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BACKGROUND Syphilis has increased in prevalence in the United States by 72.7% from 2013 to 2017, with the highest rates recorded in men who have sex with men. There is an increased incidence of syphilis in patients with a concomitant HIV infection, estimated at a 77-fold increase. CASE REPORT This report documents an unusual case of neurosyphilis manifesting as syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a 56-year-old man with HIV/AIDS. A 56-year-old man who has sex with men with HIV/AIDS presented with a 4-day history of periumbilical abdominal pain, nausea, and constipation. A physical exam revealed slowing of baseline cognition, but was otherwise unremarkable. Urine and serum osmolality studies were consistent with SIADH as defined by the Bartter and Schwartz Criteria serum osmolality 20-40 mmol/L, euvolemia, and no other cause for hyponatremia identified. He was fluid-restricted, with improvement in laboratory abnormalities, further supporting the diagnosis of SIADH. A diagnostic work-up included a CT abdomen/pelvis with perirectal lymphadenopathy, colonoscopy negative for malignancy, chest CT with lymphadenopathy, and a head MRI negative for intracranial processes. The patient was ultimately found to have positive results on rapid plasma reagin (RPR) and Venereal Disease Research Laboratory (VDRL) tests, and was diagnosed as having neurosyphilis. He underwent penicillin desensitization and received a 14-day course of penicillin G, with recovery of sodium to normal range on discharge. CONCLUSIONS Our case highlights SIADH as an initial presenting sign of neurosyphilis with HIV infection, which has only been documented in 2 prior case reports. Our case highlights the importance of recognizing atypical presentations of neurosyphilis in patients with HIV to prevent long-term complications.BACKGROUND Congestive heart failure is a challenging problem due to increasing prevalence in developed countries. Patients admitted due to decompensated congestive heart failure symptoms who do not respond to medical treatment require mechanical circulatory support. Patients with biventricular failure are at particularly high mortality risk. click here MATERIAL AND METHODS We analyzed the function of 49 pumps (POLVAD-MEV, FRK Intra-cordis, Poland) implanted to rescue INTERMACS 1 and 2 profile patients referred to our department due to severe congestive heart failure. All patients were waiting for heart transplantation and were readmitted due to acute decompensations of congestive biventricular heart failure with resistance to medical therapy. RESULTS During the observational period, there were no technical problems in pump function. The mean duration of pump therapy was 30.6±8.3 (5-49) days. The risk for right-sided pump complications included clots formation on the following parts of the pump outflow tract (1, 2%), membrane (13, 27%), dome (6, 12.5%), and periphery (1, 2%). The overall risk for device thrombosis was 41%. The risk for thromboembolic complications was CRP-dependent regarding conglomerates of fibrin and platelets formation (p less then 0.05). The risk for left-sided pump complications included clots formation on the outflow tract (1, 2%), membrane (9, 19%) and dome (3, 6%). The overall risk for device thrombosis was 27%. The risk for clots formation on the membrane (P less then 0.05) and dome of the pump depended on time (P less then 0.07). CONCLUSIONS Mechanical circulatory support with a paracorporeal pump is a safe option for biventricular heart dysfunction as a bridge to heart transplantation. The risk for thrombi formation is relatively high but acceptable within 30 days after implantation.Exogenous factors influence embryo development. Enniatin B1 (EB1), one emerging mycotoxin of Fusarium fungi, can cause damage to cells and mouse blastocysts. However, the toxicity of EB1 on porcine embryo development and whether melatonin can eliminate the detrimental effects of EB1 on embryos remain unclear. Here, this work demonstrated that EB1 significantly decreased the cleavage and blastocyst rates and blastocyst cell number of embryos in a dose and time dependent manner. Further study displayed that EB1 obviously destroyed nuclear remodeling dynamics. Importantly, EB1 triggered embryo apoptosis through downregulating the expression of Sod1,Gpx4, Cat and Bcl2l1 while upregulating the transcription of Bax and Caspase3. Moreover, EB1 significantly disrupted the transcription of Dnmt1, Dnmt3a, Tet1 and Tet3, further leading to incomplete DNA demethylation of CenRep, Oct4, Nanog and Sox2, thus, the expression of Eif1a, Oct4, Nanog and Sox2 remarkably decreased. Whereas EB1-exposed embryos were treated with melatonin, these disorders were obviously ameliorated, and the development ability of embryos was also rescued. In conclusion, EB1 exerted detrimental effects on porcine early embryos, while melatonin effectively rescued EB1-mediated defects in embryos. This work provides a novel insight into the improvement of embryo quality and the promotion of human and animal reproduction.

Glioma, one of the most prevalent and aggressive cancers, is regulated by long noncoding RNAs (lncRNAs). This study aims to research the functional mechanism of lncRNA PCGEM1 involved in glioma progression.

Expression levels of PCGEM1, miR-539-5p and CDK6 were analyzed by qRT-PCR in NHA, U251, U87, and LN229 cells or glioma tissues. shRNAs were used to knock down PCGEM1 in U251 and LN229 cells. Kaplan-Meier curve and log rank test were utilized to examine survival rate. CCK8 (Cell Counting Kit-8) assay, colony formation assay and EdU staining were conducted to detect cell proliferation. Transwell assay was performed to evaluate cell migration and invasion. Luciferase reporter assay was conducted to assess RNA interaction between PCGEM1 and miR-539-5p. Nude mice were used for tumor xenograft assay.

LncRNA PCGEM1 was upregulated in glioma tissues and tumor cell lines. PCGEM1 upregulation predicted unsatisfactory prognosis. PCGEM1 knockdown inhibited proliferation, colony formation, migration and invasion. PCGEM1 knockdown delayed tumor growth

. PCGEM1 played as a competing endogenous RNA (ceRNA) for miR-539-5p to promote CDK6 expression. MiR-539-5p mimics repressed glioma progression while CDK6 overexpression reversed the roles of PCGEM1 knockdown.

PCGEM1 knockdown suppressed glioma progression through sponging miR-539-5p and regulating CDK6 expression, implying PCGEM1 as a potential therapeutic target.

PCGEM1 knockdown suppressed glioma progression through sponging miR-539-5p and regulating CDK6 expression, implying PCGEM1 as a potential therapeutic target.