Thirty Years of Radio Observations of Type Ia SN 1972E and SN 1895B: Constraints on Circumstellar Shells

We have imaged over 35 years of archival Very Large Array (VLA) observations of the nearby (d$_{\rm{L}}$ $=$ 3.15 Mpc) Type Ia supernovae SN\,1972E and SN\,1895B between 9 and 121 years post-explosion. No radio emission is detected, constraining the 8.5 GHz luminosities of SN\,1972E and SN\,1895B to be L$_{\nu,8.5\rm{GHz}}$ $<$ 6.0 $\times$ 10$^{23}$ erg s$^{-1}$ Hz$^{-1}$ 45 years post-explosion and L$_{\nu,8.5\rm{GHz}}$ $<$ 8.9 $\times$ 10$^{23}$ erg s$^{-1}$ Hz$^{-1}$ 121 years post-explosion, respectively. These limits imply a clean circumstellar medium (CSM), with $n$ $<$ 0.9 cm$^{-3}$ out to radii of a few $\times$ 10$^{18}$ cm, if the SN blastwave is expanding into uniform density material. Due to the extensive time coverage of our observations, we also constrain the presence of CSM shells surrounding the progenitor of SN\,1972E. We rule out essentially all medium and thick shells with masses of 0.05$-$0.3 M$_\odot$ at radii between $\sim$10$^{17}$ and 10$^{18}$ cm, and thin shells at specific radii with masses down to $\lesssim$0.01 M$_\odot$. These constraints rule out swaths of parameter space for a range of single and double degenerate progenitor scenarios, including recurrent nova, core-degenerate objects, ultra-prompt explosions and white dwarf (WD) mergers with delays of a few hundred years between the onset of merger and explosion. Allowed progenitors include WD-WD systems with a significant ($>$ 10$^{4}$ years) delay from the last episode of common envelope evolution and single degenerate systems undergoing recurrent nova, provided that the recurrence timescale i short and the system has been in the nova phase for $\gtrsim$10$^{4}$ yr, such that a large ($>$ 10$^{18}$ cm) cavity has been evacuated. Future multi-epoch observations of additional intermediate-aged Type Ia SNe will provide a comprehensive view of the large-scale CSM environments around these explosions.Comment: Accepted for publication in the Astrophysical Journa

Mesial Temporal Lobe Epilepsy Syndrome: An Updated Overview

Mesial temporal lobe epilepsy (MTLE) is the most common form of partial epilepsy in young adults and also the most frequent type of epilepsy reported in surgical series worldwide. Mesial temporal lobe sclerosis (MTS) is the major underlying cause of MTLE, and it is present in 60-70% of patients with MTLE who undergo surgery for treatment of medically refractory seizures. Pathogenetic mechanisms underlying this distinct hippocampal pathology remains undetermined. Recent findings suggest a developmental malformation of hippocampus (inherited or acquired) that in association with subsequent injury (e.g. trauma, infection, complex febrile seizures) could develop ongoing seizures, resulting in the full-blown neuropathological features of MTS. Genetic background, age and type of initial precipitating injury, and vulnerability related to programmed cell death pathways are probable mechanisms involved in the development of MTS. Definitions for medical intractability may vary among centers, but usually include failure to achieve seizure control with two or more AEDs with adequate dosage and posology. The decision as to when one should perform surgery in patients with MTLE is a relevant issue that needs more investigation. Recent evidence discussed in this review indicates that longer duration of uncontrolled seizures is associated with an increased risk of unsuccessful surgery.113141144Cendes F, Kahane P, Brodie MJ, Andermann F. The mesio-temporal lobe epilepsy syndrome. In: Roger J, Bureau M, Dravet C, Genton P, Tassinari CA, Wolf P, editors. Epileptic syndromes in infancy, childhood and adolescence. 3 rd ed. Eastleigh UK: John Libbey &ampCo Ltd2002. p.513-30Kobayashi, E., Lopes-Cendes, I., Guerreiro, C.A., Sousa, S.C., Guerreiro, M.M., Cendes, F., Seizure outcome and hippocampal atrophy in familial mesial temporal lobe epilepsy (2001) Neurology, 56, pp. 166-172Gloor, P., Mesial temporal sclerosis: Historical background and an overview from a modern perspective (1991) Epilepsy surgery, pp. 689-703. , Luders H, editor, New York: Raven Press;Meencke, H.J., Veith, G., Hippocampal sclerosis in epilepsy (1991) Epilepsy surgery, pp. 705-715. , Luders H, ed, New York: Raven Press;Bruton, C.J., (1988) The neuropathology of temporal lobe epilepsy, , New York: Oxford University Press;Camfield, C.S., Camfield, P.R., Gordon, K., Wirrell, E., Dooley, J.M., Incidence of epilepsy in childhood and adolecesce - A population-based study in Nova Scotia from 1977 to 1985 (1996) Epilepsia, 37, pp. 19-23Camfield, P., Camfield, C., Gordon, K., Dooley, J., What types of epilepsy are preceded by febrile seizures? A population-based study of children (1994) Dev Med Child Neurol, 36, pp. 887-892Cendes, F., Febrile seizures and mesial temporal sclerosis (2004) Curr Opin Neurol, 17, pp. 161-164VanLandingham, K.E., Heinz, E.R., Cavazos, J.E., Lewis, D.V., Magnetic resonance imaging evidence of hippocampal injury after prolonged focal febrile convulsions (1998) Ann Neurol, 43, pp. 413-426Kobayashi, E., D'Agostino, M.D., Lopes-Cendes, I., Berkovic, S.F., Li, M.L., Andermann, E., Hippocampal atrophy and T2-weighted signal changes in familial mesial temporal lobe epilepsy (2003) Neurology, 60, pp. 405-409Cendes, F., Progressive hippocampal and extrahippocampal atrophy in drug resistant epilepsy (2005) Curr Opin Neurol, 18, pp. 173-177Blumcke, I., Thom, M., Wiestler, O.D., Ammon's horn sclerosis: A maldevelopmental disorder associated with temporal lobe epilepsy (2002) Brain Pathol, 12, pp. 199-211Mathern, G.W., Pretorius, J.K., Babb, T.L., Influence of the type of initial precipitating injury and at what age it occurs on course and outcome in patients with temporal lobe seizures (1995) J Neurosurg, 82, pp. 220-227Mathern, G.W., Babb, T.L., Leite, J.P., Pretorius, K., Yeoman, K.M., Kuhlman, P.A., The pathogenic and progressive features of chronic human hippocampal epilepsy (1996) Epilepsy Res, 26, pp. 151-161Shinoda, S., Schindler, C.K., Meller, R., So, N.K., Araki, T., Yamamoto, A., Bim regulation may determine hippocampal vulnerability after injurious seizures and in temporal lobe epilepsy (2004) J Clin Invest, 113, pp. 1059-1068Kobayashi, E., Li, L.M., Lopes-Cendes, I., Cendes, F., Magnetic resonance imaging evidence of hippocampal sclerosis in asymptomatic, first-degree relatives of patients with familial mesial temporal lobe epilepsy (2002) Arch Neurol, 59, pp. 1891-1894Kim, W.J., Park, S.C., Lee, S.J., Lee, J.H., Kim, J.Y., Lee, B.I., The prognosis for control of seizures with medications in patients with MRI evidence for mesial temporal sclerosis (1999) Epilepsia, 40, pp. 290-293Montenegro, M.A., Ferreira, C.M., Cendes, F., Li, L.M., Guerreiro, C.A., Clobazam as add-on therapy for temporal lobe epilepsy and hippocampal sclerosis (2005) Can J Neurol Sci, 32, pp. 93-96Rodin, E.A., (1968) The prognosis of patients with epilepsy, , Springfield: Charles C. Thomas;Sillanpaa, M., Remission of seizures and predictors of intractability in long-term follow-up (1993) Epilepsia, 34, pp. 930-936Camfield, C., Camfield, P., Smith, B., Gordon, K., Dooley, J., Biologic factors as predictors of social outcome of epilepsy in intellectually normal children: A population-based study (1993) J Pediatr, 122, pp. 869-873Semah, F., Picot, M.C., Adam, C., Broglin, D., Arzimanoglou, A., Bazin, B., Is the underlying cause of epilepsy a major prognostic factor for recurrence? (1998) Neurology, 51, pp. 1256-1262Wiebe, S., Blume, W.T., Girvin, J.P., Eliasziw, M., A randomized, controlled trial of surgery for temporal-lobe epilepsy (2001) N Engl J Med, 345, pp. 311-318Yoon, H.H., Kwon, H.L., Mattson, R.H., Spencer, D.D., Spencer, S.S., Long-term seizure outcome in patients initially seizure-free after resective epilepsy surgery (2003) Neurology, 61, pp. 445-450Trevathan, E., Gilliam, F., Lost years: Delayed referral for surgically treatable epilepsy (2003) Neurology, 61, pp. 432-433Gilliam, F., Kuzniecky, R., Meador, K., Martin, R., Sawrie, S., Viikinsalo, M., Patient-oriented outcome assessment after temporal lobectomy for refractory epilepsy (1999) Neurology, 53, pp. 687-694Berg, A.T., Langfitt, J., Shinnar, S., Vickrey, B.G., Sperling, M.R., Walczak, T., How long does it take for partial epilepsy to become intractable? (2003) Neurology, 60, pp. 186-19

Striatal and extrastriatal atrophy in Huntington's disease and its relationship with length of the CAG repeat

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that affects the striatum most severely. However, except for juvenile forms, relative preservation of the cerebellum has been reported. The objective of the present study was to perform MRI measurements of caudate, putamen, cerebral, and cerebellar volumes and correlate these findings with the length of the CAG repeat and clinical parameters. We evaluated 50 consecutive patients with HD using MRI volumetric measurements and compared them to normal controls. Age at onset of the disease ranged from 4 to 73 years (mean: 43.1 years). The length of the CAG repeat ranged from 40 to 69 (mean: 47.2 CAG). HD patients presented marked atrophy of the caudate and putamen, as well as reduced cerebellar and cerebral volumes. There was a significant correlation between age at onset of HD and length of the CAG repeat, as well as clinical disability and age at onset. The degree of basal ganglia atrophy correlated with the length of the CAG repeat. There was no correlation between cerebellar or cerebral volume and length of the CAG repeat. However, there was a tendency to a positive correlation between duration of disease and cerebellar atrophy. While there was a negative correlation of length of the CAG repeat with age at disease onset and with striatal degeneration, its influence on extrastriatal atrophy, including the cerebellum, was not clear. Extrastriatal atrophy occurs later in HD and may be related to disease duration.1129113

Thalamic metabolic abnormalities in patients with Huntington's disease measured by magnetic resonance spectroscopy

Huntington's disease (HD) is a neurologic disorder that is not completely understood; its fundamental physiological mechanisms and chemical effects remain somewhat unclear. Among these uncertainties, we can highlight information about the concentrations of brain metabolites, which have been widely discussed. Concentration differences in affected, compared to healthy, individuals could lead to the development of useful tools for evaluating the progression of disease, or to the advance of investigations of different/alternative treatments. The aim of this study was to compare the thalamic concentration of metabolites in HD patients and healthy individuals using magnetic resonance spectroscopy. We used a 2.0-Tesla magnetic field, repetition time of 1500 ms, and echo time of 135 ms. Spectra from 40 adult HD patients and 26 control subjects were compared. Quantitative analysis was performed using the LCModel method. There were statistically significant differences between HD patients and controls in the concentrations of N-acetylaspartate+N-acetylaspartylglutamate (NAA+NAAG; t-test, P&lt;0.001), and glycerophosphocholine+phosphocholine (GPC+PCh; t-test, P=0.001) relative to creatine+phosphocreatine (Cr+PCr). The NAA+NAAG/Cr+PCr ratio was decreased by 9% and GPC+PCh/Cr+PCr increased by 17% in patients compared with controls. There were no correlations between the concentration ratios and clinical features. Although these results could be caused by T1 and T2 changes, rather than variations in metabolite concentrations given the short repetition time and long echo time values used, our findings point to thalamic dysfunction, corroborating prior evidence.72272

The Re-Acceleration of the Shock Wave in the Radio Remnant of SN 1987A

We report on updated radio imaging observations of the radio remnant of Supernova 1987A (SN 1987A) at 9 GHz, taken with the Australia Telescope Compact Array (ATCA), covering a 25-year period (1992-2017). We use Fourier modeling of the supernova remnant to model its morphology, using both a torus model and a ring model, and find both models show an increasing flux density, and have shown a continuing expansion of the remnant. As found in previous studies, we find the torus model most accurately fits our data, and has shown a change in the remnant expansion at Day 9,300 $\pm$210 from 2,300 $\pm$200 km/s to 3,610 $\pm$240 km/s. We have also seen an increase in brightness in the western lobe of the remnant, although the eastern lobe is still the dominant source of emission, unlike what has been observed at contemporary optical and X-ray wavelengths. We expect to observe a reversal in this asymmetry by the year $\sim$2020, and note the south-eastern side of the remnant is now beginning to fade, as has also been seen in optical and X-ray data. Our data indicate that high-latitude emission has been present in the remnant from the earliest stages of the shockwave interacting with the equatorial ring around Day 5,000. However, we find the emission has become increasingly dominated by the low-lying regions by Day 9,300, overlapping with the regions of X-ray emission. We conclude that the shockwave is now leaving the equatorial ring, exiting first from the south-east region of the remnant, and is re-accelerating as it begins to interact with the circumstellar medium beyond the dense inner ring.Comment: 22 pages, 14 figures. Accepted to Ap

Pharmacogenetics Reality Or Fction? Or Are We There Yet?

[No abstract available]6902:00:00151152Twardowschy, C.A., Werneck, L.C., Scola, R.H., Depaola, L., Silvado, C.E., CYP2C9 polymorphisms in patients with epilepsy. Genotypic frequency analyzes and phe-nytoin adverse reactions correlations (2011) Arq Neurop-siquiatr, 69, pp. 153-158Glauser, T., Bem-Menachen, E., Bourgeois, B., ILAE treatment guidelines: Evidence-based analysis of an-tiepileptic drug efcacy and efectiveness as initialmonotherapy for epileptic seizures and syndromes (2006) Epilepsia, 47, pp. 1094-1120Gidal, B.E., French, J.A., Grossman, P., le Teuf, G., Assessment of potential drug interactions in patients with epilepsy:Impact of age and sex (2009) Neurology, 72, pp. 419-425Vogel, F., Moderne probleme der humangenetik (1959) Ergeb Inn Med Kinder-heilkd, 12, pp. 52-125Johnson, J.A., Pharmacogenetics: Potential for individualized drug therapy through genetics (2003) Trends Genet, 19, pp. 660-666Initial sequencing and analysis of the human genome (2001) Nature, 409, pp. 860-921. , International Human Genome Sequence ConsortiumJordan, D.M., Ramensky, V.E., Sunyaev, S.R., Human allelic variation: Perspective from protein function, structure, and evolution (2010) Curr Opin Struct Biol, 20, pp. 342-350Evans, B.J., Establishing clinical utility of pharmacogenetic tests in the post-FDAAA era (2010) Clin Pharmacol Ther, 88, pp. 749-751Hamburg, M.A., Collins, F.S., The path to personalized medicine (2010) N Engl J Med, 363, pp. 301-304(2009) Carbamazepine (market As Car-batrol, Equetro, Tegretol and Generics), , http:www.fda.gov/cder/drug/InfoSheet/HCP/carba-mazepineHCP.htm, Information for healthcare professionals, FDA Alert 12/12/07, updated 1/31/0

Espectroscopia De Fósforo Por Ressonância Magnética Na Investigação De Epilepsia Do Lobo Temporal: lendo Nas Entrelinhas Das Alterações Metabólicas

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Формування маркетингових підрозділів на підприємствах Харківського регіону

У статті розглянуто ситуацію формування маркетингових підрозділів на підприємствах Харківського регіону, розвиток їх структури, проаналізовано підходи до формування кадрового складу маркетингових підрозділів та динаміку їх розвитку, визначені тенденції щодо подальших напрямків вдосконалення маркетингу та виявлені ніші для перспективного розвитку маркетингу у Харківському регіоні.The article deals with the situation forming marketing departments in enterprises of Kharkov region, the development of structure analysis approaches to staffing marketing departments and the dynamics of their development trends identified areas for further improvement of marketing and found a niche for the future of marketing in the Kharkiv region

Indomethacin treatment prior to pentylenetetrazole-induced seizures downregulates the expression of Il1b and cox2 and decreases seizure-like behavior in zebrafish larvae

It has been demonstrated that the zebrafish model of pentylenetetrazole (PTZ)‑evoked seizures and the well‑established rodent models of epilepsy are similar pertaining to behavior, electrographic features, and c‑fosexpression. Although this zebrafish mode1712FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ - CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO2014/15640‑8; 2013/19151‑9475405/2010‑

Late Onset Temporal Lobe Epilepsy With Mri Evidence Of Mesial Temporal Sclerosis Following Acute Neurocysticercosis: Case Report.

The objective of this case report is to describe magnetic resonance imaging (MRI) evidence of mesial temporal sclerosis (MTS) in a patient with new onset temporal lobe epilepsy (TLE) and acute neurocysticercosis with multiple cysts. A 56 years old man with new onset headache, Simple Partial Seizures and Complex Partial Seizures underwent CT scan and lumbar puncture as diagnose proceeding. Multiple cysts and meningitis were identified, with a positive immunology for cysticercosis. Seizures were recorded over the left temporal region in a routine EEG. Treatment with albendazole was performed for 21 days, with clinical improvement and seizure remission after 4 months. An MRI scan 11 months after treatment, showed complete resolution of those cystic lesions and a left hippocampal atrophy (HA) with hyperintense T2 signal. The presence of HA and hyperintense T2 signal in this patient has not, to date, been associated with a poor seizure control. This patient presented with MRI evidence of left MTS after new onset partial seizures of left temporal lobe origin. Although we did not have a previous MRI scan, it is likely that this hippocampal abnormality was due to the acute inflammatory response to cysticercosis associated to repeated partial seizures. This suggests that acute neurocysticercosis associated with repeated seizures may cause MTS and late onset TLE.59255-