bluuebunny/crossref_metadata_2025_split huggingface dataset:
Frying Performance of No‐trans, Low‐Linolenic Acid Soybean Oils
Authors: Gerde Jose , Hardy Connie , Fehr Walter , White Pamela J. 
Published: May 2007

AbstractTwo extruded‐expelled physically refined soybean oils with reduced contents of linolenic acid, ultra‐low‐ linolenic acid (ULL, 1.5%) and low‐linolenic acid (LL, 2.6%), and a extruded‐expelled physically refined control oil (control, 5.3% linolenic acid) were evaluated by frying French fries in a commercial‐like setting for 6 h day−1 during 23 days. The oils became darker, increased in yellow color at the beginning, and became redder and less green throughout the process. Free fatty acids levels were not different among the oils until day 14, after which, ULL was different from the control for the remainder of frying. The conjugated dienoic acid values were greatest in the control. Generally, ULL and LL oils had lower percentages of polar compounds than did the control, providing a frying life 2 days longer than the control and ~30% increase in frying time. A trained sensory panel evaluated the French fries on days 2, 5, and 6. Buttery and potato flavors decreased, and rancid and painty flavors increased over frying time for all products. Rancid flavor was highest in the fries from the control oil. Overall, the ULL and LL oils performed better than did the control oil and ULL tended to perform better than the LL.
Baclofen‐enhanced spinal cord stimulation and intrathecal baclofen alone for neuropathic pain: Long‐term outcome of a pilot study
Authors: Lind Göran , Schechtmann Gastón , Winter Jaleh , Meyerson Björn A. , Linderoth Bengt 
Published: May 2007

AbstractIn a previously published pilot study, we addressed the possibility to increase the effectiveness of spinal cord stimulation (SCS) applied for neuropathic pain by using adjunct pharmacological therapy. This combined treatment approach was a direct spin‐off from animal experiments aiming at the exploration of transmitter and receptor mechanisms involved in the pain relieving effect of SCS. Out of 48 patients with neuropathic pain of peripheral origin responding poorly to SCS, seven received pumps for intrathecal baclofen (GABA‐B receptor agonist) delivery together with SCS, and four had pumps alone. In order to assess the long‐term effect a follow‐up has been performed, with an average, total treatment time of 67 months. At the follow‐up the remaining nine patients still enjoy about the same pain relief as initially, but with a mean, further dose increase of about 30%. This study demonstrates that a deficient SCS effect in neuropathic pain may be considerably improved by intrathecal baclofen administration, and that this enhanced effect persists for a long‐time. On‐going and future animal studies may provide new and even more efficient pharmaceutical candidates for such combined therapy.
Quetiapine versus risperidone in elderly patients with behavioural and psychological symptoms of dementia: Efficacy, safety and cognitive function
Authors: Rainer M. , Haushofer M. , Pfolz H. , Struhal C. , Wick W. 
Published: May 2007

AbstractObjectiveIn this study we directly compared the efficacy and tolerability of the atypical antipsychotics quetiapine and risperidone in elderly patients with dementia and symptoms of disturbed perception, thought content, mood or behaviour (behavioural and psychological symptoms of dementia—BPSD).MethodsWe conducted an 8-week, rater-blinded, randomised study of 72 outpatients (55–85 years) with BPSD (assessed by NPI baseline score), who received flexibly-dosed quetiapine (50–400 mg/day) or risperidone (0.5–2 mg/day). Primary efficacy measure: Neuropsychiatric Inventory (NPI) Parts 1 and 2; secondary efficacy measures: Clinical Global Impression (CGI), Cohen-Mansfield Agitation Inventory (CMAI), Mini-Mental State Examination (MMSE), Age-adjusted concentration test (AKT). Safety evaluations included the incidence of extrapyramidal symptoms (EPS) and adverse events (AEs).ResultsSixty-nine of 72 patients were evaluable for efficacy (72 were evaluated for safety), 4 patients discontinued (3 due to AEs: quetiapine 2, risperidone 1; 1 lost to follow-up). Sixty-five patients received quetiapine (n = 34; mean dose 77 ± 40 mg/day) or risperidone (n = 31; mean dose 0.9 ± 0.3 mg/day). There was no significant difference between treatments on NPI scores; within treatment groups, NPI scores decreased significantly from baseline to Week 8 (P ≤ 0.05 vs. baseline). Most patients (quetiapine arm 67.6%, risperidone arm 71.0%) experienced clinical improvement (CGI-Improvement scores); both agents reduced agitation (CMAI scores); and there was no cognitive impairment (MMSE and AKT scores). There were no significant differences between treatments in any safety measures, including EPS. Four patients experienced serious AEs (quetiapine arm 3; risperidone arm 1); none were considered treatment-related by the study investigator. There were no cerebrovascular AEs or deaths.ConclusionsQuetiapine or risperidone, at low doses, were equally effective and generally well tolerated (including no cognitive impairment) in the treatment of BPSD in elderly patients.
Integrin-linked kinase is required for epidermal and hair follicle morphogenesis
Authors: Lorenz Katrin , Grashoff Carsten , Torka Robert , Sakai Takao , Langbein Lutz , Bloch Wilhelm , Aumailley Monique , Fässler Reinhard 
Published: May 2007

Integrin-linked kinase (ILK) links integrins to the actin cytoskeleton and is believed to phosphorylate several target proteins. We report that a keratinocyte-restricted deletion of the ILK gene leads to epidermal defects and hair loss. ILK-deficient epidermal keratinocytes exhibited a pronounced integrin-mediated adhesion defect leading to epidermal detachment and blister formation, disruption of the epidermal–dermal basement membrane, and the translocation of proliferating, integrin-expressing keratinocytes to suprabasal epidermal cell layers.
The mutant hair follicles were capable of producing hair shaft and inner root sheath cells and contained stem cells and generated proliferating progenitor cells, which were impaired in their downward migration and hence accumulated in the outer root sheath and failed to replenish the hair matrix. In vitro studies with primary ILK-deficient keratinocytes attributed the migration defect to a reduced migration velocity and an impaired stabilization of the leading-edge lamellipodia, which compromised directional and persistent migration. We conclude that ILK plays important roles for epidermis and hair follicle morphogenesis by modulating integrin-mediated adhesion, actin reorganization, and plasma membrane dynamics in keratinocytes.
Strong suppression of tumor growth by insulin‐like growth factor‐binding protein‐related protein 1/tumor‐derived cell adhesion factor/mac25
Authors: Sato Yuichiro , Chen Zhaoxin , Miyazaki Kaoru 
Published: May 2007

Insulin‐like growth factor binding protein‐related protein 1 (IGFBP‐rP1) has been shown to induce cellular senescence or apoptosis of breast and prostate cancer cell lines in vitro. To examine whether IGFBP‐rP1 acts as a tumor‐suppressive protein in vivo, we established two model systems. Expression of IGFBP‐rP1 in the human bladder carcinoma cell line EJ‐1 was blocked by RNA interference. Human colon cancer cell line DLD‐1, which did not express endogenous IGFBP‐rP1, was transfected with an IGFBP‐rP1 expression vector. When injected intraperitoneally or subcutaneously into nude mice, the IGFBP‐rP1‐expressing EJ‐1 and DLD‐1 cell lines grew poorly, whereas the IGFBP‐rP1 non‐producers grew rapidly and produced large tumors. In monolayer culture the IGFBP‐rP1 producers and non‐producers grew similarly in each model, whereas in soft agar culture the former produced far less colonies than the latter. The IGFBP‐rP1 producers had IGFBP‐rP1 bound to the cell surface, and adhered more efficiently to fibronectin and laminin‐5 than the respective non‐producers. Expression of IGFBP‐rP1 did not affect the efficiency of insulin signaling. These results demonstrate that IGFBP‐rP1 strongly suppresses tumor growth by an insulin‐independent or insulin‐like growth factor‐independent mechanism. Cell surface IGFBP‐rP1 may reduce the anchorage‐independent growth ability, leading to the marked loss of tumorigenicity. (Cancer Sci 2007; 98: 1055–1063)
Complex ABCC8 DNA variations in congenital hyperinsulinism: lessons from functional studies
Authors: Muzyamba Morris , Farzaneh Tabasum , Behe Phillip , Thomas Alison , Christesen Henrik B. T. , Brusgaard Klaus , Hussain Khalid , Tinker Andrew 
Published: May 2007

SummaryObjective  Congenital hyperinsulinism (CHI) is a cause of persistent and severe hypoglycaemia in infancy. Mutations in the genes ABCC8 and KCNJ11 encoding SUR1 and Kir6·2, respectively, are the commonest cause of CHI. We investigated whether the possession of two DNA variants leading to coding changes in a single allele of ABCC8 can affect the potential mechanism of disease pathogenesis.Design and patients  We studied two patients with complex mutations in the ABCC8 gene with CHI and used in vitro studies to explore the potential disease mechanism and the contribution of the various mutant allelles.Results  The first case had diffuse disease and was homozygous for the mutations D1193V and R1436Q in SUR1. Channel complexes containing the D1193V mutant were delivered to the plasma membrane and were functional and those containing R1436Q were also present at the plasma membrane but were nonfunctional. Combining the two mutations (SUR1D1193V/R1436Q) led to intracellular retention of the channel complex. In a second family, the patient had histologically focal disease and was heterozygous for two mutations from his father (G228D and D1471N) and one from his mother (V1572I). SUR1 G228D and D1471N singly or in combination led to intracellular retention of the channel complex and loss of function. By contrast, V1572I is trafficked appropriately and is functional, consistent with a mechanism of reduction to hemizygosity of paternal ABCC8 in focal disease. V1572I is likely to be a benign DNA variant.Conclusion  In one patient the combination of two coding variants led to intracellular retention of channel complex. In a second patient, functional studies allowed us to unravel the DNA variants likely to be causing the abrogation of ATP‐sensitive K+ channel function.
Perioperative plasma active and total ghrelin levels are reduced in acromegaly when compared with in nonfunctioning pituitary tumours even after normalization of serum GH
Authors: Kawamata Takakazu , Inui Akio , Hosoda Hiroshi , Kangawa Kenji , Hori Tomokatsu 
Published: May 2007

SummaryObjective Ghrelin is a novel gastric peptide known to stimulate GH secretion, but the relationship between ghrelin and the GH‐insulin‐like growth factor (IGF)‐1 axis in GH excess or deficiency is poorly understood. This study investigated dysregulation of ghrelin secretion in acromegaly and its short‐term postoperative recovery.Methods A prospective study was conducted on eight patients who underwent complete transsphenoidal resection of GH‐producing pituitary adenomas (acromegaly group) and 22 for endocrinologically nonfunctioning pituitary tumours (control group). Active and total plasma ghrelin levels were measured serially before and after surgery.Results Preoperative active and total plasma ghrelin concentrations (mean ± SD; fmol/ml) were significantly reduced in acromegalic patients when compared with those in the controls (9·6 ± 4·3 and 157·4 ± 65·6vs.21·8 ± 13·0 and 267·1 ± 111·4;P = 0·023 andP = 0·021, respectively). Both levels were still significantly suppressed on postoperative Day 7 in the acromegaly group when compared with those in the control group (11·7 ± 4·3 and 197·8 ± 68·9vs.22·5 ± 12·6 and 302·7 ± 100·0;P = 0·038 andP = 0·018, respectively). The ratios of active to total ghrelin were not significantly different between the two groups before and after operation. In acromegalic patients, active and total ghrelin levels remained significantly suppressed even after normalization of serum GH levels.Conclusions The putative negative feedback mechanism of GH on ghrelin secretion may in part account for the low ghrelin levels observed in acromegalic patients, and the mechanism may persist even after normalization of serum GH.
Adaptive versus non‐adaptive phenotypic plasticity and the potential for contemporary adaptation in new environments
Authors: GHALAMBOR C. K. , McKAY J. K. , CARROLL S. P. , REZNICK D. N. 
Published: May 2007

SummaryThe role of phenotypic plasticity in evolution has historically been a contentious issue because of debate over whether plasticity shields genotypes from selection or generates novel opportunities for selection to act. Because plasticity encompasses diverse adaptive and non‐adaptive responses to environmental variation, no single conceptual framework adequately predicts the diverse roles of plasticity in evolutionary change.Different types of phenotypic plasticity can uniquely contribute to adaptive evolution when populations are faced with new or altered environments. Adaptive plasticity should promote establishment and persistence in a new environment, but depending on how close the plastic response is to the new favoured phenotypic optimum dictates whether directional selection will cause adaptive divergence between populations. Further, non‐adaptive plasticity in response to stressful environments can result in a mean phenotypic response being further away from the favoured optimum or alternatively increase the variance around the mean due to the expression of cryptic genetic variation. The expression of cryptic genetic variation can facilitate adaptive evolution if by chance it results in a fitter phenotype.We conclude that adaptive plasticity that places populations close enough to a new phenotypic optimum for directional selection to act is the only plasticity that predictably enhances fitness and is most likely to facilitate adaptive evolution on ecological time‐scales in new environments. However, this type of plasticity is likely to be the product of past selection on variation that may have been initially non‐adaptive.We end with suggestions on how future empirical studies can be designed to better test the importance of different kinds of plasticity to adaptive evolution.
Fault locking, block rotation and crustal deformation in the Pacific Northwest
Authors: McCaffrey Robert , Qamar Anthony I. , King Robert W. , Wells Ray , Khazaradze Giorgi , Williams Charles A. , Stevens Colleen W. , Vollick Jesse J. , Zwick Peter C. 
Published: May 2007

SummaryWe interpret Global Positioning System (GPS) measurements in the northwestern United States and adjacent parts of western Canada to describe relative motions of crustal blocks, locking on faults and permanent deformation associated with convergence between the Juan de Fuca and North American plates. To estimate angular velocities of the oceanic Juan de Fuca and Explorer plates and several continental crustal blocks, we invert the GPS velocities together with seafloor spreading rates, earthquake slip vector azimuths and fault slip azimuths and rates. We also determine the degree to which faults are either creeping aseismically or, alternatively, locked on the block-bounding faults. The Cascadia subduction thrust is locked mainly offshore, except in central Oregon, where locking extends inland. Most of Oregon and southwest Washington rotate clockwise relative to North America at rates of 0.4–1.0 ° Myr−1. No shear or extension along the Cascades volcanic arc has occurred at the mm/yr level during the past decade, suggesting that the shear deformation extending northward from the Walker Lane and eastern California shear zone south of Oregon is largely accommodated by block rotation in Oregon. The general agreement of vertical axis rotation rates derived from GPS velocities with those estimated from palaeomagnetic declination anomalies suggests that the rotations have been relatively steady for 10–15 Ma. Additional permanent dextral shear is indicated within the Oregon Coast Range near the coast. Block rotations in the Pacific Northwest do not result in net westward flux of crustal material—the crust is simply spinning and not escaping. On Vancouver Island, where the convergence obliquity is less than in Oregon and Washington, the contractional strain at the coast is more aligned with Juan de Fuca—North America motion. GPS velocities are fit significantly better when Vancouver Island and the southern Coast Mountains move relative to North America in a block-like fashion. The relative motions of the Oregon, western Washington and Vancouver Island crustal blocks indicate that the rate of permanent shortening, the type that causes upper plate earthquakes, across the Puget Sound region is 4.4 ± 0.3 mm yr−1. This shortening is likely distributed over several faults but GPS data alone cannot determine the partitioning of slip on them. The transition from predominantly shear deformation within the continent south of the Mendocino Triple Junction to predominantly block rotations north of it is similar to changes in tectonic style at other transitions from shear to subduction. This similarity suggests that crustal block rotations are enhanced in the vicinity of subduction zones possibly due to lower resisting stress.
Significant high expression of CD23 in follicular lymphoma of the inguinal region
Authors: Thorns C , Kalies K , Fischer U , Höfig K , Krokowski M , Feller A C , Merz H , Bernd H‐W 
Published: May 2007

Aims:  Inguinal lymph nodes are considered to be problematic for the diagnosis of lymphoma due to architectural changes resulting from previous inflammatory processes. The aim was to investigate the morphology and immunophenotype of follicular lymphomas (FL) in order to clarify whether FL presenting in inguinal nodes differs from FL biopsies from other sites.Methods and results:  A total of 219 FLs were studied, comprising 78 biopsy specimens of inguinal lymph nodes and 141 from other sites. All samples were assessed for growth pattern, grade, sclerosis and immunophenotype (Bcl‐2, CD10, CD23, Mib‐1). Cases negative for Bcl‐2 were analysed by polymerase chain reaction and fluorescence in situ hybridization. In comparison with the biopsies from other regions, we found a significantly increased number of CD23+ FLs in samples of inguinal lymph nodes (38% versus 21%). Expression of CD23 was more frequently detected in grade 1 FLs than in other grades (grade 1, 37%; grade 2, 18%; grade 3, 23%; transformed, 6%). Other immunohistochemical parameters, however, did not differ between the two groups.Conclusion:  There is an unexpectedly high frequency of CD23 expression in FL in general, which is even more pronounced in inguinal nodes.
Histopathology of graft versus host disease of the liver
Authors: Quaglia A , Duarte R , Patch D , Ngianga‐Bakwin K , Dhillon A P 
Published: May 2007

Aims:  To analyse the histological features of 33 patients (48 biopsy specimens) with a clinicopathological diagnosis of graft vs. host disease of the liver (L‐GVHD).Results:  The time of biopsy post‐haematopoietic stem cell transplantation (HSCT) ranged from 22 to 1082 days (median 144 days). Bile duct damage (BDD) was present in all biopsies except one. The bile duct to portal ratio ranged from 0.3 to 1 (median 0.8). Moderate/severe lobular hepatitis was present in 11 biopsies. Endotheliitis was present in four biopsies (8%). The majority of the biopsies showed none [25 (52%)] or mild [17 (35%)] fibrosis. The only significant difference between biopsies earlier (‘acute’) or later (‘chronic’ GVHD) than 100 days post‐HSCT was the presence of portal inflammation in the ‘chronic’ GVHD group.Conclusion:  BDD is the predominant change in L‐GVHD. In about a quarter of biopsies the appearance may be of a lobular hepatitis. L‐GVHD is not a fibrogenic process. The significance of separating acute versus chronic L‐GVHD based on a cut‐off of 100 days post‐HSCT is questionable. Further studies are needed to understand the relationships between the mechanisms of BDD, bile duct loss and regeneration.
Cytoarchitectural and kinetic features in the histological evaluation of follicular thyroid neoplasms
Authors: Arif S , Patel J , Blanes A , Diaz‐Cano S J 
Published: May 2007

Aims:  The diagnosis of follicular thyroid carcinomas is mainly based on capsular and vascular invasion. The aim of this study was to determine the diagnostic relevance of nuclear features, inflammation and stromal changes.Methods and results:  Anisokaryosis, chromatin pattern, nucleolus, nuclear pleomorphism, nuclear/cytoplasmic ratio, necrosis, stromal changes and tumour interstitial lymphocytes (TIL) were analysed in adenomatous hyperplastic nodules (39), adenomas (43) and carcinomas (28 minimally invasive, 48 widely invasive and 27 anaplastic). Ki67 immunostaining, in situ end labelling (ISEL) for apoptosis and the Ki67/ISEL index were analysed by topographical compartments. Variables were compared by histological diagnosis using Fisher's exact test, analysis of variance and Student's t‐tests and considered significant if P < 0.05. TIL were absent in 96% of neoplasms and 54% of adenomatous hyperplastic nodules. Conspicuous nucleoli, increased nuclear–cytoplasmic ratio and coexistent apoptosis–myxoid changes distinguished minimally invasive carcinomas from adenomas. The most specific variables of high‐grade carcinoma were vasculonecrotic patterns, nuclear hyperchromatism and pleomorphism. A kinetic advantage predominated in the internal compartments of benign lesions and in the peripheral compartments of malignant lesions.Conclusions:  Follicular carcinomas show up‐regulation of proliferation markers and the distinctive topographical kinetic profiles provide a basis for the distinction between benign and malignant and an explanation for the circumscription and encapsulation of benign lesions.
BALB/c mice resistant to Toxoplasma gondii infection proved to be highly susceptible when previously infected with Myocoptes musculinus fur mites
Authors: Welter Áurea , Mineo José Roberto , De Oliveira Silva Deise Aparecida , Lourenço Elaine Vicente , Vieira Ferro Eloísa Amália , Roque‐Barreira Maria Cristina , Maria da Silva Neide 
Published: May 2007

SummaryThe immune response induced by Toxoplasma gondii is characterized by Th1 immune mechanisms. We previously demonstrated that C57BL/6 mice infested with Myocoptes musculinus and infected with T. gondii by intraperitoneal route undergo accelerated mortality according to Th2 immune mechanisms induced by the acarian. To evaluate whether infection with M. musculinus influences T. gondii‐induced Th1 response in a resistant mouse lineage, BALB/c, which develops latent chronic toxoplasmosis in a way similar to that observed in immunocompetent humans, this study was done. The animals were infected with T. gondii ME‐49 strain 1 month after M. musculinus infestation, being the survival and the immune response monitored. The double‐infected displayed higher mortality rate if compared with the mono‐infected mice. In addition, infection with M. musculinus changed the T. gondii‐specific immune response, converting BALB/c host to a susceptible phenotype. Spleen cells had increased the levels of IL‐4 in double‐infected mice. This alteration was associated with severe pneumonia, encephalitis and wasting condition. In addition, a higher tissue parasitism was observed in double‐infected animals. It can be concluded that infection with these two contrasting parasites, M. musculinus and T. gondii, may convert an immunocompetent host into a susceptible one, and such a host will develop severe toxoplasmosis.