The curse of the Romanovs a study of the lives and reigns of two tsars Paul I and Alexander I of Russia: 1754-1825.

Bibliography: p. 413-416.

H.R.M. Prince Henry Maurice of Battenberg K.G. : a memoir /

Mode of access: Internet.

The comedies, histories, and tragedies of Mr. William Shakespeare as presented at the Globe and Blackfriars Theatres, circa 1591-1623 : being the text furnished the players, in parallel pages with the first revised folio text, with critical introductions : the Bankside Shakespeare /

"Five hundred copies only"--V. 1, p. [43].

Congress of arts and science, Universal exposition, St. Louis, 1904;

"Special works of reference" (accompanying particularly Professor Boltzmann's address)": v. 1, p. [625]-626.

Diary and correspondence of John Evelyn, F.R.S., to which is subjoined the private correspondence between King Charles I and Sir Edward Nicholas, and between Sir Edward Hyde, afterwards Earl of Clarendon, and Sir Richard Browne.

Half-title of v. 4: Bohn's historical library.

Autobiography and life of George Tyrrell

I. Autobiography of George Tyrrell, 1861-1884.--II. Life of George Tyrrell from 1884 to 1909.

Monte Carlo Study of Particle Transport Problem in Air Pollution

2002 Mathematics Subject Classification: 65C05.

The syntheses and characterization of nickel complexes; investigation of Ni(dppp)2 and [NiX(dppp)n]x, potentially catalytically active nickel(0)/(I) species for cross-coupling reactions

This thesis describes an investigation in which we compare Ni(0), Ni(I) and Ni(II) complexes containing 1,3-bis(diphenylphosphino)propane (dppp) as a phosphine ligand for their abilities to effect three types of cross-coupling reactions: Buchwald-Hartwig Amination, Heck-Mizoroki, and Suzuki-Miyaura cross-coupling reactions with different types of substrates. The Ni(0) complex Ni(dppp)2 is known and we have synthesized it via a new procedure involving zinc reduction of the known NiCl2(dppp) in the presence of an excess of dppp. The Ni(0) complex was characterized by NMR spectroscopy and X-ray crystallography. Since Ni(I) complexes of dppp seem unknown, we have synthesized what at this stage appear to be NiXdpppn/[NiX(dppp)n]x (X = Cl, Br, I; n = 1,2, x = 1, 2) by comproportionation of molar equivalents of Ni(dppp)2 and NiX2dppp, X= Cl, Br, I.

Посланието на патриарх Фотий до българския княз Борис-Михаил и неговият славянски превод

Статията разглежда славянския превод на Посланието на патриарх Фотий до българския княз Борис- Михаил, запазен само в руски преписи от началото на XVI до началото на XX в. Специално внимание се отделя на езика на славянския превод (правопис, морфосинтаксис, лексика и словообразуване), чрез който става възможно датирането на превода, тъй като липсват всякакви други (литературни, исторически, палеографски, кодикологични) сведения за това. Изследването на езика позволява пре- водът да се отнесе към книжовната продукция на XIV в. и по-точно към школата на Евтимий Търновски. Причината за появата на славянския превод на Фотиевия трактат трябва да се търси в основното послание на съчинението – запазване устоите на християнската вяра и въплъщаването й в държавното управление.

Life without complex I: proteome analyses of an Arabidopsis mutant lacking the mitochondrial NADH dehydrogenase complex

The mitochondrial NADH dehydrogenase complex (complex I) is of particular importance for the respiratory chain in mitochondria. It is the major electron entry site for the mitochondrial electron transport chain (mETC) and therefore of great significance for mitochondrial ATP generation. We recently described an Arabidopsis thaliana double-mutant lacking the genes encoding the carbonic anhydrases CA1 and CA2, which both form part of a plant-specific 'carbonic anhydrase domain' of mitochondrial complex I. The mutant lacks complex I completely. Here we report extended analyses for systematically characterizing the proteome of the ca1ca2 mutant. Using various proteomic tools, we show that lack of complex I causes reorganization of the cellular respiration system. Reduced electron entry into the respiratory chain at the first segment of the mETC leads to induction of complexes II and IV as well as alternative oxidase. Increased electron entry at later segments of the mETC requires an increase in oxidation of organic substrates. This is reflected by higher abundance of proteins involved in glycolysis, the tricarboxylic acid cycle and branched-chain amino acid catabolism. Proteins involved in the light reaction of photosynthesis, the Calvin cycle, tetrapyrrole biosynthesis, and photorespiration are clearly reduced, contributing to the significant delay in growth and development of the double-mutant. Finally, enzymes involved in defense against reactive oxygen species and stress symptoms are much induced. These together with previously reported insights into the function of plant complex I, which were obtained by analysing other complex I mutants, are integrated in order to comprehensively describe 'life without complex I'.

The origins of the Inquisition in Andalusia

Es bien conocido que los primeros tribunales de la nueva Inquisición fueron establecidos por Fernando e Isabel en Andalucía, tanto en Sevilla como en Córdoba. Su introducción fue, por supuesto, el resultado de un claro propósito de lograr la ortodoxia religiosa entre los cristianos de origen judío los llamados «cristianos nuevos» o conversos. Pero el contexto político también influyó en la nueva institución porque contribuyó a asegurar el régimen de Isabel tras la amenaza que había representado su rival Juana “La- Beltraneja” y su marido portugués, al tiempo que podía servir para controlar mejor los conflictos entre «bandos», especialmente en Andalucía. Con todo, no debería pensarse que la Inquisición y sus horrores fueron una cuestión solamente atribuible a España. Por el contrario, tuvo sus precedentes y paralelos en otros países europeos, entre ellos Francia, Italia e Inglaterra.

Toxicological impact of JWH-018 and its phase I metabolite N-(3-hydroxypentyl) on human cell lines

"The emergence and abuse of synthetic cannabinoids has been increasing as an alternative to cannabis, mainly among youth. As their appearance on the drug market has been recent, the pharmacological and toxicological profiles of these psychoactive substances are poorly understood. Current studies suggest that they have stronger effects compared to their natural alternatives and their metabolites retain affinity towards CB1 receptors in CNS. Since studies on its toxicological properties are scarce, the effects of the drug in human derived cell lines were investigated. The present study was designed to explore the toxicological impact of parent drug versus phase I metabolites of synthetic cannabinoids on human cells with and without CB1 receptor. The human cell line of neuroblastoma SH-SY5Y and human kidney cell line HEK-293T were exposed to JWH-018 and to its N-(3-hydroxypentyl) metabolite. Cell toxicity was evaluated using the MTT and LDH assay. Additionally, a dual staining methodology with fluorescent Annexin V-FITC and propidium iodide was performed to address the question of whether JWH-018 N-(3-hydroxypentyl) metabolite is inducing cell death through apoptosis or necrosis, in HEK293T and SH-SY5Y cell lines. The obtained results show that JWH-018 does not cause a statistically significant decrease in cell viability, in contrast to its N-(3-hydroxypentyl) metabolite, which at ≥25μM causes a significant decrease in cell viability. Both cell lines are affected by JWH-018 metabolite. Our results point to higher toxicity of JWH-018 metabolite when compared to its parent drug, suggesting a non-CB1 receptor mediated toxicological mechanism. Comparing the results from Annexin V/PI with MTT and LDH assays of SH-SY5Y and HEK293T in the presence of the synthetic cannabinoid metabolite, emerges the picture that cellular viability decreases and associated death is occurring through necrosis."

Rapamycin reverses age-related increases in mitochondrial ROS production at complex I, oxidative stress, accumulation of mtDNA fragments inside nuclear DNA, and lipofuscin level, and increases autophagy, in the liver of middle-aged mice

Rapamycin consistently increases longevity in mice although the mechanism of action of this drug is unknown. In the present investigation we studied the effect of rapamycin on mitochondrial oxidative stress at the same dose that is known to increase longevity in mice (14 mg of rapamycin/kg of diet). Middle aged mice (16 months old) showed significant age-related increases in mitochondrial ROS production at complex I, accumulation of mtDNA fragments inside nuclear DNA, mitochondrial protein lipoxidation, and lipofuscin accumulation compared to young animals (4 months old) in the liver. After 7 weeks of dietary treatment all those increases were totally or partially (lipofuscin) abolished by rapamycin, middle aged rapamycin-treated animals showing similar levels in those parameters to young animals. The decrease in mitochondrial ROS production was due to qualitative instead of quantitative changes in complex I. The decrease in mitochondrial protein lipoxidation was not due to decreases in the amount of highly oxidizable unsaturated fatty acids. Rapamycin also decreased the amount of RAPTOR (of mTOR complex) and increased the amounts of the PGC1-α and ATG13 proteins. The results are consistent with the possibility that rapamycin increases longevity in mice at least in part by lowering mitochondrial ROS production and increasing autophagy, decreasing the derived final forms of damage accumulated with age which are responsible for increased longevity. The decrease in lipofuscin accumulation induced by rapamycin adds to previous information suggesting that the increase in longevity induced by this drug can be due to a decrease in the rate of aging. © 2016 Elsevier Inc.

FY 2014-15 & 2015-16 Evaluation of State-Funded Full-Day 4K, part I

This report documents the expansion of 4K and expenditure of funds in Fiscal Years 2014-15 and 2015-16; provides 2015-16 projections for the number of at-risk four-year-olds in each school district and the number of at-risk four-year-olds served in a publicly funded program using available information; details the results of the CIRCLE assessment, which was administered to children in publicly-funded four-year-old (4K) and five-year-old (5K) kindergarten during the 2014-15 school year; describes the four language and literacy assessments that measure 4K and 5K students’ abilities during the 2015-16 school year; and discusses how 4K quality can be defined and the important role of teacher-child instructional interactions in assessing quality of publicly-funded 4K.

Participation of neuronal nitric oxide synthase in experimental neuropathic pain induced by sciatic nerve transection

Nerve injury leads to a neuropathic pain state that results from central sensitization. This phenomenom is mediated by NMDA receptors and may involve the production of nitric oxide (NO). In this study, we investigated the expression of the neuronal isoform of NO synthase (nNOS) in the spinal cord of 3-month-old male, Wistar rats after sciatic nerve transection (SNT). Our attention was focused on the dorsal part of L3-L5 segments receiving sensory inputs from the sciatic nerve. SNT resulted in the development of neuropathic pain symptoms confirmed by evaluating mechanical hyperalgesia (Randall and Selitto test) and allodynia (von Frey hair test). Control animals did not present any alteration (sham-animals). The selective inhibitor of nNOS, 7-nitroindazole (0.2 and 2 µg in 50 µL), blocked hyperalgesia and allodynia induced by SNT. Immunohistochemical analysis showed that nNOS was increased (48% by day 30) in the lumbar spinal cord after SNT. This increase was observed near the central canal (Rexed’s lamina X) and also in lamina I-IV of the dorsal horn. Real-time PCR results indicated an increase of nNOS mRNA detected from 1 to 30 days after SNT, with the highest increase observed 1 day after injury (1469%). Immunoblotting confirmed the increase of nNOS in the spinal cord between 1 and 15 days post-lesion (20%), reaching the greatest increase (60%) 30 days after surgery. The present findings demonstrate an increase of nNOS after peripheral nerve injury that may contribute to the increase of NO production observed after peripheral neuropathy.