Choriocarcinoma That Had Transferred to the Right Inferior Pulmonary Vein and Left Atrium: A Case Report.

Here, we present a case of choriocarcinoma with metastasis only to the right inferior pulmonary vein and heart, which is unusual, as the skipping of lung metastasis is extremely rare. The 34-year-old patient presented with cough and hemoptysis. The diagnosis was challenging due to the absence of gynecological abnormalities and elevated ß-HCG levels, only revealing a cardiac mass upon imaging. While no abnormalities were found through gynecological ultrasound or gynecological examination, the serum human chorionic gonadotropin ß subunit (ß-HCG) level was abnormally raised. Echocardiography showed a left atrial myxoma with a size of approximately 6.3×1.81 cm. A left atrial mass resection was performed during cardiac surgery, where it was found that the left atrial mass had originated from the right inferior pulmonary vein. It was approximately 6×3×3 cm in size, with a flesh-red color and firm tissue. Postoperative pathology and immunohistochemistry indicated choriocarcinoma. The cardiac surgery unearthed a mass originating from the right inferior pulmonary vein. Its size and characteristics, along with the chemotherapy regimens that followed, are crucial details for understanding treatment approaches for such atypical cases. Highlight the patient's recovery post-treatment and the effectiveness of the chemotherapy regimen. This offers insights into the potential for successful treatment outcomes in atypical choriocarcinoma cases. The patient underwent chemotherapy regimens with etoposide, cisplatin (EP) ,etoposide, and methotrexate, and dactinomycin alternating with cyclophosphamide and vincristine (EMACO). A satisfactory result was achieved. This case enhances understanding of choriocarcinoma metastasis patterns. It underscores the need for a multidisciplinary approach in diagnosing and managing such rare presentations.

Subacromial osteolysis following hook plate fixation for acromioclavicular dislocation: a systematic review and meta-analysis.

BACKGROUND: Clavicular hook plates are extensively used in the treatment of acromioclavicular (AC) dislocation. Subacromial osteolysis is a typical complication following hook plate fixation. We performed a systematic review and meta-analysis to determine the incidence of subacromial osteolysis and analyzed the associated characteristics of subacromial osteolysis to guide surgeons. METHODS: PubMed, EMBASE, and Cochrane Library databases were comprehensively searched for relevant literature. We screened the literature based on the eligibility criteria, extracted relevant data and assessed the quality of the included studies. Pooled odds ratios (ORs) or mean differences (MDs) with 95% confidence intervals were calculated by a fixed-effects or random-effects model. Heterogeneity was evaluated by the chi-squared test and I2 statistics. A meta-regression analysis was performed to explore the potential source of heterogeneity. RESULTS: Thirty-two studies met the inclusion criteria. The total pooled incidence of subacromial osteolysis was 29%, and the only covariate that could influence the incidence of subacromial osteolysis was the radiological measurement method (P=0.017). Patients in the hook plate fixation with coracoclavicular (CC) ligament reconstruction group had lower odds of subacromial osteolysis (OR, 2.54, 95% CI 1.54 to 4.18; P < 0.001). There were no significant differences in the Constant-Murley scores at the final follow-up between patients with and without subacromial osteolysis (SMD, -0.17; 95% CI, -0.50 to 0.15; P= 0.294). CONCLUSIONS: Subacromial osteolysis has a relatively high and variable incidence, and the primary factor influencing the reported incidence is the radiological assessment method. The current analysis suggests CC ligament reconstruction as an effective surgical approach for decreasing the incidence of subacromial osteolysis. The presence or absence of subacromial osteolysis did not significantly impact the functional outcomes observed during the final follow-up period.

Environmental taxes, eco-innovation, and environmental sustainability in EU member countries.

Environmental taxes and renewable energy consumption are becoming central policy instruments in countries especially in European Union (EU) countries to enhance environmental sustainability; however, no attention has been given to eco-innovations in the nexus between environmental taxes and carbon dioxide emission. This study investigates the effect of environmental taxes, innovations, and renewable energy consumption on CO2 emissions in 26 EU countries from 2000 to 2020. Panel quantile regression was employed for analysis where the results show that environmental taxes have both positive and negative influence on CO2 emissions across quantiles in different models, whereas renewable energy consumption considerably reduces carbon emissions. Economic growth causes an increase in CO2 emissions; however, the financial progress greatly reduces CO2 emissions. Eco-innovations and its square term have a negative influence on carbon emissions which shows that eco-innovations significantly reduce carbon dioxide emission. The findings have significant implications for public policy in the sample countries, notably in terms of promoting renewable energy sources and transitioning to green growth through eco-innovations in order to achieve environmental sustainability.

The role of quality institutions and technological innovations in environmental sustainability: Panel data analysis of BRI countries.

The majority of countries struggle to accomplish sustainable development and environmental sustainability; nevertheless, environmental degradation issues can be resolved by enhancing technological innovations and institutional effectiveness. This study assesses the impact of technological innovations and institutional quality on carbon dioxide emission in the Belt and road initiative countries for the time period of 2002 to 2019. Fixed effect, OLS, and generalized method of moment estimators were applied to the panel data for analysis. The results shows that energy from fossil fuels, economic growth and technological innovations increase environmental degradation by rising carbon dioxide emission. Renewable energy consumption, the rule of law, and the quality of institutions make a significant contribution to the improvement of environmental quality. In particular, the Environmental Kuznets Curve and Innovation Claudia curve is valid in the Belt and Road Initiative countries. In the presence of quality institutions, countries can achieve sustainable growth and environmental sustainability by expanding their use of green technology and renewable energy. The findings provide suggestions to the sample countries on the improvement of institutional framework and technological innovations in order to achieve sustainable development.

The effect of income inequality and economic growth on carbon dioxide emission.

Most of the developing and emerging countries are focusing to increase economic growth, enhance the living standard of the people, and reduce income inequality. Increasing economic growth through the factors such as agriculture, energy use for production, and other related activities can harm the environment. Considering this situation, this study utilizes data from the Belt and Road Initiative countries for the period of 1999 and 2018 to explore the nexus between income inequality, agricultural value added, and carbon dioxide using two-step system GMM model. The findings of the study indicate that income inequality, economic growth, energy consumption, and agriculture significantly contribute to an increase in carbon emissions and a decrease in environmental quality. On the other hand, the findings also indicate that manufacturing and service industries significantly contribute to an improvement in environmental quality by reducing carbon emissions. The findings lend even more credence to the environmental Kuznets curve, but the results do not indicate that there is a strong relationship between income inequality and economic growth. The outcomes of this study have crucial policy implications for the sample countries to build environmental regulations.

Efficient Tb3+-to-Eu3+ energy transfer for colorimetric luminescence sensing.

State-of-the-art Tb-to-Eu energy transfer (TEET) efficiency (>90%) under ultralow Eu3+ proportion (<6%) has been achieved in Eu/Tb bimetallic lanthanide coordination polymers (LnCPs). The yellow-light-emitting sample as sensor exhibits micromolar l-phenylalanine (l-Phe) in water and serum via obvious yellow-to-green luminometric behavior, meanwhile nanomolar-level detection limits are determined in terms of an updated Stern-Volmer equation with high selectivity and competitiveness. Excited-state inter-ligand photon transfer (ESILPT) greatly contributes to superior TEET property and outstanding luminometric behavior. This work opens a window for developing sensitive and stable visualization sensing, being of values on monitoring biochemical markers.

The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1.

Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p in vivo. Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend in vitro and in vivo. The novel miR-582-3p represses the malignant properties of OC via the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC.

Cisplatin remodels the tumor immune microenvironment via the transcription factor EB in ovarian cancer.

The mortality rate of ovarian cancer (OC) remains the highest among all gynecological malignancies. Platinum-based chemotherapies are effective in treating most OC cases. However, chemoresistance is still a major challenge for successful OC treatments. Emerging evidence has highlighted that the modulation of the tumor immune microenvironment is involved in chemoresistance, but the mechanism remains unclear. This study aimed to investigate whether resistance to cisplatin (CDDP), the standard treatment for OC, is due to the remodeling of the tumor immune microenvironment by the transcription factor EB (TFEB). We hypothesized that TFEB is not essential for tumor survival but is associated with CDDP resistance. We collected 20 tissue samples of OC patients who had not undergone chemotherapy or radiotherapy prior to surgery. We cultured OC cell lines and performed cell transfection and assays as well as analytical, fluorescence microscopy, and immunohistochemical techniques to explore a novel function of TFEB in remodeling the tumor immune microenvironment in OC. We found a positive correlation between TFEB and programmed cell death-ligand 1 (PD-L1), PD-L2, and HLA-A expression in OC cells and tissues. We also found that CDDP treatment induced TFEB nuclear translocation, thus increasing PD-L1 and PD-L2 expression to foster an immunosuppressive tumor microenvironment, which mediates tumor immune evasion and drug resistance. Interestingly, TFEB also regulated HLA-A expression, which increases the tumor immunogenicity of OC. Finally, in a syngenic murine model of OC, we observed the therapeutic benefit of CDDP plus programmed cell death-1 (PD-1) inhibitor, which enhanced the cytolytic activity of CD8+ T cells and inhibited tumor growth. Our study illustrates the important role of TFEB in regulating the tumor immune microenvironment in OC.

MicroRNA-324-5p affects the radiotherapy response of cervical cancer via targeting ELAV-like RNA binding protein 1.

Cervical cancer (CC) seriously threatens the health of women. Radiation therapy (RT) is the major treatment for CC. However, the recurrent CC can acquire resistance to RT. Thus, it is necessary to find a new method for reversing RT resistance in CC. It has been reported that miR-324-5p can suppress the progression of multiple cancers. However, whether it can reverse resistance to RT in CC remains unclear. qRT-PCR and Western blotting were used to detect gene and protein expression in CC cells, respectively. Cell proliferation was tested by CCK-8 assay and colony formation assay. In addition, cell apoptosis was detected by flow cytometry. Transwell assays were performed to detect cell migration. Dual luciferase reporter assay and TargetScan were used to explore the targets of microRNA-324-5p (miR-324-5p). MiR-324-5p was downregulated in CC cells. Overexpression of miR-324-5p sensitized CC cells to RT. In addition, miR-324-5p mimics significantly induced apoptosis and inhibits the migration of CC cells in the presence of 137 Cs ionizing radiation. Furthermore, miR-324-5p sensitized CC cells to ionizing radiation by targeting ELAV-like RNA binding protein 1 (ELAVL1). MiR-324-5p overexpression affects the radiotherapy response of CC by targeting ELAVL1, which may serve as a new target for the treatment of CC.

Response of Vallisneria natans to aluminum phytotoxicity and their synergistic effect on nitrogen, phosphorus change in sediments.

Increasing aluminum (Al) use and its effects on aquatic systems have been a global issue, however the Al impacts on submerged plants and their ecological functions were poorly understood. Aquatic simulation experiments were performed to study Al-toxicity on the germination and seedling morphological and physiological characteristics of Vallisneria natans, and investigate their synergistic effect on nitrogen (N), phosphorus (P) change and microbial community in sediment. The seeds germination characteristics, growth and physiological parameters of seedlings, including root activity, were significantly affected by alum treatments and the inhibition levels increased with Al3+ concentration. The Al accumulation in roots and leaves were significantly different. Al3+ concentration above 0.3 mg/L showed toxic to V. natans. TN, TP, IP, Fe/Al-P contents in sediments varied markedly under co-existence of Al and V. natans. Additionally, the relative abundance of sediment microbial community related to N, P cycle was effected. Results concluded that the increasing aquatic Al-concentration inhibits growth and propagation of submerged plants and the ecological restoration effect, and exerts synergistic effect with submerged plants on N, P components in sediments. Such findings were helpful for Al ecological evaluation, and were instructive for the submerged plants restoration in shallow eutrophic lakes with Al input.

Dusp6 inhibits epithelial-mesenchymal transition in endometrial adenocarcinoma via ERK signaling pathway.

Background Endometrial adenocarcinoma (EAC) is one of the most commonly diagnosed gynaecological malignancies among female population of the developed countries. DUSP6 is a negative regulator of ERK signaling, which is a molecular switch involved in MAPK signaling during the progress of malignancies. DUSP6 was previously found to inhibit tumorigenesis and EMT-associated properties in several cancers, however, its exact role in EAC remains unclear Methods The level of DUSP6, (E-cad) and (N-cad) in EAC cancerous tissues and respective adjacent non-cancerous tissues were examined by western-blot or immunohistochemistry. The cell growth, invasion and migration abilities were measured in Ishikawa 3H12 endometrial cancer cell lines with overexpressed or knock down DUSP6. Protein levels of EMT-associated markers E-cadherin, N-cadherin and Vimentin were also determined. The impacts of DUSP6 on ERK signaling was assessed by detection of ERK and p-ERK. Results Down-regulation of DUSP6 was observed in EAC compared with the normal controls. The overexpression of DUSP6 significantly attenuated tumor cell growth, invasion, migration abilities and inhibited EMT-associated markers, while knock down of DUSP6 showed opposite trends. Overexpression of DUSP6 also down-regulated p-ERK and the knock down of DUSP6 inversely up-regulated p-ERK level. Conclusions DUSP6 inhibited cell growth, invasion and migration abilities in Ishikawa 3H12 cells as well as attenuating EMT-associated properties. This tumor suppressive effect of DUSP6 in EAC is achieved by inhibiting ERK signaling pathway.

Long non-coding RNA SPRY4-IT1 promotes epithelial-mesenchymal transition of cervical cancer by regulating the miR-101-3p/ZEB1 axis.

BACKGROUND: Emerging evidences have indicated that long non-coding RNAs (LncRNAs) play vital roles in cancer development and progression. Previous studies have suggested that overexpression of SPRY4 intronic transcript 1 (SPRY4-IT1) predicates poor prognosis and promotes tumor progress in cervical cancer (CC). However, the underlying mechanism of SPRY4-IT1 in CC remains unknown. The aim of the present study is to evaluate the function and mechanism of SPRY4-IT1 in CC. METHODS: SPRY4-IT1 was detected by quantitative PCR. Wound-healing assay and Transwell assay were performed to detect cell migration and invasion, respectively. Western blotting assays were used to analyze the protein expression of E-cadherin, N-cadherin and vimentin. Tumor xenografts experiments were performed to detect the effect of SPRY4-IT1 in vivo. Dual luciferase reporter assay was used to investigate potential molecular mechanism of SPRY4-IT1 in CC cells. RESULTS: SPRY4-IT1 was up-regulated in CC cell lines. Knockdown of SPRY4-IT1 significantly inhibited CC cells migration and invasion in vitro and in vivo Moreover, knockdown of SPRY4-IT1 significantly suppressed the epithelial-mesenchymal transition (EMT) of CC by increased E-cadherin expression and decreased the N-cadherin and vimentin expression. Mechanically, SPRY4-IT1 could directly bind to miR-101-3p and effectively act as a competing endogenous RNA (ceRNA) for miR-101-3p to regulate the expression of the target gene ZEB1Conclusions: Our findings indicate that the SPYR4-IT1/miR-101-3p/ZEB1 axis contributes to CC migration and invasion, which may provide novel insights into the function of lncRNA-driven tumorigenesis of CC.

Knockdown of long noncoding RNA-taurine-upregulated gene 1 inhibits tumor angiogenesis in ovarian cancer by regulating leucine-rich α-2-glycoprotein-1.

To investigate the role of long noncoding RNA taurine-upregulated gene 1 (TUG1) on ovarian cancer-induced angiogenesis and to explore possible signaling pathways. Ovarian cancer cell line SKOV3 or CAOV3 was transfected with short hairpin-TUG1 to suppress TUG1 expression. Supernatant from cultured cancer cells was used as a condition medium to incubate endothelial cell line human umbilical vein endothelial cells, whose proliferation rate was quantified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Migration and invasion of endothelial cells were examined by wound healing and Transwell assays, followed by in-vitro angiogenesis assay. One of the secretory factors mediating angiogenesis, leucine-rich α-2-glycoprotein-1 (LRG1), was measured in ovarian cancer cells. Signaling pathway mediating angiogenesis was further detected by western blotting. TUG1 was down-regulated in ovarian cancer cells by short hairpin RNA. Conditional medium originating from TUG1-knockdown cancer cells led to suppressed proliferation, migration, or invasion of endothelial cell line human umbilical vein endothelial cells. LRG1 expression and secretion was suppressed in ovarian cancer cells after TUG1 knockdown. Moreover, recombinant LRG1 rescued TUG1 knockdown-induced angiogenesis inhibition, and LRG1 probably mediated angiogenesis by tumor growth factor-ß signaling pathway in endothelial cells. Long noncoding RNA-TUG1 mediates angiogenesis of endothelial cells by regulating LRG1 secretion from ovarian cancer cells partially through tumor growth factor-ß pathway. Our results indicate the potency of TUG1 as a biomarker and therapeutic target for tumor-induced angiogenesis.

Knockdown of METTL14 inhibits the growth and invasion of cervical cancer.

BACKGROUND: Increasing evidence has revealed that N 6-methyladenosine (m6A) modification is implicated in multiple biological functions in mammals. Methyltransferase-like 14 (METTL14), an important component of m6A modification, has been reported to play important roles in the pathogenesis of acute myeloid leukaemia and hepatocellular carcinoma metastasis. However, its role in cervical cancer remains unclear. METHODS: Expression of METTL14 was knocked down by shRNA-METTL14 interference in HPV-positive and HPV-negative cervical cancer cell lines SiHa and C33a. CCK8, colony formation, wound-healing, and Transwell assays were performed to evaluate the effects of METTL14 knockdown on the proliferation, migration and invasion abilities of SiHa and C33a cells. Flow cytometry analysis was utilized to detect cell cycle distribution, and the expression of related proteins was examined by western blot analysis. RESULTS: Bioinformatics analysis demonstrated that up-regulation of METTL14 acted as an adverse prognostic factor for overall survival in cervical cancer patients. We demonstrated that down-regulation of METTL14 inhibited the proliferation, migration and invasion abilities of SiHa and C33a cells. Moreover, silencing METTL14 induced cell cycle arrest in cervical cancer cells. METTL14 knockdown suppressed the PI3K/Akt/mTOR signaling pathway by decreasing the phosphorylation of Akt and mTOR, and the expression of downstream apoptosis-related proteins was also impacted. CONCLUSIONS: In conclusion, these data suggest an important oncogenic role of METTL14 in the growth and invasion of both HPV-positive and HPV-negative cervical cancer cells.

Draft genome of the lined seahorse, Hippocampus erectus.

Background: The lined seahorse, Hippocampus erectus , is an Atlantic species and mainly inhabits shallow sea beds or coral reefs. It has become very popular in China for its wide use in traditional Chinese medicine. In order to improve the aquaculture yield of this valuable fish species, we are trying to develop genomic resources for assistant selection in genetic breeding. Here, we provide whole genome sequencing, assembly, and gene annotation of the lined seahorse, which can enrich genome resource and further application for its molecular breeding. A total of 174.6 Gb (Gigabase) raw DNA sequences were generated by the Illumina Hiseq2500 platform. The final assembly of the lined seahorse genome is around 458 Mb, representing 94% of the estimated genome size (489 Mb by k-mer analysis). The contig N50 and scaffold N50 reached 14.57 kb and 1.97 Mb, respectively. Quality of the assembled genome was assessed by BUSCO with prediction of 85% of the known vertebrate genes and evaluated using the de novo assembled RNA-seq transcripts to prove a high mapping ratio (more than 99% transcripts could be mapped to the assembly). Using homology-based, de novo and transcriptome-based prediction methods, we predicted 20 788 protein-coding genes in the generated assembly, which is less than our previously reported gene number (23 458) of the tiger tail seahorse ( H. comes ). We report a draft genome of the lined seahorse. These generated genomic data are going to enrich genome resource of this economically important fish, and also provide insights into the genetic mechanisms of its iconic morphology and male pregnancy behavior.

The Asian arowana (Scleropages formosus) genome provides new insights into the evolution of an early lineage of teleosts.

The Asian arowana (Scleropages formosus), one of the world's most expensive cultivated ornamental fishes, is an endangered species. It represents an ancient lineage of teleosts: the Osteoglossomorpha. Here, we provide a high-quality chromosome-level reference genome of a female golden-variety arowana using a combination of deep shotgun sequencing and high-resolution linkage mapping. In addition, we have also generated two draft genome assemblies for the red and green varieties. Phylogenomic analysis supports a sister group relationship between Osteoglossomorpha (bonytongues) and Elopomorpha (eels and relatives), with the two clades together forming a sister group of Clupeocephala which includes all the remaining teleosts. The arowana genome retains the full complement of eight Hox clusters unlike the African butterfly fish (Pantodon buchholzi), another bonytongue fish, which possess only five Hox clusters. Differential gene expression among three varieties provides insights into the genetic basis of colour variation. A potential heterogametic sex chromosome is identified in the female arowana karyotype, suggesting that the sex is determined by a ZW/ZZ sex chromosomal system. The high-quality reference genome of the golden arowana and the draft assemblies of the red and green varieties are valuable resources for understanding the biology, adaptation and behaviour of Asian arowanas.

Mudskipper genomes provide insights into the terrestrial adaptation of amphibious fishes.

Mudskippers are amphibious fishes that have developed morphological and physiological adaptations to match their unique lifestyles. Here we perform whole-genome sequencing of four representative mudskippers to elucidate the molecular mechanisms underlying these adaptations. We discover an expansion of innate immune system genes in the mudskippers that may provide defence against terrestrial pathogens. Several genes of the ammonia excretion pathway in the gills have experienced positive selection, suggesting their important roles in mudskippers' tolerance to environmental ammonia. Some vision-related genes are differentially lost or mutated, illustrating genomic changes associated with aerial vision. Transcriptomic analyses of mudskippers exposed to air highlight regulatory pathways that are up- or down-regulated in response to hypoxia. The present study provides a valuable resource for understanding the molecular mechanisms underlying water-to-land transition of vertebrates.

Dual-specificity phosphatase 6 (Dusp6), a negative regulator of FGF2/ERK1/2 signaling, enhances 17ß-estradiol-induced cell growth in endometrial adenocarcinoma cell.

Dual-specificity phosphatase 6 (Dusp6) is a negative feedback mechanism of fibroblast growth factors (FGFs)/mitogen-activated protein kinase (MAPK)/ERK1/2 signaling. The aim of this study was to explore the expression of Dusp6 in human endometrial adenocarcinomas and the role of Dusp6 expression in the growth regulation of endometrial adenocarcinoma cell. We found that Dusp6 was over-expressed in human endometrial adenocarcinomas. In Ishikawa cells, plasmid-driven Dusp6 expression efficiently blocked the activity of FGF2-induced MAPK/ERK1/2 signaling. Unexpectedly, Dusp6 expression significantly enhanced the growth of Ishikawa cells. In Dusp6 forced-expression cells, 17ß-estradiol stimulation increased the cell growth by all most threefolds. In addition, progesterone treatment reduced the cell growth to about half both in Ishikawa cells with and without forced-Dusp6-expression. Dusp6 over-expression is involved in the pathogenesis and development of human endometrial adenocarcinomas. Dusp6 functions as a negative regulator of FGF2/ERK1/2 signaling but enhances the growth and 17ß-estradiol-induced cell growth in endometrial adenocarcinoma cell.