25 research outputs found
354: Stem cell transplantation (SCT) with and without conditioning for primary immune deficiency (PID) in children
Geometric representation of graphs in low dimension
An axis-parallel kâdimensional box is a Cartesian product R1 Ă R2 à · · · Ă Rk where Ri (for 1 †i †k) is a closed interval of the form [ai, bi] on the real line. For a graph G, its boxicity box(G) is the minimum dimension k, such that G is representable as the intersection graph of (axisâparallel) boxes in kâdimensional space. The concept of boxicity finds applications in various areas such as ecology, operation research etc. A number of NP-hard problems are either polynomial time solvable or have much better approximation ratio on low boxicity graphs. For example, the max-clique problem is polynomial time solvable on bounded boxicity graphs and the maximum independent set problem has log n approximation ratio for boxicity 2 graphs. In most cases, the first step usually is computing a low dimensional box representation of the given graph. Deciding whether the boxicity of a graph is at most 2 itself is NP-hard. We give an efficient randomized algorithm to construct a box representation of any graph G on n vertices in 1.5( â + 2) ln n dimensions, where â is the maximum degree of G. We also show that box(G) †(â+2) lnn for any graph G. Our bound is tight up to a factor of ln n. The only previously known general upper bound for boxicity was given by Roberts, namely box(G) †n/2. Our result gives an exponentially better upper bound for bounded degree graphs. We also show that our randomized algorithm can be derandomized to get a polynomial time deterministic algorithm. Though our general upper bound is in terms of maximum degree â, we show that for almost all graphs on n vertices, its boxicity is upper bound by c · (dav + 1) lnn where dav is the average degree and c is a small constant. Also, we show that for any graph G, box(G) †â 8ndav ln n, which is tight up to a factor of b â ln n for a constant b
Immunohistological studies of lymphoproliferative lesions in a fatal case of Epstein-Barr virus infection.
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Viral Load and CD4 T Cell Percentage Predict Sleep Disturbances in HIV-Infected Children
Analysis of HIV- type 1 protease and reverse transcriptase in Brazilian children failing highly active antiretroviral therapy (HAART) AnĂĄlise da protease e transcriptase reversa do HIV-1 em crianças com falha terapĂȘutica em uso de terapia anti-retroviral altamente eficaz (HAART)
The aim of this study was to evaluate the genotypic resistance profiles of HIV-1 in children failing highly active antiretroviral therapy (HAART). Forty-one children (median age = 67 months) receiving HAART were submitted to genotypic testing when virological failure was detected. cDNA was extracted from PBMCs and amplified by nested PCR for the reverse transcriptase and protease regions of the pol gene. Drug resistance genotypes were determined from DNA sequencing. According to the genotypic analysis, 12/36 (33.3%) and 6/36 (16.6%) children showed resistance and possible resistance, respectively, to ZDV; 5/36 (14%) and 4/36 (11.1%), respectively, showed resistance and possible resistance to ddI; 4/36 (11.1%) showed resistance to 3TC and D4T; and 3/36 (8.3%) showed resistance to Abacavir. A high percentage (54%) of children exhibited mutations conferring resistance to NNRTI class drugs. Respective rates of resistance and possible resistance to PIs were: RTV (12.2%, 7.3%); APV (2.4%, 12.1%); SQV(0%, 12.1%); IDV (14.6%, 4.9%), NFV (22%, 4.9%), LPV/RTV (2.4%, 12.1%). Overall, 37/41 (90%) children exhibited virus with mutations related to drug resistance, while 9% exhibited resistance to all three antiretroviral drug classes.<br>O objetivo deste estudo foi avaliar o perfil de resistĂȘncia genotĂpica do HIV-1 em crianças com falha terapĂȘutica ao tratamento anti-retroviral (HAART). Quarenta e uma crianças (idade mediana = 67 meses) em uso de HAART foram submetidas ao teste de genotipagem no momento da detecção de falha ao tratamento. Foi realizada extração de cDNA de cĂ©lulas perifĂ©ricas mononucleares e amplificação do mesmo (regiĂ”es da transcriptase reversa e protease do gene pol) atravĂ©s de PCR-nested. O perfil genotĂpico foi determinado atravĂ©s do seqĂŒenciamnto de nucleotĂdeos. De acordo com a anĂĄlise genotĂpica, 12/36 (33,3%) e 6/36 (16,6%) crianças apresentaram, respectivamente, resistĂȘncia e possĂvel resistĂȘncia ao AZT; 5/36 (14%) e 4/36 (11,1%), respectivamente, eram resistentes e possivelmente resistentes ao ddI; 4/36 %11,1%) apresentaram resistĂȘncia ao 3TC e D4T, e 3/36 (8,3%) eram resistentes ao ABC. Uma alta porcentagem de crianças (54%) apresentou mutaçÔes relacionadas Ă resistĂȘncia aos inibidores da trancriptase reversa nĂŁo-anĂĄlogos de nucleosĂdeos. As taxas de resistĂȘncia e possĂvel resistĂȘncia aos inibidores da protease foram, respectivamente: RTV (12,2%; 7,3%); APV (2,4%; 12,1%); SQV (0%; 12,1%); IDV (14,6%; 4,9%); NFV (22%; 4,9%); LPV/RTV (2,4%; 12,1%). No total, 37/41 (90%) crianças apresentaram vĂrus com mutaçÔes relacionadas Ă resistĂȘncia a alguma droga, sendo que 9% delas tinham vĂrus resistentes Ă s trĂȘs classes de drogas anti-retrovirais disponĂveis