Biomedical subjects

J Ribeiro

Publications and source records attributed to J Ribeiro.

40 records · Page 3Linked to original sources

PubMedDate not supplied

Overweight and obesity in children and adolescents: relationship with blood pressure, and physical activity.

OBJECTIVE: Using body mass index (BMI) quartiles, the present study's aims were (1) to describe and evaluate the relationship between overweight/obesity with cardiovascular disease (CVD) risk factors, such as systolic blood pressure (SBP), diastolic blood pressure (DBP) and physical activity; (2) to provide information on the prevalence of high blood pressure and physical activity according to BMI quartiles; and (3) to examine the relationship of risk of obesity to adverse levels of high blood pressure and physical activity. METHODS: The sample consisted of 1439 children (758 males and 681 females), 8-16 years old. Participants were classified as being at 'risk of obesity' according to age- and sex-adjusted fourth quartile of BMI values. Blood pressure was measured using the Dinamap monitor. An adapted version of the Weekly Activity Checklist was applied for the diagnosis of physical activity index (PAI). RESULTS: Systolic and diastolic blood pressures were significantly (p < 0.05) and positively related to BMI, whereas no significant associations were reported between BMI and PAI in both genders. Overall, the proportion of subjects with adverse levels of blood pressure (SBP or DBP) ranged from 21.3% in the first BMI quartile (BMI-1Q) to 30.4% in BMI-4Q (p < 0.05). The PAI ranged from 24.5% in BMI-1Q to 20.6 in BMI-4Q and no significant differences were found. Children and adolescents at 'risk of obesity' were 1.5 times as likely to have at least one risk factor (high blood pressure or low level of activity). CONCLUSIONS: Our data suggest that higher BMI is associated with higher values of SBP and DBP. Children and adolescents in the upper quartile of BMI are 1.5 times as likely to have at least one risk factor. Furthermore our data confirmed previous findings that higher levels of BMI are associated with a unfavourable risk profile for CVD risk factors.

Adolescent↗

PubMedDate not supplied

[Von Recklinghausen neurofibromatosis and malignant pheochromocytoma: presentation of 3 cases].

Neurofibromatosis may involve every organ. Manifestations vary greatly and different kind of neoplasia may be associated with excessive frequency; it's the case of pheochromocytoma that, as a benign tumor, coexists in 10%. Description of coexistency as a malignant tumor is a rarity; therefore, we think it's interesting to publish our experience. Nevertheless the association of Von Recklinghausen's disease with hypertension is not always dependent of that kind of association.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

[Von Recklinghausen's neurofibromatosis].

Neurofibromatosis is a multisystemic disease in which the multiple possible clinical manifestations may have important diagnostic and prognostic implications; if arterial hypertension coexists, many pathogenic mechanisms justify that the possible secondary etiology must be considered. In this report we review the pathogenic and clinical mechanisms and we point to the diagnostic strategy to reveal anomalies and diseases that, although present, may be occult.

Bone Diseases↗

PubMedDate not supplied

Regulation and deregulation of G2 checkpoint proteins with cisplatin.

BACKGROUND: The G2 checkpoint has a key role in the response to DNA damage. G2 arrest following DNA damage is associated with inactivation of the protein kinase cyclin B-cdc2. The role of changes in protein expression in enzyme inhibition is controversial. METHODS: Expression of cyclin B1, cdc2, cdc25c, total protein and DNA content were examined by flow cytometry in two lung cancer cell lines. Changes in protein expression were compared to cell cycle matched controls under conditions associated with and without G2 arrest. RESULTS: Total protein increased with G2 arrest and decreased with cell death. Changes in cdc2, cdc25c and p16 paralleled changes in total protein. A larger increase in cyclin B1 was seen which was due to cell cycle redistribution. Deregulation of cyclin B1 was seen with a sublethal dose of cisplatin. CONCLUSIONS: Our results do not support the model that changes in expression of cyclin B1 or other checkpoint proteins mediate G2 arrest after cisplatin.

Animals↗