Albrightmouritsen0566

Increasing evidence confirms that long non-coding RNA (lncRNA) has a vital impact on the procession of cervical cancer (CC). The present study aimed to investigate the clinical significance of LINC01089 in CC, as well as explore its biological functions and potential molecular mechanisms.

A quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to investigate the expression of LINC01089 and miR-27a-3p in CC cells and tissues. Analysis of the correlation between the expression level of LINC01089 and the clinical pathological parameters of CC was then conducted. The human CC cell lines HeLa and SiHa were utilized for transfection to establish a gain-of-function model and loss-of-function models. Pepstatin A Western blotting and a qRT-PCR were performed to detect B-cell translocation gene-2 (BTG2) expression in CC cells. Cell counting kit (CCK)-8 and 5-bromo-2-deoxyuridine (BrdU) assays were performed to detect the proliferation of CC cells. The transwell method was employed to evaluate the migration and invasion of CC cells. The interactions between LINC01089 and miR-27a-3p were verified by bioinformatics, a dual luciferase reporter gene experiment and a RNA immunoprecipitation experiment, respectively.

The expression of LINC01089 in CC was markedly down-regulated. The low expression of LINC01089 in CC was closely associated with a larger tumor size and positive lymph node metastasis. Moreover, overexpression of LINC01089 impeded the proliferation and metastasis of CC cells, whereas knockdown of LINC01089 had the opposite biological functions. In terms of mechanism, LINC01089 could sponge miR-27a-3p and indirectly up-regulate BTG2 expression.

LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to up-regulate BTG2 expression.

LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to up-regulate BTG2 expression.Although individuals with posttraumatic stress disorder (PTSD) are at an increased risk for suicidal ideation (SI), it is unclear what factors might influence this association. Investigators have hypothesized that posttraumatic cognitions (PTCs), such as self-blame (SB) or negative cognitions about the self (NCAS) or world (NCAW), would play a role, but this has not been investigated empirically. Accordingly, we evaluated a model in which the association between PTSD symptoms and SI was moderated by PTCs in a sample of trauma-exposed undergraduate students (N = 410). To identify the specific source of this hypothesized moderation effect, we ran the moderation model separately for PTSD total severity, PTSD total severity without the cognition-related items, and each of four DSM PTSD symptom clusters in combination with each of three types of PTCs (i.e., NCAS, NCAW, SB), accounting for quadratic effects. The results revealed that NCAW moderated the positive association between all six of the PTSD variables and SI, f2 s less then .01 to .04. Analyses of simple slopes generally revealed strong positive associations between PTSD symptoms with SI at high levels of NCAW, no associations at moderate levels, and negative associations at low levels. We also found one statistically significant quadratic effect when examining avoidance and NCAW. In contrast, neither NCAS nor SB emerged as a significant moderator in any of our regression models. These findings highlight the importance of addressing PTCs-particularly NCAW-in trauma survivors.Drug allergy is associated with adverse short-term perinatal outcomes such as caesarian delivery and preterm delivery. The aim of the present study was to determine whether being born to a mother with known drug allergy increases the risk for long-term dermatological morbidity of the offspring. A population-based cohort study, comparing long-term dermatological morbidity of offspring to mothers with and without known drug allergy, was conducted. Dermatological morbidity was assessed up to the age of 18 years according to a predefined set of ICD-9 codes associated with hospitalization of the offspring. A Kaplan-Meier survival curve was used to compare cumulative incidence of long-term dermatological morbidity, and a Cox proportional hazards model was constructed to control of confounders. During the study period, 243,682 deliveries met the inclusion criteria, of them 4% (n = 9756) were of mothers with known drug allergy. Offspring born to mothers with known drug allergy had higher rates of long-term dermatological morbidity Likewise, the cumulative incidence of long-term dermatological morbidity was higher as compared with those without known drug allergy (Kaplan-Meier log-rank P = .021). Using a Cox proportional hazards model, controlling for confounders, being born to a mother with known drug allergy was found to be an independent risk factor for long-term dermatological morbidity of the offspring (adjusted HR 1.2, 95% CI 1.03-1.33, P = .016). Being born to a mother with known drug allergy is independently associated with higher risk for long-term dermatological morbidity of the offspring.

To analyse the expression and clinical role of the phosphatase PTPN1 (PTP1B) in serous effusions.

PTPN1 mRNA expression by quantitative RT-PCR was analysed in 83 high-grade serous carcinoma (HGSC) and 15 malignant mesothelioma (MM) effusions. PTP1B and phospho-PTP1B (pPTP1B) protein expression by immunohistochemistry was analysed in 62 HGSC and 44 MM effusions.

PTPN1 mRNA (P=.048), PTP1B protein (P=.047) and pPTP1B protein (P<.001) were overexpressed in HGSC compared to MM effusions. PTPN1 mRNA was additionally overexpressed in post-chemotherapy HGSC effusions compared to chemo-naïve effusions (P=.005). However, pPTP1B protein expression was higher in effusions from patients with FIGO stage III compared to stage IV (P=.006), and higher expressions of both PTPN1 mRNA (P=.041) and PTP1B protein (P=.035) in HGSC effusions were associated with better (complete) chemotherapy response at diagnosis. PTPN1 RNA and protein expression was unrelated to survival in HGSC, whereas a trend for shorter overall survival (P=.06) was found for MM patients whose tumours expressed pPTP1B protein.

PTPN1 is overexpressed in HGSC compared to MM effusions, and may be a marker of better chemotherapy response in the former. Whether PTPN1 activation is informative of adverse outcome in MM merits further investigation.

PTPN1 is overexpressed in HGSC compared to MM effusions, and may be a marker of better chemotherapy response in the former. Whether PTPN1 activation is informative of adverse outcome in MM merits further investigation.