Yttrium atomically incorporated into Co(OH)F nanowires enables efficient electrochemical reduction of nitrate to ammonia.

A new kind of electrocatalyst consisting of yttrium-doped Co(OH)F (Y-Co(OH)F) nanowires was synthesized by one hydrothermal method for nitrate electroreduction to ammonia. It was demonstrated that the rare earth element Y, as an oxophilic metal, can be approximated as Lewis acid sites enhancing nitrate adsorption on the catalyst surface. Therefore, the Y-Co(OH)F exhibits excellent nitrate reduction performance, reaching an optimal ammonia production rate of 0.2149 mmol h-1 cm-2 and ammonia faradaic efficiency of 91.81%.

Electrochemical Postmodification-Induced Surface Atom Rearrangement over Cu Nanodendrites for Enhanced Electrosynthesis of Ammonia from Nitrate.

Utilizing nitrate from wastewater as a N-source for ammonia synthesis via electrocatalysis is of significance for both environmental protection and ecological nitrogen cycle balance, which requires high-performance electrocatalysts to drive selective nitrate-to-ammonia transformation. In this work, an electrochemical postmodification strategy was developed to regulate the surface structure of presynthesized Cu nanodendrites at the atomic level. A combination of physicochemical characterization and electrochemical study demonstrates that such a treatment could induce surface Cu atom rearrangement and result in increased electrochemically active surface area and high density of surface-active sites, disclosing a high electrocatalytic nitrate-to-ammonia capability, with an optimal NH3 yield rate of 0.2238 mmol h-1 cm-2 and a corresponding Faradaic efficiency of 94.43%. This study may provide a guiding design avenue for atomic arrangement engineering of metallic nanocrystals via electrochemical postmodification for nitrate reduction reaction and other energy conversion electrocatalysis.

Cavernous hemangioma of the cisternal segment of the auditory nerve: case report.

BACKGROUND: Extraaxial cerebellopontine angle cavernous hemangiomas are rare and their diagnosis and treatment are challenging. CASE PRESENTATION: A 43-year-old female was admitted to the hospital who had repeated hearing loss in her left ear accompanied by tinnitus. Magnetic resonance imaging revealed a hemangioma-like lesion in the left cerebellopontine angle extra-axial cisternal segment. During the surgery, it was found that the lesion was located in the cisternal segment of the root of the auditory nerve. Postoperative pathological examination confirmed that the lesion was a cavernous hemangioma. CONCLUSION: We report a case of cavernous hemangioma in the brain spatula cisternal segment of the left auditory nerve. For cranial nerve CMs early diagnosis and surgical removal may maximize the chance of a positive outcome.

Sustainable Ammonia Electrosynthesis from Nitrate Wastewater Coupled to Electrocatalytic Upcycling of Polyethylene Terephthalate Plastic Waste.

Integrating the nitrate reduction reaction (NO3RR) with polyethylene terephthalate (PET) hydrolysate oxidation to construct the nitrate/PET hydrolysate coelectrolysis system holds a great promise of realizing the simultaneous upcycling of nitrate wastewater and PET plastic waste, which, however, is still an almost untouched research area. Herein, we develop an ultralow content of Ru-incorporated Co-based metal-organic frameworks as a bifunctional precatalyst, which can be in situ reconstructed to Ru-Co(OH)2 at the cathode and Ru-CoOOH at the anode under electrocatalytic environments, and function as real active catalysts for the NO3RR and PET hydrolysate oxidation, respectively. With a two-electrode nitrate/PET hydrolysate coelectrolysis system, the current density of 50 mA cm-2 is achieved at a cell voltage of only 1.53 V, realizing the simultaneous production of ammonia and formate at a lower energy consumption. This study provides a concept for the construction of coelectrolysis systems for upcycling of nitrate wastewater and PET plastic waste.

Multifocal brain abscesses caused by invasive Streptococcus intermedia: A case report.

Multifocal brain abscesses caused by invasive Streptococcus intermedia are relatively rare. Here, we present a 67-year-old male was admitted to the hospital for unconsciousness and fever. The computed tomography (CT) examination showed multiple intracranial space-occupying and "cavity-like" changes in the right lower lung. The examination of cerebrospinal fluid (CSF) was consistent with typical bacterial meningitis, CSF analyses revealed leukocytosis (10,300 × 106/L), elevated protein levels (140.39 mg/dL), decreased glucose levels (0.27 mmol/L), and normal chloride concentration level (120.2 mmol/L), however, pathogens were not detected in the cultures. Then, the CSF and sputum samples were analyzed using meta-genomic next-generation sequencing (mNGS), and S. intermedia was detected in both samples. We adjusted the use of antibiotics according to the results of mNGS in time. After anti-infective treatment, the patient achieved good treatment results in a very short time. This case highlights the mNGS can identify pathogens of brain abscess, and provide strong evidence for clinical diagnosis and treatment strategy.

High Levels of Progesterone Receptor B in MCF-7 Cells Enable Radical Anti-Tumoral and Anti-Estrogenic Effect of Progestin.

The widely reported conflicting effects of progestin on breast cancer suggest that the progesterone receptor (PR) has dual functions depending on the cellular context. Cell models that enable PR to fully express anti-tumoral properties are valuable for the understanding of molecular determinant(s) of the anti-tumoral property. This study evaluated whether the expression of high levels of PR in MCF-7 cells enabled a strong anti-tumoral response to progestin. MCF-7 cells were engineered to overexpress PRB by stable transfection. A single dose of Promegestone (R5020) induced an irreversible cell growth arrest and senescence-associated secretory phenotype in MCF-7 cells with PRB overexpression (MCF-7PRB cells) but had no effect on MCF-7 cells with PRA overexpression. The growth-arresting effect was associated with downregulations of cyclin A2 and B1, CDK2, and CDK4 despite an initial upregulation of cyclin A2 and B1. R5020 also induced an evident activation of Nuclear Factor κB (NF-κB) and upregulation of interleukins IL-1α, IL-1ß, and IL-8. Although R5020 caused a significant increase of CD24+CD44+ cell population, R5020-treated MCF-7PRB cells were unable to form tumorspheres and underwent massive apoptosis, which is paradoxically associated with marked downregulations of the pro-apoptotic proteins BID, BAX, PARP, and Caspases 7 and 8, as well as diminution of anti-apoptotic protein BCL-2. Importantly, R5020-activated PRB abolished the effect of estrogen. This intense anti-estrogenic effect was mediated by marked downregulation of ERα and pioneer factor FOXA1, leading to diminished chromatin-associated ERα and FOXA1 and estrogen-induced target gene expression. In conclusion, high levels of agonist-activated PRB in breast cancer cells can be strongly anti-tumoral and anti-estrogenic despite the initial unproductive cell cycle acceleration. Repression of ERα and FOXA1 expression is a major mechanism for the strong anti-estrogenic effect.

Tetratricopeptide repeat domain 9A knockout induces social anxiety and impairs offense behaviors in female mice.

Objectives: The involvement of tetratricopeptide repeat domain 9A (TTC9A) in anxiety-like behaviors through estrogen action has been reported in female mice, this study further investigated its effects on social anxiety and aggressive behaviors. Materials and sMethods: Using female Ttc9a knockout (Ttc9a-/-) mice, the role of TTC9A in anxiety was investigated in non-social and social environments through home-cage emergence and social interaction tests, respectively, whereas aggressive behaviors were examined under the female intruder test. Results: We observed significant social behavioral deficits with pronounced social and non-social anxiogenic phenotypes in female Ttc9a-/- mice. When tested for aggressive-like behaviors, we found a reduction in offense in Ttc9a-/- animals, suggesting that TTC9A deficiency impairs the offense responses in female mice. Conclusion: Future study investigating mechanisms underlying the social anxiety-like behavioral changes in Ttc9a-/- mice may promote the understanding of social and anxiety disorders.

Effect of long-term adjuvant temozolomide chemotherapy on primary glioblastoma patient survival.

OBJECTIVE: Glioblastoma multiforme (GBM) is the most common primary malignant central nervous system (CNS) tumor. The Stupp regimen is the standard treatment, although the optimal number of temozolomide (TMZ) treatment cycles remains controversial. We compared the effects of standard 6 cycles versus > 6 cycles of TMZ chemotherapy post-surgery with concurrent chemoradiotherapy on primary GBM patient survival. PATIENTS AND METHODS: We performed a single center retrospective study of GBM patients that underwent total resection, concurrent chemoradiotherapy, and at least 6 cycles of adjuvant TMZ chemotherapy from June 2011 to August 2018. Patients were divided into 2 groups based on adjuvant TMZ treatment plan: Group A(n = 27): standard 6-cycle adjuvant TMZ therapy and Group B(n = 26): > 6 cycles of adjuvant TMZ therapy. Primary endpoints were progression-free survival (PFS) and overall survival (OS). Continuous variables were analyzed by ANOVA, and the Kaplan-Meier method was used to evaluate PFS and OS. Univariate and multivariate COX analyses determined correlation between survival rates and covariates. We used The Mini Mental State Examination (MMSE) and Karnofsky Performance Status (KPS) to assess patients' neurocognitive function and quality of life. RESULTS: After follow-up, median PFS was 15 months in in Group A (95%CI 9.5-20.5) and 20.1 months in Group B (95%CI 15.9-24.4). Group A median OS was 19.4 months (95%CI 15.5-23.2), compared to 25.6 months in Group B (95%CI 20.4-30.8). The 2-year survival rate of Groups A and B was 36% was 66%, respectively (P = 0.02). and 5-year survival was 7% in both. Multivariate COX regression analysis showed association between patient PFS and long-period adjuvant chemotherapy, but not OS. There were no significant difference in disability or quality of life during treatment with Stupp protocol, but differences in MMSE and KPS were in favour of the Groups B after year 1 of the treatment (P < 0.05). CONCLUSIONS: Long-term adjuvant TMZ chemotherapy was beneficial for PFS and 2-year survival rate in GBM patients, and improved their quality of life contemporarily. But OS was not significantly improved.

Radiation-induced cavernous malformation after stereotactic radiosurgery for cavernous sinus meningioma: a case report.

BACKGROUND: Radiation-induced cavernous malformation (RICM) is a rare sequela of stereotactic radiosurgery (SRS) treatment of intracranial tumors. To date, no study reported on RICM after SRS for meningiomas originating from the skull base. The relationship between locus of initial meningioma and RICM has not been studied. CASE PRESENTATION: A 57-year-old woman presented with persistent headaches and blepharoptosis at initial episode. MRI disclosed a right parasellar lesion, diagnosed as a cavernous sinus meningioma (CSM). After receiving a single-fractionated SRS, headache relieved, but blepharoptosis did not significantly improve. Three years and three months later, she returned with headaches and dizziness. MRI showed an enlarged CSM. Moreover, a new mass-like lesion, suspected hemangioma, appeared in the nearby right temporal lobe. After surgical removal of the new lesion and the CSM, the patient's neurological symptoms significantly improved. Pathology confirmed CSM and temporal RICM. CONCLUSIONS: We report the first rare case of RICM occurring after SRS for CSM. The RICM may be in the same region as the initial tumor. Surgical intervention was preferred for symptomatic RICM and initial meningioma. We recommend long-term regular followup MRIs for patients with meningioma after SRS treatment.

Estrogen exacerbates mammary involution through neutrophil-dependent and -independent mechanism.

There is strong evidence that the pro-inflammatory microenvironment during post-partum mammary involution promotes parity-associated breast cancer. Estrogen exposure during mammary involution drives tumor growth through neutrophils' activity. However, how estrogen and neutrophils influence mammary involution are unknown. Combined analysis of transcriptomic, protein, and immunohistochemical data in BALB/c mice showed that estrogen promotes involution by exacerbating inflammation, cell death and adipocytes repopulation. Remarkably, 88% of estrogen-regulated genes in mammary tissue were mediated through neutrophils, which were recruited through estrogen-induced CXCR2 signalling in an autocrine fashion. While neutrophils mediate estrogen-induced inflammation and adipocytes repopulation, estrogen-induced mammary cell death was via lysosome-mediated programmed cell death through upregulation of cathepsin B, Tnf and Bid in a neutrophil-independent manner. Notably, these multifaceted effects of estrogen are mostly mediated by ERα and unique to the phase of mammary involution. These findings are important for the development of intervention strategies for parity-associated breast cancer.

TTC9A deficiency induces estradiol-mediated changes in hippocampus and amygdala neuroplasticity-related gene expressions in female mice.

The involvement of tetratricopeptide repeat domain 9A (TTC9A) deficiency in anxiety-like responses and behavioral despair through estradiol action on the serotonergic system has been reported. Emerging evidence suggests that estradiol is a potent modulator of neuroplasticity. As estradiol and neuroplasticity changes are both implicated in mood regulation, and estradiol activity is negatively regulated by TTC9A, we hypothesized that the behavioral changes induced by Ttc9a-/- is also mediated by neuroplasticity-related mechanisms. To understand the effects of TTC9A and estradiol modulation on neuroplasticity functions, we performed a behavioral analysis of tail suspension immobility and neuroplasticity-related gene expression study of brain samples collected in a previous study involving ovariectomized (OVX) Ttc9a-/- mice with estradiol or vehicle treatment. We observed that OVX-Ttc9a-/- mice had significantly reduced the tail suspension immobility compared to OVX-Ttc9a-/- estradiol-treated mice. Interestingly, there was an upregulation in gene expression of tropomyosin receptor kinase B (Trkb) in the ventral hippocampus, as well as brain-derived neurotrophic factor (Bdnf) and postsynaptic density protein-95 (Psd-95) in the amygdala of OVX-Ttc9a-/- mice compared to those treated with estradiol. These findings indicate that estradiol plays an inhibitory role in neuroplasticity in Ttc9a-/- mice. These observations were not found in the wildtype mice, as the presence of TTC9A suppressed the effects of estradiol. Our data suggest the behavioral alterations in Ttc9a-/- mice were mediated by estradiol regulation involving neuroplasticity-related mechanisms in both the hippocampus and amygdala regions.

Estrogen reprograms the activity of neutrophils to foster protumoral microenvironment during mammary involution.

Epidemiological studies have indicated increased risk for breast cancer within 10 years of childbirth. Acute inflammation during mammary involution has been suggested to promote this parity-associated breast cancer. We report here that estrogen exacerbates mammary inflammation during involution. Microarray analysis shows that estrogen induces an extensive proinflammatory gene signature in the involuting mammary tissue. This is associated with estrogen-induced neutrophil infiltration. Furthermore, estrogen induces the expression of protumoral cytokines/chemokines, COX-2 and tissue-remodeling enzymes in isolated mammary neutrophils and systemic neutrophil depletion abolished estrogen-induced expression of these genes in mammary tissue. More interestingly, neutrophil depletion diminished estrogen-induced growth of ERα-negative mammary tumor 4T1 in Balb/c mice. These findings highlight a novel aspect of estrogen action that reprograms the activity of neutrophils to create a pro-tumoral microenvironment during mammary involution. This effect on the microenvironment would conceivably aggravate its known neoplastic effect on mammary epithelial cells.

Tetratricopeptide repeat domain 9A modulates anxiety-like behavior in female mice.

Tetratricopeptide repeat domain 9A (TTC9A) expression is abundantly expressed in the brain. Previous studies in TTC9A knockout (TTC9A-/-) mice have indicated that TTC9A negatively regulates the action of estrogen. In this study we investigated the role of TTC9A on anxiety-like behavior through its functional interaction with estrogen using the TTC9A-/- mice model. A battery of tests on anxiety-related behaviors was conducted. Our results demonstrated that TTC9A-/- mice exhibited an increase in anxiety-like behaviors compared to the wild type TTC9A+/+ mice. This difference was abolished after ovariectomy, and administration of 17-ß-estradiol benzoate (EB) restored this escalated anxiety-like behavior in TTC9A-/- mice. Since serotonin is well-known to be the key neuromodulator involved in anxiety behaviors, the mRNA levels of tryptophan hydroxylase (TPH) 1, TPH2 (both are involved in serotonin synthesis), and serotonin transporter (5-HTT) were measured in the ventromedial prefrontal cortex (vmPFC) and dorsal raphe nucleus (DRN). Interestingly, the heightened anxiety in TTC9A-/- mice under EB influence is consistent with a greater induction of TPH 2, and 5-HTT by EB in DRN that play key roles in emotion regulation. In conclusion, our data indicate that TTC9A modulates the anxiety-related behaviors through modulation of estrogen action on the serotonergic system in the DRN.