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101.
Lara Kevorkian David A. Young Clare Darrah Simon T. Donell Lee Shepstone Sarah Porter Sarah Brockbank Dylan R. Edwards rew E. Parker Ian M. Clark 《International journal of experimental pathology》2004,85(1):A23-A23
Objective To profile the expression of all known members of the matrix metalloproteinase ( MMP ), a disintegrin and metalloproteinase with thrombospondin motifs ( ADAMTS ), and tissue inhibitor of metalloproteinases ( TIMP s) gene families in normal cartilage and that from patients with osteoarthritis (OA).
Methods Human cartilage was obtained from femoral heads at joint replacement for either osteoarthritis or following fracture to the neck of femur. Total RNA was purified and expression of genes assayed using quantitative real-time PCR.
Results Several members of the above gene families were regulated in OA. Genes increasing in expression in OA were: at P < 0.001, MMP-13 , MMP-28 , ADAMTS-16 ; at P < 0.01, MMP-9 , MMP-16 , ADAMTS-2 , ADAMTS-14 and at P < 0.05, MMP-2 , TIMP-3 , ADAMTS-12 . Genes decreasing in expression in OA were: at P < 0.001, MMP-1 , MMP-3 , ADAMTS-1 ; at P < 0.01, MMP-10 , TIMP-1 , ADAMTS-9 and at P < 0.05, TIMP-4 , ADAMTS-5 , ADAMTS-15 . Correlation analysis revealed that groups of genes across the gene families are co-expressed in cartilage.
Conclusion This is the first comprehensive expression profile of all known MMP , ADAMTS and TIMP genes in cartilage. Patterns of expression provide a foundation on which to understand mechanisms of gene regulation in OA and potentially for refining the specificity of anti-proteolytic therapies. 相似文献
Methods Human cartilage was obtained from femoral heads at joint replacement for either osteoarthritis or following fracture to the neck of femur. Total RNA was purified and expression of genes assayed using quantitative real-time PCR.
Results Several members of the above gene families were regulated in OA. Genes increasing in expression in OA were: at P < 0.001, MMP-13 , MMP-28 , ADAMTS-16 ; at P < 0.01, MMP-9 , MMP-16 , ADAMTS-2 , ADAMTS-14 and at P < 0.05, MMP-2 , TIMP-3 , ADAMTS-12 . Genes decreasing in expression in OA were: at P < 0.001, MMP-1 , MMP-3 , ADAMTS-1 ; at P < 0.01, MMP-10 , TIMP-1 , ADAMTS-9 and at P < 0.05, TIMP-4 , ADAMTS-5 , ADAMTS-15 . Correlation analysis revealed that groups of genes across the gene families are co-expressed in cartilage.
Conclusion This is the first comprehensive expression profile of all known MMP , ADAMTS and TIMP genes in cartilage. Patterns of expression provide a foundation on which to understand mechanisms of gene regulation in OA and potentially for refining the specificity of anti-proteolytic therapies. 相似文献
102.
Jessica Lasky-Su Tobias Banaschewski Jan Buitelaar Barbara Franke Keeley Brookes Edmund Sonuga-Barke Richard Ebstein Jacques Eisenberg Michael Gill Iris Manor Ana Miranda Fernando Mulas Robert D Oades Herbert Roeyers Aribert Rothenberger Joseph Sergeant Hans-Christoph Steinhausen Eric Taylor Kaixin Zhou Margaret Thompson Philip Asherson Stephen V Faraone 《Neuropsychopharmacology》2007,62(9):985-990
BACKGROUND: Previous research found an association between single nucleotide polymorphisms (SNPs) in the promoter region of DRD4 and statistically derived phenotypes generated from attention-deficit/hyperactivity disorder (ADHD) symptoms. We sought to replicate this finding by using the same methodology in an independent sample of ADHD individuals. METHODS: Four SNPs were genotyped in and around DRD4 in 2631 individuals in 642 families. We developed a quantitative phenotype at each SNP by weighting nine inattentive and nine hyperactive-impulsive symptoms. The weights were selected to maximize the heritability at each SNP. Once a quantitative phenotype was generated at each SNP, the screening procedure implemented in PBAT was used to select and test the five SNPs/genetic model combinations with the greatest power to detect an association for DRD4. RESULTS: One of the four SNPs was associated with the quantitative phenotypes generated from the ADHD symptoms (corrected p-values = .02). A rank ordering of the correlation between each of the ADHD symptoms and the quantitative phenotype suggested that hyperactive-impulsive symptoms were more strongly correlated with the phenotype; however, including inattentive symptoms was necessary to achieve a significant result. CONCLUSIONS: This study partially replicated a previous finding by identifying an association between rs7124601 and a quantitative trait generated from ADHD symptoms. The rs7124601 is in linkage disequilibrium (LD) with the SNPs identified previously. In contrast to the previous study, this finding suggests that both hyperactive-impulsive and inattentive symptoms are important in the association. 相似文献
103.
This paper reviews the literature on colorectal cancer from a sex and gender-based perspective. Colorectal cancer is a major cause of death in the developed world, with rates increasing in developing countries. Although described by some writers as an ‘equal opportunity’ disease, it presents more risk to men than women. Both biological, or sex-linked factors, and gender-linked factors play a part in the aetiology of the disease, while gender differences in the use of screening and treatment also help shape the mortality gap between women and men for this condition. Without an appreciation of the part played by sex and gender in the risk of colorectal cancer, and without a gender-sensitive approach to screening in particular, it is possible that the mortality gap between men and women for this condition will widen in the future. 相似文献
104.
Sarah M Cowgill Desiree V Villadolid Sam Al-Saadi Alexander S Rosemurgy 《JSLS, Journal of the Society of Laparoendoscopic Surgeons》2007,11(3):336-343
OBJECTIVES: The impact of preoperative endoscopic therapy on the difficulty of laparoscopic Heller myotomy and the impact of the difficulty of the myotomy on long-term outcome has not been determined. This study was undertaken to determine whether preoperative therapy impacts the difficulty of laparoscopic Heller myotomy and whether preoperative therapy or difficulty of myotomy impacts long-term outcomes. METHODS: Since 1992, 305 patients, 56% male, median age 49 years, underwent laparoscopic Heller myotomy and were prospectively followed. The difficulty of the laparoscopic Heller myotomy was scored by the operating surgeon for the most recent 170 consecutive patients on a scale of 1 (easiest) to 5 (most difficult). Patients scored their symptoms before and after myotomy using a Likert scale from 0 (never/not bothersome) to 10 (always/very bothersome). RESULTS: Before myotomy, 66% of patients underwent endoscopic therapy: 33% dilation, 11% Botox, and 22% both. Preoperative endoscopic therapy did not correlate with the difficulty of the myotomy (P=NS). Median follow-up was 25 months. Regardless of the difficulty of the myotomy, dysphagia improved with myotomy (P<0.0001). By regression analysis, the frequency and severity of post-myotomy dysphagia correlated with neither preoperative endoscopic therapy nor the difficulty of the myotomy. CONCLUSIONS: Laparoscopic Heller myotomy improves the frequency and severity of dysphagia. The difficulty of laparoscopic Heller myotomy is not impacted by preoperative therapy, and neither preoperative therapy nor difficulty of the myotomy impact long-term outcome. 相似文献
105.
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107.
John L Waddington Aiden P Corvin Gary Donohoe Colm M P O'Tuathaigh Kevin J Mitchell Michael Gill 《The Psychiatric clinics of North America》2007,30(3):365-399
This article summarizes the rationale, methods, and results of gene discovery programs in schizophrenia research and describes functional methods of investigating potential candidate genes. It focuses next on the most prominent current candidate genes and describes (1) evidence for their association with schizophrenia and research into the function of each gene; (2) investigation of the clinical phenotypes and endophenotypes associated with each gene, at the levels of psychopathologic, neurocognitive, electrophysiologic, neuroimaging, and neuropathologic findings; and (3) research into the ethologic, cognitive, social, and psychopharmacologic phenotype of mutants with targeted deletion of each gene. It examines gene-gene and gene-environment interactions. Finally, it looks at future directions for research. 相似文献
108.
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110.
Holly L Rosenzweig Manabu Minami Nikola S Lessov Sarah C Coste Susan L Stevens David C Henshall Robert Meller Roger P Simon Mary P Stenzel-Poore 《Journal of cerebral blood flow and metabolism》2007,27(10):1663-1674
Lipopolysaccharide (LPS) preconditioning provides neuroprotection against subsequent cerebral ischemic injury. Tumor necrosis factor-alpha (TNFalpha) is protective in LPS-induced preconditioning yet exacerbates neuronal injury in ischemia. Here, we define dual roles of TNFalpha in LPS-induced ischemic tolerance in a murine model of stroke and in primary neuronal cultures in vitro, and show that the cytotoxic effects of TNFalpha are attenuated by LPS preconditioning. We show that LPS preconditioning significantly increases circulating levels of TNFalpha before middle cerebral artery occlusion in mice and show that TNFalpha is required to establish subsequent neuroprotection against ischemia, as mice lacking TNFalpha are not protected from ischemic injury by LPS preconditioning. After stroke, LPS preconditioned mice have a significant reduction in the levels of TNFalpha (approximately threefold) and the proximal TNFalpha signaling molecules, neuronal TNF-receptor 1 (TNFR1), and TNFR-associated death domain (TRADD). Soluble TNFR1 (s-TNFR1) levels were significantly increased after stroke in LPS-preconditioned mice (approximately 2.5-fold), which may neutralize the effect of TNFalpha and reduce TNFalpha-mediated injury in ischemia. Importantly, LPS-preconditioned mice show marked resistance to brain injury caused by intracerebral administration of exogenous TNFalpha after stroke. We establish an in vitro model of LPS preconditioning in primary cortical neuronal cultures and show that LPS preconditioning causes significant protection against injurious TNFalpha in the setting of ischemia. Our studies suggest that TNFalpha is a twin-edged sword in the setting of stroke: TNFalpha upregulation is needed to establish LPS-induced tolerance before ischemia, whereas suppression of TNFalpha signaling during ischemia confers neuroprotection after LPS preconditioning. 相似文献