TALITA ROJAS CUNHA SANCHES
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/12 - Laboratório de Pesquisa Básica em Doenças Renais, Hospital das Clínicas, Faculdade de Medicina
LIM/08 - Laboratório de Anestesiologia, Hospital das Clínicas, Faculdade de Medicina
LIM/12 - Laboratório de Pesquisa Básica em Doenças Renais, Hospital das Clínicas, Faculdade de Medicina
LIM/08 - Laboratório de Anestesiologia, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
Agora exibindo 1 - 4 de 4
- Vitamin D deficiency aggravates ischemic acute kidney injury in rats(2015) BRAGANCA, Ana Carolina de; VOLPINI, Rildo A.; CANALE, Daniele; GONCALVES, Janaina G.; SHIMIZU, Maria Heloisa M.; SANCHES, Talita R.; SEGURO, Antonio C.; ANDRADE, LuciaVitamin D deficiency (VDD) increases the risk of death in hospitalized patients. Renal ischemia/reperfusion injury (IRI) induces acute kidney injury (AKI), which activates cell cycle inhibitors, including p21, a cyclindependent kinase inhibitor and genomic target of 25-hydroxyvitamin D, which is in turn a potent immunomodulator with antiproliferative effects. In this study, we assess the impact of VDD in renal IRI. Wistar rats were divided into groups, each evaluated for 30 days: control (receiving a standard diet); VDD (receiving a vitamin D-free diet); IRI (receiving a standard diet and subjected to 45-min bilateral renal ischemia on day 28); and VDD + IRI (receiving a vitamin D-free diet and subjected to 45-min bilateral renal ischemia on day 28). At 48 h after IRI, animals were euthanized; blood, urine, and kidney tissue samples were collected. Compared with IRI rats, VDD + IRI rats showed a more severe decrease in glomerular filtration rate, greater urinary protein excretion, a higher kidney/body weight ratio and lower renal aquaporin 2 expression, as well as greater morphological damage, characterized by increased interstitial area and tubular necrosis. Our results suggest that the severity of tubular damage in IRI may be associated with downregulation of vitamin D receptors and p21. VDD increases renal inflammation, cell proliferation and cell injury in ischemic AKI.
- CHRONIC NICOTINE EXPOSURE DOWNREGULATES RENAL KLOTHO EXPRESSION AND TRIGGERS DIFFERENT RENAL AND AUTONOMIC RESPONSES ACCORDING TO THE KLOTHO STATUS IN MICE(2015) COELHO, Fernanda O.; JORGE, Lecticia B.; BRAGANCA, Ana Carolina de; SANCHES, Talita R. C.; CANALE, Daniele; HELOU, Claudia M. B.; IRIGOYEN, Maria Claudia; KUROO, Makoto; ANDRADE, Lucia
- Serum and Urinary Values of CA 19-9 and TGF beta 1 in a Rat Model of Partial or Complete Ureteral Obstruction(2015) LOPES, Roberto Iglesias; DENES, Francisco Tibor; BARTOLAMEI, Matheus Gesualdo; REIS, Sabrina; SANCHES, Talita Rojas; LEITE, Katia Ramos; SROUGI, Miguel; SEGURO, Antonio CarlosIntroduction Abnormal levels of serum and urinary markers occur in the presence of renal damage associated to obstructive uropathy. Urinary and serum transforming growth factor beta 1 (TGF beta 1) and carbohydrate antigen (CA 19-9) have not yet been evaluated in an experimental model of obstructive uropathy. Material and Methods Rats were divided into seven groups: reference, sham operation, unilateral nephrectomy, complete unilateral ureteral obstruction, partial unilateral ureteral obstruction, partial bilateral ureteral obstruction, and unilateral nephrectomy with contralateral partial ureteral obstruction. Kidney and ureter morphometry, TGF beta 1 and CA 19-9 serum and urinary concentrations and CA 19-9 renal tissue expression were analyzed. Correlation of these markers to complete, partial obstruction, or unobstructed groups was performed. Results Pathological findings correlated positively with the degree of ureteral obstruction, but negatively with urinary CA 19-9 levels. Marked underexpression of CA 19-9 was observed in kidneys with complete ureteral obstruction. No statistically significant differences were found for urinary and serum TGF beta 1 and also for serum CA 19-9. Conclusion Urinary CA 19-9 correlated negatively with ureteral obstruction grade. Immunohistochemistry depicted CA 19-9 expression on epithelial tubular cells cytoplasm, suggesting renal origin. Serum and urinary TGF beta 1 did not show alterations in response to severity and length of urinary obstruction, which might be associated with less intense renal remodeling.
- Effects of terlipressin as early treatment for protection of brain in a model of haemorrhagic shock(2015) IDA, Keila Kazue; OTSUKI, Denise Aya; SASAKI, Adolfo Toshiro Cotarelli; BORGES, Emilyn Silva; CASTRO, Letcia Urbano Cardoso; SANCHES, Talita Rojas; SHIMIZU, Maria-Heloisa Massola; ANDRADE, Lcia Conceicao; AULER JR., Jose-Otavio Costa; DYSON, Alex; SMITH, Kenneth John; ROCHA FILHO, Joel Avancini; MALBOUISSON, Luiz-Marcelo SaIntroduction: We investigated whether treatment with terlipressin during recovery from hypotension due to haemorrhagic shock (HS) is effective in restoring cerebral perfusion pressure (CPP) and brain tissue markers of water balance, oxidative stress and apoptosis. Methods: In this randomised controlled study, animals undergoing HS (target mean arterial pressure (MAP) 40 mmHg for 30 minutes) were randomised to receive lactated Ringer's solution (LR group; n = 14; volume equal to three times the volume bled), terlipressin (TERLI group; n = 14; 2-mg bolus), no treatment (HAEMO group; n = 12) or sham (n = 6). CPP, systemic haemodynamics (thermodilution technique) and blood gas analyses were registered at baseline, shock and 5, 30, 60 (T60), 90 and 120 minutes after treatment (T120). After the animals were killed, brain tissue samples were obtained to measure markers of water balance (aquaporin-4 (AQP4)), Na+-K+-2Cl(-) co-transporter (NKCC1)), oxidative stress (thiobarbituric acid reactive substances (TBARS) and manganese superoxide dismutase (MnSOD)) and apoptotic damage (Bcl-x and Bax). Results: Despite the HS-induced decrease in cardiac output (CO) and hyperlactataemia, resuscitation with terlipressin recovered MAP and resulted in restoration of CPP and in cerebral protection expressed by normalisation of AQP4, NKCC1, TBARS and MnSOD expression and Bcl-x/Bax ratio at T60 and T120 compared with sham animals. In the LR group, CO and blood lactate levels were recovered, but the CPP and MAP were significantly decreased and TBARS levels and AQP4, NKCC1 and MnSOD expression and Bcl-x/Bax ratio were significantly increased at T60 and T120 compared with the sham group. Conclusions: During recovery from HS-induced hypotension, terlipressin was effective in normalising CPP and cerebral markers of water balance, oxidative damage and apoptosis. The role of this pressor agent on brain perfusion in HS requires further investigation.