Unsuccessful laparoscopic resection of a large pelvic solitary fibrous tumor: A case report.

We present a rare case of a female pelvic solitary fibrous tumor unsuccessfully resected using single-port laparoscopy, requiring conversion to laparotomy. Although the resection was successful, the surgical approach could have been improved. For large tumors, minimally invasive results are possible with flexible choices of equipment and incision position.

Treatment of heterotopic cervical pregnancy by ultrasound-guided hysteroscopy: A case report and literature review.

BACKGROUND: Heterotopic cervical pregnancy is a rare event of ectopic pregnancy with an incidence rate of < 1%. Herein, we report a rare case of successful treatment of heterotopic pregnancy following an in vitro fertilization-embryo transfer using ultrasound-guided hysteroscopy. In order to choose the best treatment option, we reviewed the clinical treatments and discussion of heterotopic cervical pregnancy over the last 15 years. METHODS: The heterotopic pregnancy was terminated using ultrasound-guided hysteroscopy; however, the intrauterine pregnancy was maintained. We searched for the keywords "cervical pregnancy combined with intrauterine pregnancy," "compound pregnancy," "assisted reproductive technology," "cervical pregnancy," and "ectopic pregnancy" on PubMed to include articles published in the last 15 years. RESULTS: The patient underwent an emergency cervical cerclage at 22 weeks' gestation for cervical insufficiency and delivered a healthy newborn at 38 weeks' gestation by transvaginal compliance. Twenty-one relevant case reports were selected. After analysis and discussion, we found that assisted reproductive technology is more likely to lead to heterotopic pregnancy than unassisted reproduction. Most women requesting the preservation of intrauterine embryos opted for surgical termination of cervical pregnancy and achieved the ideal outcomes. CONCLUSION: More attention should be paid to the diagnosis and treatment of heterotopic pregnancies to obtain the most optimal pregnancy outcome and long-term prognosis. Hysteroscopic surgery is a completely feasible cervical pregnancy treatment option with less postoperative impact on the mother and the intrauterine fetus.

Enhanced postoperative cancer therapy by iron-based hydrogels.

Surgical resection is a widely used method for the treatment of solid tumor cancers. However, the inhibition of tumor recurrence and metastasis are the main challenges of postoperative tumor therapy. Traditional intravenous or oral administration have poor chemotherapeutics bioavailability and undesirable systemic toxicity. Polymeric hydrogels with a three-dimensional network structure enable on-site delivery and controlled release of therapeutic drugs with reduced systemic toxicity and have been widely developed for postoperative adjuvant tumor therapy. Among them, because of the simple synthesis, good biocompatibility, biodegradability, injectability, and multifunctionality, iron-based hydrogels have received extensive attention. This review has summarized the general synthesis methods and construction principles of iron-based hydrogels, highlighted the latest progress of iron-based hydrogels in postoperative tumor therapy, including chemotherapy, photothermal therapy, photodynamic therapy, chemo-dynamic therapy, and magnetothermal-chemical combined therapy, etc. In addition, the challenges towards clinical application of iron-based hydrogels have also been discussed. This review is expected to show researchers broad perspectives of novel postoperative tumor therapy strategy and provide new ideas in the design and application of novel iron-based hydrogels to advance this sub field in cancer nanomedicine.

Idiopathic Granulomatous Mastitis: Etiology, Clinical Manifestation, Diagnosis and Treatment.

Idiopathic granulomatous mastitis (IGM) is a rare form of chronic inflammatory breast disease. Although it is a benign breast lesion, it may be sometimes difficult to distinguish from breast cancer. The cause of IGM is unknown, but may be associated with autoimmunity, abnormal hormone levels and infection. While the clinical manifestations of IGM involve various manifestations of inflammation, the diagnosis is principally established by histopathology, characterized by non-caseating granulomas and microabscess formation centered on the breast lobules. Therapeutic options for IGM range from observation to various medical treatments, such as steroids, immunosuppressants, and antibiotics, to surgical intervention, particularly if secondarily infected. Given that the controversy on etiology and treatment choices, we accomplished the present review through reviewing IGM-related literature published in 'Pubmed' and 'Web of science' databases during 1997 to 2020, aiming to provide the basis for rational clinical diagnosis and treatment.

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.

The role of EMT-related lncRNA in the process of triple-negative breast cancer metastasis.

Triple-negative breast cancer (TNBC) is the most malignant and fatal subtype of breast cancer, which has characterized by negativity expression of ER, PR, and HER2. Metastasis is the main factor affecting the prognosis of TNBC, and the process of metastasis is related to abnormal activation of epithelial-mesenchymal transition (EMT). Recent studies have shown that long non-coding RNA (LncRNA) plays an important role in regulating the metastasis and invasion of TNBC. Therefore, based on the metastasis-related EMT signaling pathway, great efforts have confirmed that LncRNA is involved in the molecular mechanism of TNBC metastasis, which will provide new strategies to improve the treatment and prognosis of TNBC. In this review, we summarized many signal pathways related to EMT involved in the transfer process. The advances from the most recent studies of lncRNAs in the EMT-related signal pathways of TNBC metastasis. We also discussed the clinical research, application, and challenges of LncRNA in TNBC.

Polysaccharides extracted from Rheum tanguticum ameliorate radiation-induced enteritis via activation of Nrf2/HO-1.

Radiation-induced enteritis is a major side effect in cancer patients undergoing abdominopelvic radiotherapy. The Nrf2/HO-1 pathway is a critical endogenous antioxidant stress pathway, but its precise role in radiation-induced enteritis remains to be clarified. Polysaccharides extracted from Rheum tanguticum (RTP) can protect the intestinal cells from radiation-induced damage, but the underlying mechanism is unknown. SD rats and IEC-6 cells were exposed to 12 or 10 Gy X-ray radiation. Rat survival, and histopathological and immunohistochemical profiles were analyzed at different time points. Indicators of oxidative stress and inflammatory response were also assessed. Cell viability, apoptosis and Nrf2/HO-1 expression were evaluated at multiple time points. Significant changes were observed in the physiological and biochemical indexes of rats after radiation, accompanied by significant oxidative stress response. The mRNA and protein expression of Nrf2 peaked at 12 h after irradiation, and HO-1 expression peaked at 48 h after irradiation. RTP administration reduced radiation-induced intestinal damage, upregulated Nrf2/HO-1, improved physiological indexes, significantly decreased apoptosis and inflammatory factors, and upregulated HO-1, particularly at 48 h after irradiation. In conclusion, Nrf2 is activated in the early stage of radiation-induced intestinal injury and plays a protective role. RTP significantly ameliorates radiation-induced intestinal injury via the regulation of Nrf2 and its downstream protein HO-1.

Computing Univariate Neurodegenerative Biomarkers with Volumetric Optimal Transportation: A Pilot Study.

Changes in cognitive performance due to neurodegenerative diseases such as Alzheimer's disease (AD) are closely correlated to the brain structure alteration. A univariate and personalized neurodegenerative biomarker with strong statistical power based on magnetic resonance imaging (MRI) will benefit clinical diagnosis and prognosis of neurodegenerative diseases. However, few biomarkers of this type have been developed, especially those that are robust to image noise and applicable to clinical analyses. In this paper, we introduce a variational framework to compute optimal transportation (OT) on brain structural MRI volumes and develop a univariate neuroimaging index based on OT to quantify neurodegenerative alterations. Specifically, we compute the OT from each image to a template and measure the Wasserstein distance between them. The obtained Wasserstein distance, Wasserstein Index (WI) for short to specify the distance to a template, is concise, informative and robust to random noise. Comparing to the popular linear programming-based OT computation method, our framework makes use of Newton's method, which makes it possible to compute WI in large-scale datasets. Experimental results, on 314 subjects (140 Aß + AD and 174 Aß- normal controls) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) baseline dataset, provide preliminary evidence that the proposed WI is correlated with a clinical cognitive measure (the Mini-Mental State Examination (MMSE) score), and it is able to identify group difference and achieve a good classification accuracy, outperforming two other popular univariate indices including hippocampal volume and entorhinal cortex thickness. The current pilot work suggests the application of WI as a potential univariate neurodegenerative biomarker.

Investigating the biomechanical function of the plate-type external fixator in the treatment of tibial fractures: a biomechanical study.

BACKGROUND: The design of an external fixator with the optimal biomechanical function and the lowest profile has been highly pursued, as fracture healing is dependent on the stability and durability of fixation, and a low profile is more desired by patients. The plate-type external fixator, a novel prototype of an external tibial fixation device, is a low profile construct. However, its biomechanical properties remain unclear. The objective of this study was to investigate the stiffness and strength of the plate-type external fixator and the unilateral external fixator. We hypothesized that the plate-type external fixator could provide higher stiffness while retaining sufficient strength. METHODS: Fifty-four cadaver tibias underwent a standardized midshaft osteotomy to create a fracture gap model to simulate a comminuted diaphyseal fracture. All specimens were randomly divided into three groups of eighteen specimens each and stabilized with either a unilateral external fixator or two configurations of the plate-type external fixator. Six specimens of each configuration were tested to determine fixation stiffness in axial compression, four-point bending, and torsion, respectively. Afterwards, dynamic loading until failure was performed in each loading mode to determine the construct strength and failure mode. RESULTS: The plate-type external fixator provided higher stiffness and strength than the traditional unilateral external fixator. The highest biomechanics were observed for the classical plate-type external fixator, closely followed by the extended plate-type external fixator. CONCLUSIONS: The plate-type external fixator is stiffer and stronger than the traditional unilateral external fixator under axial compression, four-point bending and torsion loading conditions.

A novel biscoumarin compound ameliorates cerebral ischemia reperfusion-induced mitochondrial oxidative injury via Nrf2/Keap1/ARE signaling.

Some phytochemical-derived synthetic compounds have been shown to improve neurological disorders, especially in ischemic stroke. In this study, we identified a novel biscoumarin compound, known as COM 3, which had substantial antioxidant effects in neurons. Next, we found that COM 3 occupies a critical binding site between the Nrf2 and Keap1 dipolymer, impairing the inhibitory effects of Keap1 on Nrf2, both of which play central roles in increasing endogenous antioxidant activity. We verified that COM 3 could increase the survival of neurons experiencing oxygen and glucose deprivation (OGD) from 51.1% to 77.2% when exposure to 2.5 and 10 µg/mL of COM 3, respectively. In addition, the same concentrations of COM 3 could reduce brain infarct volumes by 33.8%to13.7%, respectively, while also reducing the neurobehavioral score from 3.3 to 1.4 on average in mice with a middle cerebral artery occlusion (MCAO). COM 3 reduced neuronal death from 36.5% to 13.9% and apoptosis from 35.1% to 18.2%. In addition, COM 3 could improve the neuronal mitochondrial energy metabolism after experiencing oxidative stress caused by OGD or MCAO. The present study suggests that COM 3 protects against OGD in neurons and MCAO in mice by interfering with the structure of Keap1 to activate the nuclear transcription of Nrf2, which balances endogenous redox activity and restores mitochondrial function. Hence, COM 3 might be a potential therapeutic agent for ischemic stroke in the clinic.

microRNA-mediated GAS1 downregulation promotes the proliferation of synovial fibroblasts by PI3K-Akt signaling in osteoarthritis.

Hyperplastic synovial fibroblasts (SFs) serve a critical role in the pathogenesis of knee osteoarthritis (OA); however, the molecular mechanism involved in OA during synovial tissue hyperproliferation remains unclear. Growth arrest-specific gene 1 (GAS1), a cell growth repressor gene, was found to be downregulated in OASFs according to previous preliminary experiments. It was therefore hypothesized that reduced GAS1 expression may participate in the hyperproliferation of SFs in OA development, downstream of possible microRNA (miR) regulation, in hyperplastic OASFs. In the present study, GAS1 expression was indeed decreased in OASFs and interleukin-1ß-induced SFs by reverse transcription-quantitative PCR and western blot analysis. Further cell viability assays, cell cycle and apoptosis analyses revealed that the overexpression of GAS1 can inhibited proliferation, induced cell cycle arrest and promoted apoptosis in SFs. In contrast, GAS1 knockdown in SFs accelerated cell proliferation, enhanced cell cycle progression and suppressed apoptosis. Notably, the suppressive effects of GAS1 were mediated through the inactivation of the PI3K-Akt pathway. Finally, miR-34a-5p and miR-181a-5p were predicted and subsequently verified to directly target the 3'-untranslated region of the GAS1 gene, downregulating GAS1 levels in OASFs and IL-1ß-induced SFs. In conclusion, the present study demonstrated that downregulation of GAS1 can lead to the hyperproliferation of SFs in OA pathogenesis through the PI3K-Akt pathway, and miR-34a-5p and miR-181a-5p are potential regulators of GAS1 expression in OA. Therefore, it may be promising to investigate the potential of GAS1 as a novel therapeutic target for preventing SF hyperplasia in OA.

Downregulation of the long non­coding RNA FOXD2­AS1 inhibits cell proliferation, migration and invasion in osteosarcoma.

Increasing amounts of long noncoding RNAs (lncRNAs) have been shown to be involved in the development of cancer. Recently, aberrant expression of the lncRNA forkhead box D2 adjacent opposite strand RNA1 (FOXD2­AS1) has been reported to be involved in the progression of several types of human cancer. However, the function and mechanism of FOXD2­AS1 in osteosarcoma (OS) are currently unclear. The present study aimed to investigate the function and mechanism of FOXD2­AS1 in OS. Firstly, it was revealed that the expression levels of FOXD2­AS1 were significantly upregulated in OS tissues and cells, compared with in adjacent tissues and normal cells, as determined using reverse transcription­quantitative polymerase chain reaction. Notably, the overall survival of patients with relatively high FOXD2­AS1 expression in OS tissues was significantly lower than that of patients with relatively low expression, as determined using Kaplan­Meier analysis. In addition, loss­of­function experiments were performed in vivo and in vitro to study the biological effects of FOXD2­AS1. The SOSP­9607 and U2OS OS cell lines were infected with lentivirus­mediated FOXD2­AS1 short hairpin RNA; subsequently, the alterations in cell phenotype and downstream molecules were evaluated. Knockdown of FOXD2­AS1 inhibited the proliferation, migration and invasion of OS cells. Furthermore, the number of cells in the S phase was significantly decreased, which was consistent with the results of the Cell Counting kit 8 proliferation assay. The expression levels of ribonucleotide reductase regulatory subunit M2 and phosphoglycerate dehydrogenase were decreased, as determined by western blotting, following FOXD2­AS1 knockdown. Finally, in a nude mouse model of tumorigenesis, it was revealed that, when FOXD2­AS1 expression was downregulated, tumor growth was significantly reduced and pulmonary metastatic nodules were markedly reduced. The results of the present study suggested that decreased FOXD2­AS1 expression may inhibit the growth, migration and invasion of tumor cells, and it may regulate downstream gene expression. In conclusion, these findings indicated that FOXD2­AS1 may be used as a potential therapeutic target and early tumor marker for the diagnosis and prognosis of OS.