Nipped-B-like protein plays a pivotal role as a cohesin loading factor in the segregation of chromosomes when cells divide.  https://www.selleckchem.com/products/bp-1-102.html  Accumulating evidence indicates that alterations of this protein are involved in human carcinogenesis, especially in the regulation of chemotherapeutic drug response. However, the role of Nipped-B-like protein in esophageal squamous cell carcinoma remains unknown. In this study, we investigated the relevance of Nipped-B-like protein in the regulation of cisplatin sensitivity in esophageal squamous cell carcinoma. Ectopic expression of Nipped-B-like protein inhibited the growth of COLO-680N cells with low endogenous expression levels of Nipped-B-like protein, and increased sensitivity to cisplatin, a commonly used chemotherapy drug for patients with esophageal squamous cell carcinoma. In contrast, loss of Nipped-B-like protein stimulated the growth of EC9706 and Eca-109 cells with high levels of the protein, and resulted in resistance to cisplatin. P53-upregulated modulator of apoptosis, which is essential in the modulation of cisplatin sensitivity in a variety of cancers, acts as a downstream effector of Nipped-B-like protein. Restoration of this pro-apoptotic protein in Nipped-B-like protein-overexpressing esophageal squamous cell carcinoma cells effectively increased cisplatin sensitivity. Conversely, the silencing of P53-upregulated modulator of apoptosis in Nipped-B-like protein-depleted esophageal squamous cell carcinoma rendered cells resistant to cisplatin. Moreover, Nipped-B-like protein could bind directly to the promoter region of P53-upregulated modulator of apoptosis. In summary, our study addresses the involvement of Nipped-B-like protein in the development of esophageal squamous cell carcinoma, and the modulation of cisplatin sensitivity via regulation of P53-upregulated modulator of apoptosis.Endometrial cancer (EC) is one of the most common cancers among women worldwide. Kinesin family member C1 (KIFC1) has been demonstrated to play crucial roles in various tumors. However, the function of KIFC1 in EC remains to be revealed. In this study, upregulation of KIFC1 expression in human EC tissues was found from analysis on data from The Cancer Genome Atlas (TCGA), and positively correlated with short survival outcome of EC patients. In addition, the mRNA and protein levels of KIFC1 were confirmed to be up-regulated in EC cells (Ishikawa, HEC-1B, HEC-1A and KLE) compared to human normal endometrial stromal cells (hESCs) by quantitative real time PCR and western blot. In vitro functional experiments showed that overexpression of KIFC1 promoted proliferation, migration and invasion of EC cells, while KIFC1 depletion showed the opposite results. Moreover, KIFC1 knockdown suppressed tumor growth in mice. Further mechanism analysis showed that KIFC1 participated in the regulation of EC progression through regulating the PI3K/AKT signaling pathway. Collectively, KIFC1 promoted proliferation and invasion through modulating PI3K/AKT signaling pathway in EC, implying that KIFC1 might provide a promising therapeutic target for the therapy of EC.In this study, an intelligent knowledge base (IKB) is developed based on a model developed by Fu et al. for identification of accident causes, which may play a significant role in preventing accidents. This IKB has been generated using eight sample accidents reported in the literature and tested by two additional accidents. The causes of these sample accidents were identified according to a model taxonomy developed by Fu et al. For the test, an oil spill and a refinery accident are considered in two case studies. This study proved 89.47 and 73.01% success rates, respectively, for the identification of additional accidents causes based on the developed IKB. These results obtained from only eight sample accidents are considered promising because as the number of sample accidents increases, the success rates are expected to increase further. This IKB was prepared as part of a more comprehensive intelligent system to be developed.
  Early-life adversity impacts on the offspring's brain development and is associated with a higher risk of developing age-associated diseases. In particular, perinatal protein malnutrition appears to be one of the most critical nutritional deficiencies affecting the individual's health and survival, but little is known about its effects on the persistence of behavioral alterations throughout life. Thus, the aim of the present study was to investigate how perinatal protein malnutrition impacts on age-related changes in the neuromuscular, cognitive and behavioral functions throughout life in a mouse model.
 
  One group of CF-1 dams received a normal-protein diet (NP 20% casein) during gestation and lactation, whereas another group received a low-protein diet (LP 10% casein). The offspring of both groups were analyzed by means of several behavioral tests at four different ages (young 6-10 weeks old, mature 22-26 weeks old, middle age 39-43 weeks old, and old 55-59 weeks old).
 
  Regarding neuromuscular functions, LP mice showed an early deterioration in muscular strength and a reduction in the body weight throughout life. Regarding behavior, while NP mice showed an age-related reduction of exploratory behavior, LP mice showed a constantly low level of this behavior, as well as high anxiety-like behavior, which remained at high levels throughout life. Regarding cognitive functions, LP mice showed deteriorated working memory at middle age. Finally, LP mice died 3.4 times earlier than NP mice. Analysis of the sex-related vulnerability showed that females and males were equally affected by perinatal protein malnutrition throughout life.
 
  Our results demonstrate that perinatal protein malnutrition induces enduring and age-related impairment behaviors, which culminate in higher death risk, affecting males and females equally.
 Our results demonstrate that perinatal protein malnutrition induces enduring and age-related impairment behaviors, which culminate in higher death risk, affecting males and females equally.
  Circulating tumor cells (CTCs) hold huge potential for both clinical applications and basic research into the management of cancer, but the relationship between CTC count and cervical cancer prognosis remains unclear. Therefore, research on this topic is urgently required.
 
  This study investigated whether CTCs were detectable in patients with cervical cancer and whether CTC count was an indicator of prognosis.
 
  We enrolled 107 patients with pathologically confirmed cervical cancer. CTCs were detected after radiotherapy or concurrent cisplatin-containing chemotherapy in all patients. We evaluated all medical records and imaging data as well as follow-up information to calculate progression-free survival (PFS). PFS was defined as the time until first diagnosis of tumor progression or death. We also analyzed the relationship between CTC count and patient age, disease stage, histological differentiation, tumor size, and pathological type.
 
  CTCs were identified in 86 of 107 patients (80%), and the CTC count ranged from 0 to 27 cells in 3.