Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters










Database
Language
Publication year range
1.
Sao Paulo Med J ; 138(6): 490-497, 2020.
Article in English | MEDLINE | ID: mdl-33263706

ABSTRACT

BACKGROUND: Since February 2020, data on the clinical features of patients infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and their clinical evolution have been gathered and intensively discussed, especially in countries with dramatic dissemination of this disease. OBJECTIVE: To assess the clinical features of Brazilian patients with SARS-CoV-2 and analyze its local epidemiological features. DESIGN AND SETTING: Observational retrospective study conducted using data from an official electronic platform for recording confirmed SARS-CoV-2 cases. METHODS: We extracted data from patients based in the state of Pernambuco who were registered on the platform of the Center for Strategic Health Surveillance Information, between February 26 and May 25, 2020. Clinical signs/symptoms, case evolution over time, distribution of confirmed, recovered and fatal cases and relationship between age group and gender were assessed. RESULTS: We included 28,854 patients who were positive for SARS-CoV-2 (56.13% females), of median age 44.18 years. SARS-CoV-2 infection was most frequent among adults aged 30-39 years. Among cases that progressed to death, the most frequent age range was 70-79 years. Overall, the mortality rate in the cohort was 8.06%; recovery rate, 30.7%; and hospital admission rate (up to the end of follow-up), 17.3%. The average length of time between symptom onset and death was 10.3 days. The most commonly reported symptoms were coughing (42.39%), fever (38.03%) and dyspnea/respiratory distress with oxygen saturation < 95% (30.98%). CONCLUSION: Coughing, fever and dyspnea/respiratory distress with oxygen saturation < 95% were the commonest symptoms. The case-fatality rate was 8.06% and the hospitalization rate, 17.3%.


Subject(s)
COVID-19/epidemiology , Adult , Aged , Brazil/epidemiology , COVID-19/mortality , Female , Fever , Hospitalization/statistics & numerical data , Humans , Male , Middle Aged , Retrospective Studies
2.
Gut ; 68(9): 1676-1687, 2019 09.
Article in English | MEDLINE | ID: mdl-31315892

ABSTRACT

BACKGROUND & OBJECTIVES: Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide. Several types of chronic liver disease predispose to HCC, and several different signalling pathways have been implicated in its pathogenesis, but no common molecular event has been identified. Ca2+ signalling regulates the proliferation of both normal hepatocytes and liver cancer cells, so we investigated the role of intracellular Ca2+ release channels in HCC. DESIGN: Expression analyses of the type 3 isoform of the inositol 1, 4, 5-trisphosphate receptor (ITPR3) in human liver samples, liver cancer cells and mouse liver were combined with an evaluation of DNA methylation profiles of ITPR3 promoter in HCC and characterisation of the effects of ITPR3 expression on cellular proliferation and apoptosis. The effects of de novo ITPR3 expression on hepatocyte calcium signalling and liver growth were evaluated in mice. RESULTS: ITPR3 was absent or expressed in low amounts in hepatocytes from normal liver, but was expressed in HCC specimens from three independent patient cohorts, regardless of the underlying cause of chronic liver disease, and its increased expression level was associated with poorer survival. The ITPR3 gene was heavily methylated in control liver specimens but was demethylated at multiple sites in specimens of patient with HCC. Administration of a demethylating agent in a mouse model resulted in ITPR3 expression in discrete areas of the liver, and Ca2+ signalling was enhanced in these regions. In addition, cell proliferation and liver regeneration were enhanced in the mouse model, and deletion of ITPR3 from human HCC cells enhanced apoptosis. CONCLUSIONS: These results provide evidence that de novo expression of ITPR3 typically occurs in HCC and may play a role in its pathogenesis.


Subject(s)
Carcinoma, Hepatocellular/metabolism , Inositol 1,4,5-Trisphosphate Receptors/metabolism , Liver Neoplasms/metabolism , Adult , Animals , Apoptosis/physiology , Calcium Signaling/physiology , Carcinogenesis/genetics , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , Cell Proliferation/physiology , Cells, Cultured , DNA Methylation , Female , Gene Expression Regulation, Neoplastic/physiology , Hepatocytes/metabolism , Humans , Inositol 1,4,5-Trisphosphate Receptors/deficiency , Inositol 1,4,5-Trisphosphate Receptors/genetics , Liver/metabolism , Liver Neoplasms/genetics , Liver Neoplasms/pathology , Liver Regeneration/physiology , Male , Mice, Knockout , Middle Aged , Survival Analysis
3.
Hypertension ; 41(3 Pt 2): 737-43, 2003 Mar.
Article in English | MEDLINE | ID: mdl-12623989

ABSTRACT

Angiotensin-(1-7) [Ang-(1-7)] has biological actions that can often be distinguished from those of angiotensin II (Ang II). Recent studies indicate that the effects of Ang-(1-7) are mediated by specific receptor(s). We now report the partial characterization of a new antagonist selective for Ang-(1-7), D-Pro7-Ang-(1-7). D-Pro7-Ang-(1-7) (50 pmol) inhibited the hypertensive effect induced by microinjection of Ang-(1-7) [4+/-1 vs 21+/-2 mm Hg, 25 pmol Ang-(1-7) alone] into the rostral ventrolateral medulla without changing the effect of Ang II (16+/-2.5 vs 19+/-2.5 mm Hg after 25 pmol Ang II alone). At 10(-7) mol/L concentration, it completely blocked the endothelium-dependent vasorelaxation produced by Ang-(1-7) (10(-10) to 10(-6) mol/L) in the mouse aorta. The antidiuresis produced by Ang-(1-7) (40 pmol/100 g body weight) in water-loaded rats was also blocked by its analog [1 microg/100 g body weight; 3.08+/-0.8 vs 1.27+/-0.33 mL in Ang-(1-7)-treated rats]. D-Pro7-Ang-(1-7) at a molar ratio of 40:1 did not change the hypotensive effect of bradykinin. Moreover, D-Pro7-Ang-(1-7) did not affect the dipsogenic effect produced by intracerebroventricular administration of Ang II (11.4+/-1.15 vs 8.8+/-1.2 mL/h after Ang II) and did not show any demonstrable angiotensin-converting enzyme inhibitory activity in assays with the synthetic substrate Hip-His-Leu and rat plasma as a source of enzyme. Autoradiography studies with 125I-Ang-(1-7) in mouse kidney slices showed that D-Pro7-Ang-(1-7) competed for the binding of Ang-(1-7) to the cortical supramedullary region. In Chinese hamster ovary cells stably transfected with the AT1 receptor subtype, D-Pro7-Ang-(1-7) did not compete for the specific binding of 125I-Ang-II in concentrations up to 10(-6) mol/L. There was also no significant displacement of Ang II binding to angiotensin type 2 receptors in membrane preparations of adrenal medulla. These data indicate that D-Pro7-Ang-(1-7) is a selective antagonist for Ang-(1-7), which can be useful to clarify the functional role of this heptapeptide.


Subject(s)
Angiotensin I/antagonists & inhibitors , Angiotensin I/pharmacology , Peptide Fragments/antagonists & inhibitors , Peptide Fragments/pharmacology , Renal Agents/antagonists & inhibitors , Angiotensin I/metabolism , Angiotensin II/metabolism , Animals , Aorta/drug effects , Aorta/metabolism , Aorta/physiology , Culture Techniques , Male , Peptide Fragments/metabolism , Rats , Rats, Wistar , Renal Agents/metabolism , Vasodilation/drug effects
SELECTION OF CITATIONS
SEARCH DETAIL
...