Serum oxidative biomarkers associated with genital HPV infection and cervical lesions in women.

Human papillomavirus (HPV) infection is a major cause of cervical cancer. Studies showed HPV carcinogenesis may be induced by oxidative stress affecting the host immune system. The objective of this study is to evaluate levels of four circulating oxidative stress biomarkers associated with the HPV infection, persistence, and cervical lesion status in women. The three serum biomarkers measuring oxidative damage to biomolecules (8-oxodG, 8-oxo-7,8-dihydro-2'-deoxyguanosine [8-oxodG] for DNA, 4-hydroxy-2-nonenal [4-HNE] for lipid, and protein carbonyl [PC] for protein) and one antioxidant (glutathione, GSH) collected from 38 women were evaluated. The PC levels were significantly higher for women with oncogenic HPV infection (p = 0.047) and persistence (p = 0.053) based on the unadjusted linear model. In particular, women with ≥3 oncogenic HPV types had a higher PC level than those without HPV infection (p = 0.041). Women with low-grade squamous intraepithelial lesions showed an elevated PC (p = 0.058). These trends remained similar after adjusting for age. The GSH levels were lower for women infected with ≥3 oncogenic HPV types based on age-adjusted results (p = 0.061). This study supported that serum PC was associated with HPV infection, persistence, and cervical lesions, so it can potentially be used to monitor HPV carcinogenesis. Further large-scale studies will be needed to confirm these findings.

Impact of Dietary Quality on Genital Oncogenic Human Papillomavirus Infection in Women.

BACKGROUND: Most cervical cancers are directly linked to oncogenic or high-risk human papillomavirus (HR-HPV) infection. This study evaluates associations between diet quality and genital HPV infection in women. METHODS: This study included 10 543 women from the 2003-2016 National Health and Nutrition Examination Survey. The outcome was the genital HPV infection status (HPV-negative, low-risk [LR] HPV, and HR-HPV). Dietary quality was evaluated using the Healthy Eating Index (HEI), in which a higher score indicates a better diet quality. RESULTS: Women who did not consume total fruits (15.8%), whole fruits (27.5%), or green vegetables and beans (43%) had a significantly higher risk of HR-HPV infection than women who complied with the Dietary Guidelines for Americans (HR-HPV odds ratio = 1.76, 1.63, and 1.48 for a HEI score of 0 vs 5, respectively) after adjusting confounding factors. Similar results of these food components on LR-HPV infection were found. In addition, intake of whole grains and dairy was inversely associated with LR-HPV infection. CONCLUSIONS: This study showed that women who did not eat fruits, dark-green vegetables, and beans had a higher risk of genital HR-HPV infection. Intake of these food components is suggested for women to prevent HPV carcinogenesis.

Lesion size as a prognostic factor in the antifungal treatment of pulmonary cryptococcosis: a retrospective study with chest CT pictorial review of 2-year follow up.

BACKGROUND: Pulmonary cryptococcosis (PC) is a fungal infection that can have a variable prognosis depending on several factors. The objective of this study was to analyse the characteristics of pulmonary lesions and identify prognostic factors in patients with PC who were human immunodeficiency virus (HIV) -negative and underwent antifungal treatment. METHODS: The study enrolled patients diagnosed with PC who were negative for HIV. Symptoms, CT characteristics of pulmonary lesions, serum cryptococcal capsular antigen (CrAg) titre, underlying diseases, and duration of antifungal treatment were evaluated over a 2-year follow-up. RESULTS: A total of 63 patients (40 men and 23 women) with a mean age of 50.4 years were included. Half of the patients (50.8%) were asymptomatic, and the most common symptoms were cough (44.4%), expectoration (27.0%), and fever (17.5%). Pulmonary lesions were mainly present in the peripheral and lower lobes of the lung, with 35 cases classified as nodular-type lesions and 28 cases classified as mass-type lesions. At the first, third, sixth, 12th, and 24th-month follow-ups, the median proportion of residual pulmonary lesions were 59.6%, 29.9%, 12.2%, 9.6%, and 0.0%, respectively. During antifungal treatment, the lesions of 33 patients achieved complete response, while the remaining 30 patients did not. Compared with the non-CR group, the CR group had a lower baseline serum CrAg titre (median, 1:20 vs 1:80, P < 0.01), smaller pulmonary lesion size (median area, 1.6 cm2 vs 6.3 cm2, P < 0.01), lower Hounsfield-units (HU) radiodensity (median, - 60.0 HU vs - 28.5 HU, P < 0.05), more nodular-type lesions (72.7% vs 36.7%, P < 0.01), and fewer air-bronchogram signs (18.2% vs 43.3%, P < 0.05). Multivariate logistic regression analysis showed that a larger lesion size on chest CT scans was associated with a lower likelihood of achieving complete response [OR: 0.89; 95% CI (0.81-0.97); P < 0.05]. CONCLUSIONS: PC was more commonly observed in HIV-negative men, and chest CT scans mostly revealed nodular-type lesions. After antifungal treatment, patients with smaller lesions had a better prognosis.

Aquaporins in Respiratory System.

Aquaporins (AQPs) are water channel proteins facilitating fluid transport in alveolar space, airway humidification, pleural fluid absorption, and submucosal gland secretion. In this chapter, we mainly focus on the expression of four AQPs in the lungs, which include AQP1, AQP2, AQP4, and AQP5 in normal and disease status, and the experience of AQPs function from various model and transgenic mice were summarized in detail to improve our understanding of the role of AQPs in fluid balance of respiratory system. It has been suggested that AQPs play important roles in various physiology and pathophysiology conditions of different lung diseases. There still remains unclear the exact role of AQPs in lung diseases, and thus continuous efforts on elucidating the roles of AQPs in lung physiological and pathophysiological processes are warranted.

Ticlopidine induces embryonic development toxicity and hepatotoxicity in zebrafish by upregulating the oxidative stress signaling pathway.

Ticlopidine exerts its anti-platelet effects mainly by antagonizing platelet p2y12 receptors. Previously, a few studies have shown that ticlopidine can induce liver injury, but the exact mechanism of hepatotoxicity remains unclear. Oxidative stress, metabolic disorders, hepatocyte apoptosis, lipid peroxidation, and inflammatory responses can all lead to hepatic liver damage, which can cause hepatotoxicity. In this study, in order to deeply explore the potential molecular mechanisms of ticlopidine -induced hepatotoxicity, we used zebrafish as a model organism to comprehensively evaluate the hepatotoxicity of ticlopidine and its associated mechanism. Three days post-fertilization, zebrafish larvae were exposed to varying concentrations (1.5, 1.75 and 2 µg/mL) of ticlopidine for 72 h, in contrast, adult zebrafish were exposed exposure to 4 µg/mL of ticlopidine for 28 days. Ticlopidine-exposed zebrafish larvae showed changes in liver morphology, shortened body length, and delayed development of the swim bladder development. Liver tissues of ticlopidine-exposed zebrafish larvae and adults stained with Hematoxylin & Eosin revealed vacuolization and increased cellular interstitial spaces in liver tissues. Furthermore, using Oil Red O and periodic acid-Schiff staining methods and evaluating different metabolic enzymes of ticlopidine-exposed zebrafish larvae and adults suggested abnormal liver metabolism and liver injury in both ticlopidine-exposed zebrafish larvae and adults. Ticlopidine also significantly elevated inflammation and oxidative stress and reduced hepatocyte proliferation. During the rescue intervention using N-acetylcysteine, we observed significant improvement in ticlopidine-induced morphological changes in the liver, shortened body length, delayed swim bladder development, and proliferation of liver tissues showed significant improvement. In conclusion, ticlopidine might inhibit normal development and liver proliferation in zebrafish by upregulation of oxidative stress levels, thus leading to embryonic developmental toxicity and hepatotoxicity. In this study, we used zebrafish as a model organism to elucidate the developmental toxicity and hepatotoxicity induced by ticlopidine upregulation of oxidative stress signaling pathway in zebrafish, providing a theoretical basis for clinical application.

Protective Effect and Mechanism of Autophagy in Endothelial Cell Injury Induced by Hyperoxia.

OBJECTIVE: Bronchopulmonary dysplasia is a chronic lung disease in premature infants with alveolar simplification and pulmonary vascular development disorder as the main pathological feature and hyperoxia as the main etiology. Autophagy is a highly conserved cytological behavior of self-degrading cellular components and is accompanied by oxidative stress. Studies have reported that autophagy is regulated by FOXO1 posttranslational modification. However, whether autophagy can be involved in the regulation of endothelial cell injury induced by hyperoxia and its mechanism are still unclear. STUDY DESIGN: We have activated and inhibited autophagy in human umbilical vein endothelial cells under hyperoxia and verified the role of autophagy in endothelial cell-related functions from both positive and negative aspects. RESULTS: Our research showed that the expression level of autophagy-related proteins decreased, accompanied by decreased cell migration ability and tube formation ability and increased cell reactive oxygen species level and cell permeability under hyperoxia conditions. Using an autophagy agonist alleviated hyperoxia-induced changes and played a protective role. However, inhibition of autophagy aggravated the cell damage induced by hyperoxia. Moreover, the decrease in autophagy proteins was accompanied by the upregulation of FOXO1 phosphorylation and acetylation. CONCLUSION: We concluded that autophagy was a protective mechanism against endothelial cell injury caused by hyperoxia. Autophagy might participate in this process by coregulating posttranslational modifications of FOXO1. KEY POINTS: · Hyperoxia induces vascular endothelial cell injury.. · Autophagy may has a protective role under hyperoxia conditions.. · FOXO1 posttranslational modification may be involved in the regulation of autophagy..

Change to Hearing Loss-Related Risks and Screening in Preterm Infants.

Hearing loss is one of the most common congenital defects in infancy; it increases speech and language delays and adversely affects academic achievement and socialemotional development. The risk of hearing loss in premature infants is higher than that in normal newborns, and because of the fragility of the auditory nervous system, it is more vulnerable to different risk factors. The hearing screening guidelines in current use were proposed by the American Academy of Pediatrics and updated in 2007, but there are no uniform guidelines for hearing screening in preterm infants. This review focuses on the risk factors related to hearing loss in premature infants, hearing screening strategies, and reasons for failure. The aim is to provide a more comprehensive understanding of hearing development in preterm infants to achieve early detection and early intervention. At the same time, attention should be paid to delayed auditory maturation in preterm infants to avoid excessive intervention. KEY POINTS: · Hearing loss is very common in infancy, especially in premature infants.. · Genetic factors, infection, hyperbilirubinemia, drugs, and noise are the main causes.. · We should pay attention to the delayed hearing maturity of premature infants and avoid excessive intervention..

Resveratrol Attenuates Hyperoxia Lung Injury in Neonatal Rats by Activating SIRT1/PGC-1α Signaling Pathway.

OBJECTIVES: Our previous study showed that resveratrol (Res) attenuates apoptosis and mitochondrial dysfunction in alveolar epithelial cell injury induced by hyperoxia by activating the SIRT1/PGC-1α signaling pathway. In the present study, we investigated whether Res protects against hyperoxia-induced lung injury in neonatal rats by activating SIRT1/PGC-1α signaling pathway. METHODS: Naturally delivered neonatal rats were randomly divided into six groups: normoxia + normal saline, normoxia + dimethyl sulfoxide (DMSO), normoxia + Res, hyperoxia + normal saline, hyperoxia + DMSO, and hyperoxia + Res. Lung tissue samples were collected on postnatal days 1, 7, and 14. Hematoxylin and eosin staining was used to evaluate lung development. Dual-immunofluorescence staining, real-time polymerase chain reaction, and western blotting were used to evaluate the levels of silencing information regulator 2-related enzyme 1 (SIRT1), peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α), nuclear respiratory factor 1 (Nrf1), Nrf2, transcription factor A (TFAM) and citrate synthase, the number of mitochondrial DNA (mtDNA) and mitochondria, the integrity of mtDNA, and the expression of TFAM in mitochondria. RESULTS: We found that hyperoxia insulted lung development, whereas Res attenuated the hyperoxia lung injury. Res significantly upregulated the levels of SIRT1, PGC-1α, Nrf1, Nrf2, TFAM, and citrate synthase; promoted TFAM expression in the mitochondria; and increased the copy number of ND1 and the ratio of ND4/ND1. CONCLUSIONS: Our data suggest that Res attenuates hyperoxia-induced lung injury in neonatal rats, and this was achieved, in part, by activating the SIRT1/PGC-1α signaling pathway to promote mitochondrial biogenesis. KEY POINTS: · Hyperoxia insulted lung development in neonatal rats.. · Resveratrol promoted mitochondrial biogenesis to attenuate hyperoxia lung injury in neonatal rats.. · Resveratrol, at least in part, promoted mitochondrial biogenesis by activating the SIRT1/PGC-1α signaling pathway..

circ_0008797 attenuates non-small cell lung cancer proliferation, metastasis, and aerobic glycolysis by sponging miR-301a-3p/SOCS2.

PURPOSE: This paper firstly reported the exact function of circ_0008797 on non-small cell lung cancer (NSCLC) progression. METHODS: NSCLC tissues/matched normal tissues were harvested from 88 NSCLC patients. RNA fluorescence in situ hybridization experiment was applied to detect circ_0008797 localization in NSCLC cells. circ_0008797 effect on NSCLC cells proliferation, migration, invasion, glucolysis, and apoptosis was researched by cell counting kit-8 assay, 5-ethynyl-2'deoxyuridine assay, Transwell experiment, glycolysis assay, and TUNEL assay. Dual luciferase reporter gene assay, RNA pull-down assay and RNA immunoprecipitation assay were used to verify the binding relationship between two genes. In vivo tumorigenesis and lung metastasis was performed using nude mice. Quantitative reverse transcription-polymerase chain reaction, immunohistochemistry and western blot were applied for genes expression detection. Hematoxylin and eosin staining was performed on lung tissues. RESULTS: circ_0008797 was low expressed in NSCLC tissues and cell lines, associating with poor outcome (p <.05). circ_0008797 was mainly expressed in NSCLC cells cytoplasm. circ_0008797 inhibited proliferation, migration, invasion, and glycolysis, but enhanced apoptosis of NSCLC cells (p <.05). circ_0008797 attenuated malignant phenotype of NSCLC cells by sponging miR-301a-3p. circ_0008797 facilitated SOCS2 expression by sponging miR-301a-3p. SOCS2 knockdown partially reversed the inhibitory effect of miR-301a-3p inhibition on NSCLC cells malignant phenotype (p <.05). circ_0008797 attenuated NSCLC prolifearion and metastasis in vivo (p <.05). CONCLUSION: circ_0008797 attenuates NSCLC proliferation, metastasis and aerobic glycolysis by sponging miR-301a-3p/SOCS2.

IV segment portal vein reconstruction in split-liver transplantation with extended right grafts.

BACKGROUND: Liver transplantation is one of the most effective treatments for end-stage liver disease. Split liver transplantation (SLT) can effectively improve the utilization efficiency of grafts. However, split liver transplantation still faces shortcomings and is not widely used in surgery. How to improve the effective transplantation volume of split liver transplantation and promote the postoperative recovery of patients has important clinical significance. METHODS: In our study, the donor's liver was split into the extended right graft and left lateral sector, and the IV segment occur ischemia. To guarantee the functional graft size, and avoid complications, we reconstructed the IV segment portal vein and left portal vein. And we analyzed the operation time, intraoperative bleeding, liver function, and postoperative complications. RESULTS: In our research, 14 patients underwent IV segment portal vein reconstruction, and 8 patients did not undergo vascular reconstruction. We found that the ischemic area of the IV segment decreased significantly after IV segment portal vein reconstruction. We found that there was no significant difference in operation time and postoperative complications between the patients of the groups. There were significant differences in ALT on the 1st day and albumin on the 6th day after the operation. CONCLUSION: It indicates that IV segment reconstruction in SLT surgery can alleviate the graft ischemic and promote the recovery of liver function after the operation. And, IV segment reconstruction as a novel operating procedure may be widely used in SLT.

Conditional standards for the quantification of foetal growth in an ethnic Chinese population: a longitudinal study.

This was an observational study of low-risk singleton pregnancies in an ethnic Chinese population. Foetal biometric variables which included biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC) and femur length (FL) were measured repeatedly. The standard views for measurement were obtained according to INTERGROWTH-21st criteria. A linear mixed model with fractional polynomial regression was used to describe the longitudinal design. The study included 1289 foetuses and a total of 5125 ultrasound scans, of which each foetus was scanned at least three times, the intervals between scans being at least two weeks. The parameters of the linear mixed models were estimated by Stata v.16 (College Station, TX). Using these parameters, the equations of the mean and variance for BPD, HC, AC and FL were constructed. The conditional percentiles or Z scores could be calculated based on the above equations and previous measurements of the same foetus. A spreadsheet was provided for implementation.Impact StatementWhat is already known on this subject? Longitudinal data derived from serial measurements are therefore appropriate for assessing both foetal size and foetal growth. At present, most reference charts of ethnic Chinese foetal biometry are derived from cross-sectional data, which can only assess foetal size.What do the results of this study add? In this study, we have constructed conditional standards for foetal biometry in an ethnic Chinese population and provided a spreadsheet for querying.What are the implications of these findings for clinical practice and/or further research? The conditional standards can be used to assess foetal growth in clinical practice. In the future, we hope that these foetal growth standards can be applied to determine whether abnormal growth increases the risk of adverse outcomes.

Chronic intermittent hypoxia promoted lung cancer stem cell-like properties via enhancing Bach1 expression.

BACKGROUND: An adverse role for obstructive sleep apnea (OSA) in cancer aggressiveness and mortality has recently emerged from clinical and animal studies, and the reasons have not been fully determined. Cancer stem cells (CSCs) are regarded as the main cause of carcinoma metastasis. So far, the relationship between OSA and lung CSCs has not been explored. METHOD: In the present study, we established an orthotopic mouse model of primary lung cancer and utilized chronic intermittent hypoxia (CIH) exposure to mimic OSA status. RESULTS: We observed that CIH endows lung cancer with greater metastatic potential, evidenced by increased tumor growth, tumor seeding, and upregulated CSC-related gene expression in the lungs. Notably, the transcription factor BTB and CNC homology 1 (Bach1), a key factor in responding to conditions of oxidative stress, is increased in lung cancer after CIH exposure in vitro and in vivo. Meanwhile, exposing lung cancer cells to CIH promoted cell proliferation, clonal diversity, induced stem-like cell marker expression, and gave rise to CSCs at a relatively higher frequency. Furthermore, the increase of mitochondrial ROS (mtROS) and CSC-marker expression induced by CIH exposure was abolished in Bach1 shRNA-treated lung cancer cells. CONCLUSIONS: Our results indicated that CIH promoted lung CSC-like properties by activating mtROS, which was partially mediated by Bach1.

Clinically significant genomic alterations in the Chinese and Western patients with intrahepatic cholangiocarcinoma.

BACKGROUND: The goal of this study is to disclose the clinically significant genomic alterations in the Chinese and Western patients with intrahepatic cholangiocarcinoma. METHODS: A total of 86 Chinese patients were enrolled in this study. A panel of 579 pan-cancer genes was sequenced for the qualified samples from these patients. Driver genes, actionability, and tumor mutational burden were inferred and compared to a cohort of Western patients. RESULTS: Totally, 36 and 12 driver genes were identified in the Chinese and Western cohorts, respectively. Of them, seven driver genes (IDH1, KRAS, TP53, BAP1, PBRM1, ARID1A, and NRAS) were shared by the two cohorts. Four driver genes (SPTA1, ARID2, TP53, and GATA1) were found significantly correlated with the tumor mutational burden. For both cohorts, half of the patients had actionable mutations. The two cohorts shared the most actionable genes but differed much in their frequency. Though KRAS mutations were at the first and second actionable rank respectively for the Chinese and Western populations, they were still at a relatively low level of actionable evidence. CONCLUSIONS: The study on the clinical significance of genomic alterations directs the future development of precision medicine for intrahepatic cholangiocarcinoma treatment.

Added value of contrast-enhanced ultrasound (CEUS) in the diagnosis of primary retroperitoneal serous adenocarcinoma: a case report.

BACKGROUND: Primary retroperitoneal serous adenocarcinoma (PRSA) is a rare malignant disease. Given the rarity of the disease, the imaging features of PRSA are unclear. Contrast-enhanced ultrasound (CEUS) also plays an important role in the evaluation of the differential diagnosis of retroperitoneal lesions. CASE PRESENTATION: We report the case of a 62-year-old woman of with increased CA125 levels for 1 year who was referred to our hospital. After conducting contrast-enhanced computed tomography and magnetic resonance imaging, the mass was misdiagnosed as a chocolate cyst. After transvaginal ultrasound (TUS) combined with CEUS, cystadenocarcinoma was considered as the initial diagnosis. Pathology results confirmed PRSA as the final diagnosis. CONCLUSIONS: CEUS features of PRSA are reported for the first time based on this case, potentially aiding in the differential diagnosis of this rare entity before surgery.

Can Radiographic Tumor Volume of Oral Squamous Cell Carcinoma Help Predict Clinical and Pathological Tumor Features?

PURPOSE: Radiographic tumor volume (RTV) of oral squamous cell carcinoma (SCC) is seldom measured in practice. Aims of the study are to estimate RTV of SCC and to investigate its relationship with clinical and pathological stage, tumor margin status, recurrence, and need for chemo/radiation. METHODS: The design is a retrospective cohort study. The predictor variable is SCC RTV. The primary outcome variables are clinical and pathological tumor size. The secondary outcomes are margin status and postoperative chemo/radiation. Tumor dimensions were measured on preoperative maxillofacial or neck computer tomography images with contrast. Information on patient and tumor characteristics was obtained. Pearson correlation, t test, ANOVA and log rank test were used for statistical analysis. The significance level was set at .05. RESULTS: Thirty-six subjects aged 36 to 86 were included in the study. Positive association was found between clinical T stage and RTV (P = .0003) and between pathologic T stage and RTV (P = .002). Mean value of RTV was significantly higher in the group with positive margins (P = .0004). RTV was significantly higher in cancers requiring adjuvant chemo/radiation (P = .033). Mean RTV for patients with recurrence was 1.86 cm3 as compared to 1.29 cm3 for patients with no recurrence. Higher tumor volumes were more likely to be associated with recurrence. CONCLUSIONS: RTV is a variable that is readily available to head and neck surgeons. RTV is associated with clinical and pathological tumor sizes, margin status, need for adjuvant chemo/radiation and tumor recurrence.

Tiotropium in Early-Stage Chronic Obstructive Pulmonary Disease.

BACKGROUND: Patients with mild or moderate chronic obstructive pulmonary disease (COPD) rarely receive medications, because they have few symptoms. We hypothesized that long-term use of tiotropium would improve lung function and ameliorate the decline in lung function in patients with mild or moderate COPD. METHODS: In a multicenter, randomized, double-blind, placebo-controlled trial that was conducted in China, we randomly assigned 841 patients with COPD of Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 1 (mild) or 2 (moderate) severity to receive a once-daily inhaled dose (18 µg) of tiotropium (419 patients) or matching placebo (422) for 2 years. The primary end point was the between-group difference in the change from baseline to 24 months in the forced expiratory volume in 1 second (FEV1) before bronchodilator use. Secondary end points included the between-group difference in the change from baseline to 24 months in the FEV1 after bronchodilator use and the between-group difference in the annual decline in the FEV1 before and after bronchodilator use from day 30 to month 24. RESULTS: Of 841 patients who underwent randomization, 388 patients in the tiotropium group and 383 in the placebo group were included in the full analysis set. The FEV1 in patients who received tiotropium was higher than in those who received placebo throughout the trial (ranges of mean differences, 127 to 169 ml before bronchodilator use and 71 to 133 ml after bronchodilator use; P<0.001 for all comparisons). There was no significant amelioration of the mean (±SE) annual decline in the FEV1 before bronchodilator use: the decline was 38±6 ml per year in the tiotropium group and 53±6 ml per year in the placebo group (difference, 15 ml per year; 95% confidence interval [CI], -1 to 31; P=0.06). In contrast, the annual decline in the FEV1 after bronchodilator use was significantly less in the tiotropium group than in the placebo group (29±5 ml per year vs. 51±6 ml per year; difference, 22 ml per year [95% CI, 6 to 37]; P=0.006). The incidence of adverse events was generally similar in the two groups. CONCLUSIONS: Tiotropium resulted in a higher FEV1 than placebo at 24 months and ameliorated the annual decline in the FEV1 after bronchodilator use in patients with COPD of GOLD stage 1 or 2. (Funded by Boehringer Ingelheim and others; Tie-COPD ClinicalTrials.gov number, NCT01455129 .).

Uterine mass after caesarean section: a report of two cases.

BACKGROUND: Caesarean scar pregnancy (CSP) is a rare complication of caesarean delivery and a special type of ectopic pregnancy. Gestational trophoblastic neoplasia (GTN) is an uncommon complication of pregnancy. Early diagnosis of the two diseases is crucial because a delay or misdiagnosis can lead to increased maternal morbidity and mortality. CASE PRESENTATION: We report two cases of uterine isthmus lesions with a previous caesarean section (CS). Two patients were misdiagnosed based on the first ultrasound exam. The first case of trophoblastic tumour was initially diagnosed as CSP, while the second case, which had a scar pregnancy, was misdiagnosed as GTN. The misdiagnoses were due to the particularity of the locations of the lesions in the two patients, complicating the ultrasound-based diagnosis and hindering early clinical diagnosis and treatment. CONCLUSIONS: A medical history, ß-hCG measurements and transvaginal ultrasound are necessary to diagnose lesions in the lower anterior wall of the uterus early. However, when the location cannot be determined, magnetic resonance imaging (MRI) can be further performed to determine whether the lesion is located at the uterine scar. Combined with the degree of increased ß-hCG, differentiate CSP, myometrial GTN or caesarean scar GTN is helpful.

Interfacial States and Fano-Feshbach Resonance in Graphene-Silicon Vertical Junction.

Interfacial quantum states are drawing tremendous attention recently because of their importance in design of low-dimensional quantum heterostructures with desired charge, spin, or topological properties. Although most studies of the interfacial exchange interactions were mainly performed across the interface vertically, the lateral transport nowadays is still a major experimental method to probe these interactions indirectly. In this Letter, we fabricated a graphene and hydrogen passivated silicon interface to study the interfacial exchange processes. For the first time we found and confirmed a novel interfacial quantum state, which is specific to the 2D-3D interface. The vertically propagating electrons from silicon to graphene result in electron oscillation states at the 2D-3D interface. A harmonic oscillator model is used to explain this interfacial state. In addition, the interaction between this interfacial state (discrete energy spectrum) and the lateral band structure of graphene (continuous energy spectrum) results in Fano-Feshbach resonance. Our results show that the conventional description of the interfacial interaction in low-dimensional systems is valid only in considering the lateral band structure and its density-of-states and is incomplete for the ease of vertical transport. Our experimental observation and theoretical explanation provide more insightful understanding of various interfacial effects in low-dimensional materials, such as proximity effect, quantum tunneling, etc. More important, the Fano-Feshbach resonance may be used to realize all solid-state and scalable quantum interferometers.

Xiaoyaosan, a traditional Chinese medicine, inhibits the chronic restraint stress-induced liver metastasis of colon cancer in vivo.

CONTEXT: Xiaoyaosan (XYS), a traditional Chinese medicine (TCM), has been widely used to relieve a variety of disorders caused by depression. OBJECTIVE: This study evaluates the effect of XYS against tumour metastasis in a chronic restraint stress mouse model. METHODS AND MATERIALS: Forty C57BL/6J mice were randomly divided into four groups, including blank-control (BC), blank-stress (BS), XYS-control (XC) and XYS-stress (XS). BS and XS groups were exposed to immobilization stress for 2 h per day for 28 days commencing seven days before tumour cell injection. XC and XS groups were given a gavage of XYS (1516.67 mg/kg) before chronic immobilization stress. Mice were injected with HT-29 colon cancer cells in the spleen to produce liver metastasis. After 28 days of injecting with HT-29 cells, flow cytometry, western blot, PCR and immunohistochemical staining were performed to uncover the role of chronic restraint stress and XYS in the liver metastasis of colon cancer. RESULTS: Metastatic liver weight of mice in XS group (3.33 ± 0.18 g) was significantly lower than BS group (4.01 ± 0.27 g). Chronic restraint stress significantly increased CD11b+F4/80+ and CD11b+GrloLy6Chi cell infiltration. XYS treatment significantly decreased the CD11b+F4/80+ tumour-associated macrophage (TAM) population and CD11b+GrloLy6Chi myeloid-derived suppressor cell (MDSC). TGF-ß, IL-6, MMP-9 and VEGF in spleen tumours significantly decreased in XYS group. XYS also reduced VEGF and CD31 in hepatic metastatic tissue, which were elevated by chronic restraint stress. CONCLUSIONS: XYS may successfully inhibit chronic-stress-induced liver metastasis. Results suggest that XYS may have therapeutic value for colorectal cancer treatment.

Rs1894720 polymorphism in MIAT increased susceptibility to age-related hearing loss by modulating the activation of miR-29b/SIRT1/PGC-1α signaling.

BACKGROUND: MIAT may be implicated in the pathogenesis of age-related hearing loss (AHL). This study aimed to clarify the effect of a MIAT signaling pathway on the risk of AHL. METHODS: Terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, auditory brainstem response (ABR) and quantitative hair cell counts were used to compare the hearing functions in different groups of mice. 5,5,6,6-Tetrachloro-1,1,3,3-tetraethylbenzimidazolylcarbocyanine iodide (JC-1) dye method was used to establish the potential association between mitochondrial dysfunction and aging. Real-time polymerase chain reaction, Western blot analysis, computational analysis, and luciferase assay were conducted to establish a myocardial infarction associated transcript (MIAT) signaling pathway, whose role in the pathogenesis of AHL was further validated by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay and flow cytometry. RESULTS: Aged C57BL/6 mice were associated with a more severe level of hair cell loss, while exhibiting a higher ABR threshold at various frequencies as well as a lower percentage of inner/outer hair cells. A reduced mitochondrial membrane potential in the cochleae of aged C57BL/6 mice indicated the presence of mitochondrial dysfunction in these mice. Relative expression of MIAT, Sirtuin1 (SIRT1), and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) was downregulated in aged mice, with microRNA-29b (miR-29b) being highly expressed. Also, MIAT binds to miR-29b, an inhibitor of SIRT1 expression. The regulatory relationship among MIAT, miR-29b, and SIRT1 was further validated by comparing the differentiated expression of these factors in cells treated with phosphate-buffered saline + H2 O2, a negative control + H2 O2, MIAT + H2 O2 , or H2 O2 + anti-miR-29b. CONCLUSION: MIAT could elevate the expression of SIRT1/PGC-1α via downregulating miR-29b. And the downregulated SIRT/PGC-1α increased the incidence of AHL via promoting the apoptosis of cochlear hair cells.