Changes in medical management and colectomy rates: a population-based cohort study on the epidemiology and natural history of ulcerative colitis in Örebro, Sweden, 1963-2010.

BACKGROUND: Whether the epidemiology of ulcerative colitis (UC) has changed during recent decades is partly unknown. AIM: To depict temporal trends in the epidemiology and medical treatment of UC as well as the long-term risk of progression in disease extent and colectomy, during 1963-2010. METHODS: Patients were identified by evaluation of all medical records in the archive of the Colitis Clinic, Örebro University Hospital. Comparisons were made between three time periods, 1963-1975, 1976-1990 and 1991-2005. RESULTS: The annual age-standardised incidence increased from 3.5 to 18.5 per 100 000 during the study period (P < .01). Correspondingly, the prevalence increased from 44 to 474 per 100 000 between 1965 and 2010. A higher proportion of males than females had extensive colitis at diagnosis (odds ratio: 1.55; 95% CI 1.17-2.05; P < .01). The risk for progression in disease extent was 34.5% and 18.5% at 10 years, for patients with proctitis and left-sided colitis, respectively (P < .01). The use of 5-aminosalicylates, within 10 years, rise from 79% to 92% between 1963-1975 and 1976-1990 (P < .01). Thiopurine use increased from 7% in 1976-1990 to 34% during 1991-2005 (P < .01). The colectomy rate at 10 years was 13.5% (95% CI 11.1%-15.8%), and the risk was lower among patients diagnosed in 1991-2005 compared to 1963-1975 (adjusted hazard ratio: 0.61; 95% CI 0.39-0.94; P = .02). CONCLUSION: The incidence and prevalence of UC increased over time, and the observed prevalence in 2010 is among the highest reported. In parallel, a decrease in colectomy rates was observed during the most recent decades, potentially reflecting improved medical treatment.

Increased lipid accumulation and adipogenic gene expression of adipocytes in 3D bioprinted nanocellulose scaffolds.

Compared to standard 2D culture systems, new methods for 3D cell culture of adipocytes could provide more physiologically accurate data and a deeper understanding of metabolic diseases such as diabetes. By resuspending living cells in a bioink of nanocellulose and hyaluronic acid, we were able to print 3D scaffolds with uniform cell distribution. After one week in culture, cell viability was 95%, and after two weeks the cells displayed a more mature phenotype with larger lipid droplets than standard 2D cultured cells. Unlike cells in 2D culture, the 3D bioprinted cells did not detach upon lipid accumulation. After two weeks, the gene expression of the adipogenic marker genes PPARγ and FABP4 was increased 2.0- and 2.2-fold, respectively, for cells in 3D bioprinted constructs compared with 2D cultured cells. Our 3D bioprinted culture system produces better adipogenic differentiation of mesenchymal stem cells and a more mature cell phenotype than conventional 2D culture systems.

[Changes in regional wall contractility induced by effort in women with normal coronary angiography --report of a clinical case]. / Alterações da contractilidade segmentar induzidas pelo esforço em mulheres com coronárias angiograficamente normais--caso clínico.

The diagnosis of coronary artery disease in women has been thought to be more difficult than in men, owing to the lower overall prevalence of disease in women, as well as more subtle clinical presentations and unspecific changes in ST segment. The authors report a clinical case of a 61-year old woman, with low cardiovascular risk and history of atypical chest pain and a positive treadmill exercise test on the inferior leads. She did an exercise echocardiogram that revealed severe hypokinesis on the anterior wall and septum with late normalization. The patient was submitted to a coronary angiography that revealed normal arteries. An echocardiogram with hyperventilation was later performed and showed the same ischemic changes as exercise did, on the inferior leads but no regional wall motions abnormalities occurred. The patient is currently asymptomatic under calcium antagonist treatment.

In vivo intrinsic efficacy of the 5-HT1A receptor antagonists NAD-299, WAY-100,635 and (S)-(-)-UH-301 at rat brain monoamine receptors.

The receptor-mediated control of brain monoamine synthesis was used to examine the in vivo intrinsic efficacy of the 5-HT1A receptor antagonists NAD-299, S(-)-UH-301 and WAY-100,635. The rate of monoamine synthesis was estimated by measuring the accumulation of DOPA and 5-HTP in the ventral neostriatum and the ventral hippocampus in rats pretreated with an inhibitor of cerebral aromatic L-amino acid decarboxylase. S(-)-UH-301 (2.0-32.0 micromol kg(-1)), but not WAY-100,635 (0.08-1.2 micromol kg(-1)), produced a decreased 5-HTP accumulation in the neostriatum and in the hippocampus. The administration of NAD-299 (0.75-12.0 micromol kg(-1)) resulted in a slight increase in neostriatal, but not hippocampal, 5-HTP accumulation. Neostriatal DOPA accumulation was decreased by S(-)-UH-301, whereas treatment with WAY- 100,635 resulted in an increase. NAD-299 did not affect neostriatal DOPA levels. There were no effects by any of these agents on DOPA levels in the ventral hippocampus. It is concluded that S(-)-UH-301, but not WAY-100,635 or NAD-299, displays intrinsic efficacy at brain 5-HT1A and DA D2/3 receptors, whereas WAY-100,635 behaves as a DA D2/3 receptor antagonist. By this comparison, NAD-299 appears to be the most selective and specific 5-HT1A receptor antagonist.

[Is the stress test useful in the detection of post-angioplasty restenosis?]. / Será a prova de esforço útil na detecção de reestenose pós-angioplastia?

Restetenosis is still the greatest limitation of coronary angioplasty (PTCA). The systematic use of ergometry (PE) with the objective of identifying restenosis is controversial and, namely, the ACC/AHA does not recommend its routine use. Our objective was to conduct a retrospective study of the use of PE when performed late (3 to 6 months) for the detection of restenosis. As a protocol, our group performed "late" PE on all the patients without contraindications, the patients with positive ergometry or CCS class II-IV angor submitted to angiographic control. Between January 1996 and July 1997, 121 patients (pts) were submitted to PTCA. Our study population was composed of patients submitted to complete revascularisation with follow-up in our centre: 59 pts (49%) with an average age of 58 +/- 12 years, 82% male. Eighty-three percent of the pts had revascularisation in a context of unstable angina, 10% in the acute phase of myocardial infarction and 7% due to chronic angina. Stents were implanted in 42% of the pts. In the follow-up after six months, 7 pts complained of CCS class II or III angor. The ergometry showed positive electrocardiographic criteria in 11 pts (18.6%). All pts with angor had positive PE. All these pts were submitted to angiographic control; restenosis (residual stenosis equal to or above 50%) was observed in all the patients who complained of angor (100% positive predictive value); restenosis occurred in 9 pts with positive ergometry (82% positive predictive value). In asymptomatic pts, PE indicated 2 pts with restenosis (2/59-3.4%) and two false positive (2/11-18%). At six months, PE detected 22% of the pts with restenosis. In conclusion, complete post-revascularisation angor due to coronary angioplasty has a higher positive predictive value than ergometry. However, the stress test, performed systematically, can identify an additional percentage of pts with restenosis with an acceptable percentage of false positives.

Infantile autism--fragile X: molecular findings support genetic heterogeneity.

Twenty-two members of 18 families with autism have been examined for the presence of mutations and abnormal methylation in the FMR-1 region at Xq27.3. All patients fulfilled diagnostic criteria of infantile autism. A characteristic pattern of insertion and methylation were detected after Southern blot analysis in 7 autistic individuals expressing the fragile site at Xq27.3. Normal DNA patterns were observed in 15 autistic boys cytogenetically negative for the fragile site. The results indicate a lack of involvement of the FMR-1 region in infantile autists negative for fragile X expression.