bluuebunny/crossref_metadata_2025_split huggingface dataset:
An evaluation of the impact of a tracheostomy weaning protocol on extubation time
Authors: Clifford Collette , Spencer Alison 
Published: April 2009

AbstractBackground:  To avoid the possible complications of prolonged intubation, it is necessary and advisable to attempt weaning from the tracheostomy tube at the earliest opportunity. However, while weaning protocols have proven successful in reducing ventilation time of critical care patients, there is little evidence of their use and impact on tracheostomy tube weaning time.Aims:  This pilot study sought to determine if the introduction of a new tracheostomy weaning protocol would reduce the time to extubation of the tracheostomy.Method:  A quasi‐experimental design used two groups of patients. A retrospective control group of patients (n = 20) who had been weaned using standard practice were identified by a search of medical records. A prospective experimental group (n = 20) had care planned using a new tracheostomy weaning protocol. Data relating to time to extubation were collected on both groups who were all patients in an eight‐bedded Critical Care Unit of a District General Hospital. The same inclusion and exclusion criteria were applied to both groups.Results:  The results revealed a reduction of 1·35 days from commencement of weaning to extubation in the prospective (experimental) group. This was not statistically significant (P = 0·181)Conclusion:  Although the findings from the study were not statistically significant, they can be seen as clinically significant in terms of patient comfort and reduced dependency in care by a reduction of time with a tracheostomy. It is recommended that a larger scale study be carried out to determine if a tracheostomy weaning protocol does make an impact on length of time to extubation in wider care settings.
Feline Ilial Fractures: A Prospective Study of Dorsal Plating and Comparison with Lateral Plating
Authors: LANGLEY‐HOBBS SORREL J. , MEESON RICHARD L. , HAMILTON MICHAEL H. , RADKE HEIDI , LEE KARLA 
Published: April 2009

Objective— To (1) report a technique for repair of feline ilial fractures using a dorsally applied bone plate and (2) compare outcome with cats treated by a lateral plate.Study Design— Prospective study.Animals— Cats (n=10) with iliac fractures.Methods— Cats with ilial fractures (January 2005–December 2006) were treated by application of a dorsally applied bone plate. Immediate postoperative radiographs were compared with those taken 4–6 weeks later to assess screw loosening, screw purchase, and pelvic canal narrowing. Owners were contacted for medium‐term (>3 month) follow‐up. Data were compared with a report of outcome after lateral plating (LP) in 21 cats.Results— Mean (± SD) screw purchase (89 ± 11 mm) was significantly greater (P<.01) with a dorsal plate compared with a lateral plate (33 ± 8 mm). Significantly more screws (P<.01) were used with a dorsal plate (median, 7) compared with a lateral plate (median, 6). Significantly less postoperative pelvic canal narrowing developed in the dorsal plating group between postoperative and 4–6‐week follow‐up radiography compared with the LP group (2% versus 15%, P<.01).Conclusion— Dorsal plating of feline ilial fractures results in significantly less screw loosening and pelvic canal narrowing at 4–6 weeks after surgery compared with LP.Clinical Relevance— Dorsal plating of feline iliac fractures may reduce complications associated with pelvic canal narrowing such as constipation and megacolon.
Sacroiliac Luxation in the Cat: Defining a Safe Corridor in the Dorsoventral Plane for Screw Insertion in Lag Fashion
Authors: SHALES CHRIS J. , WHITE LINDSAY , LANGLEY‐HOBBS SORREL J. 
Published: April 2009

Objective—To define a safe corridor in the dorsoventral plane within the feline sacral body for placement of screws inserted in lag fashion for repair of sacroiliac luxation.Study Design—Anatomic study.Sample Population—Frozen cadaveric feline sacra.Methods—Feline sacra (n=20) were used to perform a radiographic study to define a safe corridor to a depth of 66% of the sacral body width. Two drill start points (A and B) were evaluated. Dorsal exit from the safe corridor was considered unacceptable.Results—Forty safe corridors were measured. The mean articular surface was 100±6.4° from horizontal. Mean maximum, optimum, and minimum safe corridor drill angles from drill point A were 107±6.8°, 97±6.9°, and 87±7.2°, respectively, from the articular surface. Mean maximum, optimum, and minimum angles from drill point B were 109±7.2°, 99±7.1°, and 89.5±7.2°, respectively. Point B increased the risk of ventral exit from the sacral body.Conclusions—Point A and a drill angle of 90±4° for drilling of the feline sacral body is recommended. This margin for error risks ventral exit from the body in 23/40 (58%) of the sacra in this study. Reduction of the margin for error to ±2° would reduce the risk of ventral exit to 14/40 (35%) of the sacra in this study.Clinical Relevance—Drilling at 90° to the feline sacral articular surface is recommended. Findings from this study present a strong case for use of angled drill guides.
Decision Analysis for Choosing the Hemodynamically Optimum Pacemaker
Authors: GARBER GARY R. , POPP HANS , LEVINE PAUL A. 
Published: April 2009

The current and future generation of pacemakers present a bewildering array of options for the implanting physician. The current economical and legal climate makes it imperative that the appropriate pacemaker is chosen. We developed an algorithm based on our experiences and published data for choosing the optimum pacing mode. This algorithm was programmed into a commercially available expert system shell on a PC platform. Determination was made through a question‐and‐answer session, with the system prompting the physician with questions and appropriate answer choices. Program output included “Recommended”, “Possible But Not Optimal”, and “Not Recommended” pacemakers. Only the general category of pacer type was suggested, not any particular manufacturer. Explanations and reasonings are also displayed during the consultation for educational purposes.The system was then tested retrospectively on 30 consecutive pacemaker implantations. The number of times that the computer recommendation and pacer received agreed was 27. The number of times that the computer recommended a pacer type, but the patient received a different one was 3. The computer did not recommend incorrectly in any instance. There were three different implants: 1 patient was unable to receive suggested pacer for technical reasons; 2 patients had physicians that did not have programmers for the appropriate pacemaker. Based upon this retrospective analysis we conclude that a decision algorithm can be accurately applied to choose the appropriate pacemaker for implantations.
ORIGINAL ARTICLE: Modulation of Expression of Toll‐like receptors in the Human Endometrium
Authors: Lin Zhenyun , Xu Jian , Jin Xiuming , Zhang Xudong , Ge Fenfen 
Published: April 2009

Problem  The purpose of the study was to investigate the different expressions of toll‐like receptors (TLRs) in the proliferative and the secretory phase of endometrial tissue.Method of study  Eight infertile women were included in this study. The endometrial tissues of proliferative and secretory phase were obtained from each woman. The tissues were evaluated for the expression of mRNA for TLR1–10 by reverse transcribed polymerase chain reaction (RT‐PCR). The proteins of TLR2, 3, 4, and 9 were evaluated by Western blot. The mRNA and protein level of proliferative and secretory endometrial tissue from the same woman was compared. The data were analysed with SPSS15.0.Results  TLR1–7, 9, and 10 mRNA were expressed throughout the menstrual cycle, but in the same woman, the expression of TLR2–6, 9, and 10 mRNA was higher during the secretory phase than that in the proliferative phase. The Western blot also showed that the protein expression of TLR2, 3, 4, and 9 was stronger in the secretory phase than that in the proliferative phase in the same woman.Conclusion  The expression of TLRs is cycle dependent in human endometrial tissue. The expressions of TLRs were higher in the secretory phase than that in the proliferative phase: this indicated that TLRs may be regulated by sex hormones throughout the menstrual cycle.
‘FORENSIC GROUP PSYCHOTHERAPY’: ESTELA WELLDON'S CONTRIBUTION TO WORKING WITH GROUPS AT THE PORTMAN CLINIC
Authors: Hakeem Az 
Published: April 2009

abstractIn this paper the author gives a summary of the contributions made by Dr Estela Welldon to the Group Psychotherapy at The Portman Clinic. He describes how clinicians working at the Portman Clinic have evolved and adapted the principles and practices from group psychotherapy in order to work with perverse, violent, delinquent, transsexual and other specialist patient groups in what is described as ‘forensic group psychotherapy’. Attention is drawn to the selection of patients, composition of the group, particular differences of dynamic administration of the group, the style of the conductor, and the observed and expected group processes. The author describes his personal experience as a specialist registrar in forensic psychotherapy at the Portman Clinic working with Dr Welldon, and his continued work there as a consultant, and the continual development and evolution of forensic group psychotherapy.
Diagnosis of Active Tuberculosis in China Using an In-House Gamma Interferon Enzyme-Linked Immunospot Assay
Authors: Chen Xinchun , Yang Qianting , Zhang Mingxia , Graner Michael , Zhu Xiuyun , Larmonier Nicolas , Liao Mingfeng , Yu Weiye , Deng Qunyi , Zhou Boping 
Published: April 2009

ABSTRACT

Gamma interferon (IFN-γ) release assays have been proven to be useful in the diagnosis of
Mycobacterium tuberculosis
infection. Nevertheless, their specificity and sensitivity vary among the different populations studied. Here, we evaluate the value of an in-house IFN-γ enzyme-linked immunospot (ELISPOT) assay in the diagnosis of active tuberculosis (TB) in Shenzhen, China, where the prevalence of tuberculosis is severe and
Mycobacterium bovis
BCG vaccination is mandatory at birth. A total of 305 patients with active tuberculosis, 18 patients with nontuberculosis lung diseases, and 202 healthy controls were recruited in this study. Among them, 156 individuals were simultaneously tested for IFN-γ responses by the commercial QuantiFERON-TB Gold in-tube (QFT-IT) assay. Tuberculin skin tests (TST) were performed with 202 healthy controls. The overall sensitivities of the ELISPOT and QFT-IT assays for active tuberculosis were 83.60% and 80.85%, respectively; the specificities were 76.6% and 73.26%, respectively. The IFN-γ ELISPOT responses, but not those of the TST, were significantly correlated with TB exposure (
r
= −0.6040,
P
< 0.0001). The sensitivities of the ELISPOT assay varied for patients with different forms of tuberculosis, with the highest sensitivity for patients with sputum-positive pulmonary tuberculosis (89.89%) and the lowest for those with tuberculous meningitis (62.5%). In conclusion, the IFN-γ ELISPOT assay is a useful adjunct to current tests for diagnosis of active TB in China. The ELISPOT assay is more accurate than TST in identifying TB infections.
Synthesis and binding characteristics of novel calix[4]arene(amidocrown) diquinones
Authors: Chawla Har Mohindra , Sahu Satya Narayan , Shrivastava Rahul 
Published: April 2009

A series of new calix[4]arene(amidocrown) diquinones (3a–3d) have been synthesized, characterized, and evaluated for cation recognition. It has been observed that 3b interacts with alkali metal ions (Li+, Na+, and K+) and ammonium ions to induce an unprecedented downfield shift in the NH proton resonance, which can be attributed to polarization of the amidocrown ring of the calix[4]arene diquinone receptor. The observation has been confirmed by a significant anodic shift (Li+ > NH4+ > Na+> K+) of the corresponding amidocrown-diquinone redox couple in cyclic and square wave voltammetric experiments. Both NMR and electrochemical studies of the binding characteristics of 3b with alkali metal cations and ammonium ions revealed a 1:1 binding stoichiometry for all and exhibited the highest association constant for lithium ions. This indicated that the receptor 3b selectively binds the lithium ion in preference to other alkali metal cations and ammonium ions.
Epidermal Growth Factor Receptor/β-Catenin/T-Cell Factor 4/Matrix Metalloproteinase 1: A New Pathway for Regulating Keratinocyte Invasiveness after UVA Irradiation
Authors: Jean Christine , Blanc Amandine , Prade-Houdellier Naïs , Ysebaert Loïc , Hernandez-Pigeon Hélène , Al Saati Talal , Haure Marie-José , Coluccia Addolorata-Maria-Luce , Charveron Marie , Delabesse Eric , Laurent Guy 
Published: April 2009

Abstract
Previous studies have established that UV irradiation results in epidermal growth factor receptor (EGFR) activation in keratinocytes. However, the signaling pathways and cellular effects related to this process remain incompletely elucidated. Herein, we describe for the first time that UVA-mediated EGFR activation results in β-catenin tyrosine phosphorylation at the Y654 residue responsible for the dissociation of E-cadherin/α-catenin/β-catenin complexes. Moreover, UVA induces an EGFR-dependent, but Wnt-independent, β-catenin relocalization from the membrane to the nucleus followed by its association with T-cell factor 4 (TCF4). This newly formed β-catenin/TCF4 complex binds to a specific site on matrix metalloproteinase 1 (MMP1) promoter and governs MMP1 gene and protein expression, as well as cell migration in collagen and gelatin. Altogether, these results suggest that UVA stimulates keratinocyte invasiveness through two coordinated EGFR-dependent processes: loss of cell-to-cell contact due to β-catenin/E-cadherin/α-catenin dissociation and increased cell migration through extracellular matrix component degradation due to β-catenin/TCF4–dependent MMP1 regulation. These events may represent an important step in epidermis repair following UVA injury and their abnormal regulation could contribute to photoaging and photocarcinogenesis. [Cancer Res 2009;69(8):3291–9]
Atg5 Regulates Phenethyl Isothiocyanate–Induced Autophagic and Apoptotic Cell Death in Human Prostate Cancer Cells
Authors: Bommareddy Ajay , Hahm Eun-Ryeong , Xiao Dong , Powolny Anna A. , Fisher Alfred L. , Jiang Yu , Singh Shivendra V. 
Published: April 2009

Abstract
Phenethyl isothiocyanate (PEITC) is a promising cancer chemopreventive agent but the mechanism of its anticancer effect is not fully understood. We now show, for the first time, that PEITC treatment triggers Atg5-dependent autophagic and apoptotic cell death in human prostate cancer cells. Exposure of PC-3 (androgen independent, p53 null) and LNCaP (androgen responsive, wild-type p53) human prostate cancer cells to PEITC resulted in several specific features characteristic of autophagy, including appearance of membranous vacuoles, formation of acidic vesicular organelles, and cleavage and recruitment of microtubule-associated protein 1 light chain 3 (LC3) to autophagosomes. A normal human prostate epithelial cell line (PrEC) was markedly more resistant toward PEITC-mediated cleavage and recruitment of LC3 compared with prostate cancer cells. Although PEITC treatment suppressed activating phosphorylations of Akt and mammalian target of rapamycin (mTOR), which are implicated in regulation of autophagy by different stimuli, processing and recruitment of LC3 was only partially/marginally reversed by ectopic expression of constitutively active Akt or overexpression of mTOR-positive regulator Rheb. The PEITC-mediated apoptotic DNA fragmentation was significantly attenuated in the presence of a pharmacologic inhibitor of autophagy (3-methyl adenine). Transient transfection of LNCaP and PC-3 cells with Atg5-specific small interfering RNA conferred significant protection against PEITC-mediated autophagy as well as apoptotic DNA fragmentation. A xenograft model using PC-3 cells and Caenorhabditis elegans expressing a lgg-1:GFP fusion protein provided evidence for occurrence of PEITC-induced autophagy in vivo. In conclusion, the present study indicates that Atg5 plays an important role in regulation of PEITC-induced autophagic and apoptotic cell death. [Cancer Res 2009;69(8):3704–12]
Aldehyde Dehydrogenase 1 Is a Marker for Normal and Malignant Human Colonic Stem Cells (SC) and Tracks SC Overpopulation during Colon Tumorigenesis
Authors: Huang Emina H. , Hynes Mark J. , Zhang Tao , Ginestier Christophe , Dontu Gabriela , Appelman Henry , Fields Jeremy Z. , Wicha Max S. , Boman Bruce M. 
Published: April 2009

AbstractAlthough the concept that cancers originate from stem cells (SC) is becoming scientifically accepted, mechanisms by which SC contribute to tumor initiation and progression are largely unknown. For colorectal cancer (CRC), investigation of this problem has been hindered by a paucity of specific markers for identification and isolation of SC from normal and malignant colon. Accordingly, aldehyde dehydrogenase 1 (ALDH1) was investigated as a possible marker for identifying colonic SC and for tracking them during cancer progression. Immunostaining showed that ALDH1+ cells are sparse and limited to the normal crypt bottom, where SCs reside. During progression from normal epithelium to mutant (APC) epithelium to adenoma, ALDH1+ cells increased in number and became distributed farther up the crypt. CD133+ and CD44+ cells, which are more numerous and broadly distributed in normal crypts, showed similar changes during tumorigenesis. Flow cytometric isolation of cancer cells based on enzymatic activity of ALDH (Aldefluor assay) and implantation of these cells in nonobese diabetic–severe combined immunodeficient mice (a) generated xenograft tumors (Aldefluor− cells did not), (b) generated them after implanting as few as 25 cells, and (c) generated them dose dependently. Further isolation of cancer cells using a second marker (CD44+ or CD133+ serially) only modestly increased enrichment based on tumor-initiating ability. Thus, ALDH1 seems to be a specific marker for identifying, isolating, and tracking human colonic SC during CRC development. These findings also support our original hypothesis, derived previously from mathematical modeling of crypt dynamics, that progressive colonic SC overpopulation occurs during colon tumorigenesis and drives CRC development. [Cancer Res 2009;69(8):3382–9]
Guanylyl Cyclase C Prevents Colon Cancer Metastasis by Regulating Tumor Epithelial Cell Matrix Metalloproteinase-9
Authors: Lubbe Wilhelm J. , Zuzga David S. , Zhou Zengyi , Fu Weili , Pelta-Heller Joshua , Muschel Ruth J. , Waldman Scott A. , Pitari Giovanni M. 
Published: April 2009

AbstractMatrix metalloproteinase-9 (MMP-9) produced by colorectal cancer cells is a critical determinant of metastatic disease progression and an attractive target for antimetastatic strategies to reduce colon cancer mortality. Cellular signaling by cyclic GMP (cGMP) regulates MMP-9 dynamics in various cell systems, and the bacterial enterotoxin receptor guanylyl cyclase C (GCC), the principle source of cGMP in colonocytes, which is overexpressed in colorectal cancers, inhibits tumor initiation and progression in the intestine. Here, we show that ligand-dependent GCC signaling through cGMP induces functional remodeling of cancer cell MMP-9 reflected by a compartmental redistribution of this gelatinase, in which intracellular retention resulted in reciprocal extracellular depletion. Functional remodeling of MMP-9 by GCC signaling reduced the ability of colon cancer cells to degrade matrix components, organize the actin cytoskeleton to form locomotory organelles and spread, and hematogenously seed distant organs. Of significance, GCC effects on cancer cell MMP-9 prevented establishment of metastatic colonies by colorectal cancer cells in the mouse peritoneum in vivo. Because endogenous hormones for GCC are uniformly deficient in intestinal tumors, reactivation of dormant GCC signaling with exogenous administration of GCC agonists may represent a specific intervention to target MMP-9 functions in colon cancer cells. The notion that GCC-mediated regulation of cancer cell MMP-9 disrupts metastasis, in turn, underscores the unexplored utility of GCC hormone replacement therapy in the chemoprevention of colorectal cancer progression. [Cancer Res 2009;69(8):3529–36]
Regulation of RUNX3 Tumor Suppressor Gene Expression in Cutaneous Melanoma
Authors: Kitago Minoru , Martinez Steve R. , Nakamura Takeshi , Sim Myung-Shin , Hoon Dave S.B. 
Published: April 2009

Abstract
Purpose: RUNX3 is a known tumor suppressor gene in several carcinomas. Aberration in RUNX3 expression has not been described for cutaneous melanoma. Therefore, we assessed the expression of RUNX3 in cutaneous melanoma and its regulatory mechanisms relative to tumor progression.
Experimental Design: The expression of RUNX3 mRNA and miR-532-5p (microRNA) was assessed in melanoma lines and in primary and metastatic melanoma tumors.
Results: RUNX3 mRNA expression was down-regulated in 11 of 11 (100%) metastatic melanoma lines relative to normal melanocytes (P &lt; 0.001). Among 123 primary and metastatic melanoma tumors and 12 normal skin samples, RUNX3 expression was significantly down-regulated in primary melanomas (n = 82; P = 0.02) and in melanoma metastasis (n = 41; P &lt; 0.0001) versus normal skin (n = 12). This suggested that RUNX3 down-regulation may play a role in the development and progression of melanoma. RUNX3 promoter region hypermethylation was assessed as a possible regulator of RUNX3 expression using methylation-specific PCR. Assessment of RUNX3 promoter region methylation showed that only 5 of 17 (29%) melanoma lines, 2 of 52 (4%) primary melanomas, and 5 of 30 (17%) metastatic melanomas had hypermethylation of the promoter region. A microRNA (miR-532-5p) was identified as a target of RUNX3 mRNA sequences. miR-532-5p expression was shown to be significantly up-regulated in melanoma lines and metastatic melanoma tumors relative to normal melanocytes and primary melanomas, respectively. To investigate the relation between RUNX3 and miR-532-5p, anti–miR-532-5p was transfected into melanoma lines. Inhibition of miR-532-5p up-regulated both RUNX3 mRNA and protein expression.
Conclusions: RUNX3 is down-regulated during melanoma progression and miR-532-5p is a regulatory factor of RUNX3 expression.
Energy Homeostasis and Cancer Prevention: The AMP-Activated Protein Kinase
Authors: Fay Judith R. , Steele Vernon , Crowell James A. 
Published: April 2009

Abstract
Caloric restriction has long been recognized as an extremely effective cancer preventive. Current population demographics suggest that caloric excess and obesity will lead to increased cancer incidence, underscoring the need to elucidate the molecular mechanisms that couple dysregulated energy homeostasis to aberrant cell growth. The AMP-activated protein kinase (AMPK) is a critical monitor of cellular energy status, largely studied for its importance in metabolic regulation. AMPK also controls processes relevant to tumor development, including cell cycle progression, protein synthesis, cell growth, and survival. Several tumor suppressors impinge on AMPK signaling, and activation of the kinase inhibits tumor growth. However, AMPK can also promote cancer in some settings, necessitating a more complete understanding of the complexities of this signaling network. Because dysregulated energy balance is a nexus for multiple chronic diseases of aging, drugs that target these pathways may find broad utility in aging populations.