the control cell line. The γ2‐expressing T‐24 cells often produced ascites fluid, but scarcely the control cells. In culture, the γ2‐expressing cells migrated through Matrigel more efficiently than the control cells. These findings imply that the γ2 monomer is induced in human cancers by inflammatory and stromal cytokines and promotes their invasive growth in vivo.
Elevated expression of tumor necrosis factor‐α signaling molecules in colonic tumors of Zucker obese (fa/fa) rats
Authors: Jain Swati S. , Bird Ranjana P. 
Published: February 2010

AbstractZucker obese rats are highly sensitive to colon cancer and possess a plethora of metabolic abnormalities including elevated levels of cytokine tumor necrosis factor‐α (TNF‐α). The main objective of this study was to determine if physiologically elevated TNF‐α affects colonic tumor phenotype with regard to an altered TNF‐α signaling pathway. Zucker obese (fa/fa, homozygous recessive for dysfunctional leptin receptors), Zucker lean (Fa/fa, Fa/Fa) and Sprague–Dawley (SD) rats were injected twice with azoxymethane (10 mg/kg) over 2 weeks. After 30 weeks, the animals were terminated and physiological and tumor parameters were assessed. Obese rats had notably higher body and organ weights as well as plasma TNF‐α, insulin and leptin levels than lean or SD animals. A 100% tumor incidence and significantly higher tumor size, multiplicity and burden were found in obese rats compared to the lean group that had 47.8% tumor incidence. The SD group had the lowest tumor incidence (20.0%). Tumors from obese animals had higher protein levels of TNF‐α, TNF‐α‐receptor‐2 (TNFR2), nuclear transcription factor‐κB (NF‐κB) and IκB‐kinaseβ (IKKβ) compared to lean animals. In both obese and lean groups, expression levels of these proteins were higher in tumors than in surrounding, normal‐appearing colonic mucosae. These findings support an important role for TNF‐α signaling in tumorigenesis and demonstrate that tumors growing in an obese state had significantly different expression levels of TNFR2 and NF‐κB, proteins known to play a critical role in growth and survival, than those growing in the lean state. It is concluded that the physiological state of the host intricately affects tumor phenotype.
The BCR/ABL‐inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity
Authors: Salih Julia , Hilpert Julia , Placke Theresa , Grünebach Frank , Steinle Alexander , Salih Helmut Rainer , Krusch Matthias 
Published: February 2010

AbstractIn chronic myeloid leukemia (CML), BCR/ABL‐mediated oncogenic signaling can be targeted with the BCR/ABL‐inhibitors Imatinib, Nilotinib and Dasatinib. However, these agents may also affect anti‐tumor immunity. Here, we analyzed the effects of the 3 BCR/ABL‐inhibitors on natural killer (NK) cell reactivity. Exposure of CML cells (K562, Meg‐01) to pharmacological concentrations of Imatinib, Nilotinib and Dasatinib diminished expression of ligands for the activating immunoreceptor NKG2D to a similar extent. This resulted in comparably reduced NK cell cytotoxicity and IFN‐γ production. When direct effects on NK cell responses to K562 and primary CML cells as well as activating cytokines were studied, Dasatinib was found to abrogate NK cytotoxicity and cytokine production. Nilotinib did not alter cytotoxicity but, at high levels, impaired NK cytokine production, while Imatinib had no direct influence on NK cell reactivity. Of note, Nilotinib, but not the other BCR/ABL‐inhibitors increased cell death within the preferentially cytokine‐secreting CD56brightCD16− NK cell subset, which may, at least in part, serve to explain the effect of Nilotinib on NK cytokine production. Analysis of NK cell signaling revealed that Dasatinib inhibited proximal signaling events leading to decreased phosphorylation of PI3K and ERK that are crucial for NK cell reactivity. Imatinib and Nilotinib, in contrast, showed no relevant effect on NK cell PI3K or ERK activity. In light of the potential role of NK cells in the immunesurveillance of residual leukemia and for future combinatory immunotherapeutic approaches, our data indicate that choice and dosing of the most suitable BCR/ABL‐inhibitor for a given patient require careful consideration.
Deficiency or blockade of angiotensin II type 2 receptor delays tumorigenesis by inhibiting malignant cell proliferation and angiogenesis
Authors: Clere Nicolas , Corre Isabelle , Faure Sébastien , Guihot Anne‐Laure , Vessières Emilie , Chalopin Marie , Morel Alain , Coqueret Olivier , Hein Lutz , Delneste Yves , Paris François , Henrion Daniel 
Published: February 2010

AbstractDespite significant expression level in cancer cells, the role of the angiotensin II Type 2 receptor (AT2R) in cancer progression remains poorly understood. We aimed to investigate the involvement of AT2R in tumorigenesis, hypothesizing a role in tumor cell proliferation and/or tumor angiogenesis. Two animal tumor models were used: fibrosarcoma induced by 3‐methylcholanthrene (3‐MCA) in FVB/N mice invalidated for AT2R (AT2R‐KO) and carcinoma LL/2 cells injected in C57BL/6N mice treated with AT2R antagonist PD123,319. Tumor growth was monitored, microvascular density (MVD) evaluated by CD31 staining. Proliferation index of LL/2 and 3‐MCA tumor cells was evaluated by expression of Ki‐67. Angiogenesis was assessed by aorta ring assay and angiogenic mediators' expression by real‐time RT‐PCR. Tumor induction by 3‐MCA was significantly delayed in AT2R‐KO compared to wild‐type mice (56 days vs. 28 days). Tumorigenesis following LL/2 cell injection in mice was also significantly reduced by early administration of the antagonist PD123,319. In vitro, inactivation or invalidation of AT2R inhibited proliferation of LL/2 and 3‐MCA tumor cells, respectively. Tumor MVD was reduced in mice treated early with PD123,319. Ex vivo experiments revealed a significant decrease in angiogenesis after PD123,319 treatment or in AT2R‐KO mice. Finally, we identified vascular endothelial growth factor (VEGF) as a soluble proangiogenic factor produced by LL/2 cells and we showed that in LL/2 and 3‐MCA tumor cells, inhibition or deficiency of AT2R was associated with impaired production of proangiogenic factors included VEGF. This study uncovered novel mechanisms by which AT2R would promote tumor development, favoring both malignant cell proliferation and tumor angiogenesis.
Substantial regional differences in human herpesvirus 8 seroprevalence in sub‐Saharan Africa: Insights on the origin of the “Kaposi's sarcoma belt”
Authors: Dollard Sheila C. , Butler Lisa M. , Jones Alison M. Graves , Mermin Jonathan H. , Chidzonga Midion , Chipato Tsungai , Shiboski Caroline H. , Brander Christian , Mosam Anisa , Kiepiela Photini , Hladik Wolfgang , Martin Jeffrey N. 
Published: February 2010

AbstractEquatorial Africa has among the highest incidences of Kaposi's sarcoma (KS) in the world, thus earning the name “KS Belt.” This was the case even before the HIV epidemic. To date, there is no clear evidence that HHV‐8 seroprevalence is higher in this region but interpretation of the available literature is tempered by differences in serologic assays used across studies. We examined representatively sampled ambulatory adults in Uganda, which is in the “KS Belt,” and in Zimbabwe and South Africa which are outside the Belt, for HHV‐8 antibodies. All serologic assays were uniformly performed in the same reference laboratory by the same personnel. In the base‐case serologic algorithm, seropositivity was defined by reactivity in an immunofluorescence assay or in 2 enzyme immunoassays. A total of 2,375 participants were examined. In Uganda, HHV‐8 seroprevalence was high early in adulthood (35.5% by age 21) without significant change thereafter. In contrast, HHV‐8 seroprevalence early in adulthood was lower in Zimbabwe and South Africa (13.7 and 10.8%, respectively) but increased with age. After age adjustment, Ugandans had 3.24‐fold greater odds of being HHV‐8 infected than South Africans (p < 0.001) and 2.22‐fold greater odds than Zimbabweans (p < 0.001). Inferences were unchanged using all other serologic algorithms evaluated. In conclusion, HHV‐8 infection is substantially more common in Uganda than in Zimbabwe and South Africa. These findings help to explain the high KS incidence in the “KS Belt” and underscore the importance of a uniform approach to HHV‐8 antibody testing.
Plasma decorin predicts the presence of esophageal squamous cell carcinoma
Authors: Wu I‐Chen , Wu Deng‐Chyang , Huang Chun‐Chi , Lin Hung‐Shun , Chen Yu‐Kuei , Tsai Hui‐Jen , Lu Chieh‐Yu , Chou Shah‐Hwa , Chou Yi‐Ping , Li Ling‐Hui , Tai Shu‐Yu , Wu Ming‐Tsang 
Published: February 2010

AbstractUsing a microarray technique, we found decorin to be underexpressed, but osteopontin (OPN) to be overexpressed, in esophageal squamous cell carcinoma (ESCC). This study aims to examine whether plasma decorin and OPN plus personal substances use (tobacco, alcohol and areca) can serve as suitable clinical markers to predict the presence of ESCC. In total, 570 archived plasma specimens (275 patients and 295 controls) were collected from 2 medical centers in Taiwan between 2000 and 2008. Decorin and OPN protein levels were measured by ELISA. Means and standard deviation of plasma decorin were 5.6 ± 3.6 ng/ml in case patients, which were significantly lower than those in controls (7.8 ± 3.1, p < 0.0001). Plasma OPN levels in case patients were not significantly different from controls (p = 0.33). When compared to subjects with the lowest quartile of plasma decorin, those with the highest quartile one had a significantly lower risk to have ESCC (Adjusted OR = 0.03, p < 0.001). Receiver operator characteristic (ROC) analysis was performed for the combination of plasma decorin and 3 substances use (smoke, alcohol and areca) for the patients compared with the controls. The area under the curve was 88.6% and the optimal cut‐point of ROC curve (any 3 factors) had 73.5% sensitivity and 90.2% specificity with ∼82% of corrected classification. Plasma decorin, but not OPN, is a potential clinical marker for the detection of ESCC. When plasma decorin plus the use of the 3 substances are combined, this factor cluster could be used to detect the presence of ESCC.
Allergies, obesity, other risk factors and survival from pancreatic cancer
Authors: Olson Sara H. , Chou Joanne F. , Ludwig Emmy , O'Reilly Eileen , Allen Peter J. , Jarnagin William R. , Bayuga Sharon , Simon Jennifer , Gonen Mithat , Reisacher William R. , Kurtz Robert C. 
Published: February 2010

AbstractSurvival from pancreatic adenocarcinoma remains extremely poor, approximately 5% at 5 years. Risk factors include smoking, high body mass index (BMI), family history of pancreatic cancer, and long‐standing diabetes; in contrast, allergies are associated with reduced risk. Little is known about associations between these factors and survival. We analyzed overall survival in relation to risk factors for 475 incident cases who took part in a hospital based case–control study. Analyses were conducted separately for those who did (160) and did not (315) undergo tumor resection. Kaplan‐Meier methods were used to describe survival according to smoking, BMI, family history, diabetes, and presence of allergies. Cox proportional hazards models were used to adjust for covariates. There was no association with survival based on smoking, family history, or history of diabetes in either group. Among patients with resection, those with allergies showed nonstatistically significant longer survival, a median of 33.1 months (95% CI: 19.0–52.5) vs. 21.8 months (95% CI: 18.0–33.1), p = 0.25. The adjusted hazard ratio (HR) was 0.72 (95% CI: 0.43–1.23), p = 0.23. Among patients without resection, those with self‐reported allergies survived significantly longer than those without allergies: 13.3 months (95% CI: 10.6–16.9) compared to 10.4 months (95% CI: 8.8–11.0), p = 0.04, with an adjusted HR of 0.68 (95% CI: 0.49–0.95), p = 0.02. Obesity was nonsignificantly associated with poorer survival, particularly in the resected group (HR = 1.62, 95% CI: 0.76–3.44). The mechanisms underlying the association between history of allergies and improved survival are unknown. These novel results need to be confirmed in other studies.
Check your cultures! A list of cross‐contaminated or misidentified cell lines
Authors: Capes‐Davis Amanda , Theodosopoulos George , Atkin Isobel , Drexler Hans G. , Kohara Arihiro , MacLeod Roderick A.F. , Masters John R. , Nakamura Yukio , Reid Yvonne A. , Reddel Roger R. , Freshney R. Ian 
Published: February 2010

AbstractContinuous cell lines consist of cultured cells derived from a specific donor and tissue of origin that have acquired the ability to proliferate indefinitely. These cell lines are well‐recognized models for the study of health and disease, particularly for cancer. However, there are cautions to be aware of when using continuous cell lines, including the possibility of contamination, in which a foreign cell line or microorganism is introduced without the handler's knowledge. Cross‐contamination, in which the contaminant is another cell line, was first recognized in the 1950s but, disturbingly, remains a serious issue today. Many cell lines become cross‐contaminated early, so that subsequent experimental work has been performed only on the contaminant, masquerading under a different name. What can be done in response—how can a researcher know if their own cell lines are cross‐contaminated? Two practical responses are suggested here. First, it is important to check the literature, looking for previous work on cross‐contamination. Some reports may be difficult to find and to make these more accessible, we have compiled a list of known cross‐contaminated cell lines. The list currently contains 360 cell lines, drawn from 68 references. Most contaminants arise within the same species, with HeLa still the most frequently encountered (29%, 106/360) among human cell lines, but interspecies contaminants account for a small but substantial minority of cases (9%, 33/360). Second, even if there are no previous publications on cross‐contamination for that cell line, it is essential to check the sample itself by performing authentication testing.
The calcium-sensing receptor and 25-hydroxyvitamin D–1α-hydroxylase interact to modulate skeletal growth and bone turnover
Authors: Richard Christian , Huo Rujuan , Samadfam Rana , Bolivar Isabel , Miao Dengshun , Brown Edward M , Hendy Geoffrey N , Goltzman David 
Published: February 2010

Abstract
We examined parathyroid and skeletal function in 3-month-old mice expressing the null mutation for 25-hydroxyvitamin D–1α-hydroxylase [1α(OH)ase−/−] and in mice expressing the null mutation for both the 1α(OH)ase and the calcium-sensing receptor [Casr−/−1α(OH)ase−/−] genes. On a normal diet, all mice were hypocalcemic, with markedly increased parathyroid hormone (PTH), increased trabecular bone volume, increased osteoblast activity, poorly mineralized bone, enlarged and distorted cartilaginous growth plates, and marked growth retardation, especially in the compound mutants. Osteoclast numbers were reduced in the Casr−/−1α(OH)ase−/− mice. On a high-lactose, high-calcium, high-phosphorus “rescue” diet, serum calcium and PTH were normal in the 1α(OH)ase−/− mice but increased in the Casr−/−1α(OH)ase−/− mice with reduced serum phosphorus. Growth plate architecture and mineralization were improved in both mutants, but linear growth of the double mutants remained abnormal. Mineralization of bone improved in all mice, but osteoblast activity and trabecular bone volume remained elevated in the Casr−/−1α(OH)ase−/− mice. These studies support a role for calcium-stimulated maturation of the cartilaginous growth plate and mineralization of the growth plate and bone and calcium-stimulated CaSR-mediated effects on bone resorption. PTH-mediated bone resorption may require calcium-stimulated CaSR-mediated enhancement of osteoclastic activity. © 2010 American Society for Bone and Mineral Research. © 2010 American Society for Bone and Mineral Research