A nomogram based on 4-lncRNAs signature for improving prognostic prediction of hepatocellular carcinoma.

PURPOSE: Long noncoding RNAs (lncRNAs) with abnormal expression are frequently seen in hepatocellular cancer patients (HCC). Previous studies have reported the correlation between lncRNA and prognosis processes of HCC patients. In this research, a graphical nomogram with lncRNAs signatures, T, M phases was developed using the rms R package to estimate the survival rates of HCC patients in year 1, 3, and 5. METHODS: To find the prognostic lncRNA and create the lncRNA signatures, univariate Cox survival analysis and multivariate Cox regression analysis were chosen. The rms R software package was used to build a graphical nomogram based on lncRNAs signatures to predict the survival rates in of HCC patients in 1, 3, and 5 years. Using "edgeR", "DEseq" R packages to find the differentially expressed genes (DEGs). RESULTS: Firstly, a total of 5581 DEGs including 1526 lncRNAs and 3109 mRNAs were identified through bioinformatic analysis, of which 4 lncRNAs (LINC00578, RP11-298O21.2, RP11-383H13.1, RP11-440G9.1) were identified to be strongly related to the prognosis of liver cancer (P < 0.05). Moreover, we constructed a 4-lncRNAs signature by using the calculated regression coefficient. 4-lncRNAs signature is identified to significantly correlated with clinical and pathological characteristics (such as T stage, and death status of HCC patients). CONCLUSIONS: A prognostic nomogram on the base of 4-lncRNAs markers was built, which is capable to accurately predict the 1-year, 3-year, and 5-year survival of HCC patients after the construction of the 4-lncRNAs signature linked with prognosis of HCC.

MicroRNA-128 acts as a suppressor in the progression of gastrointestinal stromal tumor by targeting B-lymphoma Mo-MLV insertion region 1.

INTRODUCTION: The critical role of microRNA-128 (miR-128) in gastrointestinal-related diseases has been documented. In the current study, we tried to clarify the specific role miR-128 in gastrointestinal stromal tumor (GIST) and the underlying mechanism. METHODS: Differentially expressed genes in GIST were identified following bioinformatics analysis. Then, expression patterns of miR-128 and B-lymphoma Mo-MLV insertion region 1 (BMI-1) in clinical tissue samples and cell lines were characterized, followed by validation of their correlation. GIST-T1 cells were selected and transfected with different mimic, inhibitor, or siRNA plasmids, after which the biological functions were assayed. RESULTS: We identified low miR-128 and high BMI-1 expression in GIST tissues of 78 patients and 4 GIST cell lines. Ectopic expression of miR-128 or silencing of BMI-1 suppressed the malignant potentials of GIST-T1 cells. As a target of miR-128, BMI-1 re-expression could partly counteract the suppressive effect of miR-128 on the malignancy of GIST-T1 cells. CONCLUSION: Our study provided evidence that miR-128-mediated silencing of BMI-1 could prevent malignant progression of GIST, highlighting a promising anti-tumor target for combating GIST.

Maternal exposure to metal components of PM2.5 and low birth weight in New Mexico, USA.

Infants with low birth weight (LBW) are more likely to have health problems than normal weight infants. In studies examining the associations between particulate matter (PM) exposures and LBW, there is a tendency to focus on PM2.5 as a whole. However, insufficient information is available regarding the effects of different components of PM2.5 on birth weight. This study identified the associations between maternal exposure to 10 metal components of PM2.5 and LBW in offspring based on small area (divided by population size) level data in New Mexico, USA, from 2012 to 2016. This study used a pruned feed-forward neural network (pruned-FNN) approach to estimate the annual average exposure index to each metal component in each small area. The linear regression model was employed to examine the association between maternal PM2.5 metal exposures and LBW rate in small areas, adjusting for the female percentage and race/ethnicity compositions, marriage status, and educational level in the population. An interquartile range increase in maternal exposure to mercury and chromium of PM2.5 increased LBW rate by 0.43% (95% confidence interval (CI): 0.18-0.68%) and 0.63% (95% CI: 0.15-1.12%), respectively. These findings suggest that maternal exposure to metal components of air pollutants may increase the risk of LBW in offspring. With no similar studies in New Mexico, this study also posed great importance because of a higher LBW rate in New Mexico than the national average. These findings provide critical information to inform further epidemiological, biological, and toxicological studies.

Maternal exposure to metal components of PM2.5 and low birth weight in New Mexico, USA.

Infants with low birth weight (LBW) are more likely to have health problems than normal weight infants. In studies examining the associations between particulate matter (PM) exposures and LBW, there is a tendency to focus on PM 2.5 as a whole. However, insufficient information is available regarding the effects of different components of PM 2.5 on birth weight. This study identified the associations between maternal exposure to 10 metal components of PM 2.5 and LBW in offspring based on small area (divided by population size) level data in New Mexico, USA, from 2012 to 2016. This study used a pruned feed-forward neural network (pruned-FNN) approach to estimate the annual average exposure index to each metal component in each small area. The linear regression model was employed to examine the association between maternal PM 2.5 metal exposures and LBW rate in small areas, adjusting for the female percentage and race/ethnicity compositions, marriage status and educational level in the population. An interquartile range increase in maternal exposure to mercury and chromium of PM 2.5 increased LBW rate by 0.43% (95% confidence interval (CI): 0.18%-0.68%) and 0.63% (95% CI: 0.15%-1.12%), respectively. These findings suggest that maternal exposure to metal components of air pollutants may increase the risk of LBW in offspring. With no similar studies in New Mexico, this study also posed great importance because of a higher LBW rate in New Mexico than the national average. These findings provide critical information to inform further epidemiological, biological, and toxicological studies.

The neuroprotective effects of Lutongkeli in traumatic brain injury rats by anti-apoptosis mechanism.

PURPOSE: To explore the neuroprotective effects of Lutongkeli (LTKL) in traumatic brain injury (TBI) and detect the related mechanism. METHODS: TBI model was established with LTKL administration (2 and 4 g/kg/d, p.o.). Motor function of rats was examined by Rotarod test. Nissl staining was used to show neuron morphology. Furthermore, the disease-medicine common targets were obtained with the network pharmacology and analyzed with Kyoto Encyclopedia of Genes and Genomes. Lastly, the predicted targets were validated by real-time polymerase chain reaction. RESULTS: After LTKL administration, neural behavior was significantly improved, and the number of spared neurons in brain was largely increased. Moreover, 68 bioactive compounds were identified, corresponding to 148 LTKL targets; 2,855 genes were closely associated with TBI, of which 87 overlapped with the LTKL targets and were considered to be therapeutically relevant. Functional enrichment analysis suggested LTKL exerted its pharmacological effects in TBI by modulating multiple pathways including apoptosis, inflammation, etc. Lastly, we found LTKL administration could increase the mRNA level of Bcl-2 and decrease the expression of Bax and caspase-3. CONCLUSIONS: This study reported the neuroprotective effect of LTKL against TBI is accompanied with anti-apoptosis mechanism, which provides a scientific explanation for the clinical application of LTKL in the treatment of TBI.

The neuroprotective effects of Lutongkeli in traumatic brain injury rats by anti-apoptosis mechanism

Purpose: To explore the neuroprotective effects of Lutongkeli (LTKL) in traumatic brain injury (TBI) and detect the related mechanism. Methods: TBI model was established with LTKL administration (2 and 4 g/kg/d, p.o.). Motor function of rats was examined by Rotarod test. Nissl staining was used to show neuron morphology. Furthermore, the disease-medicine common targets were obtained with the network pharmacology and analyzed with Kyoto Encyclopedia of Genes and Genomes. Lastly, the predicted targets were validated by real-time polymerase chain reaction. Results: After LTKL administration, neural behavior was significantly improved, and the number of spared neurons in brain was largely increased. Moreover, 68 bioactive compounds were identified, corresponding to 148 LTKL targets; 2,855 genes were closely associated with TBI, of which 87 overlapped with the LTKL targets and were considered to be therapeutically relevant. Functional enrichment analysis suggested LTKL exerted its pharmacological effects in TBI by modulating multiple pathways including apoptosis, inflammation, etc. Lastly, we found LTKL administration could increase the mRNA level of Bcl-2 and decrease the expression of Bax and caspase-3. Conclusions: This study reported the neuroprotective effect of LTKL against TBI is accompanied with anti-apoptosis mechanism, which provides a scientific explanation for the clinical application of LTKL in the treatment of TBI.

IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells.

BACKGROUND: The present study aimed to investigate the underlying role of interferon-regulatory factor 2 (IRF2)-inositol polyphosphate-4-phosphatase, type-II (INPP4B) axis in the regulation of autophagy in acute myeloid leukemia (AML) cells. METHODS: Quantitative real time PCR (QRT-PCR) and western blot were performed to determine the expression levels of IRF2, INPP4B and autophagy-related markers in AML cell lines. Autophagy was assessed by elevated Beclin-1 expression, the conversion of light chain 3 (LC3)-I to LC3-II, downregulated p62 expression and green fluorescent protein (GFP)-LC3 puncta formation. The colony formation and apoptosis assays were performed to determine the effects of IRF2 and INPP4B on the growth of AML cells. RESULTS: IRF2 and INPP4B were highly expressed in AML cell lines, and were positively correlated with autophagy-related proteins. Overexpression of IRF2 or INPP4B stimulated autophagy of AML cells, whereas inhibition of IRF2 or INPP4B resulted in the attenuation of autophagy. More importantly, IRF2 or INPP4B overexpression reversed autophagy inhibitor, 3-methyladenine (3-MA)-induced proliferation-inhibitory and pro-apoptotic effects, while IRF2 or INPP4B silencing overturned the proliferation-promoting and anti-apoptotic effects of autophagy activator rapamycin. CONCLUSION: IRF2-INPP4B signaling axis attenuated apoptosis through induction of autophagy in AML cells.

IRF2-INPP4B-mediated autophagy suppresses apoptosis in acute myeloid leukemia cells

BACKGROUND: The present study aimed to investigate the underlying role of interferon-regulatory factor 2 (IRF2)-inositol polyphosphate-4-phosphatase, type-II (INPP4B) axis in the regulation of autophagy in acute myeloid leukemia (AML) cells. METHODS: Quantitative real time PCR (QRT-PCR) and western blot were performed to determine the expression levels of IRF2, INPP4B and autophagy-related markers in AML cell lines. Autophagy was assessed by elevated Beclin-1 expression, the conversion of light chain 3 (LC3)-I to LC3-II, downregulated p62 expression and green fluorescent protein (GFP)-LC3 puncta formation. The colony formation and apoptosis assays were performed to determine the effects of IRF2 and INPP4B on the growth of AML cells. RESULTS: IRF2 and INPP4B were highly expressed in AML cell lines, and were positively correlated with autophagy-related proteins. Overexpression of IRF2 or INPP4B stimulated autophagy of AML cells, whereas inhibition of IRF2 or INPP4B resulted in the attenuation of autophagy. More importantly, IRF2 or INPP4B overexpression reversed autophagy inhibitor, 3-methyladenine (3-MA)-induced proliferation-inhibitory and pro-apoptotic effects, while IRF2 or INPP4B silencing overturned the proliferation-promoting and anti-apoptotic effects of autophagy activator rapamycin. CONCLUSION: IRF2-INPP4B signaling axis attenuated apoptosis through induction of autophagy in AML cells.

Crown-to-root ratios in terms of length, surface area and volume: a pilot study of premolars / Relaciones de la corona y raíz dentaria en términos de longitud superficie y volumen: un estudio piloto de dientes premolares

The objective of this study was to construct three-dimensional (3D) images of premolars to measure the length, surface area and volume of crown and root and to analyze the mathematical relation among crown-to-root ratios in terms of length, surface area and volume. Twenty-five premolars were scanned using micro-computed tomography (micro CT) in vitro to build 3D models. The long axis and enamelo-cemental junction of each tooth were determined with the help of Geomagic Studio software, and the length, surface and volume of crown and root were measured. The crown-to-root ratios in terms of length, surface and volume were calculated and the relationship among length, surface area and volume of crown and root as well their ratios were analyzed using SPSS software. The interrelationship among crown length (x), surface area (y) and volume (z) could be expressed as z= -808.2 0+ 124.80x +3.35y -5.59x2-0.14xy+3.47y 2*10-4 (R2 = 0.99) and that of root length (x1), surface area (y1) and volume (z1), as z1= -207.50 +13.87x1+1.75y1 + 5.03x12*10-2-8.05x 1y1 *10-2+ 2.58*10-3y12 (R2 = 0.93) . The correlation among crown-to-root ratio in length(x2), crown-to-root ratio in surface area (y2) and crown-to-root ratio in volume (z2) could be expressed in z2= -4.48*10-2 -1.25x2*10-2+1.20y2 + 3.29x22-5.05x2y2 + 2.00y22 (R2 = 0.96). The length, surface area and volume of crown and root of premolars share a close relationship, while, a definite mathematical relation could be observed amongst their ratios. Crown to root ratio in terms of length, surface and volume, may provide a novel multi-criterion method for evaluating tooth function.

El objetivo de este estudio fue construir imágenes tridimensionales (3D) de los dientes premolares para medir la longitud, superficie y volumen de la corona y raíz, junto con analizar la relación matemática entre las proporciones de la corona a la raíz en términos de longitud, superficie y volumen. Veinticinco premolares fueron escaneados mediante microtomografía computadorizada (microTC) in vitro para construir modelos en 3D. Con el software Geomagic se determinaron el eje y la unión amelo-cementaria de cada diente, y se midieron la longitud, superficie y volumen de la corona y la raíz de los dientes premolares. Con el programa SPSS se calcularon y analizaron las proporciones de la corona a la raíz en términos de longitud, superficie y volumen y la relación entre la longitud, superficie y volumen de la corona y de la raíz. La interrelación entre la longitud de la corona (x), superficie (y) y el volumen (z) puede ser expresado como z= -808,2 0+ 124,80x + 3,35y -5,59x2-0,14xy + 3.47y2*10-4 (R2= 0,99) y la de longitud de la raíz (x1), área de superficie (y1) y el volumen (z1), como z1= -207,50 + 13.87x1 + 1.75y1 + 5.03x12 * 10-2-8.05x1y1 * 10-2 + 2,58 * 10-3y12 (R2= 0,93). La correlación entre la relación de corona a raíz en longitud (x2), la relación corona a raíz en superficie (y2) y la relación corona a raíz en volumen (Z2) podría expresarse en z2 = -4,48 * 10-2 * 10-2 -1.25x2 + 1.20y2 3.29x22-5.05x2y2 + 2.00y22 (R2= 0,96). La longitud, superficie y volumen de la corona y la raíz de los dientes premolares comparten una estrecha relación, mientras que, una relación matemática definida se pudo observar entre sus proporciones. La relación entre la corona y raíz en términos de longitud, superficie y volumen, puede proporcionar un nuevo método multi-criterio para evaluar la función de los dientes.

Effect of slaughter methods on the quality of Chilean jack mackerel (Trachurus murphyi) during refrigerated storage.

The main objective of this study was to assess the influence of slaughter methods on the quality of Chilean jack mackerel (Trachurus murphyi) during refrigerated storage on board. Fishes were slaughtered by asphyxia in air (AA), asphyxia in ice water (AI) or stunning fish heads (SH), and the rigor mortis, pH, total volatile basic nitrogen (TVB-N), trimethylamine (TMA), 2-thiobarbituric acid reactive substances (TBARS) and sensory properties for the fishes were analyzed. On day 0, Chilean jack mackerel samples of AI group displayed higher pH values than those of AA and SH groups. TVB-N, TMA and TBARS values of all samples increased with the storage time, and these values of AI had a lower increase than AA and SH. Moreover, samples of AI had a better sensory score than AA and SH during storage. It can be concluded that slaughter method of asphyxia in ice water for Chilean jack mackerel exhibit the better efficiency on maintaining the fish quality during refrigerated storage on board.

Acute hyperglycemia prevents dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury.

PURPOSE: To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury. METHODS: Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 µg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected. RESULTS: I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05). CONCLUSION: Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats.

Acute hyperglycemia prevents dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury

PURPOSE: To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury. METHODS: Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 μg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected. RESULTS: I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05). CONCLUSION: Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats. .

Acute hyperglycemia prevents dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury

PURPOSE:To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury.METHODS:Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 μg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected.RESULTS:I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05).CONCLUSION:Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats.(AU)

The Sirius project.

The lattice design and beam dynamics optimization for Sirius, a new low-emittance synchrotron light source presently under construction at the Brazilian Synchrotron Light Laboratory (LNLS) in Campinas, Brazil, is presented. The electron storage ring is based on a five-bend achromat (5BA) design achieving a bare lattice emittance of 0.28 nm rad for a 3 GeV beam. The circumference of 518 m contains 20 achromatic straight sections of alternating 7 m and 6 m in length. An innovative approach is adopted to enhance the performance of the storage ring dipoles by combining low-field (0.58 T) magnets for the main beam deflection with a very short 2 T permanent-magnet superbend sandwiched in the center dipole. This superbend creates 12 keV critical photon energy dipole sources with modest total energy loss from dipoles. In addition it also creates a longitudinal dipole field gradient that reduces the emittance by about 10%. The optimized dynamic aperture allows for top-up operation with off-axis injection and the optimized energy acceptance allows for a total beam lifetime of around 11 h at nominal current with a third-harmonic cavity.

Population pharmacokinetics of oral baclofen in pediatric patients with cerebral palsy.

OBJECTIVE: To characterize the population pharmacokinetics (PK) of oral baclofen and assess impact of patient-specific covariates in children with cerebral palsy (CP) in order to support its clinical use. SUBJECTS DESIGN: Children (2-17 years of age) with CP received a dose of titrated oral baclofen from 2.5 mg 3 times a day to a maximum tolerated dose of up to 20 mg 4 times a day. PK sampling followed titration of 10-12 weeks. Serial R- and S-baclofen plasma concentrations were measured for up to 16 hours in 49 subjects. Population PK modeling was performed using NONMEM 7.1 (ICON PLC; Ellicott City, Maryland). RESULTS: R- and S-baclofen showed identical concentration-time profiles. Both baclofen enantiomers exhibited linear and dose/kg-proportional PK, and no sex differences were observed. Average baclofen terminal half-life was 4.5 hours. A 2-compartment PK model with linear elimination and transit absorption steps adequately described concentration-time profiles of both baclofen enantiomers. The mean population estimate of apparent clearance/F was 0.273 L/h/kg with 33.4% inter-individual variability (IIV), and the apparent volume of distribution (Vss/F) was 1.16 L/kg with 43.9% IIV. Delayed absorption was expressed by a mean transit time of 0.389 hours with 83.7% IIV. Body weight, a possible genetic factor, and age were determinants of apparent clearance in these children. CONCLUSION: The PK of oral baclofen exhibited dose-proportionality and were adequately described by a 2-compartment model. Our population PK findings suggest that baclofen dosage can be based on body weight (2 mg/kg per day) and the current baclofen dose escalation strategy is appropriate in the treatment of children with CP older than 2 years of age.

The increased but non-predominant expression of Th17- and Th1-specific cytokines in Hashimoto’s thyroiditis but not in Graves’ disease

Hashimoto’s thyroiditis (HT) is considered to be mediated mainly by Th1 cells, but it is not known whether Graves’ disease (GD) is associated with Th1 or Th2 predominance. Th17 cells, a novel subset of Th cells, play a crucial role in the pathogenesis of various autoimmune disorders. In the present study, the expression of IL-17A and IFN-γ was investigated in patients with HT or GD. mRNA expression of IL-17A and IFN-γ in peripheral blood mononuclear cells (PBMC) from 43 patients with autoimmune thyroid disease (AITD) and in thyroid tissues from 40 AITD patients were measured by real-time qRT-PCR. The protein expression of IL-17A and IL-23p19 was examined by immunohistochemistry in thyroid tissues from 28 AITD patients. The mRNA levels of IL-17A and IFN-γ were higher in both PBMC and thyroid tissues of HT patients than in controls (mRNA levels are reported as the cytokine/β-actin ratio: IL-17 = 13.58- and 2.88-fold change and IFN-γ = 16.54- and 2.74-fold change, respectively, P < 0.05). Also, the mRNA levels of IL-17A and IFN-γ did not differ significantly in GD patients (P > 0.05). The high protein expression of IL-17A (IOD = 15.17 ± 4.8) and IL-23p19 (IOD = 16.84 ± 7.87) in HT was confirmed by immunohistochemistry (P < 0.05). The similar high levels of IL-17A and IFN-γ suggest a mixed response of Th17 and Th1 in HT, where both cells may play important roles in the destruction procedure by cell-mediated cytotoxicity.

The increased but non-predominant expression of Th17- and Th1-specific cytokines in Hashimoto's thyroiditis but not in Graves' disease.

Hashimoto's thyroiditis (HT) is considered to be mediated mainly by Th1 cells, but it is not known whether Graves' disease (GD) is associated with Th1 or Th2 predominance. Th17 cells, a novel subset of Th cells, play a crucial role in the pathogenesis of various autoimmune disorders. In the present study, the expression of IL-17A and IFN-γ was investigated in patients with HT or GD. mRNA expression of IL-17A and IFN-γ in peripheral blood mononuclear cells (PBMC) from 43 patients with autoimmune thyroid disease (AITD) and in thyroid tissues from 40 AITD patients were measured by real-time qRT-PCR. The protein expression of IL-17A and IL-23p19 was examined by immunohistochemistry in thyroid tissues from 28 AITD patients. The mRNA levels of IL-17A and IFN-γ were higher in both PBMC and thyroid tissues of HT patients than in controls (mRNA levels are reported as the cytokine/ß-actin ratio: IL-17 = 13.58- and 2.88-fold change and IFN-γ = 16.54- and 2.74-fold change, respectively, P < 0.05). Also, the mRNA levels of IL-17A and IFN-γ did not differ significantly in GD patients (P > 0.05). The high protein expression of IL-17A (IOD = 15.17 ± 4.8) and IL-23p19 (IOD = 16.84 ± 7.87) in HT was confirmed by immunohistochemistry (P < 0.05). The similar high levels of IL-17A and IFN-γ suggest a mixed response of Th17 and Th1 in HT, where both cells may play important roles in the destruction procedure by cell-mediated cytotoxicity.

Sangrado postmenopaúsico: alternativa de Abordaje / Postmenopausal bleeding: alternative of approach

Reporte de una paciente de 56 años, quien toma tratamiento hormonal sustitutivo y presentó sangrado postmenopáusico. En ultrasonido transvaginal se documentó endometrio de 23mm de grosor. Se realizó legrado uterino instrumental, donde se reporta biopsia con endometrio atrófico; debido a la discordancia encontrada entre el grosor del endometrio por ultrasonido y la biopsia, se hizo histerosonografía demostrando pólipo endometrial, por lo cual se le realizó histeroscopía terapéutica. Se hace una revisión acerca de los métodos visuales existentes para valorar patologías de cavidad uterina. Y sugerimos realizar histerosonografía a pacientes con sangrado postmenopáusico con endometrio mayor de 5 mm.