RESUMO A função e proteção das glândulas paratireoidianas é um tópico de pesquisa cada vez mais popular. Coelhos brancos da Nova Zelândia são o modelo animal mais comumente usada para isquemia da paratireóide. Porém, informação sobre a vasculatura de suas glândulas paratireóides é limitada. Foram usados 94 coelhos brancos da Nova Zelândia saudáveis, com 3-4 meses de idade, 2-3kg de peso, para exploração das glândulas paratireóides, que foram coradas com hematoxilina e eosina (HE) após a remoção. Os seguintes tipos foram classificados de acordo com a relação entre a posição da glândula paratireoidiana inferior e a tireoide: Tipo A, Tipo Próximo, Tipo B e Tipo Distante. Houve 188 casos, 4 em que as glândulas paratireoidianas inferiores estavam localizadas próximas ao lado dorsal da tireoide (2.13%), 8 onde as glândulas paratireoidianas inferiores estavam localizadas superiores ao polo superior da tireoide (4.26%), 20 onde as glândulas paratireoidianas inferiores estavam localizadas paralelo à tireoide (10.64%) e 155 casos em que as glândulas paratireoidianas inferiores estavam localizadas inferiores ao polo inferior da tireoide (82.45%). A identificação da localização e a classificação da vasculatura das glândulas paratireóides em coelhos brancos da Nova Zelândia fornecerão um modelo anatômico para auxiliar em pesquisas futuras.

ABSTRACT The function and protection of the parathyroid glands are increasingly popular research topics. New Zealand white rabbits are the most commonly used animal model of parathyroid ischemia. However, information on the vasculature of their parathyroid glands is limited. We used 94 healthy New Zealand white rabbits, 3-4 months of age and 2-3kg in weight, for exploration of the parathyroid glands, which were stained using hematoxylin and eosin (HE) after removal. The following types were classified according to the relationship between the position of the inferior parathyroid gland and the thyroid: Type A, Close Type, Type B, and Distant Type. There were 188 cases, 4 where the inferior parathyroid glands were located near the dorsal side of thyroid (2.13%), 8 where the inferior parathyroid glands were located superior to the upper pole of the thyroid (4.26%), 20 where the inferior parathyroid glands were located parallel to the thyroid (10.64%), and 155 cases where the inferior parathyroid glands were located inferior to the lower pole of thyroid (82.45%). Identifying the location and classifying the vasculature of the parathyroid glands in New Zealand white rabbits will provide an anatomical model to assist in future research.

Alkaline sulphide leaching was adopted to extract tellurium from tellurium-bearing gold concentrate for the first time. The tellurium leaching kinetics were studied. The influence of average particle size, stirring speed, leaching temperature, Na2S concentration, and NaOH concentration on the tellurium extraction were investigated. It was found that tellurium extraction could reach 79.14% under the optimum conditions: 17.77 μηι average particle size, 500 r/min stirring speed, 80 g/L Na2S concentration, 30g/L NaOH concentration, 80°C leaching temperature, 4:1 liquid to solid ratio, and 180 minutes leaching time. The interface transfer and diffusion through the product layer or insoluble substance layer were the rate-controlling steps. The leaching kinetics equation was established, and the activation energy was 34.384 kJ/mol.

The modes of occurrence of arsenic and the effects of low-intensity leaching-flotation on arsenic removal from coal slime from the Tanggongta Plant, Inner Mongolia, China were investigated. The coal slime was examined using hydride generation inductively coupled plasma optical emission spectrometry and X-ray diffraction to obtain the content of elements and the major minerals. The modes of occurrence of arsenic in minerals were determined using selective leaching, float-and-sink analysis, and polarized light microscopy. The results indicate that pyrite is the dominant carrier of arsenic in the coal slime, which predominantly exists in association with clay. Significant proportion of the arsenic is removed by a low-intensity leaching-flotation process, consistent with the data from selective leaching and flotation of gangue. The results show that low intensity leaching-alkali washing-flotation is more efficient than direct flotation and low-intensity leaching-flotation.

Colorectal cancer (CRC) is the fourth leading cause of cancer-induced mortality. Histone deacetylase 2 (HDAC2) is involved in prognosis and therapy of CRC. This study aimed to explore novel therapeutic targets for CRC. The alteration of HDAC2 expression in CRC tissues was estimated by qRT-PCR. After lentivirus transfection, HDAC2 knockdown was confirmed by western blot analysis. The effect of HDAC2 knockdown on cell proliferation was then assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Screened by TargetScan, microRNA (miR)-455 was predicted to bind to 3′UTR of HDAC2 and the prediction was verified by luciferase assay. Finally, cells were transfected, respectively, with miR-455 mimics or miR-455 negative control (miR-NC) and the expression of HDAC2, cell proliferation and apoptosis of transfected cells were respectively evaluated by western blot analysis, MTT assay and flow cytometry. Results showed that the HDAC2 expression was up-regulated in CRC tissues (P<0.05). HDAC2 knockdown significantly decreased cell viability at day 3 (P<0.05), day 4 (P<0.01), and day 5 (P<0.001) after infection. Then, miR-455 was verified to directly target HDAC2, resulting in a significant difference in luciferase activity (P<0.01). Moreover, miR-455 decreased the expression of HDAC2 (P<0.01). miR-455 remarkably decreased cell viability at day 3 (P<0.05), day 4 (P<0.01), and day 5 (P<0.001) after transfection while inducing cell apoptosis (P<0.001). In conclusion, miR-455 inhibited cell proliferation while inducing cell apoptosis by targeting HDAC2 in CRC cells.

Background and objectives: Left ventricular hypertrophy secondary to hypertension has been perceived as a protective mechanism to reduce wall stress and prevent heart failure. However, its presence is paradoxically associated with increased cardiovascular morbidity and mortality The aim of this study was to evaluate whether chronic antihypertensive treatment inhibits the development of left ventricular hypertrophy and normalize the reverting impaired cardiac beta-adrenergic response, and its possible association with changes in myocardial oxidative metabolism. Methods: Spontaneously hypertensive male rats (SHR, 2 months old) were divided into groups (n grupo = 18) according to (mg/ group kg, p.o): losartan 30 (L), hydralazine-11 (H), rosuvastatin 10 (R), carvedilol 20 (C), and water (control treatment). The control hypertension group consisted of 18 normotensive rats (Wistar-Kyoto, WKY). Systolic blood pressure (SBP) (plethysmography in awake animals) and body weight (BW) were measured periodically. The animals were sacrificed at 16 months and 50% of the hearts were mounted in a Langendorff system to measure contractility before and after beta-adrenergic stimulation [isoproterenol (Iso): 10-9 M, 10-7 M, and 10-5 M]. In the remaining hearts left ventricular weight (LVW) was measured and normalized by B W. Immunohistochemical expression of thioredoxin 1 (Trx-1), peroxyredoxin 2 (Prx-2) and glutaredoxin 3 (Grx-3) (antioxidant indicators) was quantified. Results: Body weight was similar in all groups. Systolic blood pressure (mm Hg) was 154 ± 3 (L), 137 ± 1 (H), 190 ± 3 (R)**, 206 ± 3 (SHR)*, 183 ± 1 (C)**, and 141 ± 1 (WKY) (* p < 0.05 vs. L, H, WKY, ** p < 0.05 vs. L, H, WKY, SHR). LVW/BW was higher in SHR and R (p < 0.05) compared with L, H, C and WKY. In C, there was no correlation between hypertension and left ventricular hypertrophy. SHR, R and C evidenced baseline contractile depression vs. L, H and WKY. The response to 10-5 M Iso was similar in WKY and L, and reduced in C, H, R and SHR. The expression of Trx-1, Prx-2 and Grx-3 increased in C, H, R and L (average increase: 1.5-2 times; p < 0.01 vs. SHR and WKY). Conclusions: Treatment with losartan, hydralazine, and carvedilol prevented the development of left ventricular hypertrophy. Losartan normalized the response to isoproterenol in SHR. Additional factors might participate in the development of left ventricular hypertrophy with impaired inotropic response to beta-adrenergic stimulation in hypertension. The increased ex-pression of thioredoxins as a result of antihypertensive treatment suggests an additional benefit, increasing the antioxidant response against oxidative stress in hypertension.

Introducción y objetivos: La hipertrofia ventricular izquierda secundaria a hipertensión arterial se ha interpretado como un mecanismo de protección para reducir el estrés parietal y prevenir la insuficiencia cardíaca. Sin embargo, paradójicamente, su presencia se acompaña de un incremento de la morbimortalidad cardiovascular. El presente estudio se llevó a cabo con el propósito de evaluar si el tratamiento antihipertensivo crónico inhibe el desarrollo de hipertrofia ventricular izquierda y revierte el deterioro de la respuesta betaadrenérgica cardíaca y su posible relación con cambios en el metabolismo oxidativo del miocardio. Material y métodos: Ratas macho espontáneamente hipertensas (REH, 2 meses de edad) se distribuyeron en grupos (n grupo = 18) grupo según (mg/kg, v.o.): losartán 30 (L), hidralazina 11 (H), rosuvastatina 10 (R), carvedilol 20 (C), agua (control tratamiento). Control hipertensión: 18 ratas normotensas (Wistar-Kyoto, WKY). Periódicamente se registraron la presión arterial sistólica (PAS) (pletismografía, en animales despiertos) y el peso corporal (PC). Luego de 16 meses se practicó eutanasia. El 50% de los corazones se montaron en preparación de Langendorff para medir contractilidad preestímulo y posestímulo betaadrenérgico [isoproterenol (Iso): 10-9M, 10-7M, 10-5M]. En los corazones restantes se registró el peso del ventrículo izquierdo (PVI), que se normalizó por el PC. Se cuantificó la expresión inmunohistoquímica de tiorredoxina 1(Trx-1), peroxirredoxina 2 (Prx-2) y glutarredoxina 3 (Grx-3) (indicadores antioxidantes). Resultados: Peso corporal: similar en todos los grupos. PAS (mm Hg): 154 ± 3 (L), 137 ± 1 (H), 190 ± 3 (R)**, 206 ± 3 (REH)*, 183 ± 1 (C)**, 141 ± 1 (WKY) (*p < 0,05 vs. L, H, WKY; **p < 0,05 vs. L, H, WKY, REH). El PVI/PC de REH y R fue mayor (p < 0,05) respecto de L, H, C y WKY. En C no se observó correlación entre hipertensión e hipertrofia ventricular izquierda. Grupos REH, R y C: mostraron depresión de contractilidad basal vs. L, H y WKY. Respuesta a Iso 10-5 M: similar en WKY y L; disminuida en C, H, R y REH. Expresión de Trx-1, Prx-2 y Grx-3: aumentó en C, H, R y L (1,5-2 veces promedio; p < 0,01 vs. REH y WKY). Conclusiones: El tratamiento con losartán, hidralazina y carvedilol previno el desarrollo de hipertrofia ventricular izquierda. El losartán normalizó la respuesta al isoproterenol en REH. Factores adicionales participarían en el desarrollo de hipertrofia ventricular izquierda con deterioro de la respuesta inotrópica a la estimulación betaadrenérgica en hipertensión. El aumento en la expresión de tiorredoxinas por tratamientos antihipertensivos sugiere un beneficio asociado, aumentando la respuesta antioxidante frente al estrés oxidativo en hipertensión.

Neuroblastoma is a solid tumor that occurs mainly in children. Malignant neuroblastomas have a poor prognosis because conventional chemotherapeutic agents are not very effective. Survivin, a member of the inhibitor of the apoptosis protein family, plays a significant role in cell division, inhibition of apoptosis, and promotion of cell proliferation and invasion. Previous studies found that survivin is highly expressed in some malignant neuroblastomas and is correlated with poor prognosis. The aim of this study was to investigate whether survivin could serve as a potential therapeutic target of human neuroblastoma. We employed RNA interference to reduce survivin expression in the human neuroblastoma SH-SY5Y cell line and analyzed the effect of RNA interference on cell proliferation and invasion in vitro and in vivo. RNA interference of survivin led to a significant decrease in invasiveness and proliferation and increased apoptosis in SH-SY5Y cells in vitro. RNA interference of survivin inhibited tumor growth in vivo by 68±13% (P=0.002) and increased the number of apoptotic cells by 9.8±1.2% (P=0.001) compared with negative small interfering RNA (siRNA) treatment controls. Moreover, RNA interference of survivin inhibited the formation of lung metastases by 92% (P=0.002) and reduced microvascular density by 60% (P=0.0003). Survivin siRNA resulted in significant downregulation of survivin mRNA and protein expression both in vitro and in vivo compared with negative siRNA treatment controls. RNA interference of survivin was found to be a potent inhibitor of SH-SY5Y tumor growth and metastasis formation. These results support further clinical development of RNA interference of survivin as a treatment of neuroblastoma and other cancer types.

In longitudinal multi-mode pushover analysis of bridges with elevated pile foundation systems, the inelastic contributions of the second mode cannot be neglected. Generalized pushover analysis cannot be applied directly in this condition. A modified generalized pushover procedure is developed for estimating seismic demands of bridges with elevated pile foundation systems. Modified generalized pushover procedure, modal pushover analysis and incremental dynamic analysis of a bridge with elevated pile foundation systems are conducted. The results show that the modified generalized pushover procedure can provide reasonable estimations of moments and predict more accurate plastic hinge rotations compared with modal pushover analysis.