BackgroundThe diagnostic criteria for Parkinson's disease (PD) remain complex, which is especially problematic for nonmovement disorder experts. A test is required to establish a diagnosis of PD with improved accuracy and reproducibility.ObjectiveThe study aimed to investigate the sensitivity and specificity of tests using sniffer dogs to diagnose PD.MethodsA prospective, diagnostic case‐control study was conducted in four tertiary medical centers in China to evaluate the accuracy of sniffer dogs to distinguish between 109 clinically established medicated patients with PD, 654 subjects without PD, 37 drug‐naïve patients with PD, and 185 non‐PD controls. The primary outcomes were sensitivity and specificity of sniffer dog's identification.ResultsIn the study with patients who were medicated, when two or all three sniffer dogs yielded positive detection results in a sample tested, the index test sensitivity, specificity, and positive and negative likelihood ratios were 91% (95% CI: 84%–96%), 95% (95% CI: 93%–97%), and 19.16 (95% CI: 13.52–27.16) and 0.10 (95% CI: 0.05–0.17), respectively. The corresponding sensitivity, specificity, and positive and negative likelihood ratios in patients who were drug‐naïve were 89% (95% CI: 75%–96%), 86% (95% CI: 81%–91%), and 6.6 (95% CI: 4.51–9.66) and 0.13 (95% CI: 0.05–0.32), respectively.ConclusionsTests using sniffer dogs may be a useful, noninvasive, fast, and cost‐effective method to identify patients with PD in community screening and health prevention checkups as well as in neurological practice. © 2022 International Parkinson and Movement Disorder Society.

ObjectiveTo uncover the specific function of linc00511 in the progression of liver hepatocellular carcinoma (LIHC) and the underlying mechanism.Patients and methodsGEPIA dataset containing 9736 LIHC samples and 857 normal samples were downloaded from TCGA. Expression pattern and prognostic potential of linc00511 in LIHC were analyzed. Subsequently, expression level of linc00511 in LIHC tissues collected in our hospital and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Differential expressions of linc00511 in LIHC with different tumor grades and metastatic status were compared. After transfection of si-linc00511, proliferative and migratory changes in Huh7 and Hep3B cells were assessed by cell counting kit-8 (CCK-8), 5-ethynyl-2ʹ-deoxyuridine (EdU) and Transwell assay. Lastly, Pearson correlation analysis and qRT-PCR were conducted to investigate the interaction between linc00511 and miR-29c.ResultsLinc00511 was upregulated in LIHC tissues and cell lines. Its level was positively correlated to TNM staging, lymphatic metastasis and poor prognosis in LIHC patients. Knockdown of linc00511 attenuated proliferative and migratory abilities in Huh7 and Hep3B cells. In addition, miR-29c was downregulated in LIHC and negatively linked to linc00511 level. A negative interaction between linc00511 and miR-29c could be a regulatory feedback influencing the progression of LIHC.ConclusionLinc00511 accelerates the proliferation and migration in LIHC, thus aggravating tumor progression. Meanwhile, linc00511 could be utilized as a hallmark predicting poor prognosis in LIHC patients.

Liver cancer is one of the most common and aggressive tumors, and usually leads to a poor clinical outcome. Increasing evidence has demonstrated the important functions of microRNAs (miRs) in tumor progression. miR-574-3p has been reported as a tumor suppressor and potential therapeutic target in various types of cancer. However, the underlying mechanism of the effects of miR-574-3p in liver cancer remains unknown. In the present study, reverse transcription-quantitative PCR was performed to detect miR-574-3p expression in liver cancer tissues, and the influence of miR-574-3p on cell growth was evaluated using the Cell Counting Kit-8 assay, and cell migration and flow cytometry analyses. The present study revealed that miR-574-3p expression was downregulated in liver cancer tissues and cell lines. miR-574-3p overexpression, achieved by transfecting miR-574-3p mimics into liver cancer cells, reduced cell proliferation and migration, and promoted cell apoptosis. Mechanistically, ADAM metallopeptidase domain 28 (ADAM28) was identified as a miR-574-3p target via binding to the 3'-untranslated region of the ADAM28 mRNA. Gain-of-function of miR-574-3p downregulated the expression levels of ADAM28 in liver cancer cells. Additionally, overexpression of ADAM28 significantly attenuated the suppressive effect of miR-574-3p on the growth of liver cancer cells. The present results provide novel insights into the function of the miR-574-3p/ADAM28 signaling pathway in liver cancer.

Abstract. Neuropeptide Y (NPY) is an important neurotransmitter in the control of energy metabolism. Several studies have shown that obesity is associated with increased levels of NPY in the hypothalamus. We hypothesized that the release of NPY has coordinated and integrated effects on energy metabolism in different tissues, such as adipocyte tissue, resulting in increased energy storage and decreased energy expenditure. Whether NPY has role in the molecular mechanism of human adipocyte tissue remains unclear. We established the model of human adipose derived stem cells (hADSCs) from human adipose tissue and differentiated it into adipocytes in the presence of NPY at different concentrations (10 -15 -10 -6 mmol/L). We then assessed hADSCs proliferation and differentiation by quantifying lipid accumulation and examining the expression levels of related adipocyte markers after differentiation. Furthermore, the specific markers of white adipocyte tissue (WAT) in hADSCs were also analyzed. The results showed that low doses of NPY stimulated hADSCs proliferation (p < 0.05), while high doses of NPY inhibited hADSCs proliferation (p < 0.05). NPY significantly promoted lipid accumulation and increased the size of lipid droplets during human adipogenic differentiation; the levels of adipocyte markers PPAR-γ and C/EBPα were also increased. At the same time, NPY also increased the levels of WAT markers Cidec and RIP140 after adipocyte differentiation. The results suggested high dose NPY inhibits the proliferation of hADSCs while promotes adipocyte differentiation and increases the expression of WAT markers. This may be the reason why increased levels of NPY can lead to a rise in body weight.Key words: Neuropeptide Y, Human adipose-derived stem cells, Adipocyte differentiation, White adipose tissue NEUROPEPTIDE Y (NPY) is a 36-amino acid neuropeptide, which is widely expressed in the central and peripheral nervous system. In the brain, NPY is found in many brain areas [1], including the hypothalamus, dentate gyrus, lateral thalamus and striatum, with the highest concentrations in the arcuate nucleus of the hypothalamus (Arc). NPY is implicated in the regulation of many physiological processes, including food intake and body energy balance. NPY also regulates cardiovascular, gastrointestinal, reproductive, endocrine and behavioural function [2][3][4]. Recently, studies have revealed that administration of NPY has profound metabolic effects throughout the body. One characteristic of obesity is the This overproduction of fat is associated with increased lipogenesis in different organs, such as liver and white adipose tissue (WAT). Several studies found that obesity is associated with elevated levels of NPY in the hypothalamus [5][6][7][8][9]. Adipose tissue is important for regulation of energy metabolism. A disturbance of metabolic processes, such as thermogenesis, lipogenesis and fatty acid oxidation, may contribute to the pathology of obesity. In order to increase our understanding of how NPY could be involved in the adipoc...

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