Fine-needle aspiration cytology is the standard technique to diagnose thyroid pathologies. However, this method results in a high percentage of inconclusive and false negatives. The use of time-resolved fluorescence techniques to detect biochemical composition and tissue structure alterations could help to develop a portable, minimally invasive, and nondestructive method to assist during surgical procedures. This study aimed to use fluorescence lifetimes to differentiate healthy and benign tissues from malignant thyroid tissue. The thyroid tissue was excited at 298-300 nm and the fluorescence decay registered at 340 and 450 nm. We observed fluorescence lifetimes at 340 nm emission of 0.80 ± 0.26 and 3.94 ± 0.47 ns for healthy tissue; 0.90 ± 0.24 and 4.05 ± 0.46 ns for benign lesions; and 1.21 ± 0.14 and 4.63 ± 0.25 ns for malignant lesions. For 450 nm emissions, we obtain lifetimes of 0.25 ± 0.18 and 3.99 ± 0.39 ns and for healthy tissue, 0.24 ± 0.17 and 4.20 ± 0.48 ns for benign lesions, 0.33 ± 0.32 and 4.55 ± 0.55 ns for malignant lesions. Employing analysis of variance, we differentiate malignant lesions from benign and healthy tissues. In addition, we use quadratic discriminant analysis to distinguish malignant from benign and healthy tissues with an accuracy of 76.1%, sensitivity of 74.7%, and specificity of 83.3%. These results indicate that time-resolved fluorescence can assist medical evaluation of thyroid pathologies during surgeries.
Fine-needle aspiration cytology is the standard technique to diagnose thyroid pathologies. However, this method has a high percentage of inconclusive and false-negative results for benign and malignant lesions. Hence, it is important to search for a new method to assist medical evaluation during these surgical procedures. The use of time-resolved fluorescence techniques to detect biochemical composition and tissue structure alterations could help to develop a portable, minimally invasive, and non-destructive method to assist medical evaluation. In this study, we investigated 17 human thyroid samples by absorbance, fluorescence, excitation, and time-resolved fluorescence measurements. This initial investigation has demonstrated that thyroid fluorescence originates from many endogenous fluorophores and culminates in several bands. The fluorescence lifetimes of benign and malignant lesions were significantly different, as attested by analysis of variance using Tukey test with individual confidence level of 98.06%. Our results suggest that fluorescence lifetimes of benign and malignant lesions can potentially assist diagnosis. After further investigations, fluorescence methods could become a tool for the surgeon to identify differences between normal and pathological thyroid tissues.
BackgroundFamilial partial lipodystrophy of the Dunnigan type is one of the most common inherited lipodystrophies variables. These individuals have important metabolic disorders that cause predisposition to various diseases. In this study we aimed to demonstrate the relation between the metabolic abnormalities, inflammatory profile and the expression of genes involved in the activation of the endoplasmic reticulum stress (ERS) in subjects with FPLD.MethodsWe evaluated 14 female FPLD patients and compared with 13 female healthy individuals. The subjects were paired with their respective BMI and age and categorized into two groups: Familial partial lipodystrophy of the Dunnigan type (FPLD) and control. Patients were fasted for 12 h before blood collection for measurement of HbA1c, glucose, insulin, lipids and inflammatory markers. Subcutâneous adipose tissue was collected by puncture aspiration of submental region during ambulatorial surgical aesthetic procedure.ResultsWe demonstrate that patients with FPLD show increased HbA1c (p < 0.01), fasting glucose (p < 0.002) and triglycerides (p < 0.005) while HDL/cholesterol (p < 0.001) was lower when compared to healthy individuals. We found that 64.2% FPLD patients had metabolic syndrome according to International Diabetes Federation definition. We also observe increased AUC of glucose (p < 0.001) and insulin during oGTT, featuring a frame of hyperglycemia and hyperinsulinemia, suggesting insulin resistance. Also we found hyperactivation of several genes responsible for ERS such as ATF-4 (p < 0.01), ATF-6 (p < 0.01), EIF2α3K (p < 0.005), CCT4 (p < 0.001), CHOP (p < 0.01), CALR (p < 0.001) and CANX (p < 0.005), that corroborate the idea that diabetes mellitus and metabolic syndrome are associated with direct damage to the endoplasmic reticulum homeostasis. Ultimately, we note that individuals with lipodystrophy have an increase in serum interleukins, keys of the inflammatory process, as IL-1β, TNF-α and IL-6 (p < 0.05 all), compared with healthy individuals, which can be the trigger to insulin resistance in this population.ConclusionIndividuals with FPLD besides having typical dysfunctions of metabolic syndrome, show a hyperactivation of ERS associated with increased systemic inflammatory profile, which together may explain the complex clinical aspect of this diseases.Trial registration HCRP no 6711/2012Electronic supplementary materialThe online version of this article (10.1186/s13098-017-0301-6) contains supplementary material, which is available to authorized users.
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