Phonolite Material as Catalyst Support for the Hydrotreatment of Gas Oil and Vegetable Oil Type Feedstocks

Phonolite material has shown to be promising catalyst support for the deoxygenation of triglycerides. In this work, we continue with our previous research by synthesising and testing three acid-treated phonolite-supported Co-Mo, Ni-Mo and Ni-W catalysts for the hydrotreating of atmospheric gas oil and co-processing with rapeseed oil at industrial operating conditions (350–370 °C, WHSV 1–2 h⁻¹, 5.5 MPa) in the continuous regime for more than 270 h. The phonolite-supported catalysts showed hydrotreating activity comparable with commercial catalysts, together with a complete conversion of triglycerides into n-alkanes. During co-processing, the Ni-promoted catalyst showed strong stability, with similar activity previous to the rapeseed oil addition. Our results enable us to evaluate the suitability of phonolite as catalyst support for the development of plausible alternatives to conventional hydrotreating catalysts for the co-processing of middle distillates with vegetable oils.     

Post-immunization pneumococcal antibody titers and IgG subclasses

IgG antibodies against pneumococcal polysaccharides are found predominantly within IgG subclass 2. We wished to evaluate retrospectively IgG subclasses and post-immunization pneumococcal antibody titers in children with recurrent respiratory infections. We examined total immunoglobulin levels and IgG subclasses, as well as pneumococcal antibody titers against serotypes 3, 7F, 9N, and 14 present 4–6 weeks after pneumococcal immunization in 56 children 2–18 years old. Titers >200 ng Ab N/ml to any of the 4 serotypes tested were arbitrarily considered protective. Four patients did not have protective antibody levels against any of the 4 serotypes tested following vaccination. Of those, 3 had normal IgG subclass levels and 1 had an IgG2 subclass deficiency. Of 3 additional patients with IgG2 deficiency, 2 had protective antibody levels to only 1 serotype and 1 had protective antibody levels to 2 serotypes. Furthermore, in 2 patients with undetectable IgG2 at the time of immunization, the response was only transient. We conclude that patients with IgG2 deficiency may not develop protective antibody levels to all pneumococcal serotypes and that some may have deficient memory for IgG anti-pneumococcal polysaccharide antibodies. Pediatr Pulmonol. 1996; 22:167–173. © 1996 Wiley-Liss, Inc.     

Lipotoxicity,neuroinflammation, glial cells and oestrogenic compounds

The high concentrations of free fatty acids as a consequence of obesity and being overweight have become risk factors for the development of different diseases, including neurodegenerative ailments. Free fatty acids are strongly related to inflammatory events, causing cellular and tissue alterations in the brain, including cell death, deficits in neurogenesis and gliogenesis, and cognitive decline. It has been reported that people with a high body mass index have a higher risk of suffering from Alzheimer's disease. Hormones such as oestradiol not only have beneficial effects on brain tissue, but also exert some adverse effects on peripheral tissues, including the ovary and breast. For this reason, some studies have evaluated the protective effect of oestrogen receptor (ER) agonists with more specific tissue activities, such as the neuroactive steroid tibolone. Activation of ERs positively affects the expression of pro‐survival factors and cell signalling pathways, thus promoting cell survival. This review aims to discuss the relationship between lipotoxicity and the development of neurodegenerative diseases. We also elaborate on the cellular and molecular mechanisms involved in neuroprotection induced by oestrogens.     

Giant intracranial germinoma

Journal of Neuro-Oncology -     

Involvement of ryanodine receptors in neurotrophin-induced hippocampal synaptic plasticity and spatial memory formation

Ryanodine receptors (RyR) amplify activity-dependent calcium influx via calcium-induced calcium release. Calcium signals trigger postsynaptic pathways in hippocampal neurons that underlie synaptic plasticity, learning, and memory. Recent evidence supports a role of the RyR2 and RyR3 isoforms in these processes. Along with calcium signals, brain-derived neurotrophic factor (BDNF) is a key signaling molecule for hippocampal synaptic plasticity and spatial memory. Upon binding to specific TrkB receptors, BDNF initiates complex signaling pathways that modify synaptic structure and function. Here, we show that BDNF-induced remodeling of hippocampal dendritic spines required functional RyR. Additionally, incubation with BDNF enhanced the expression of RyR2, RyR3, and PKMζ, an atypical protein kinase C isoform with key roles in hippocampal memory consolidation. Consistent with their increased RyR protein content, BDNF-treated neurons generated larger RyR-mediated calcium signals than controls. Selective inhibition of RyR-mediated calcium release with inhibitory ryanodine concentrations prevented the PKMζ, RyR2, and RyR3 protein content enhancement induced by BDNF. Intrahippocampal injection of BDNF or training rats in a spatial memory task enhanced PKMζ, RyR2, RyR3, and BDNF hippocampal protein content, while injection of ryanodine at concentrations that stimulate RyR-mediated calcium release improved spatial memory learning and enhanced memory consolidation. We propose that RyR-generated calcium signals are key features of the complex neuronal plasticity processes induced by BDNF, which include increased expression of RyR2, RyR3, and PKMζ and the spine remodeling required for spatial memory formation.     

Mechanisms involved in the effects of phenidone, diclofenac and ethacrynic acid in rat uterus in vitro.

1. The effects of phenidone (P, 10(-4)-10(-3) M), sodium diclofenac (D, 10(-5)-10(-4) M) and ethacrynic acid (E, 10(-5)-10(-4) M), proposed as inhibitors of eicosanoid synthesis, on the contractions of rat uterus induced by several agonists have been studied. 2. P, D and E inhibit the motility induced by oxytocin (4 mU/ml) (IC50: 4.62 x 10(-4), 2.55 x 10(-4) and 2.98 x 10(-5) M, respectively). 3. P (10(-3) M), D (10(-4) M) and E (10(-4) M) also inhibit the contraction induced by methacholine (10(-5) M), prostaglandin F2a (10(-6) M) and CaCl2 (6 mM), and relaxed, in a dose-dependent way, the tonic component of contraction to KCl (60 mM) (IC50: 5.81 x 10(-4), 6.67 x 10(-5) and 7.55 x 10(-5) M, respectively). 4. The CaCl2 (0.1-10 mM) reverted the relaxation of KCl contraction produced by P, but not by D or E. None of the inhibitions on CaCl2 (6 mM) are reverted by Bay K 8644. 5. D and E also relaxed the tonic contraction to vanadate (10(-4) M) in uterus incubated in calcium free solution P, enhances the vanadate-induced contractions.     

Effects of antiandrogens and progesterone on isolated rat uterus.

1. The effect of progesterone (P, 6 x 10(-6)-6 x 10(-5) M) and the antiandrogens cyproterone acetate (CPA, 10(-7)-10(-5) M), flutamide (F, 10(-6)-6 x 10(-5) M) and spironolactone (S, 10(-6)-6 x 10(-5) M) on the KCl-induced tonic contraction of the isolated rat uterus have been assayed. 2. The antiandrogens relaxed, in a dose-dependent way, the KCl-induced contraction (EC50, 2.804 +/- 0.506 x 10(-6); 1.671 +/- 0.308 x 10(-5); and 3.042 +/- 0.14 x 10(-5) M, respectively for CPA, S and F). P also relaxed the KCl-induced contraction (EC50, 2.436 +/- 0.524 x 10(-5) M). 3. CaCl2 (0.1-10 mM) counteracted the relaxing effect of CPA, S, F, and P, respectively, up to 100, 80.63, 60.66 and 90.57%. 4. The 17-OH-progesterone derivative CPA, but not S or F, reduces at small doses (6 x 10(-8) M), but not at higher concentrations (6 x 10(-7)-6 x 10(-6) M), the relaxing effect of progesterone.     

Outcome and Hepatic Hemodynamics in Liver Transplant Patients with Portal Vein Arterialization

Few cases of successful portal vein arterialization in orthotopic and auxiliary liver transplantation have been reported. AIM: To evaluate the effect of portal vein arterialization on hepatic hemodynamics and long-term clinical outcome in three patients undergoing liver transplantation. METHODS: Two patients with extensive splanchnic venous thrombosis received an orthotopic liver transplant and one with fulminant hepatic failure received an auxiliary heterotopic graft. Portal vein arterialization was performed in all cases. RESULTS: One patient died 4 months after transplant and two are still alive. Auxiliary liver graft was removed 3 months post-transplant when complete native liver regeneration was achieved. Immediate post-transplant liver function was excellent in all cases. Only one patient developed encephalopathy and variceal bleeding owing to prehepatic portal hypertension secondary to arterioportal fistula 14 months after transplant. He was successfully treated by embolization of the hepatic artery. Hepatic hemodynamic measurements demonstrated a normal pressure gradient between wedged and free hepatic venous pressures in all cases. Liver biopsy showed acceptable graft architecture in two cases and microsteatosis in one. CONCLUSIONS: Liver transplantation with portal vein arterialization is an acceptable salvage alternative when insufficient portal venous flow to the graft is present. The double arterial supply does not imply changes in hepatic hemodynamics, at least in the early months post-transplant.