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81.
Emmet J. Jordan Maeve A. Lowery Olca Basturk Peter J. Allen Kenneth H. Yu Viviane Tabar Kathryn Beal Diane L. Reidy Yoshiya Yamada Yelena Janjigian Ghassan K. Abou-Alfa Eileen M. OReilly 《Clinical colorectal cancer》2018,17(2):e315-e321
Purpose
To assess clinical characteristics of patients with metastatic pancreas ductal adenocarcinoma (PDAC) and brain metastases (BM), and to assess somatic and germ-line molecular profiles where performed.Patients and Methods
Patients with PDAC and BM between January 1990 and January 2016 were identified. Molecular characteristics of somatic and germ-line testing where performed in the subset of patients who had provided informed consent. Somatic alterations were assessed by either MSK-IMPACT testing (>340 key cancer genes) or Sequenom testing (8-gene panel). Overall survival was calculated from date of diagnosis to either date of last follow-up or death. Survival after BM was calculated from date of diagnosis of BM by radiology or pathology to either date of last follow-up or death.Results
From a total of 5824 patients with PDAC identified from January 2000 to January 2016, twenty-five patients (0.4%) had BM. Median age at PDAC diagnosis was 58 years. Median time to the development of BM from initial PDAC diagnosis was 17 months (range, 0-79 months). Median overall survival after BM diagnosis was 1.5 months (range, 1-31 months). Overall survival for patients who had craniotomy (n = 4) was 11 months (range, 1-31 months), with 2 long-term survivors at 21 and 31 months, respectively. Four patients had leptomeningeal disease. Six of 25 patients had germ-line testing, and 3 had BRCA mutations (2 BRCA1 and 1 BRCA2). Somatic profiling identified KRAS mutations in 100% (4 G12D, 2 G12V, and 1 Q61K).Conclusion
BM from PDAC is a rare event. We identified a speculative association of germ-line BRCA1/2 alterations with BM in PDAC, which requires corroboration. Survival after BM development is poor; prolonged survival occurred in selected patients via a multidisciplinary approach. 相似文献82.
Moratelli S De Sanctis V Gemmati D Serino ML Mari R Gamberini MR Scapoli GL 《Journal of pediatric endocrinology & metabolism : JPEM》1998,11(Z3):915-921
Hemostatic parameters of 495 beta-thalassemic patients (421 with thalassemia major and 74 with thalassemia intermedia) were analyzed, to assess their association with the described thrombophilic condition and to verify the role of additional risk factors (e.g. persistent postsplenectomy thrombocytosis, insulin dependent diabetes mellitus, estrogen-progestin treatment and atrial fibrillation). The prevalence of thromboembolic accidents was 5.2% and in four patients (15.3%) inherited or acquired predisposing defects were recognized. The incidence of thromboembolic events and the associated relative risk due to hemocoagulative abnormalities in these patients are discussed. 相似文献
83.
Predictors of initiation and persistence of recurrent binge eating and inappropriate weight compensatory behaviors in college men
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84.
D Gemmati M Previati M L Serino S Moratelli S Guerra S Capitani E Forini G Ballerini G L Scapoli 《Arteriosclerosis, thrombosis, and vascular biology》1999,19(7):1761-1767
Several studies have indicated that mild to moderate hyperhomocystinemia is a common cause of arterial occlusive disease. Whether hyperhomocystinemia per se is an independent risk factor for vein thromboembolism (VTE) is still somewhat controversial. Both genetic and nutritional factors influence plasma homocysteine levels. Therefore, we evaluated plasma total homocysteine (tHcy), folate, and vitamin B12 levels and established, by polymerase chain reaction, the presence of the C677T mutation (A223V) in the methylenetetrahydrofolate reductase (MTHFR) gene in 220 cases with VTE without well-established prothrombotic defects. As a control group, 220 healthy subjects from the same geographic area as the cases were investigated. Hyperhomocystinemia was defined as a plasma tHcy level above the 95th percentile in the controls (18.05 micromol/L). Hyperhomocystinemia was found in 16% of cases (odds ratio=3.59; P<0.001); deficiencies of folate (<2.47 ng/mL) or vitamin B12 (<165 pg/mL), defined as values below the 5th percentile in controls, were found in 17.7% (P<0.001) and 12.3% (P=0.015) of cases, respectively. The homozygous condition for the MTHFR mutation (VV) was present in 28.2% of cases and 17.7% of controls (odds ratio=1.82; P=0.013). Comparing only the idiopathic forms of VTE (n=80/220; 36.3%) with normal controls, individuals with hyperhomocystinemia, or individuals homozygous for MTHFR mutation increased the odds ratios to 4.03 (P=0.005) and 2.11 (P=0.018), respectively. No statistically significant difference was observed in the MTHFR genotype distribution of cases and controls with hyperhomocystinemia (P=0.386); however, the normal MTHFR genotype (AA) appeared in control subjects only when tHcy levels were below the 80th percentile (10.57 micromol/L) of the distribution, whereas in case patients, it was present at the highest tHcy levels. A strong association between mutated homozygosity (VV), low folate levels, and hyperhomocystinemia was found in both groups. We conclude that in patients with VTE who do not have coexisting prothrombotic defects, hyperhomocystinemia increases the risk of developing idiopathic and venous thrombosis; the homozygous condition for the MTHFR mutation confers a moderate risk but, together with low folate levels, it is the main determinant of mild hyperhomocystinemia in normal and thromboembolic populations. 相似文献
85.
Toyohi Isse Yoichi Ueta Ryota Serino Jun Noguchi Yukiyo Yamamoto Masayoshi Nomura Izumi Shibuya Stafford L. Lightman Hiroshi Yamashita 《Brain research》1999,846(2):5415-235
Fasting induced a reduction in neuronal nitric oxide synthase (nNOS) mRNA in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of rats. The effect of intracerebroventricular (i.c.v.) administration of leptin on the nNOS mRNA level in the PVN and SON of fasting rats was studied by in situ hybridization histochemistry. Leptin (10 microg/kg b.wt) or vehicle was administered i.c.v. at 1700 h on two successive days fasting for 2 days. Fasting for 2 days with i.c.v. administration of vehicle induced a significant reduction of nNOS mRNA in the PVN and SON. Central administration of leptin prevented the fasting-induced reduction of nNOS mRNA in the PVN and SON. Administration of leptin also prevented the fasting-induced reductions of thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) mRNAs in the parvocellular division of the PVN. These results suggest that leptin is associated with fasting-induced reduction of nNOS mRNA in the PVN and SON as well as TRH and CRH mRNAs in the PVN. 相似文献
86.
Alessandro O. Caffò Antonella Lopez Giuseppina Spano Silvia Serino Pietro Cipresso Fabrizio Stasolla 《Aging & mental health》2018,22(10):1372-1383
ABSTRACTObjectives: The study is focused on the assessment of reorientation skills in a sample of community-dwelling elderly people, manipulating landmarks and geometric (layout) information. Method: A neuropsychological assessment was administered to 286 elderly participants, divided into six groups (healthy controls, HC; four subgroups of participants with mild cognitive impairment, MCI; participants with probable dementia, Prob_D) and tested with the Virtual Reorientation Test (VReoT). VReoT manipulated different spatial cues: geometry and landmarks (proximal and distal). Result: Compared with HC, participants with MCI and Prob_D showed to be impaired in tasks involving geometry, landmarks and a combination of them. Both single and multiple domain impairment in MCI had an impact on reorientation performance. Moreover, VReoT was marginally able to discriminate between amnesic and non-amnesic MCI. The occurrence of getting lost events seemed to be associated to learning of geometric information. Conclusion: The associative strength between landmark and target plays an important role in affecting spatial orientation performance of cognitively impaired participants. Geometry significantly supports landmark information and becomes helpful with the increase of cognitive impairment which is linked to a decrement in landmark encoding. VReoT seems to represent a reliable evaluation supplement for spatial orientation deficits in prodromal stages of dementia. 相似文献
87.
Vincent Blasco-Baque Berengère Coupé Aurelie Fabre Sandra Handgraaf Pierre Gourdy Jean-François Arnal Michael Courtney Carole Schuster-Klein Beatrice Guardiola François Tercé Rémy Burcelin Matteo Serino 《Diabetologia》2017,60(4):690-700
Aims/hypothesis
Despite the current pandemic of metabolic diseases, our understanding of the diverse nature of the development of metabolic alterations in people who eat a high-fat diet (HFD) is still poor. We recently demonstrated a cardio-metabolic adaptation in mice fed an HFD, which was characterised by a specific gut and periodontal microbiota profile. Since the severity of hepatic disease is characterised by specific microRNA (miRNA) signatures and the gut microbiota is a key driver of both hepatic disease and miRNA expression, we analysed the expression of three hepatic miRNA and studied their correlation with hepatic triacylglycerol content and gut microbiota.Methods
Two cohorts of C57BL/6 4-week-old wild-type (WT) male mice (n?=?62 and n?=?96) were fed an HFD for 3 months to provide a model of metabolic adaptation. Additionally 8-week-old C57BL/6 mice, either WT or of different genotypes, with diverse gut microbiota (ob/ob, Nod1, Cd14 knockout [Cd14KO] and Nod2) or without gut microbiota (axenic mice) were fed a normal chow diet. Following which, glycaemic index, body weight, blood glucose levels and hepatic triacylglycerol levels were measured. Gut (caecum) microbiota taxa were analysed by pyrosequencing. To analyse hepatic miRNA expression, real-time PCR was performed on total extracted miRNA samples. Data were analysed using two-way ANOVA followed by the Dunnett’s post hoc test, or by the unpaired Student’s t test. A cluster analysis and multivariate analyses were also performed.Results
Our results demonstrated that the expression of miR-181a, miR-666 and miR-21 in primary murine hepatocytes is controlled by lipopolysaccharide in a dose-dependent manner. Of the gut microbiota, Firmicutes were positively correlated and Proteobacteria and Bacteroides acidifaciens were negatively correlated with liver triacylglycerol levels. Furthermore, the relative abundance of Firmicutes was negatively correlated with hepatic expression of miR-666 and miR-21. In contrast, the relative abundance of B. acidifaciens was positively correlated with miR-21.Conclusions/interpretation
We propose the involvement of hepatic miRNA, liver triacylglycerols and gut microbiota as a new triad that underlies the molecular mechanisms by which gut microbiota governs hepatic pathophysiology during metabolic adaptation to HFD.88.
89.
90.