Towards understanding of electrolyte degradation in lithium-mediated non-aqueous electrochemical ammonia synthesis with gas chromatography-mass spectrometry

Lithium-mediated electrochemical ammonia synthesis (LiMEAS) in non-aqueous media is a promising technique for efficient and green ammonia synthesis. Compared to the widely used Haber–Bosch process, the method reduces CO₂ emissions to zero due to the application of green hydrogen. However, the non-aqueous medium encounters the alkali metal lithium and organic components at high negative potentials of electrolysis, which leads to formation of byproducts. To assess the environmental risk of this synthesis method, standardized analytical methods towards understanding of the degradation level and consequences are needed. Here we report on the implementation of an approach to analyze the liquid electrolytes after electrochemical ammonia synthesis via high-resolution gas chromatography-mass spectrometry (GCMS). To characterize the molecular species formed after electrolysis, electron ionization high-resolution mass spectrometry (EI-MS) was applied. The fragmentation patterns enabled the elucidation of the mechanisms of byproduct formation. Several organic electrolytes were analyzed and compared both qualitatively and quantitatively to ascertain molecular composition and degradation products. It was found that the organic solvent in contact with metallic electrodeposited lithium induces solvent degradation, and the extent of this decomposition to different organic molecules depends on the organic solvent used. Our results show GCMS as a suitable technique for monitoring non-aqueous electrochemical ammonia synthesis in different organic electrolytes.

Lithium-mediated non-aqueous electrochemical ammonia synthesis (LiMEAS) as an efficient and green ammonia production way was studied by GCMS in different organic electrolytes to evaluate the stability of electrochemical systems.     

Targeted IL‐4 therapy synergizes with dexamethasone to induce a state of tolerance by promoting Treg cells and macrophages in mice with arthritis

F8‐IL‐4 is a recently developed immunocytokine that delivers IL‐4 to sites of inflammation by targeting the neovasculature. We previously reported that F8‐IL‐4, in combination with dexamethasone (DXM), provides a durable therapy in mice with collagen‐induced arthritis (CIA). Therefore, the objective of this study was to identify the mechanism by which IL‐4 and DXM combination therapy provides long‐lasting disease remission. F8‐IL‐4 alone attenuated inflammation in CIA and this was associated with increased T_H2 and decreased T_H17 cell numbers in the joints. Similarly, DXM alone had an antiinflammatory effect associated with lower T_H17 cell numbers. In both cases, these therapeutic benefits were reversed once treatment was stopped. On the other hand, combination therapy with F8‐IL‐4 plus DXM led to a synergistic increase in the percentage of regulatory T (Treg) cells and antiinflammatory macrophages in the arthritic joint and spleen as well as IL‐10 levels in serum and spleen. The net result of this was a more pronounced attenuation of inflammation and, more importantly, protection from arthritis relapse post therapy retraction. In conclusion, F8‐IL‐4 plus DXM is a durable treatment for arthritis that acts by promoting Treg cells in a synergistic manner, and by producing a sustained increase in antiinflammatory macrophages.     

Intraoperative radiation therapy for breast cancer: technical notes

Interest in intraoperative radiation therapy (IORT) for breast cancer is increasing as the possible benefits of this technique for the patient become apparent. The rationale for the use of this segmental radiation therapy in place of whole-breast irradiation is based on the finding that approximately 85% of breast relapses are confined to the same quadrant of the breast as the primary tumor. Phase I and II trials have demonstrated no increase in postsurgical complication rates following the use of single-dose IORT in localized breast cancers. Longer follow-up is needed to assess the cosmetic outcome. Clinical trials to evaluate the effectiveness of IORT in the treatment of breast cancer are currently under way at the European Institute of Oncology (EIO) at the University of Milan, Italy, and at Memorial Sloan-Kettering Cancer Center (MSKCC) in New York. Here we report the two different techniques in use in these trials.     

Primary therapy with ECF in combination with a GnRH analog in premenopausal women with hormone receptor-positive T2-T4 breast cancer

Patients with hormone receptor-positive tumors less often show a pathological complete response (pCR) than do those with hormone receptor-negative tumors. The addition of endocrine therapies may improve the clinical benefits of primary therapies in these patients. We investigated the efficacy of the epirubicin+cisplatin+fluorouracil (ECF) as continuous infusion) regimen in association with a gonadotropin-releasing hormone (GnRH) analog in 36 premenopausal women with T2-T4a-d N0-2 M0 ER and/or PgR-positive breast cancer. Median age was 39.5 years (range 26-53). Clinical response (complete or partial) was observed in 27 out of 36 patients (75% 95% CI 57.8-87.9%) and a pCR was observed in four patients (11%). Nine (25%) patients had stable disease and no progression was observed. Twenty-one patients (58%) were submitted for breast-conserving surgery and 15 had a radical mastectomy. No baseline clinical and biological characteristics significantly correlated with response. Thirty out of 31 patients evaluable for endocrine assessment had documented ovarian suppression, which occurred after a median of 28 days (range 20-43). We conclude that the combination of ECF and a GnRH analog is associated with a high response rate in the primary treatment of breast cancer. Further studies combining chemotherapy and endocrine agents are warranted in patients with hormone receptor-positive tumors.     

Patterns of Cerebrospinal Fluid Alzheimer’s Dementia Biomarkers in People Living with HIV: Cross-Sectional Study on Associated Factors According to Viral Control,Neurological Confounders and Neurocognition

People living with HIV (PLWH) age with an excess burden of comorbidities that may increase the incidence of age-related complications. There is controversy surrounding the hypothesis that HIV can accelerate neurodegeneration and Alzheimer’s dementia (AD). We performed a retrospective study to analyze the distribution of cerebrospinal fluid (CSF) AD biomarkers (beta amyloid 1–42 fragment, tau, and phosphorylated tau) in adult PLWH (on cART with undetectable viremia, n = 136, with detectable viremia, n = 121, and with central nervous system CNS disorders regardless of viremia, n = 72) who underwent a lumbar puncture between 2008 to 2018; HIV-negative controls with AD were included (n = 84). Five subjects (1.5%) presented CSF biomarkers that were compatible with AD: one was diagnosed with AD, whereas the others showed HIV encephalitis, multiple sclerosis, cryptococcal meningitis, and neurotoxoplasmosis. Regardless of confounders, 79.6% of study participants presented normal CSF AD biomarkers. Isolated abnormalities in CSF beta amyloid 1–42 (7.9%) and tau (10.9%) were associated with age, biomarkers of intrathecal injury, and inflammation, although no HIV-specific feature was associated with abnormal CSF patterns. CSF levels of AD biomarkers very poorly overlapped between HIV-positive clinical categories and AD controls. Despite the correlations with neurocognitive performance, the inter-relationship between amyloid and tau proteins in PLWH seem to differ from that observed in AD subjects; the main driver of the isolated increase in tau seems represented by non-specific CNS inflammation, whereas the mechanisms underlying isolated amyloid consumption remain unclear.