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PurposeEndometrial carcinoma is the most common gynecologic malignancy in both developed and some developing countries. Unlike cervical cancer, for which there is routine screening, only patients symptomatic for endometrial carcinoma typically seek medical help for its diagnosis and treatment. Dilatation and curettage (D&C) has been the standard procedure for evaluating suspicious endometrial lesions. The discomfort and injury caused by the D&C procedure, however, restrict its use as a screening method for early diagnosis of endometrial lesions. High-risk endometrial cancer patients would benefit from an effective and low-cost screening test. In recent years, several endometrial devices have been developed and proposed as screening tools.MethodsWe have reviewed and evaluated the literature relating to the endometrial sampling devices in clinical use or clinical trials, with the goal of comparing devices and identifying the most appropriate ones for screening for endometrial lesions. Eligible literature was identified from systematic PubMed searches, and the relevant data were extracted. Comments, letters, unpublished data, conference proceedings, and case reports were excluded from our search. Seventy-four articles on endometrial sampling devices were obtained for this review.ResultsThe main screening devices for endometrial carcinoma are aspiration devices (such as the Vabra aspirator), Pipelle, Tao Brush, and SAP-1 device. Among these devices, the Tao Brush is the most promising endometrial sampler for screening for endometrial lesions. However, its sampling insufficiency, cost, and unsuccessful insertion rate (20 % in nulliparous and 8 % in parous women) are problematic.ConclusionsA more accurate and low-cost endometrial sampler, with improved specimen sufficiency and higher sensitivity for endometrial lesions, needs tobe developed and clinically verified.

The aim of the present study was to characterize the role of microRNA (miR)-155 in the pathogenesis of severe preeclampsia (PE). A total of 19 severe preeclampsic and 22 normal placentas were collected to measure miR-155 and endothelial nitric oxide synthase (eNOS) expression using quantitative (q)PCR and western blot analysis. The results demonstrated a significant increase in the levels of miR-155 and decreased eNOS expression in the severe preeclampsic placentas, as compared with the normal controls. In order to examine the function of miR-155 in the human placenta, the HTR8/Svneo cell line was transiently transfected with an miR-155 mimic or its inhibitor, anti-miR-155. It was confirmed that miR-155 may suppress the expression of eNOS in HTR-8/SVneo cells. Furthermore, a transwell insert invasion assay demonstrated that miR-155 inhibited cell invasion in trophoblast cells, and the effect was rescued by over expression of eNOS. The present study revealed that miR-155 has a negative regulatory role in the migratory behavior of HTR-8/SVneo cells via modulating eNOS.

Tumor-associated neutrophils (TANs) are important inflammatory infiltrating cells in the tumor microenvironment and are closely related to the development of human tumor. However, the underlying mechanism of TANs recruiting to glioma remains unknown. Herein, we identified that LINC01116 was significantly upregulated in glioma, and positively correlated with clinical malignancy and survival prognosis. LINC01116 regulated the progression of glioma in vitro and in vivo. RNA-seq analysis demonstrated that LINC01116 knockdown affected the expression of IL-1β, which promoted glioma proliferation and neutrophil recruitment. Furthermore, the co-culture of glioma cells and neutrophils showed that the accumulation of TANs promoted tumor proliferation via producing a host of cytokines. Mechanistically, LINC01116 activated IL-1β expression by recruiting the transcriptional regulator DDX5 to the IL-1β promoter. Our findings reveal that LINC01116 can promote glioma proliferation and neutrophil recruitment by regulating IL-1β, and may be served as a novel target for glioma therapy and prognosis.

Numerous studies have used human pluripotent stem cell-derived cerebral organoids to elucidate the mystery of human brain development and model neurological diseases in vitro, but the potential for grafted organoid-based therapy in vivo remains unknown. Here, we optimized a culturing protocol capable of efficiently generating small human cerebral organoids. After transplantation into the mouse medial prefrontal cortex, the grafted human cerebral organoids survived and extended projections over 4.5 mm in length to basal brain regions within 1 month. The transplanted cerebral organoids generated human glutamatergic neurons that acquired electrophysiological maturity in the mouse brain. Importantly, the grafted human cerebral organoids functionally integrated into pre-existing neural circuits by forming bidirectional synaptic connections with the mouse host neurons. Furthermore, compared to control mice, the mice transplanted with cerebral organoids showed an increase in freezing time in response to auditory conditioned stimuli, suggesting the potentiation of the startle fear response. Our study showed that subcortical projections can be established by microtransplantation and may provide crucial insights into the therapeutic potential of human cerebral organoids for neurological diseases.

The present study aimed to investigate the role of microRNA (miR)-101 in acute lymphoblastic leukemia progression and chemoresistance. Furthermore, a novel target gene of miR-101 was identified. Here, we confirmed that miR-101 was significantly downregulated in the blood samples of patients with T-cell acute lymphoblastic leukemia (T-ALL) compared with the healthy controls, as determined by reverse transcription quantitative polymerase chain reaction (RTqPCR) analysis. The in vitro experiments demonstrated that miR-101 significantly repressed the proliferation and invasion, and induced potent apoptosis in Jurkat cells, as determined by CCK-8, flow cytometer and cell invasion assays. Luciferase assay confirmed that Notch1 was a target gene of miR-101, and western blotting showed that miR-101 suppressed the expression of Notch1 at the protein level. Moreover, functional restoration assays revealed that Notch1 mediates the effects of miR-101 on Jurkat cell proliferation, apoptosis and invasion. miR-101 enhanced the sensitivity of Jurkat cells to the chemotherapeutic agent adriamycin. Taken together, our results show for the first time that miR-101 acts as a tumor suppressor in T-cell acute lymphoblastic leukaemia and it could enhance chemotherapeutic sensitivity. Furthermore, Notch1 was identified to be a novel target of miR-101. This study indicates that miR-101 may represent a potential therapeutic target for T-cell acute lymphoblastic leukemia intervention.

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Background and Aims Recent evidence suggest that microbiota is associated with almost all major types of diseases, including cardiovascular diseases. However, its role in Acute Cerebral Infarction remains unexplored. It is important to understand the diversity and distribution of gut microbiota (GM) in patients with Acute Cerebral Infarction and the role that GM plays in this type of disease. Methods We performed pyrosequencing on the gut microbiota of 40 individuals in order to elucidate whether the composition of the microbiota differs between patients with Acute Cerebral Infarction and healthy controls: Of these individuals, there were 31 with Acute Cerebral Infarction and nine controls. We applied linear regression to calculate the correlation between the gut flora and disease risk factors. Finally, KEGG functional enrichment analysis was conducted to examine the correlation between the gut flora and Acute Cerebral Infarction. Results The overall microbial structure was similar in both the controls and the patients, but the control group had higher relative presence of Blautia obeum while the presence of Streptococcus infantis and Prevotella copri were relatively higher in the patient group. Using linear regression, we found that Blautia obeum was negatively associated with white blood cell count and Streptococcus infantis was positively correlated with creatinine and lipoprotein. The KEGG pathway analysis indicated that the bio-pathways including methane metabolism, lipopolysaccharide synthesis, bacterial secretion, and flagellar assembly of the gut microbiota in the patient group was expressed differently than that of the controls. We identified three differentially expressed gut microbial functions in Acute Cerebral Infarction and found four bacterial pathways that might be related to the development of this disease. Conclusions Our study identified three abnormally-expressed bacteria—Blautia obeum, Streptococcus infantis, and Prevotella copri—in patients with Acute Cerebral Infarction compared with healthy controls. It reveals a correlation of these bacterial species with Acute Cerebral Infarction as they relate to disease factors and functional pathways. These findings may shed light on the treatment of cerebral infarction because gut microbiota could serve as a potential therapeutic approach for the treatment of cardiovascular and metabolic diseases.