CHIN JIA LIN
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/22 - Laboratório de Patolologia Cardiovascular, Hospital das Clínicas, Faculdade de Medicina - Líder
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- Fructose ingestion impairs expression of genes involved in skeletal muscle's adaptive response to aerobic exercise(2017) GONCALVES, Natalia Gomes; CAVALETTI, Stephanie Heffer; PASQUALUCCI, Carlos Augusto; MARTINS, Milton Arruda; LIN, Chin JiaBackground: The inverse relationship between exercise capacity and its variation over time and both cardiovascular and all-cause mortality suggests the existence of an etiological nexus between cardiometabolic diseases and the molecular regulators of exercise capacity. Coordinated adaptive responses elicited by physical training enhance exercise performance and metabolic efficiency and possibly mediate the health benefits of physical exercise. In contrast, impaired expression of genes involved in mitochondrial biogenesis or protein turnover in skeletal muscle-key biological processes involved in adaptation to physical training-leads to insulin resistance and obesity. Ingestion of fructose has been shown to suppress the exercise-induced GLUT4 response in rat skeletal muscle. To evaluate in greater detail how fructose ingestion might blunt the benefits of physical training, we investigated the effects of fructose ingestion on exercise induction of genes that participate in regulation of mitochondrial biogenesis and protein turnover in rat's skeletal muscle. Methods: Eight-week-old Wistar rats were randomly assigned to sedentary (C), exercise (treadmill running)-only (E), fructose-only (F), and fructose + exercise (FE) groups and treated accordingly for 8 weeks. Blood and quadriceps femoris were collected for biochemistry, serum insulin, and gene expression analysis. Expression of genes involved in regulation of mitochondrial biogenesis and autophagy, GLUT4, and ubiquitin E3 ligases MuRF-1, and MAFbx/Atrogin-1 were assayed with quantitative real-time polymerase chain reaction. Results: Aerobic training improved exercise capacity in both E and FE groups. A main effect of fructose ingestion on body weight and fasting serum triglyceride concentration was detected. Fructose ingestion impaired the expression of PGC-1 alpha, FNDC5, NR4A3, GLUT4, Atg9, Lamp2, Ctsl, Murf-1, and MAFBx/Atrogin-1 in skeletal muscle of both sedentary and exercised animals while expression of Err alpha and Ppar delta was impaired only in exercised rats. Conclusions: Our results show that fructose ingestion impairs the expression of genes involved in biological processes relevant to exercise-induced remodeling of skeletal muscle. This might provide novel insight on how a dietary factor contributes to the genesis of disorders of glucose metabolism.
- Iodine increases and predicts incidence of thyroiditis in NOD mice: Histopathological and ultrastructural study(2013) VECCHIATTI, Stella Maria Pedrossian; GUZZO, Maria Luisa; CALDINI, Elia Garcia; BISI, Helio; LONGATTO-FILHO, Adhemar; LIN, Chin JiaProlonged intake of large amounts of iodine has been reported to increase the incidence of hypothyroidism in humans, as well as in animals which are prone to spontaneously developing autoimmune thyroiditis. We sought to investigate the histopathological consequences of large amounts of dietary iodine on the thyroid gland and observe the occurrence of lymphocytic infiltration associated with the time of exposure to iodine. An experimental model using non-obese diabetic (NOD) mice was analyzed. A potassium iodide intake of 0.2 mg/animal/day was administered via drinking water, in experimental groups of 60 and 90 days (EG60 and EG90). Distended rough endoplasmic reticulum, degenerated mitochondria, debris and amorphous spaces or 'ill-defined' spaces were observed with electron microscopy (EM). Lymphocyte infiltration was observed in the two groups and the time of exposure to iodine did not increase the appearance of lymphocyte infiltration but significantly associated with the development of necrosis. The results of the present study demonstrated that the NOD mouse is a feasible experimental model for thyroiditis induced by iodine administration and may represent an opportunity to analyze the steps and factors associated with genetic autoimmune thyroiditis. High doses of ingested iodine were observed to precdict and increase the incidence of the thyroiditis process.
- The applicability of the ""surprise question"" as a prognostic tool in patients with severe chronic comorbidities in a university teaching outpatient setting(2023) LIN, C. A.; PIRES, P. P.; FREITAS, L. V.; REIS, P. V. S.; SILVA, F. D.; HERBST, L. G.; NUNES, R.; LIN, C. J.; NUNES, M. P. T.Background Life expectancy in recent decades has increased the prevalence of chronic diseases in the population, requiring an approach to new health topics, such as discussions on quality of life and expectations about death and dying. The concept of advance directives (ADs) gives individuals the opportunity to make known their decisions about the treatments they would like to receive at the end of life. Despite the recognition of relevance in clinical practice, the applicability of the concept presents challenges, including establishing the appropriate prognosis for each patient and the ideal time to approach the patient. Some prognostic tools were developed, such as the surprise question (SQ): ""Would you be surprised if your patient died in 12 months?"", which is used in some clinical settings to predict patient deaths and to make decisions regarding ADs. The main objective of the present study was to evaluate the behavior of second-year resident physicians (PGY-2) when the SQ was applied. Method In our observational study, from July 1, 2016, to February 28, 2017, (PGY-2) in the Internal Medicine Residency Program (IMRP) applied SQ to all patients with multiple and varied chronic no communicable comorbidities, who were followed up at the general medicine outpatient clinic (GMOC) of a tertiary university hospital in Sao Paulo- Brazil. The frequency of the outcome (death or non-death within 12 months) was analyzed by correlating it with the clinical data (impact of the studied variables). Results Eight hundred forty patients entered the study. Fitfty-two of them (6.2%) died within one year. PGY-2 predicted that two hundred and fourteen patients (25.5% of total) would die within a year (answer No to SQ), of which, 32 (14.9%) did so. The correct residents' prognosis for the subgroup of 626 patients (answer ""Yes"" to SQ) was NPV = 96.8% (CI = 95.4%-98.2%) and PPV = 14.9% (CI 10.1%-19, 6%). Answering ""Yes"" to SQ correlated negatively to addressing AD while the outcomes death and the answer No to SQ were positively correlated, according to the number of comorbidities. Conclusion The SQ, in addition to care, contributed to health education, communication and care planning shared by the doctor and patient.
- Aerobic Exercise Reduces Asthma Phenotype by Modulation of the Leukotriene Pathway(2016) ALBERCA-CUSTODIO, Ricardo Wesley; GREIFFO, Flavia Regina; MACKENZIE, BreAnne; OLIVEIRA-JUNIOR, Manoel Carneiro; ANDRADE-SOUSA, Adilson Santos; GRAUDENZ, Gustavo Silveira; SANTOS, Angela Batista Gomes; DAMACENO-RODRIGUES, Nilsa Regina; CASTRO-FARIA-NETO, Hugo Caire; ARANTES-COSTA, Fernanda Magalhaes; MARTINS, Milton De Arruda; ABBASI, Asghar; LIN, Chin Jia; IDZKO, Marco; OLIVEIRA, Ana Paula Ligeiro; NORTHOFF, Hinnak; VIEIRA, Rodolfo PaulaIntroduction: Leukotrienes (LTs) play a central role in asthma. Low- to moderate intensity aerobic exercise (AE) reduces asthmatic inflammation in clinical studies and in experimental models. This study investigated whether AE attenuates LT pathway activation in an ovalbumin (OVA) model of asthma. Methods: Sixty-four male, BALB/c mice were distributed into Control, Exercise (Exe), OVA, and OVA + Exe groups. Treadmill training was performed at moderate intensity, 5x/week, 1 h/session for 4 weeks. Quantification of bronchoalveolar lavage (BAL) cellularity, leukocytes, airway remodeling, interleukin (IL)-5, IL-13, cysteinyl leukotriene (CysLT), and leukotriene B4 (LTB4) in BAL was performed. In addition, quantitative analyses on peribronchial leukocytes and airway epithelium for LT pathway agents: 5-lypoxygenase (5-LO), LTA4 hydrolase (LTA4H), CysLT(1) receptor, CysLT(2) receptor, LTC4 synthase, and LTB4 receptor 2 (BLT2) were performed. Airway hyperresponsiveness (AHR) to methacholine (MCh) was assessed via whole body plethysmography. Results: AE decreased eosinophils (p < 0.001), neutrophils (p > 0.001), lymphocytes (p < 0.001), and macrophages (p < 0.01) in BAL, as well as eosinophils (p < 0.01), lymphocytes (p < 0.001), and macrophages (p > 0.001) in airway walls. Collagen (p < 0.01), elastic fibers (p < 0.01), mucus production (p < 0.01), and smooth muscle thickness (p < 0.01), as well as IL-5 (p < 0.01), IL-13 (p < 0.01), CysLT (p < 0.01), and LTB4 (p < 0.01) in BAL were reduced. 5-LO (p < 0.05), LTA4H (p < 0.05), CysLT(1) receptor (p < 0.001), CysLT(2) receptor (p < 0.001), LTC4 synthase (p < 0.001), and BLT2 (p < 0.01) expression by peribronchial leukocytes and airway epithelium were reduced. Lastly, AHR to MCh 25 mg/mL (p < 0.05) and 50 mg/mL (p < 0.01) was reduced. Conclusion: Moderate-intensity AE attenuated asthma phenotype and LT production in both pulmonary leukocytes and airway epithelium of OVA-treated mice.