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排序方式: 共有10000条查询结果,搜索用时 15 毫秒
971.
A 66-year-old man was found to have a 7.5 cm mediastinal mass detected on routine chest X-rays as part of his preoperative work up for an inguinal hernia repair. An orthotopic (normally located) nongoitrous thyroid gland without evidence of connection to the mediastinal mass was also identified. The clinical differential diagnoses included lymphoma, thymoma, and germ cell tumor. Fine-needle aspiration (FNA) biopsy smears and touch imprints of the mediastinal mass showed a loosely cohesive, highly cellular population of relatively uniform cells with abundant granular cytoplasm, low nuclear to cytoplasmic (N/C) ratios, and prominent nucleoli consistent with a Hurthle cell (HC) neoplasm. Subsequently, the diagnosis of HC adenoma was confirmed on the surgically excised mediastinal mass. To the best of our knowledge, the surgical pathology and cytologic features of an HC adenoma of the mediastinum have not been reported in the literature. The gross, histologic, immunohistochemical, and electron microscopic (EM) findings, in addition to the cytologic features, are presented along with a differential diagnosis of this mediastinal neoplasm. 相似文献
972.
Rademakers R Melquist S Cruts M Theuns J Del-Favero J Poorkaj P Baker M Sleegers K Crook R De Pooter T Bel Kacem S Adamson J Van den Bossche D Van den Broeck M Gass J Corsmit E De Rijk P Thomas N Engelborghs S Heckman M Litvan I Crook J De Deyn PP Dickson D Schellenberg GD Van Broeckhoven C Hutton ML 《Human molecular genetics》2005,14(21):3281-3292
973.
van Duist MM Albrecht M Podswiadek M Giachino D Lengauer T Punzi L De Marchi M 《European journal of human genetics : EJHG》2005,13(6):742-747
The caspase recruitment domain gene CARD15/NOD2, encoding a cellular receptor involved in an NF-kappaB-mediated pathway of innate immunity, was first identified as a major susceptibility gene for Crohn's disease (CD), and more recently, as responsible for Blau syndrome (BS), a rare autosomal-dominant trait characterized by arthritis, uveitis, skin rash and granulomatous inflammation. While CARD15 variants associated with CD are located within or near the C-terminal leucine-rich repeat domain and cause decreased NF-kappaB activation, BS mutations affect the central nucleotide-binding NACHT domain and result in increased NF-kappaB activation. In an Italian family with BS, we detected a novel mutation E383K, whose pathogenicity is strongly supported by cosegregation with the disease in the family and absence in controls, and by the evolutionary conservation and structural role of the affected glutamate close to the Walker B motif of the nucleotide-binding site in the NACHT domain. Interestingly, substitutions at corresponding positions in another NACHT family member cause similar autoinflammatory phenotypes. 相似文献
974.
975.
Evans CM Williams OW Tuvim MJ Nigam R Mixides GP Blackburn MR DeMayo FJ Burns AR Smith C Reynolds SD Stripp BR Dickey BF 《American journal of respiratory cell and molecular biology》2004,31(4):382-394
Airway mucus hypersecretion is a prominent feature of many obstructive lung diseases. We thus determined the ontogeny and exocytic phenotype of mouse airway mucous cells. In naive mice, ciliated (approximately 40%) and nonciliated (approximately 60%) epithelial cells line the airways, and > 95% of the nonciliated cells are Clara cells that contain Clara cell secretory protein (CCSP). Mucous cells comprise < 5% of the nonciliated cells. After sensitization and a single aerosol antigen challenge, alcian blue-periodic acid Schiff's positive mucous cell numbers increase dramatically, appearing 6 h after challenge (21% of nonciliated/nonbasal cells), peaking from Days 1-7 (99%), and persisting at Day 28 (65%). Throughout the induction and resolution of mucous metaplasia, ciliated and Clara cell numbers identified immunohistochemically change only slightly. Intracellular mucin content peaks at Day 7, and mucin expression is limited specifically to a Clara cell subset in airway generations 2-4 that continue to express CCSP. Functionally, Clara cells are secretory cells that express the regulated exocytic marker Rab3D and, in antigen-challenged mice, rapidly secrete mucin in response to inhaled ATP in a dose-dependent manner. Thus, Clara cells show great plasticity in structure and secretory products, yet have molecular and functional continuity in their identity as specialized apical secretory cells. 相似文献
976.
Coluccia A Tattoli M Bizzoca A Arbia S Lorusso L De Benedictis L Buttiglione M Cuomo V Furley A Gennarini G Cagiano R 《Neuroscience》2004,123(1):155-166
We have shown that transgenic transient axonal glycoprotein (TAG)/F3 mice, in which the mouse axonal glycoprotein F3/contactin was misexpressed from a regulatory region of the gene encoding the transient axonal glycoprotein TAG-1, exhibit a transient disruption of cerebellar granule and Purkinje cell development [Development 130 (2003) 29]. In the present study we explore the neurobehavioural consequences of this mutation. We report on assays of reproductive parameters (gestation length, litter size and offspring viability) and on somatic and neurobehavioural end-points (sensorimotor development, homing performance, motor activity, motor coordination and motor learning). Compared with wild-type littermates, TAG/F3 mice display delayed sensorimotor development, reduced exploratory activity and impaired motor activity, motor coordination and motor learning. The latter parameters, in particular, were affected also in adult mice, despite the apparent recovery of cerebellar morphology, suggesting that subtle changes of neuronal circuitry persist in these animals after development is complete. These behavioural deficits indicate that the finely coordinated expression of immunoglobulin-like cell adhesion molecules such as TAG-1 and F3/contactin is of key relevance to the functional, as well as morphological maturation of the cerebellum. 相似文献
977.
978.
Interaction between a peroxisome proliferator-activated receptor gamma gene polymorphism and dietary fat intake in relation to body mass 总被引:5,自引:0,他引:5
Memisoglu A Hu FB Hankinson SE Manson JE De Vivo I Willett WC Hunter DJ 《Human molecular genetics》2003,12(22):2923-2929
The peroxisome proliferator-activated receptor gamma (PPAR gamma) is a critical regulator of adipogenesis. PPAR gamma+/- mice are resistant to high-fat diet-induced obesity and thus PPAR gamma may mediate physiological responses to dietary fat in other mammals. The aim of this study was to determine whether the human PPAR gamma proline to alanine substitution polymorphism (Pro12Ala) modifies the association between dietary fat and adiposity and plasma lipids. Subjects (n=2141) were controls selected for three case-control studies nested within the Nurses' Health Study, a large ongoing prospective cohort study. Associations between intake of total fat, fat subtypes and BMI were different in PPAR gamma 12Ala variant allele-carriers compared with non-carriers. Among homozygous wild-type Pro/Pro individuals, those in the highest quintile of total fat intake, had significantly higher mean body mass index (BMI) compared with those in the lowest quintile (27.3 versus 25.4 kg/m2, respectively; P-trend<0.0001) whereas among 12Ala variant allele-carriers there was no significant trend observed between dietary fat intake and BMI (P-trend=0.99; P-interaction=0.003). In contrast, intake of monounsaturated fat was not associated with BMI among homozygous wild-type women but was inversely associated with BMI among 12Ala variant allele-carriers (mean in lowest quintile=27.6 versus mean in highest quintile=25.5 kg/m2; P-trend=0.006; P-interaction=0.003). The relationship between dietary fat intake and plasma lipid concentrations also differed according to PPAR gamma genotype. These data suggest that PPAR gamma genotype is an important factor in physiological responses to dietary fat in humans. 相似文献
979.
980.
Multiple pathways of cell invasion are regulated by multiple families of serine proteases 总被引:5,自引:0,他引:5
Del Rosso M Fibbi G Pucci M D'Alessio S Del Rosso A Magnelli L Chiarugi V 《Clinical & experimental metastasis》2002,19(3):193-207
The complex process of tumor invasion requires the coordinated expression and activity of cell-substratum adhesive interactions
and of cell-associated protease systems, which destroy the extracellular matrix (ECM), in order to enable the invading cells
to simultaneously grip and destroy the anatomical barriers that control cell spreading. A number of data indicate that such
a `grip and go' process may be performed by an enlarging series of cell membrane-associated serine proteases and serine protease
receptors, which provide the invasive cells with a functional unit (the protease and its receptor), able to mediate cell-substratum
adhesion through specific receptor domains, to proteolytically degrade ECM and to deliver into the cell signals that up-regulate
the expression either of the protease/receptor complex, or of other adhesion molecules, such as integrins. There is evidence
that some proteases and protease receptor expression are under the control of tumor hypoxia, which is the result of an imbalance
in oxygen supply and demand. The urokinase-type plasminogen activator (u-PA) receptor (u-PAR) is under hypoxic control and
cooperates with other serine proteases of the blood coagulation pathways that may extravasate in the tumor milieu as a result
of hypoxia-simulated increase of vessel permeability. Other serine proteases and their receptors cooperate with the cell-associated
fibrinolytic system to promote cell invasion. Among these, tissue factor and its ligand coagulation factor VII, thrombin and
its protease-activated receptors, and type II trans-membrane serine proteases seem to play a crucial role. This Review takes
into consideration the complex scenario of the single serine proteases and related receptors that are involved in cell invasion,
as well as the protease receptor/adhesion molecule interplay which is necessary to focus the cell surface-driven proteolysis
where adhesion provides a grip to the invading cell.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献