RESUMO
The deepest recorded depth for trematodes currently stands at approximately 6200 m. This depth record was achieved solely through sequence datasets of Lepidapedon sp. obtained from a gastropod. Given that trematodes of this genus typically use fish as definitive hosts, the origin of the trematode sequence was thought to be larval stages. However, the specific species remained unclear owing to the absence of reported adult-stage sequences. In the present study, we definitively identified the deepest trematode as Lepidapedon oregonense by comparing 28S ribosomal DNA sequences from adult worms from the macrourid fish Coelorinchus gilberti with data from the gastropod in the previous study.
Assuntos
DNA de Helmintos , DNA Ribossômico , Filogenia , RNA Ribossômico 28S , Trematódeos , Animais , Trematódeos/classificação , Trematódeos/genética , Trematódeos/isolamento & purificação , RNA Ribossômico 28S/genética , DNA de Helmintos/genética , DNA Ribossômico/genética , Gastrópodes/parasitologia , Análise de Sequência de DNA , Peixes/parasitologia , Doenças dos Peixes/parasitologia , Infecções por Trematódeos/parasitologia , Infecções por Trematódeos/veterináriaRESUMO
We report on NMR and torque measurements on the frustrated quasi-two-dimensional spin-dimer system SrCu(2)(BO(3))(2) in magnetic fields up to 34 T that reveal a sequence of magnetization plateaus at 1/8, 2/15, 1/6, and 1/4 of the saturation and two incommensurate phases below and above the 1/6 plateau. The magnetic structures determined by NMR involve a stripe order of triplets in all plateaus, suggesting that the incommensurate phases originate from proliferation of domain walls. We propose that the magnetization process of SrCu(2)(BO(3))(2) is best described as an incomplete devil's staircase.
RESUMO
OBJECTIVES: Diabetes mellitus (DM) is known to impair fracture healing. Increasing evidence suggests that some microRNA (miRNA) is involved in the pathophysiology of diabetes and its complications. We hypothesized that the functions of miRNA and changes to their patterns of expression may be implicated in the pathogenesis of impaired fracture healing in DM. METHODS: Closed transverse fractures were created in the femurs of 116 rats, with half assigned to the DM group and half assigned to the control group. Rats with DM were induced by a single intraperitoneal injection of streptozotocin. At post-fracture days five, seven, 11, 14, 21, and 28, miRNA was extracted from the newly generated tissue at the fracture site. Microarray analysis was performed with miRNA samples from each group on post-fracture days five and 11. For further analysis, real-time polymerase chain reaction (PCR) analysis was performed at each timepoint. RESULTS: Microarray analysis showed that there were 14 miRNAs at day five and 17 miRNAs at day 11, with a greater than twofold change in the DM group compared with the control group. Among these types of miRNA, five were selected based on a comparative and extended literature review. Real-time PCR analysis revealed that five types of miRNA (miR-140-3p, miR-140-5p, miR-181a-1-3p, miR-210-3p, and miR-222-3p) were differentially expressed with changing patterns of expression during fracture healing in diabetic rats compared with controls. CONCLUSIONS: Our findings provide information to further understand the pathology of impaired fracture healing in a diabetic rat model. These results may allow the potential development of molecular therapy using miRNA for the treatment of impaired fracture healing in patients with DM.Cite this article: S. Takahara, S. Y. Lee, T. Iwakura, K. Oe, T. Fukui, E. Okumachi, T. Waki, M. Arakura, Y. Sakai, K. Nishida, R. Kuroda, T. Niikura. Altered expression of microRNA during fracture healing in diabetic rats. Bone Joint Res 2018;7:139-147. DOI: 10.1302/2046-3758.72.BJR-2017-0082.R1.
RESUMO
MicroRNAs (miRNAs ) are small non-coding RNAs that regulate gene expression. We hypothesised that the functions of certain miRNAs and changes to their patterns of expression may be crucial in the pathogenesis of nonunion. Healing fractures and atrophic nonunions produced by periosteal cauterisation were created in the femora of 94 rats, with 1:1 group allocation. At post-fracture days three, seven, ten, 14, 21 and 28, miRNAs were extracted from the newly generated tissue at the fracture site. Microarray and real-time polymerase chain reaction (PCR) analyses of day 14 samples revealed that five miRNAs, miR-31a-3p, miR-31a-5p, miR-146a-5p, miR-146b-5p and miR-223-3p, were highly upregulated in nonunion. Real-time PCR analysis further revealed that, in nonunion, the expression levels of all five of these miRNAs peaked on day 14 and declined thereafter. Our results suggest that miR-31a-3p, miR-31a-5p, miR-146a-5p, miR-146b-5p and miR-223-3p may play an important role in the development of nonunion. These findings add to the understanding of the molecular mechanism for nonunion formation and may lead to the development of novel therapeutic strategies for its treatment.
Assuntos
Fraturas do Fêmur/metabolismo , Fraturas não Consolidadas/metabolismo , MicroRNAs/metabolismo , Animais , Modelos Animais de Doenças , Masculino , Análise em Microsséries , Ratos , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase em Tempo RealRESUMO
A 16-year-old Japanese girl had desquamating erythematosquamous lesions mostly on the extensor surface of the extremities. The lesions were worse in summer. The patient also had a mild muscle pain after strenuous exercise. Her paternal and maternal grandfathers are cousins. An analysis of lactic acid dehydrogenase (LDH) isozymes in her serum revealed a single peak of LDH1. Analysis of LDH isozymes of erythrocytes demonstrated a complete lack of LDH M-subunit in the patient and a substantial lack in the parents. The epidermis of the diseased skin and scalp hair follicles of the patient were virtually devoid of LDH activity.
Assuntos
Cabelo/enzimologia , L-Lactato Desidrogenase/deficiência , Pele/enzimologia , Adolescente , Eritrócitos/enzimologia , Feminino , Cabelo/patologia , Humanos , Isoenzimas , L-Lactato Desidrogenase/sangue , L-Lactato Desidrogenase/genética , L-Lactato Desidrogenase/metabolismo , Pele/patologia , Dermatopatias/enzimologia , Dermatopatias/patologiaRESUMO
Melanoma antigen (MAGE)-encoding genes are expressed in various tumour types via demethylation of their promoter CpG islands, which are silent in all non-neoplastic tissues except for the testis and placenta. The clinicopathological significance of demethylation of MAGE genes in gastric carcinoma is not known. We investigated the promoter methylation status of MAGE-A1 and -A3 in 10 gastric cancer cell lines and in surgical specimens from 84 gastric cancer patients by methylation-specific PCR (MSP). Expression of MAGE-A1 and -A3 in the 10 gastric cancer cell lines was also investigated by RT-PCR. Any correlation between the methylation status of the MAGE promoters and clinicopathological characteristics of the gastric cancer patients was then assessed. Eight of the 10 gastric cancer cell lines showed demethylation of both MAGE-A1 and -A3, and the remaining two cell lines did either of MAGE-A1 or -A3. Expression of MAGE-A1 and -A3 was confirmed in seven and nine of the 10 gastric cancer cell lines, respectively. The MAGE-A1 and -A3 promoters were demethylated in 29% (25 out of 84) and 66% (56 out of 84) of the gastric tumour specimens, respectively. Demethylation of both MAGE-A1 and -A3 promoters (n=22) was found more frequently in gastric cancer patients in advanced clinical stages (P=0.0035), and these patients also exhibited a higher incidence of lymph node metastasis (P=0.0007) compared to those patients without demethylation (n=25). Furthermore, demethylation patients tended to have a worse prognosis, although this difference was not statistically significant (P=0.183). Demethylation of MAGE-A1 and -A3 occurs during progressive stages of gastric cancer, and may be associated with aggressive biological behaviour of gastric cancer.
Assuntos
Adenocarcinoma/genética , Adenocarcinoma/patologia , Antígenos de Neoplasias/metabolismo , Metilação de DNA , Regulação Neoplásica da Expressão Gênica , Proteínas de Neoplasias/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia , Antígenos de Neoplasias/farmacologia , Antígenos de Superfície , Progressão da Doença , Humanos , Melanoma/imunologia , Antígenos Específicos de Melanoma , Proteínas de Neoplasias/farmacologia , Regiões Promotoras Genéticas , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Células Tumorais CultivadasRESUMO
While chromosomal instability is a common feature of human solid tumours, no abnormalities in genes involved in the mitotic checkpoint have been identified. However, recently, Chfr (checkpoint with forkhead associated and ring finger), a mitotic stress checkpoint gene, has been reported to be inactivated due to promoter hypermethylation in several types of human malignancy. To clarify whether Chfr promoter hypermethylation is involved in gastric carcinogenesis, we investigated the promoter methylation status of the Chfr gene in gastric cancer cell lines and primary gastric cancers. Non-neoplastic gastric epithelia from cancer-bearing and noncancer-bearing stomachs were also examined for Chfr promoter hypermethylation to study its cancer specificity. Two of 10 gastric cancer cell lines (20%) showed Chfr promoter hypermethylation with resultant loss of expression, which could be restored by 5-aza-2' deoxycytidine treatment. Chfr promoter hypermethylation was present in 35% (25 of 71) of primary tumours and occurred at similar frequencies in early and advanced stages. As for non-neoplastic gastric epithelia, 1% (one of 91) from noncancer-bearing and 5% (four of 71) from cancer-bearing stomachs exhibited Chfr promoter hypermethylation. Thus, Chfr promoter hypermethylation is mostly cancer specific and frequently leads to chromosome instability in gastric cancer.
Assuntos
Proteínas de Ciclo Celular/genética , Transformação Celular Neoplásica , Instabilidade Cromossômica , Metilação de DNA , Proteínas de Neoplasias/genética , Neoplasias Gástricas/genética , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Autopsia , Criança , Pré-Escolar , Células Epiteliais , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Proteínas de Ligação a Poli-ADP-Ribose , Regiões Promotoras Genéticas , Estômago/citologia , Neoplasias Gástricas/fisiopatologia , Células Tumorais Cultivadas , Ubiquitina-Proteína LigasesRESUMO
Optical loss increase characteristics under lateral force were investigated to determine the load limit for coated fiber. Plastic deformation of the coating was analyzed, and the loss increase was found to occur in the large deformation region beyond a limit theoretically determined using structural dimensions (diameter and thickness) and the material constant of the coating. The optimum coating structure for preventing loss increase has been designed by introducing the result of the lateral deformation limit as well as fiber stress induced by the lateral force and fiber strain at low temperature. The nylon outer and silicone layer diameters are 0.9 and 0.4 mm, respectively.
RESUMO
Previous studies have shown that serum concentrations of lipoprotein(a) [Lp(a)] are markedly different among different ethnic groups. We examined the serum levels of total cholesterol, high density lipoprotein (HDL) cholesterol and Lp(a) in apparently healthy subjects aged 20-69 years in Japan (n = 865) and the Dominican Republic (n = 1,893). Dominicans had significantly lower levels of total cholesterol and HDL cholesterol than Japanese. The distribution of Lp(a) concentrations were markedly skewed towards low levels in both Japanese and Dominicans. However, the mean Lp(a) concentration in Dominicans was approximately 2 times higher than in Japanese (21.7 +/- 23.7 vs 12.3 +/- 15.9 mg/dl, p < 0.001). This is possibly because the majority of Dominicans are of mixed Negroid and European blood.