Quantum enhanced radio detection and ranging with solid spins.

The accurate radio frequency (RF) ranging and localizing of objects has benefited the researches including autonomous driving, the Internet of Things, and manufacturing. Quantum receivers have been proposed to detect the radio signal with ability that can outperform conventional measurement. As one of the most promising candidates, solid spin shows superior robustness, high spatial resolution and miniaturization. However, challenges arise from the moderate response to a high frequency RF signal. Here, by exploiting the coherent interaction between quantum sensor and RF field, we demonstrate quantum enhanced radio detection and ranging. The RF magnetic sensitivity is improved by three orders to 21 [Formula: see text], based on nanoscale quantum sensing and RF focusing. Further enhancing the response of spins to the target's position through multi-photon excitation, a ranging accuracy of 16 µm is realized with a GHz RF signal. The results pave the way for exploring quantum enhanced radar and communications with solid spins.

Downregulation of miR-21 is Involved in the Pathogenesis of Infection-Induced Preterm Birth by Targeting NF-κB.

Infection-induced preterm birth (PTB) is contributing to the main factors of increased maternal and fetal morbidity and mortality. Infections and inflammation are often accompanied by histologic chorioamnionitis. Recently, several studies have uncovered that miR-21 and NF-κB are associated with pathological processes of pregnant women. However, the role of miR-21 in infection-induced PTB remains unclear. This study aimed to determine whether miR-21 is involved in the pathogenesis of infection-induced PTB by regulating NF-κB. In this study, we found that the expression of miR-21 was significantly decreased in placental tissues of lipopolysaccharides (LPS)-induced infectious PTB mice model, accompanied by the increase of NF-κB, IL-6, and TNF-α (P < 0.05). Luciferase reporter gene assays showed that NF-κB was a validated target of miR-21. Furthermore, cell transfection experiments showed that miR-21 overexpression significantly decreased NF-κB mRNA expression compared with the miR-control group and blank group. Conversely, miR-21 inhibitor can enhance NF-κB mRNA expression. After the treatment of miR-21 mimics, miR-21 expression was obviously increased compared with the LPS group, accompanied by the decrease of NF-κB, TNF-α, and IL-6 mRNA expression (P < 0.05). What's more, miR-21 expression was negatively correlated with NF-κB (r=-0.87, P < 0.01). Overall, the study findings indicate that miR-21 may contribute to the pathogenesis of infection-induced PTB by upregulating the target NF-κB and that miR-21 may be a new potential therapeutic target for infection-induced PTB.

Comparison of the Effects of Intraperitoneal Injection with Carbon Tetrachloride on Acute Liver Toxicity in Male and Female Kunming Mice.

BACKGROUND Acute chemical liver injury needs to be further explored. The present study aimed to compare the effects of intraperitoneal injection with carbon tetrachloride on acute liver toxicity after 24 h in male and female Kunming mice. MATERIAL AND METHODS In this study, female and male mice were simultaneously divided into 3 different groups. Each group was treated differently, and after 24 h, blood samples were collected to check for changes in the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), which were used to assess liver toxicity. Liver samples were used for hematoxylin-eosin staining, and periodic acid Schiff reagent staining was performed to detect the pathological changes of each group. The expression level of biomarker molecules in liver cells was also systematically analyzed. RESULTS Our results showed that, compared with male mice, female mice showed more serious damage: reduced glycogen and higher degree of necrosis, and the levels of heatshock protein 27 (HSP27), heat-shock protein 70 (HSP70), proliferating cell nuclear antigen (PCNA) and B cell lymphoma/lewkmia-2 (Bcl-2) were significantly lower than in the male group (P<0.05 or P<0.01), while the results of Bcl-2-associated X protein (Bax), cysteinyl aspartate specific proteinase 3 (Caspase3), and cytochrome P450 2E1 (CYP2E1) were the opposite (P<0.05 or P<0.01). CONCLUSIONS The findings from this study showed that, compared with male mice, at 24 h after CCl4 toxicity, female mice showed more severe changes of hepatocyte necrosis and PAS-positivity, with significantly reduced expression of HSP27, HSP70, PCNA, and Bcl-2, and significantly increased expression of Bax, caspase-3, and CYP2E1.

Aberrantly up-regulated miR-142-3p inhibited the proliferation and invasion of trophoblast cells by regulating FOXM1.

INTRODUCTION: Preeclampsia is one of the main causes of morbidity and mortality in pregnant women and mothers. Numerous studies showed that microRNAs (miRNAs) played important roles in the occurrence and development of preeclampsia. However, the regulation of microRNA-142-3p (miR-142-3p) in preeclampsia has not been clarified. METHODS: The expression of miR-142-3p and FOXM1 was detected by RT-qPCR. The interaction between miR-142-3p and FOXM1 was confirmed by dual-luciferase reporter assay. The relative protein expression of FOXM1 was measured by western blot. Cell proliferation was measured using MTT assay. Cell migration was detected using transwell assay and wound healing assay. RESULTS: The expression of miR-142-3p was up-regulated, while the mRNA and protein of FOXM1 expression were down-regulated in preeclampsia tissues. Additionally, we found that miR-142-3p targeted FOXM1. Moreover, FOXM1 expression was negatively regulated by miR-142-3p. Functional experiments showed that overexpression of miR-142-3p inhibited cell growth and migration in trophoblast cells. Reverse experiments determined that overexpression of FOXM1 reversed the suppressive effects of miR-142-3p on cell proliferation and migration. DISCUSSION: Our results demonstrated that miR-142-3p regulated cell proliferation and migration through targeting FOXM1 in trophoblast cells, providing a novel therapeutic target and extending the pathogenesis of preeclampsia.

The role and significance of endomorphin-1 and µ-opioid receptor in rats with endometriosis.

Endomorphin-1 (EM-1) was reported to have very high affinity and selectivity for µ-opioid receptor (MOR). However, it remained unclear whether EM-1 and MOR were involved in the pathologies of endometriosis resulting in reduced fertility. In this study, RT-PCR, radioimmunoassay, immunohistochemistry, and Western blot were used, respectively. The results showed that the immune positive cells of EM-1 in hypothalamus, pituitary, and ovaries were significantly increased in endometriosis model rats, accompanied by the increase of plasma level of EM-1 and the decrease of follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), and progesterone (P). Interestingly, EM-1 was negatively correlated with FSH and LH (p < 0.05). More importantly, Naloxone (MOR antagonist) can significantly reduce the levels of EM-1 in serum, hypothalamus, pituitary, and ovaries, while increased the levels of FSH and LH. In conclusion, our results suggested that EM-1 may be involved in the pathogenesis of the endometriosis-associated infertility by regulating hypothalamus-pituitary-ovarian axis, and Naloxone may be a new alternative drug for the treatment of endometriosis.

Oral Propranolol for the Treatment of Infantile Hemangiomas in the Post-Proliferative Phase: A-Single Center Retrospective Study of 31 Cases.

PURPOSE: Infantile hemangiomas (IHs) are the most common benign tumors affecting infants, and most IHs are self-limiting. However, there are cases that require specific treatment. Propranolol is now widely used to treat severe IHs. Several studies have shown the efficacy and limited side effects associated with propranolol as the first-line treatment for IHs. There are a limited number of publications describing the role of propranolol in treating IHs beyond the proliferative phase (>12 months). The purpose of this study was to evaluate the effects and safety of oral high-dose (2.0 mg/kg per day) propranolol for IHs beyond the proliferative phase (>12 months). PATIENTS AND METHODS: This study enrolled patients with IHs who accepted systemic propranolol treatment from the Department of Oral and Maxillofacial Surgery, Stomatological Hospital Affiliated China Medical University. This is a single-center retrospective study conducted from April 2011 to July 2015. All children who were older than 12 months were eligible for the study. Digital photographs taken before and after treatment were analyzed by a panel of 3 plastic surgeons. The esthetic results were evaluated using a 4-point scale and ranked as poor, moderate, good, or excellent. The patient follow-up visits were scheduled monthly, and changes in the size, texture, and color of the lesions were recorded. The adverse effects after medication were evaluated and managed accordingly. RESULTS: We collected data on 31 eligible patients. The 31 patients had 32 hemangiomas (1 female patient had 2 lesions) and were treated with systemic propranolol at a high dose of 2 mg/kg per day. The mean age at the initiation of propranolol therapy was 18.4 months (range, 12 to 48 months), and the mean treatment duration was 10.1 months (range, 8 to 16 months). The treatment responses for the 32 hemangiomas included 17 excellent responses (53.1%), 8 good responses (25%), and 7 moderate responses (21.9%). There were no severe side effects encountered and recurrence was observed in 3 patients during the treatment and follow-up course. CONCLUSIONS: Oral propranolol, 2 mg/kg per day, is a safe and effective treatment for IHs beyond the proliferative phase (>12 months of age) in the Chinese population.

Dual gRNAs guided CRISPR/Cas9 system inhibits hepatitis B virus replication.

AIM: To screen and investigate the effective gRNAs against hepatitis B virus (HBV) of genotypes A-D. METHODS: A total of 15 gRNAs against HBV of genotypes A-D were designed. Eleven combinations of two above gRNAs (dual-gRNAs) covering the regulatory region of HBV were chosen. The efficiency of each gRNA and 11 dual-gRNAs on the suppression of HBV (genotypes A-D) replication was examined by the measurement of HBV surface antigen (HBsAg) or e antigen (HBeAg) in the culture supernatant. The destruction of HBV-expressing vector was examined in HuH7 cells co-transfected with dual-gRNAs and HBV-expressing vector using polymerase chain reaction (PCR) and sequencing method, and the destruction of cccDNA was examined in HepAD38 cells using KCl precipitation, plasmid-safe ATP-dependent DNase (PSAD) digestion, rolling circle amplification and quantitative PCR combined method. The cytotoxicity of these gRNAs was assessed by a mitochondrial tetrazolium assay. RESULTS: All of gRNAs could significantly reduce HBsAg or HBeAg production in the culture supernatant, which was dependent on the region in which gRNA against. All of dual gRNAs could efficiently suppress HBsAg and/or HBeAg production for HBV of genotypes A-D, and the efficacy of dual gRNAs in suppressing HBsAg and/or HBeAg production was significantly increased when compared to the single gRNA used alone. Furthermore, by PCR direct sequencing we confirmed that these dual gRNAs could specifically destroy HBV expressing template by removing the fragment between the cleavage sites of the two used gRNAs. Most importantly, gRNA-5 and gRNA-12 combination not only could efficiently suppressing HBsAg and/or HBeAg production, but also destroy the cccDNA reservoirs in HepAD38 cells. CONCLUSION: These results suggested that CRISPR/Cas9 system could efficiently destroy HBV expressing templates (genotypes A-D) without apparent cytotoxicity. It may be a potential approach for eradication of persistent HBV cccDNA in chronic HBV infection patients.

Integrative analysis of aberrant Wnt signaling in hepatitis B virus-related hepatocellular carcinoma.

AIM: To comprehensively understand the underlying molecular events accounting for aberrant Wnt signaling activation in hepatocellular carcinoma (HCC). METHODS: This study was retrospective. The HCC tissue specimens used in this research were obtained from patients who underwent liver surgery. The Catalogue of Somatic Mutations in Cancer (COSMIC) database was searched for the mutation statuses of CTNNB1, TP53, and protein degradation regulator genes of CTNNB1. Dual-luciferase reporter assay was performed with TOP/FOP reporters to detect whether TP53 gain-of-function (GOF) mutations could enhance the transcriptional activity of Wnt signaling. Methylation sensitive restriction enzyme-quantitative PCR was used to explore the methylation status of CpG islands located in the promoters of APC, SFRP1, and SFRP5 in HCCs with different risk factors. Finally, nested-reverse transcription PCR was performed to examine the integration of HBx in front of LINE1 element and the existence of HBx-LINE1 chimeric transcript in Hepatitis B virus-related HCC. All results in this article were analyzed with the software SPSS version 19.0 for Windows, and different groups were compared by χ(2) test as appropriate. RESULTS: Based on the data from COSMIC database, compared with other solid tumors, mutation frequency of CTNNB1 was significantly higher in HCC (P < 0.01). The rate of CTNNB1 mutation was significantly less frequent in Hepatitis B virus-related HCC than in other etiologies (P < 0.01). Dual-luciferase reporter system and TOP/FOP reporter assays confirmed that TP53 GOF mutants were able to enhance the transcriptional ability of Wnt signaling. An exclusive relationship between the status of TP53 and CTNNB1 mutations was observed. However, according to the COSMIC database, TP53 GOF mutation is rare in HCC, which indicates that TP53 GOF mutation is not a reason for the aberrant activation of Wnt signaling in HCC. APC and AXIN1 were mutated in HCC. By using methylation sensitive restriction enzyme-quantitative PCR, hypermethylation of APC was detected in HCC with different risk factors, whereas SFRP1 and SFRP5 were not hypermethylated in any of the HCC etiologies, which indicates that the mutation of APC and AXIN1, together with the methylation of APC could take part in the overactivation of Wnt signaling. Nested-reverse transcription PCR failed to detect the integration of HBx before the LINE1 element, or the existence of an HBx-LINE1 chimeric transcript, suggesting that integration could not play a role in the aberrant activation of Wnt signaling in HCC. CONCLUSION: In HCC, genetic/epigenetic aberration of CTNNB1 and its protein degradation regulators are the major cause of Wnt signaling overactivation.

Mattress cerclage combined with electrochemical therapy and pingyangmycin injection after embolization for management of arteriovenous malformation on oral and maxillofacial region.

BACKGROUND: The purpose of the article was to assess the clinical results of mattress cerclage combined with electrochemical therapy and pingyangmycin injection after embolization in treating arteriovenous malformations (AVMs). METHODS: During the period from January 2008 to December 2012, a total of 26 patients with AVMs were treated through mattress cerclage combined with electrochemical therapy and pingyangmycin injection after embolization and were retrospectively examined. The size of the lesions ranged from 2.5 cm × 3 cm to 8 cm × 10 cm. The follow-up time varied from 8 months to 24 months. The clinical outcome was evaluated using a 4-grade scale. RESULTS: All the lesions decreased in size after the treatment. The clinical follow-up showed excellent response in 20 of the 26 patients, whereas the remaining 6 patients also had satisfactory response. The most common complication was swelling, followed by pain and fever, without serious adverse effects being encountered. CONCLUSIONS: Mattress cerclage combined with electrochemical therapy and pingyangmycin injection after embolization was a reliable method for AVMs.

Oral propranolol for parotid infantile hemangiomas.

The aim of our study was to assess the efficacy and safety of oral propranolol for the treatment of parotid infantile hemangiomas. Between October 2009 and January 2013, propranolol was given orally to 30 infants with proliferating hemangiomas at a dose of 1.0 to 1.5 mg/kg per day in our department. The patients included 12 male infants and 18 female infants, aged between 2 and 13 months, with a median of 5.9 months. The lesions were located in the parotid region and measured from 1.5 cm × 2 cm × 0.5 cm to 6 cm × 8 cm × 3 cm in volume. Oral propranolol was administered once daily for a mean duration of 22.7 weeks (range, 14-32 wk). Follow-up times were from 1 to 10 months (median, 6.4 mo). Changes in the color and size of the tumor were recorded using hemisphere measurements and digital photographs. The treatment results were scored according to a 4-point scale. Overall response was graded scale 4 (excellent) in 18 patients, scale 3 (good) in 11 patients, scale 2 (moderate) in 1 patient, and scale 1 (poor) in none. No major collateral effects and rebounds were observed in any of the patients. Oral propranolol was a well-tolerated and effective treatment with mild adverse effects for parotid infantile hemangiomas.

Nerve invasion by epithelial cells in benign breast diseases.

Nerve invasion by glandular epithelial cells in a lesion is usually regarded as invasive carcinoma. However, some benign conditions in the pancreas, prostate, breast and other organs may show involvement of nerve bundles by benign epithelial cells. We report an 18-year-old female with nerve invasion in benign breast disease. The lesion in her right breast revealed fibrocystic changes with ductal hyperplasia and stromal sclerosis. Perineural and intraneural involvement by bland-looking small ducts lined by 2 layers of cells including an outer layer of myoepithelial cells were found, suggestive of benign nerve invasion. There was no evidence of malignant cells in any of the sections. The patient remains well after 31 months of follow-up. About 44 cases of nerve invasion in benign breast diseases have been reported in the literature. It is necessary to carefully evaluate nerve involvement in breast lesions to avoid over-diagnosis and inappropriate operation.