bluuebunny/crossref_metadata_2025_split huggingface dataset:
Membrane proteinase 3 and its interactions within microdomains of neutrophil membranes
Authors: Fridlich Ram , David Alina , Aviram Irit 
Published: April 2006

AbstractProteinase 3 (PR3) is a serine protease of neutrophil granules released to the medium or into the phagocytic vesicle upon neutrophil stimulation. A fraction of the enzyme is thought to associate with the cell membrane yielding membrane PR3 (mPR3). In autoimmune disorders characterized by the presence of antineutrophil cytoplasmic antibodies (ANCA), the reaction of the latter with their target antigen mPR3 activates the cell inflicting injuries on the surrounding tissues. In a previous communication we provided evidence for the presence of mPR3 in lipid rafts obtained by lysis of neutrophils in Triton X‐100 and for the mediation of PR3 binding to the membrane by a glycosylphosphatidylinositol (GPI)‐anchored neutrophil protein, possibly FcγRIIIb. In the current study we employed the mild detergent Brij 58 to isolate high molecular weight (HMW) protein complexes in the void volume of a Sepharose 4B gel filtration minicolumn. HMW complexes of unstimulated neutrophils comprised PR3, FcγRIIIb, the β2 integrin CD11b/CD18 as well as the membrane and cytosolic subunits of the NADPH oxidase, p22phox and p47phox/p67phox. Treatment of neutrophils with phosphatidylinositol‐specific phospholipase C (PI‐PLC) reduced amounts of PR3 and FcγRIIIb in HMW complexes isolated from the treated cells, supporting our previous suggestion that FcγRIIIb acts as a membrane adaptor for PR3. FcγRIIIb of HMW fractions co‐immunoprecipitated with PR3, indicating their presence in the same protein complex. Since HMW fractions contained also the majority of biotinylated proteins obtained by the reaction of neutrophils with a membrane impermeable biotinylating agent Sulfo‐NHS‐biotin, it was concluded that HMW proteins were derived from cell membranes. Lipid rafts isolated from Brij 58‐lysed neutrophils were similar in their protein composition to the HMW complexes but not identical. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.
17β‐estradiol (E2) induces cdc25A gene expression in breast cancer cells by genomic and non‐genomic pathways
Authors: Ru Lee Wan , Chen Chien‐Cheng , Liu Shengxi , Safe Stephen 
Published: April 2006

AbstractCdc25A is a potent tyrosine phosphatase that catalyzes specific dephosphorylation of cyclin/cyclin‐dependent kinase (cdk) complexes to regulate G1 to S‐phase cell cycle progression. Cdc25A mRNA levels are induced by 17β‐estradiol (E2) in ZR‐75 breast cancer cells, and deletion analysis of the cdc25A promoter identified the −151 to −12 region as the minimal E2‐responsive sequence. Subsequent mutation/deletion analysis showed that at least three different cis‐elements were involved in activation of cdc25A by E2, namely, GC‐rich Sp1 binding sites, CCAAT motifs that bind NF‐Y, and E2F sites that bind DP/E2F1 proteins. Studies with inhibitors and dominant negative expression plasmids show that E2 activates cdc25A expression through activation of genomic ERα/Sp1 and E2F1 and cAMP‐dependent activation of NF‐YA. Thus, both genomic and non‐genomic pathways of estrogen action are involved in induction of cdc25A in breast cancer cells. J. Cell. Biochem. © 2006 Wiley‐Liss, Inc.
The status of hospital medicine groups in the United States
Authors: Kralovec Peter D. , Miller Joseph A. , Wellikson Laurence , Huddleston Jeanne M. 
Published: April 2006

AbstractBACKGROUNDHospitalists, defined as hospital‐based physicians who take responsibility for managing the medical needs of inpatients, represent a significant trend in physician specialization. However, only limited anecdotal data quantifying the status of hospital medicine groups around the country is available.OBJECTIVETo better understand the extent and nature of the hospitalist movement, utilizing data from the 2003 Annual Survey of the American Hospital Association (AHA).STUDY POPULATION4895 acute care hospitals in the United States.MEASUREMENTSNumber and percentage of hospitals with hospital medicine groups; mean number of hospitalists per group; hospitalists per average daily census (ADC) of 100 patients; distribution of groups by employment model.DESCRIPTIVE VARIABLESCensus region; rural/urban status; number of beds; organizational control; teaching status.RESULTSThere are approximately 1415 hospital medicine groups and 11 159 hospitalists in the United States. The overall penetration of hospital medicine groups at hospitals is 29% (55% at hospitals with 200 or more beds), and the in‐hospital impact at hospitals with hospital medicine groups is 3.93 hospitalists per 100 ADC. The average hospital medicine group has 7.9 hospitalists. There is a fairly equal distribution among the 3 major employment models for hospital medicine groups: hospital employees, independent provider groups, and physician groups. All these measures can vary substantially, depending on the characteristics of individual hospitals.CONCLUSIONSHospital medicine appears to have become part of the mainstream delivery of health care in the United States. No employment model of hospital medicine group appears to dominate this specialty. We expect there will continue to be growth and diversity in the implementation of hospital medicine groups. Journal of Hospital Medicine 2006;1:75–80. © 2006 Society of Hospital Medicine.
Magnetic resonance imaging measures of brain atrophy in multiple sclerosis
Authors: Anderson Valerie M. , Fox Nick C. , Miller David H. 
Published: April 2006

AbstractMagnetic resonance imaging (MRI) has been widely used to diagnose and monitor multiple sclerosis (MS). Although MRI‐visible lesions are a key feature of MS, they are thought to correlate poorly with clinical progression. Neurodegeneration is increasingly being recognized as an important factor in the pathogenesis of MS, and MRI measures of brain atrophy have been suggested as surrogate markers of neuroaxonal loss and disease progression. This pathology may be more relevant to the progression of disability than focal inflammation. A number of MRI‐based methods have been developed for the measurement of global and regional brain atrophy. Natural‐history studies of MS and clinically isolated syndromes suggestive of MS have observed atrophy in these subjects above that seen in controls, over periods ranging from three months to years. Brain atrophy has also been incorporated as an outcome measure in therapeutic trials of disease‐modifying treatments. This paper considers neuroaxonal loss and the pathological basis of brain atrophy, methods developed to quantify brain atrophy, the findings of natural‐history and therapeutic studies, the relationship of brain atrophy to disability and cognition, and the future research directions and clinical applications of brain atrophy measurements. J. Magn. Reson. Imaging 2006. © 2006 Wiley‐Liss, Inc.
In vivo three‐dimensional motion analysis of the forearm with radioulnar synostosis treated by the kanaya procedure
Authors: Oka Kunihiro , Doi Kazuteru , Suzuki Koichi , Murase Tsuyoshi , Goto Akira , Yoshikawa Hideki , Sugamoto Kazuomi , Moritomo Hisao 
Published: April 2006

AbstractAttempts to separate congenital radioulnar synostosis and restore forearm rotation had been disappointing until a new mobilization technique was developed by Kanaya and colleagues using free vascularized fascio‐fat graft interposition. This technique provides a functional rotation arc, but postoperative forearm motion is difficult to evaluate given the inaccuracies in determining the range of motion and rotational axis using conventional x‐rays or computed tomography. This study represents an attempt to analyze in vivo three‐dimensional motion of the forearm with radioulnar synostosis treated by Kanaya's operation using a markerless bone registration technique. Six patients with seven postoperative forearms (six with congenital and one with posttraumatic radioulnar synostosis) underwent 3D computed tomography with the forearm in neutral, fully pronated, and fully supinated positions. Range of motion according to this method was 30 ± 18°, significantly smaller than the 82 ± 29° from manual examination. Improvements in range of motion were significantly greater in cases without dislocation of the radial head (46 ± 13°) than in cases with dislocation (19 ± 10°). Dislocation of the radial head was also significantly correlated with an abnormal axis of rotation of the forearm. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res
Investigation of in vivo 6DOF total knee arthoplasty kinematics using a dual orthogonal fluoroscopic system
Authors: Hanson George R. , Suggs Jeremy F. , Freiberg Andrew A. , Durbhakula Sridar , Li Guoan 
Published: April 2006

AbstractFluoroscopic techniques have been recently used to detect in vivo knee joint kinematics. This article presents a technique that uses two fluoroscopes to form a dual orthogonal fluoroscopic system for accurately measuring in vivo 6DOF total knee arthoplasty (TKA) kinematics. The system was rigorously validated and used to investigate in vivo kinematics of 12 patients after cruciate‐retaining TKA. In a repeatability study, the pose of two different TKA components was reproduced with standard deviations (SD) of 0.17 mm and 0.57° about all three axes. In an accuracy study, the reproduced component positions were compared to the known component positions. Position and rotation mean errors were all within 0.11 mm and 0.24°, with SD within 0.11 mm and 0.48°, respectively. The results of this study show that the matching process of the imaging system is able to accurately reproduce the spatial positions and orientations of both the femoral and tibial components. For CR TKA patients, a consistent anterior femoral translation was observed with flexion through 45° of flexion, and thereafter, the femur translated posteriorly with further flexion. The medial–lateral translation was measured to be less than 2 mm throughout the entire flexion range. Internal tibial rotation steadily increased through maximum flexion by approximately 6°. Varus rotation was also measured with flexion but had a mean magnitude less than 2.0°. In conclusion, the dual orthogonal fluoroscopic system accurately detects TKA kinematics and is applicable towards other joints of the musculoskeletal system, including the wrist, elbow, shoulder, ankle, and spine. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res
On double Veronese embeddings in the Grassmannian 𝔾(1, N )
Authors: Sierra José Carlos , Ugaglia Luca 
Published: April 2006

AbstractWe classify all the embeddings of ℙn in a Grassmannian of lines 𝔾(1, N ) such that the composition with Plücker is given by a linear system of quadrics of ℙn . (© 2006 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Analysis of 14 LRRK2 mutations in Parkinson's plus syndromes and late‐onset Parkinson's disease
Authors: Tan E.K. , Skipper Lisa , Chua Eva , Wong Meng‐Cheong , Pavanni Ratnagopal , Bonnard Carine , Kolatkar Prasanna , Liu Jian‐Jun 
Published: April 2006

AbstractThe pleomorphic pathology of postmortem LRRK2‐positive patients and the frequent association with late‐onset Parkinson's disease (LOPD) symptoms suggest that LRRK2 mutations may play a role in Parkinson's Plus disorders and LOPD. Published studies primarily focus on the common G2019S mutation. Analysis of a spectrum of LRRK2 mutations in Parkinson's Plus disorders has yet to be reported. We investigated 14 leucine‐rich repeat kinase 2 (LRRK2) mutations in a cohort of Parkinson's Plus disorders and LOPD. A total of 458 patients with progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal ganglionic degeneration (CBGD), atypical Parkinsonism (AP), and LOPD were screened for 14 mutations that span exons 19 to 41 of the LRRK2 gene. Among the LOPD cases, 1 patient was found to harbor the R1441C mutation. He presented with typical features of PD at age of 58 years old and responded well to levodopa. We did not detect any of the 14 mutations in PSP, MSA, CBGD, and AP patients. We highlight the first case of LRRK2 R1441C mutation in late onset sporadic PD of non‐European ancestry. Furthermore, extensive mutational screen found LRRK2 mutations to be rare among patients who presented with PSP, MSA, CBGD, and AP. © 2006 Movement Disorder Society
Perception of heaviness in Parkinson's disease
Authors: Maschke Matthias , Tuite Paul J. , Krawczewski Kim , Pickett Kristen , Konczak Jürgen 
Published: April 2006

AbstractThe present study investigated whether a specific aspect of proprioception, the sense of heaviness or weight is affected in PD. We determined detection thresholds for the perception of a gravito‐inertial load in 10 PD patients and 11 age‐matched control subjects. A gradually increasing weight was applied to the index finger by means of two slings of different width (low vs. high skin pressure). For the controls, mean detection thresholds were 31.3 g at skin high pressure and 33.0 g under low pressure. PD patients revealed significantly higher thresholds than the control group in both pressure conditions (mean high pressure,47.7 g; mean low pressure, 52.3 g; group effect, P = 0.001). Thresholds of PD patients tended to increase with disease severity as measured by the Unified Parkinson's Disease Rating Scale Motor score (r = 0.55) but did not correlate significantly with levodopa equivalent dosage. The results demonstrate that the perception of heaviness or weight is already affected in the early stages of PD. These findings underline the growing evidence that proprioceptive and possibly haptic dysfunction is a common feature of PD. © 2006 Movement Disorder Society
Concepts of nerve regeneration and repair applied to brachial plexus reconstruction
Authors: Bertelli Jayme Augusto , Ghizoni Marcos Flávio 
Published: April 2006

AbstractBrachial plexus injury is a serious condition that usually affects young adults. Progress in brachial plexus repair is intimately related to peripheral nerve surgery, and depends on clinical and experimental studies. We review the rat brachial plexus as an experimental model, together with its behavioral evaluation. Techniques to repair nerves, such as neurolysis, nerve coaptation, nerve grafting, nerve transfer, fascicular transfer, direct muscle neurotization, and end‐to‐side neurorraphy, are discussed in light of the authors' experimental studies. Intradural repair of the brachial plexus by graft implants into the spinal cord and motor rootlet transfer offer new possibilities in brachial plexus reconstruction. The clinical experience of intradural repair is presented. Surgical planning in root rupture or avulsion is proposed. In total avulsion, the authors are in favor of the reconstruction of thoraco‐brachial and abdomino‐antebrachial grasping, and on the transfer of the brachialis muscle to the wrist extensors if it is reinnervated. Surgical treatment of painful conditions and new drugs are also discussed. © 2006 Wiley‐Liss, Inc. Microsurgery, 2006.
Surgical treatment for spinal accessory nerve injury
Authors: Okajima Seiichiro , Tamai Kazuo , Fujiwara Hiroyoshi , Kobashi Hiroaki , Hirata Miyuki , Kubo Toshikazu 
Published: April 2006

AbstractWe report on the surgical results of spinal accessory nerve injuries between 1992–2003. We operated on 10 patients (9 female, and 1 male) who had injuries of the spinal accessory nerve. All injuries were iatrogenic. The mean age of patients was 39.2 years (range, 20–57 years). The average interval between date of injury and surgery was 7 months (range, 4–12 months). All patients had stiffness and pain in the shoulder girdle. The average active abduction of the shoulder joint was 79.5° (range, 60–100°) before surgery. End‐to‐end repairs were performed in 7 cases, and graft repairs were indicated in 3 cases. The mean follow‐up period was 18.4 months (range, 8–36 months). The average active abduction of the shoulder joint was 171° (range, 140–180°) at time of final follow‐up. © 2006 Wiley‐Liss, Inc. Microsurgery, 2006.
Evaluation of electrospray‐tandem mass spectrometry for the detection of phenylketonuria and other rare disorders
Authors: Lukacs Zoltan , Santer René 
Published: April 2006

AbstractSince a few years ESI‐MS/MS has been employed for the simultaneous detection of a wide range of inborn errors of metabolism. The screening center North at the Hamburg University Medical Center processes 40–50 000 samples per year. To assess current developments in neonatal screening, the Northern German Working Group on Neonatal Screening consisting of health care providers, metabolic centers, and screening laboratories was founded. Based on current literature and experience four categories of diseases were established. The first three categories were recommended for screening under constant scientific evaluation, while glutaric aciduria II, β‐ketothiolase deficiency, short‐chain acylCoA dehydrogenase deficiency, and homocystinuria were not included in the screening program. In contrast, general screening for phenylketonuria (PKU) remains undisputed and MS/MS screening reduced false positives by simultaneously detecting phenylalanine and tyrosine. Recently, (6R)‐L‐erythro‐5,6,7,8‐tetrahydrobiopterin (BH4)‐sensitive PKU has been discovered. We were able to demonstrate that BH4 treatment without dietary restrictions may be sufficient for certain BH4‐responsive PKU patients. In general, MS/MS provides a potential to rapidly screen for a wide variety of rare metabolic disorders but a close cooperation between scientists and metabolic doctors is required to constantly evaluate results in terms of improving the outcome of patients.
Genotoxicity of glycidamide in comparison to (±)‐anti‐benzo[a]pyrene‐7,8‐dihydrodiol‐9,10‐epoxide and α‐acetoxy‐N‐nitroso‐diethanolamine in human blood and in mammalian V79‐cells
Authors: Thielen Silke , Baum Matthias , Hoffmann Michelle , Loeppky Richard N. , Eisenbrand Gerhard 
Published: April 2006

AbstractGenotoxic activity of glycidamide (GA) was investigated in comparison to that of the known carcinogens (±)‐anti‐benzo[a]pyrene‐7,8‐dihydrodiol‐9,10‐epoxide ((±)‐BPDE) and α‐acetoxy‐N‐nitroso‐diethanolamine (α‐A‐NDELA), using the hypoxanthine‐phosphoribosyl‐transferase (hPRT) gene mutation assay with V79 mammalian cells and modified alkaline single cell gel electrophoresis (alkaline comet assay with and without treatment of cells with formamido‐pyrimidine‐DNA‐glycosylase (FPG)) in lymphocytes from human whole blood. As shown earlier, GA induced significant DNA damage in lymphocytes from treated whole blood at ⪈300 μM (4 h) (Baum et al., Mutat. Res. 2005, 580, 61–69). In the present study, using the alkaline comet assay with FPG treatment, increased formation of DNA strand breaks was observed in lymphocytes treated with GA (10 μM; 4 h). α‐A‐NDELA and (±)‐BPDE were genotoxic at 10–30 μM (1 h). Genotoxic activity of these compounds was not enhanced after FPG treatment. FPG treatment thus offers an enhanced sensitivity of DNA damage detection for genotoxic compounds with preference for N7‐ resp. N3‐purine alkylation. In the hPRT assay with V79 cells, mutagenic activity of (±)‐BPDE became significant at ⪈3 μM (24 h). For α‐A‐NDELA significant activity was observed at ⪈10 μM (24 h). As previously observed, GA was considerably less effective, inducing significant mutagenicity roughly at about 80–300‐fold higher concentrations (800 μM; 24 h) (Baum et al., Mutat. Res. 2005, 580, 61–69).
A new oleanane glycoside from the roots of Astragalus caprinus
Authors: Mitaine‐Offer Anne‐Claire , Miyamoto Tomofumi , Semmar Nabil , Jay Maurice , Lacaille‐Dubois Marie‐Aleth 
Published: April 2006

AbstractA novel oleanane‐type triterpene saponin (1) together with two known molecules, soyasapogenol B and astragaloside VIII were isolated from the roots of Astragalus caprinus. Their structural elucidation was performed mainly by 2D NMR techniques (COSY, TOCSY, NOESY, HSQC, HMBC) and mass spectrometry. Compound 1 was determined as 3‐O‐[α‐L‐rhamnopyranosyl‐(1 → 2)‐β‐D‐glucuronopyranosyl]‐22‐O‐β‐D‐apiofuranosyl‐soyasapogenol B. Copyright © 2006 John Wiley & Sons, Ltd.
A novel maternally transcribed homeobox gene, Eso‐1, is preferentially expressed in oocytes and regulated by cytoplasmic polyadenylation
Authors: Li Hung , Tsai Ming‐Shiun , Chen Chun‐Ying , Lian Wei‐Cheng , Chiu Yung‐Tsung , Chen Gin‐Den , Wang Sue‐Hong 
Published: April 2006

AbstractThe homeobox gene families play important roles in the transcriptional regulation of gene expression prior to and during embryo development. To identify novel homeobox genes expressed in early embryonic development, we conducted a degenerated oligonucleotide polymerase chain reaction (PCR) to screen a mouse embryonic stem (ES) cell cDNA library. A novel homeobox‐containing gene, Eso‐1, which is preferentially expressed in ES cells and ovaries, was identified. The full‐length Eso‐1 cDNA was found to be 1,710 bp with a predicted homeodomain that has no significant homology to previously reported homeodomain proteins. Eso‐1 was mapped to chromosome 14A3. Reverse transcription‐polymerase chain reaction (RT‐PCR) analyses showed that Eso‐1 was expressed through oogenesis and continuing to be expressed through to the blastocyst stage. De novo expression of Eso‐1 started at 13.5 days postcoitum in the ovaries, which coincides with the initiation of oogenesis. Northern blot analyses demonstrated that Eso‐1 is preferentially expressed in both ovaries and ES cells as a 1.7‐kb transcript. Results from whole mount in situ hybridization revealed that Eso‐1 in oocytes showed increased expression from primordial to antral follicles. The 3′‐untranslated region of Eso‐1 transcripts contained cytoplasmic polyadenylation sequences while the length of poly (A) tails changed during oocyte maturation, indicating that Eso‐1 expression is controlled by time‐dependent translational activation. We suggest that the novel homeodomain protein, Eso‐1, plays a role during oocyte maturation and early embryonic development. Mol. Reprod. Dev. © 2006 Wiley‐Liss, Inc.
Expression of a carboxy terminally truncated Stat5 with no transactivation domain in the mammary glands of transgenic mice inhibits cell proliferation during pregnancy, delays onset of milk secretion, and induces apoptosis upon involution
Authors: Iavnilovitch Elena , Eilon Tali , Groner Bernd , Barash Itamar 
Published: April 2006

AbstractSignal transducer and activator of transcription (Stat5) is a transcription factor, which transduces extracellular cytokine and growth‐factor signals to the nuclei of mammalian cells. As a major mediator of prolactin action, it is involved in the regulation of the development, function, and survival of mammary epithelial cells. The carboxyl terminal of Stat5 encodes a transactivation domain (TAD), which interacts with coactivators and is crucial for the transcriptional induction of Stat5 target genes. To study the role of the Stat5 TAD in mediating Stat5 functions, a carboxy terminally truncated Stat5 variant (Stat5Δ750) was directed for expression in the mammary glands of transgenic mice by regulatory sequences of the β‐lactoglobulin (BLG) gene. Expression of Stat5Δ750 in mammary tissue reduced the rates of cell proliferation at mid and late pregnancy. Subsequently, morphological signs of milk secretion upon parturition were delayed. In double‐transgenic mice, expression of Stat5Δ750 drastically decreased BLG/luciferase activity during lactation, but did not affect the expression and secretion of the endogenous β‐casein or α‐lactalbumin into the milk. Expression of Stat5Δ750 also caused an increase in the number of apoptotic cells during mammary involution by a factor of 3 relative to control glands. Our data established a role for the Stat5 TAD in mediating the effects of Stat5 on mammary development, regulation of milk protein gene activity, and cell survival. The full effects of Stat5Δ750 may be partially buffered by the expression of endogenous wild‐type Stat5 and the formation of truncated and wild‐type heterodimers. Mol. Reprod. Dev. © 2006 Wiley‐Liss, Inc.