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91.
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Background: Expression patterns of human β‐defensin‐2 (HBD‐2) mRNA or HBD‐2 protein concentration and periodontal diseases have been a focus of scientific research. This study compares the salivary levels of HBD‐2 protein concentration of healthy patients and patients with gingivitis and chronic periodontitis (CP) and correlates these levels with the presence of periodontopathogens. Methods: A total of 89 patients were enrolled in this study: 31 periodontally healthy, 27 with gingivitis, and 31 with CP. Plaque and gingival indices, probing depth, and clinical attachment level were measured. The presence of Campylobacter rectus, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, and Prevotella intermedia was evaluated qualitatively by conventional polymerase chain reaction. HBD‐2 quantification in saliva was performed using an immune enzymatic assay. Frequency of periodontopathogens and HBD‐2 protein concentration was assessed. Association between HBD‐2 protein concentration (≥100 pg/mL) and the simultaneous presence of one to two, three to four, or five to six periodontopathogens was tested. Results: Although periodontally healthy individuals and patients with gingivitis showed similar HBD‐2 levels, the CP group displayed an increased level of HBD‐2. P. gingivalis, P. intermedia, T. forsythia, and T. denticola were more prevalent in CP; however, their mere presence was not related to the increased levels of HBD‐2 (Pearson correlation and multinomial logistic regression model). Conclusions: Salivary HBD‐2 protein concentration was higher in patients with CP compared with healthy individuals or patients with gingivitis. These different protein concentrations were not related to the frequency of periodontopathogens. Clinical inflammatory profile had a higher impact on salivary HBD‐2 levels than bacteria.  相似文献   
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The aim of the present study was to investigate the effect of continuous positive airway pressure (CPAP) treatment on regional adipose tissue distribution in patients with moderate or severe obstructive sleep apnoea. Patients received both therapeutic and sham CPAP in a random order for 2 months each with an intervening 1-month washout. Abdominal subcutaneous, visceral and liver fat were quantified using magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS). Liver enzymes and plasma glucose were also determined. Measurements were obtained at baseline and at the end of both treatment arms. 38 eligible patients were randomly assigned to a treatment order, with 27 patients having complete MRI/MRS data. No significant difference was observed in subcutaneous (-28.6 cm(3); p=0.49) or visceral (-16.8 cm(3); p=0.59) adipose tissue, intrahepatic lipid (-0.2%; p=0.21), or fasting glucose measurements (-0.1 mmol·L(-1); p=0.46) between treatment modalities. Alkaline phosphatase decreased (-3.1 U·L(-1); p=0.02) while on therapeutic CPAP compared with sham CPAP but other liver enzymes, including aspartate aminotransferase (0.3 U·L(-1); p=0.82), alanine aminotransferase (1.34 U·L(-1); p=0.59) and γ-glutamyltransferase (-2.3 U·L(-1); p=0.33), remained unchanged. In this first randomised, sham-controlled trial, there was no change in adipose tissue distribution after 8 weeks of therapeutic CPAP compared with 8 weeks of sham CPAP. Longer duration of CPAP use may be necessary to demonstrate a difference.  相似文献   
95.
Fat mass may be modulated by the number of brown‐like adipocytes in white adipose tissue (WAT) in humans and rodents. Bone remodeling is dependent on systemic energy metabolism and, with age, bone remodeling becomes uncoupled and brown adipose tissue (BAT) function declines. To test the interaction between BAT and bone, we employed Misty (m/m) mice, which were reported be deficient in BAT. We found that Misty mice have accelerated age‐related trabecular bone loss and impaired brown fat function (including reduced temperature, lower expression of Pgc1a, and less sympathetic innervation compared to wild‐type (+/ +)). Despite reduced BAT function, Misty mice had normal core body temperature, suggesting heat is produced from other sources. Indeed, upon acute cold exposure (4°C for 6 hours), inguinal WAT from Misty mice compensated for BAT dysfunction by increasing expression of Acadl, Pgc1a, Dio2, and other thermogenic genes. Interestingly, acute cold exposure also decreased Runx2 and increased Rankl expression in Misty bone, but only Runx2 was decreased in wild‐type. Browning of WAT is under the control of the sympathetic nervous system (SNS) and, if present at room temperature, could impact bone metabolism. To test whether SNS activity could be responsible for accelerated trabecular bone loss, we treated wild‐type and Misty mice with the β‐blocker, propranolol. As predicted, propranolol slowed trabecular bone volume/total volume (BV/TV) loss in the distal femur of Misty mice without affecting wild‐type. Finally, the Misty mutation (a truncation of DOCK7) also has a significant cell‐autonomous role. We found DOCK7 expression in whole bone and osteoblasts. Primary osteoblast differentiation from Misty calvaria was impaired, demonstrating a novel role for DOCK7 in bone remodeling. Despite the multifaceted effects of the Misty mutation, we have shown that impaired brown fat function leads to altered SNS activity and bone loss, and for the first time that cold exposure negatively affects bone remodeling.  相似文献   
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Background: Patients with semantic dementia are impaired in both object naming and, to a lesser extent, in object use (Bozeat, Lambon Ralph, Patterson, & Hodges, 2002a Bozeat, S., Lambon Ralph, M. A., Patterson, K. and Hodges, J. R. 2002a. When objects lose their meaning: What happens to their use?. Cognitive, Affective & Behavioural Neurosciences, 2: 236251. [Crossref], [PubMed], [Web of Science ®] [Google Scholar]; Hodges, Graham, & Patterson, 1995 Hodges, J. R., Graham, N. and Patterson, K. 1995. Charting the progression in semantic dementia: Implications for the organisation of semantic memory.. Memory, 3: 463495. [Taylor & Francis Online], [Web of Science ®] [Google Scholar]). To date there have been relatively few studies examining the relearning of object names, and only one examining the relearning of object use. No study has examined relearning object naming, definition, and use simultaneously.

Aims: To explore the relatedness of object naming, definition, and object use in semantic dementia; to explore whether or not therapy is effective; and to explore the effectiveness of errorless learning.

Methods & Procedures: Two patients with mild to moderate semantic dementia and two matched control participants were tested in naming, defining, and demonstrating the use of 33 household objects. The quality of the definitions was rated as poor, adequate, or good by three independent raters. Three components of object use were examined: hold, orientation, and movement. The assessment was repeated with the patients following 3 weeks of therapy, and 1 month after completion of therapy. For the therapy objects were divided into individual trained and untrained sets based on familiarity and performance at initial assessment. Patients received therapy sessions twice weekly, and engaged in independent practice. During the therapy sessions, the researcher modelled the name, definition, and use of each item, which the patient then repeated. In the independent practice each patient watched a DVD in which she named and defined the object and used it correctly.

Outcomes & Results: Patients were severely impaired on object naming and definition, but less so on object use. Both patients showed some improvement as a result of therapy, which was maintained at follow‐up in one case.

Conclusions: The results show that relearning in semantic dementia is possible. Factors affecting the results and the interaction between lexical and conceptual impairments are discussed. An unexpected finding of the study was that patients performed better in verb production both in the preliminary tests and in object definition.  相似文献   
100.
Many people carry cerebral aneurysms but are generally unaware of their presence until they rupture, resulting in high morbidity or mortality. The pathogenesis and aetiology of aneurysms are largely unknown; however, a greater understanding, by analysing the genetic, molecular and haemodynamic risk factors involved in the initiation, enlargement, and rupture of aneurysms, could lead to effective prevention, early diagnosis and more effective treatment. The risk of aneurysm is increased by a family history of aneurysms, and amongst certain populations, namely in Japan and Finland. Several other risk factors are documented, including hypertension, smoking, alcohol consumption, and female sex. Studies indicate a higher occurrence of cerebral aneurysms in females compared to males. Oestrogen protects several components within the artery wall, and inhibits some of the inflammatory molecules that could cause aneurysms. At menopause, the oestrogen level decreases and the incidence of aneurysm increases. Haemodynamic stresses have been shown to be involved in the formation, growth and rupture of aneurysms. This is often associated with hypertension, which also increases the risk of aneurysm rupture. When an unruptured aneurysm is detected the decision to treat can be complicated, since only 1–2% of aneurysms eventually rupture. Haemodynamic simulation software offers an effective tool for the consideration of treatment options for patients who carry unruptured aneurysms. The assessment must consider the risks of interventional treatments versus non-interventional management options, such as controlling blood pressure.  相似文献   
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