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Long non-coding RNAs (lncRNAs) play important roles in human diseases. They control gene expression levels and influence various biological processes through multiple mechanisms. Functional abnormalities in lncRNAs are strongly associated with occurrence and development of various diseases. LINC00472, which is located on chromosome 6q13, is involved in several human diseases, particularly cancers of the breast, lung, liver, osteosarcoma, bladder, colorectal, ovarian, pancreatic and stomach. Importantly, LINC00472 can be used as a biomarker for breast cancer cell sensitivity to chemotherapeutic regimens, including doxorubicin. LINC00472 is regulated by microRNAs and several signaling pathways. However, the significance of LINC00472 in human diseases has not been clearly established. In this review, we elucidate on the significance of LINC00472 in various human diseases, indicating that LINC00472 may be a diagnostic, prognostic as well as therapeutic target for these diseases.
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PURPOSE: Our study aims to investigate the distribution of pain symptoms and the association between pain symptoms and clinical parameters in patients with adenomyosis. PATIENTS AND METHODS: The clinical and pathological data of 291 patients diagnosed with adenomyosis in the Obstetrics and Gynecology Department of Peking Union Medical College Hospital from March 2012 to September 2015 were collected, and analyzed in regard to the pain symptoms. RESULTS: The median age at disease onset was 34 years. 71.8% of the patients had pain symptoms (pain group) and 28.2% had no pain symptoms (painless group). Patients with symptoms accompanied by dysmenorrhea accounted for 68%, among which 30.3% were mild, 36.9% were moderate, and 32.8% severe, while 56.1% presented with progressive pain. Through comparison, significant differences were identified between the pain and painless groups with regard to age at diagnosis (P=0.009), age at onset of disease (P=0.008), and level of pre-surgical CA125 (P<0.001), as well as proportion of patients with rectal irritation (P=0.008), elevated CA125 level (P<0.001), thickened myometrial layer (P<0.001) and concurrent endometriosis (P=0.001). In the multivariable analysis, an elevated level of pre-surgical CA125 (P<0.001) and thickened posterior myometrial layer (P=0.023) were both independent risk factors for the morbidity of pain symptoms. Similar results except for the difference in rectal irritation were noticed when we made further comparison between the dysmenorrhea and non-dysmenorrhea groups in adenomyosis patients. CONCLUSION: Our research analyzes the clinical features related to pain symptoms in patients with adenomyosis, which may provide clues for the possible presurgical diagnosis of adenomyosis, as well as references for pain management of adenomyosis.
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Adenomiose/patologia , Endometriose/patologia , Doenças Uterinas/patologia , Adulto , Feminino , HumanosRESUMO
BACKGROUND AND OBJECTIVES: Ischemic post-conditioning (PostC) has been demonstrated as a novel strategy to harness nature's protection against myocardial ischemia-reperfusion (I/R). Hypercholesterolemia (HC) has been reported to block the effect of PostC on the heart. Angiotensin II type-1 (AT1) modulators have shown benefits in myocardial ischemia. The present study investigates the effect of a novel inhibitor of AT1, azilsartan in PostC of the heart of normocholesterolemic (NC) and HC rats. MATERIALS AND METHODS: HC was induced by the administration of high-fat diet to the animals for eight weeks. Isolated Langendorff's perfused NC and HC rat hearts were exposed to global ischemia for 30 min and reperfusion for 120 min. I/R-injury had been assessed by cardiac hemodynamic parameters, myocardial infarct size, release of tumor necrosis factor-alpha troponin I, lactate dehydrogenase, creatine kinase, nitrite in coronary effluent, thiobarbituric acid reactive species, a reduced form of glutathione, superoxide anion, and left ventricle collagen content in normal and HC rat hearts. RESULTS: Azilsartan post-treatment and six episodes of PostC (10 sec each) afforded cardioprotection against I/R-injury in normal rat hearts. PostC protection against I/R-injury was abolished in HC rat hearts. Azilsartan prevented the HC-mediated impairment of the beneficial effects of PostC in I/R-induced myocardial injury, which was inhibited by L-N5-(1-Iminoethyl)ornithinehydrochloride, a potent inhibitor of endothelial nitric oxide synthase (eNOS). CONCLUSION: Azilsartan treatment has attenuated the HC-induced impairment of beneficial effects of PostC in I/R-injury of rat hearts, by specifically modulating eNOS. Azilsartan may be explored further in I/R-myocardial injury, both in NC and HC conditions, with or without PostC.
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The Fourier interferometric spectrometer (FIS) acquires the interference data information of the spectrum and during the spectrum data processing, a series of spectrum reconstruction will be performed on the interference information to obtain the final spectrum information data. The spectral calibration is the key step to spectrum reconstruction of FIS, which directly determines accuracy and availability of the spectrum results. This paper introduces the basic ideas and calibration accuracy about the spectral calibration for the FIS and puts forward a new spectral calibration method based on calculating the precise value of the total optical path difference (TOPD). The TOPD of FIS is difficult to be precisely measured, but it is the core and key to the spectral calibration. In order to calculate the precise TOPD, this paper proposes the idea how to traverse the TOPD and analyzes the spectrum drift. During the calibration, all the possible values of the TOPD participate in the spectrum reconstruction flow to carry out spectrum recovery and analysis. Ultimately the TOPD with the minimum spectrum drift will be achieved, namely solution value of the TOPD. This method can accurately resolve the TOPD of the FIS and then calibrate the spectrum with high accuracy. In addition, the paper introduces the detailed and complete spectral calibration flow and obtains the center wavelength value of every band and wavenumber resolution. Moreover, the paper designs the main parameters of the typical FIS and generates its simulation interference data. Using the above method to calibrate the simulation data, the analysis and verification of the spectral calibration results proves that the calibration precision of wavenumber resolution achieves 0.000 25 cm⻹ or above.
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PURPOSE: To evaluate the clinical value of fluorescence in situ hybridization (FISH) for diagnosis and surveillance of bladder urothelial carcinoma (BUC). MATERIALS AND METHODS: Between November 2010 and December 2013, patients suspected of having BUC were examined using urine cytology and FISH assay. Based on histopathological examination results, FISH results were compared with urine cytology. In addition, patients with a history of non-muscle invasive BUC were also examined using urine cytology and FISH assay at the first time of visit and then monitored with cystoscopy during follow-up period. RESULTS: A total of 162 patients included in this study and 12 patients were excluded due to uninformative FISH assays. The remaining 150 patients consisted of 108 patients suspected for BUC and 42 patients with a history of non-muscle invasive BUC. The sensitivities of FISH analysis and urine cytology were 72.8% and 27.2%, respectively, and the difference was statistically significant (P <.05). Difference between specificity of urine cytology (100%) and FISH assay (85%) was not statistically significant (P >.05). At the first visit, of 42 patients, one patient had positive cystoscopy, and FISH assay was positive in 26 of 41 patients with negative cystoscopy. During the follow-up period (mean, 29.5 months), 18 of 26 patients developed recurrence, and recurrence occurred in only one of 15 patients with negative FISH analysis. CONCLUSION: Our results suggest that FISH analysis can be used as a non-invasive diagnostic tool for patients suspected of having new BUC. In addition, FISH analysis may provide important prognostic information to better define the individual risk for BUC recurrence.& nbsp;
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Carcinoma in Situ , Carcinoma de Células de Transição , Hibridização in Situ Fluorescente/métodos , Recidiva Local de Neoplasia/diagnóstico , Neoplasias da Bexiga Urinária , Adulto , Idoso , Carcinoma in Situ/diagnóstico , Carcinoma in Situ/patologia , Carcinoma de Células de Transição/diagnóstico , Carcinoma de Células de Transição/patologia , China , Cistoscopia , Células Epiteliais/patologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica , Valor Preditivo dos Testes , Prognóstico , Reprodutibilidade dos Testes , Medição de Risco/métodos , Sensibilidade e Especificidade , Bexiga Urinária/patologia , Neoplasias da Bexiga Urinária/diagnóstico , Neoplasias da Bexiga Urinária/patologiaRESUMO
This meta-analysis of published cohort studies was conducted to evaluate how closely the promoter methylation of the vimentin gene is correlated with the pathogenesis of colorectal carcinogenesis (CRC). The Web of Science (1945 ~ 2013), Cochrane Library Database (issue 12, 2013), PubMed (1966 ~ 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), and Chinese Biomedical Database (CBM) (1982 ~ 2013) were searched without language restrictions. Meta-analyses were conducted using Stata software (Version 12.0, Stata Corporation, College Station, TX, USA). Odds ratios (ORs) and 95 % confidence intervals (95 %CI) were calculated. Seven clinical cohort studies with a total of 467 CRC subjects met our inclusion criteria. Our meta-analysis results demonstrated that the frequency of vimentin promoter methylation in cancer tissues was significantly higher than in normal and benign tissues (cancer tissues vs. normal tissues: OR = 32.41, 95 %CI = 21.04 ~ 49.93, P < 0.001; cancer tissues vs. benign tissues: OR = 1.60, 95 %CI 1.05 ~ 2.42, P = 0.028). Ethnicity-stratified analysis indicated that the frequency of aberrant vimentin promoter methylation was correlated with the pathogenesis of CRC in both Asians and Caucasians. The findings of our meta-analysis confirm that vimentin methylation may play a crucial role in the pathogenesis of CRC.