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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.(AU)
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.(AU)
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Animais , Coelhos , Glândulas Paratireoides/anatomia & histologia , Glândulas Paratireoides/irrigação sanguíneaRESUMO
The retracted article is: Ji Y, Jin HH, Wang MD, Cao WX, et al. (2016). Methylation of the RASSFIA promoter in breast cancer. Genet. Mol. Res. 15: gmr.15028261. There are significant parts of this article (particularly, in the discussion section) that are copied from "Methylation of HIN-1, RASSF1A, RIL and CDH13 in breast cancer is associated with clinical characteristics, but only RASSF1A methylation is associated with outcome", by Jia Xu, Priya B Shetty, Weiwei Feng, Carol Chenault, Robert C Bast Jr, Jean-Pierre J Issa, Susan G Hilsenbeck and Yinhua Yu, published in BMC Cancer 2012; 12: 243. DOI: 10.1186/1471-2407-12-243. The first paragraphs of both discussions are identical. This is concerning. The abstract and introduction sections have much of their text plagiarized. Overall, there is high plagiarism detected. The GMR editorial staff was alerted and after a thorough investigation, we have strong reason to believe that the peer review process was failure and, after review and contacting the authors, the editors of Genetics and Molecular Research decided to retract the article in accordance with the recommendations of the Committee on Publication Ethics (COPE). The authors and their institutions were advised of this serious breach of ethics.
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Tumor suppressor genes are the key targets of hypermethylation in breast cancer and may therefore lead to malignancy by deregulation of cell growth and division. Our previous pilot study with pairs of malignant and normal breast tissues identified a correlation between RASSFIA gene methylation and breast cancer. To determine the relationship between RASSFIA methylation and breast cancer, we conducted a larger study. We took samples from 108 patients with breast cancer, 28 patients with benign breast tumors, and 33 subjects with normal breast tissues at the Second Affiliated Hospital of Nanjing Medical University at Wuxi between July 2013 and September 2015. We used the samples to investigate methylation levels of the RASSF1A gene for associations with breast cancer. Quantitative real-time polymerase chain reaction (PCR) and methylation-specific PCR were used to investigate the levels of RASSF1A mRNA expression and RASSF1A methylation, respectively. RASSFIA was not expressed in 22 of the 108 breast cancer tissue samples (20.37%), and there was no statistically significant difference (P > 0.05); however, RASSFIA expression was significantly lower than that in the normal breast tissue samples (P < 0.05). Moreover, the methylation rate of the RASSFIA gene promoter was significantly higher in the breast cancer tissues (64.81%) than in the normal breast tissues (18.18%) and benign breast tumors (17.86%) (P < 0.05). High methylation of the RASSF1A gene promoter was an important reason for its downregulation, and the gene played a critical regulated role in the incidence and development of breast cancer.
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Sex hormones play important roles in breast cancer (BC) development. This study investigated associations between BC risk and hormone-related gene variants in Chinese women. In a cohort of 336 patients with histopathologically confirmed BC and 390 age-matched controls, we genotyped seven single nucleotide polymorphisms (SNPs) in five hormone-related genes: estrogen receptor-α (ESR1), aromatase (CYP19), catechol-O-methyl transferase (COMT), sex hormone-binding globulin (SHBG), and glutathione S-transferase (GSTP1). Among these seven SNPs, the SNPs in GSTP1 rs1695 [A/G; odds ratio (OR): 1.68; 95% confidence interval (CI): 1.23-2.30] and ESR1 rs2046210 (C/T; OR: 1.39; 95%CI = 1.02-1.91) were associated with an increased risk among heterozygote carriers. Homozygotes of minor alleles of CYP19 rs10046 (CC) were associated with a reduced risk of BC with OR: 0.61 (95%CI = 0.39-0.95). In addition, a stratified analysis by menopausal status indicated that the association of the CYP19 polymorphisms (rs10046 and rs700519) with BC risk was mainly evident in premenopausal women, and the association of CYP19 rs700519 with BC risk was significant in women less than 50 years old. Haplotype analysis identified 15 common haplotypes (>1%). The haplotype TGGGGTC was significantly associated with BC risk compared with the reference haplotype CGAGGTC (OR > 1000, P < 0.0001). Our data demonstrate that these ESR1, GSTP1, and CYP19 polymorphisms are associated with risk of BC, and the risk haplotype TGGGGTC could help to identify populations with high susceptibility to BC in Chinese women.
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Aromatase/genética , Neoplasias da Mama/genética , Catecol O-Metiltransferase/genética , Receptor alfa de Estrogênio/genética , Glutationa S-Transferase pi/genética , Globulina de Ligação a Hormônio Sexual/genética , Idoso , Alelos , Povo Asiático/genética , Estudos de Casos e Controles , China , Feminino , Predisposição Genética para Doença , Variação Genética , Haplótipos , Humanos , Pessoa de Meia-Idade , Polimorfismo Genético , Polimorfismo de Nucleotídeo ÚnicoRESUMO
The function of SIRT1 in the proliferation and osteoblastic differentiation of dental stem cells is unclear. The aim of this study was to assess the roles of SIRT1 in these processes using periodontal ligament stem cells (PDLSCs) and stem cells from apical papilla (SCAPs). A defined concentration of resveratrol, an SIRT1 activator, or nicotinamide, an SIRT1 inhibitor, was administered to PDLSCs, SCAPs, and a mixed group of the two cell lines, and their effects on these processes analyzed. Cell proliferation was tested using microtitration with a tetrazolium dye (MTT). Alkaline phosphatase (ALP) activity, mineralization ability, and the expression of osteoblastic differentiation-associated genes were assessed as well. These studies demonstrated that resveratrol could promote cell proliferation of all three groups in a gradually increasing trend over time. In contrast, nicotinamide suppressed the proliferation of the three cell lines. The results also showed that the markers of osteoblastic differentiation: ALP activity, mineralization ability, and the expression levels of the osteoblastic genes ALP, osteopontin, osteocalcin, and bone sialoprotein, were enhanced in the groups with resveratrol treatment. In contrast, following addition of nicotinamide, ALP activity, mineralization ability, and the expression levels of the osteoblastic genes were down-regulated in the cells. Together, these results suggest that the SIRT1 activator and inhibitor compounds, resveratrol and nicotinamide, function at high efficiency in adjusting cell proliferation, and that SIRT1 is a powerful regulator of osteoblastic differentiation of PDLSCs and SCAPs. In addition, co-culture of the two cell lines could promote their abilities of proliferation and osteogenic differentiation.
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Diferenciação Celular/genética , Ligamento Periodontal/citologia , Sirtuína 1/metabolismo , Células-Tronco/citologia , Células-Tronco/metabolismo , Linhagem Celular , Proliferação de Células/genética , Humanos , Sirtuína 1/genéticaRESUMO
We investigated the killing effect of low-intensity ultrasound combined with 5-aminolevulinic acid (5-ALA) on the rat osteosarcoma cell line UMR-106. Logarithmic-phase UMR-106 cells were divided into a control group, ultrasound group and 5-ALA group. The cell apoptotic rate, production of reactive oxygen species, and the change in mitochondrial membrane potential were analyzed by flow cytometry; ultrastructural changes were observed by transmission electron microscopy. Using low-intensity ultrasound at 1.0 MHz and 2.0 W/cm(2) plus 5-ALA at a concentration of 2 mM, the apoptotic rate of the sonodynamic therapy group was 27.2 ± 3.4% which was significantly higher than that of the control group, ultrasound group, and 5-ALA group (P < 0.05). The production of reactive oxygen species was 32.6 ± 2.2% and the decrease in mitochondrial membrane potential was 39.5 ± 2.5%. The 33342 staining showed nuclear condensation and fragmentation in the ultrasound group and 5-ALA group. Structural changes in the cell membrane, mitochondria, Golgi apparatus, and other organelles observed by transmission electron microscopy included formation of apoptotic bodies. The killing effect of low-intensity ultrasound combined with 5-ALA on UMR-106 cells was significant. Cell apoptosis played a vital role in the killing effect, and the mitochondria pathway contributed to the apoptosis of UMR-106 cells.
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Ácido Aminolevulínico/farmacologia , Apoptose/efeitos dos fármacos , Apoptose/efeitos da radiação , Ondas Ultrassônicas/efeitos adversos , Linhagem Celular Tumoral , Citometria de Fluxo , Humanos , Osteossarcoma/metabolismo , Osteossarcoma/terapia , Espécies Reativas de Oxigênio/metabolismo , Terapia por UltrassomRESUMO
Germline mutations in identified breast cancer susceptibility genes account for less than 20% of Chinese familial breast cancers. Dicer is an essential component of the microRNA-producing machinery; germline mutations of DICER1 have been confirmed in familial pleuropulmonary blastoma, ovarian sex cord-stromal tumors, and other cancers. Low expression of DICER1 is frequently detected in breast cancer. However, whether germline mutations of DICER1 occur in familial breast cancers remain unknown. Sixty-five breast cancer probands from BRCA1/BRCA2-negative Chinese breast cancer families were screened for germline mutations in DICER1. In addition, 100 unrelated healthy females were enrolled as controls. A polymerase chain reaction sequencing assay was used to screen for mutations in coding regions and at the exon-intron boundaries of DICER1. All variants in introns were evaluated using the NNSplice software to determine the potential splicing effect. A total of 12 germline variants were found, including 11 variants in introns and 1 variant in the 3'-non-coding region. Four variants (IVS8-205 C>T, IVS11+131 delGAAA, IVS16+42 delTA, and IVS19+160 T>C) were novel. Three variants (IVS11+105 C>T, IVS16+42 delTA, and 6095 T>A) may affect splice sites. None of the observed variants appeared to be disease-related, suggesting that germline mutations in DICER1 are rare or absent in familial breast cancer patients.
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RNA Helicases DEAD-box/genética , Mutação em Linhagem Germinativa , Neoplasias Ovarianas/genética , Blastoma Pulmonar/genética , Ribonuclease III/genética , Tumores do Estroma Gonadal e dos Cordões Sexuais/genética , Adulto , Idoso , Proteína BRCA1/metabolismo , Proteína BRCA2/metabolismo , Neoplasias da Mama/genética , Neoplasias da Mama/metabolismo , China , Simulação por Computador , RNA Helicases DEAD-box/metabolismo , Feminino , Humanos , Pessoa de Meia-Idade , Neoplasias Ovarianas/metabolismo , Isoformas de Proteínas/metabolismo , Blastoma Pulmonar/metabolismo , Ribonuclease III/metabolismo , Tumores do Estroma Gonadal e dos Cordões Sexuais/metabolismo , Adulto JovemRESUMO
We aimed to summarize the results of screening protocol and prevention of neonatal glucose 6-phosphate dehydrogenase (G6PD) deficiency during a 22-year-long period to provide a basis of reference for the screening of this disease. About 1,705,569 newborn subjects in Guangzhou City were screened for this deficiency. Specimens were collected according to the conventional method of specimen acquisition for "newborn dried bloodspot screening", preserved, and inspected. The specimens were studied with fluorescent spot test and quantitative fluorescence assay. Diagnosis was performed using the modified NBTG6PD/6PGD ratio method. Bloodspot filter paper specimens were sent to the laboratory within 24 h via EMS Express, and the G6PD test was performed on the same day. The G6PD deficiency-positive rate was 4.2% in the samples screened using the fluorescent spot test, while it was 5% in case of the quantitative fluorescence assay. Neonatal screening for G6PD deficiency for 11,437 cases (6117 boys and 5320 girls) showed positive results in 481 cases. About 420 cases (318 boys and 102 girls) of G6PD deficiency were confirmed with the modified Duchenne NBT ratio method. The total detection rate was 3.7:5.2% for boys and 1.9% for girls. Quantitative fluorescence assay improved the sensitivity and detection rate. Accelerating the speed of sample delivery by using Internet network systems and ensuring online availability of screening results can aid the screening and diagnosis of this deficiency within 1 week of birth.
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Deficiência de Glucosefosfato Desidrogenase/diagnóstico , Deficiência de Glucosefosfato Desidrogenase/prevenção & controle , Triagem Neonatal/métodos , Povo Asiático/genética , China , Feminino , Fluorescência , Glucosefosfato Desidrogenase/genética , Deficiência de Glucosefosfato Desidrogenase/epidemiologia , Testes Hematológicos , Humanos , Recém-Nascido , Internet , MasculinoRESUMO
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.
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Animais , Humanos , Apoptose/efeitos dos fármacos , Inibidores de Cisteína Proteinase/farmacologia , Proteínas Inibidoras de Apoptose/efeitos dos fármacos , Neoplasias Pulmonares/secundário , Neuroblastoma/patologia , RNA Interferente Pequeno/farmacologia , Antineoplásicos/farmacologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Regulação para Baixo/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Proteínas Inibidoras de Apoptose/genética , Proteínas Inibidoras de Apoptose/metabolismo , Camundongos Nus , Invasividade Neoplásica , Neuroblastoma/secundário , Reação em Cadeia da Polimerase Via Transcriptase Reversa , RNA Neoplásico/efeitos dos fármacos , RNA Neoplásico/metabolismo , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
The secondary lymphoid tissue chemokine (CCL21) is closely associated with lymphoid homing and anti-tumor immune responses. CCL21 also has a chemotactic effect on intestinal lymphocytes. This study mainly focused on CCL21 expression in experimental ulcerative colitis and on the effects of CCL21 suppression on this disease in mice. The mouse colitis model was induced by dextran sulfate sodium (DSS) in 40 female BALB/c mice that were equally distributed into five groups: control, DSS, propylene glycol, triptolide (TL), and dexamethasone treatment groups. The disease activity index, general morphology score of the colon, and histological pathology score of colon tissues were evaluated. CCL21 expression was examined in colons of mice by immunohistochemistry, reverse transcription-polymerase chain reaction, and Western blotting analysis. CCL21 was upregulated in the mouse model of ulcerative colitis (control group vs DSS group/propylene glycol group, P<0.01). The TL and dexamethasone treatments improved colitis symptoms and decreased CCL21 expression (TL group/dexamethasone group vs DSS group/propylene glycol group, P<0.05). In conclusion, CCL21 was shown to be involved in the induction of ulcerative colitis. Suppression of CCL21 expression decreased damage induced from ulcerative colitis, indicating that CCL21 targeted therapy might be an effective treatment for this disease.