916 research outputs found

    Correlation functions of the One-Dimensional Random Field Ising Model at Zero Temperature

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    We consider the one-dimensional random field Ising model, where the spin-spin coupling, JJ, is ferromagnetic and the external field is chosen to be +h+h with probability pp and −h-h with probability 1−p1-p. At zero temperature, we calculate an exact expression for the correlation length of the quenched average of the correlation function ⟨s0sn⟩−⟨s0⟩⟨sn⟩\langle s_0 s_n \rangle - \langle s_0 \rangle \langle s_n \rangle in the case that 2J/h2J/h is not an integer. The result is a discontinuous function of 2J/h2J/h. When p=12p = {1 \over 2}, we also place a bound on the correlation length of the quenched average of the correlation function ⟨s0sn⟩\langle s_0 s_n \rangle.Comment: 12 pages (Plain TeX with one PostScript figure appended at end), MIT CTP #220

    Diagnosis and endovascular treatment of an internal mammary artery injury

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    Internal mammary artery (IMA) disruption after blunt chest trauma is rare. In some instances, it may occur after mild chest trauma with minor external physical findings. However, prompt diagnosis and treatment are necessary, as it can be associated with vascular and parenchymal injuries. We report a case of blunt chest trauma resulting in a sternal fracture associated with an IMA injury, active anterior mediastinal bleeding, bilateral lung contusions, and a left hemothorax. It was successfully treated by selective embolization to the left IMA branch and chest tube placement

    Active case-finding for TB among incarcerated women in Peru

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    Carta al editorRevisión por pare

    p-Type semiconducting properties in lithium-doped MgO single crystals

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    The phenomenally large enhancement in conductivity observed when Li-doped MgO crystals are oxidized at elevated temperatures was investigated by dc and ac electrical measurements in the temperature interval 250-673 K. The concentration of ([Li]^{0}) centers (Li^{+} ions each with a trapped hole) resulting from oxidation was monitored by optical absorption measurements. Both dc and ac experiments provide consistent values for the bulk resistance. The electricalconductivity of oxidized MgO:Li crystals increases linearly with the concentration of ([Li]^{0}) centers. The conductivity is thermally activated with an activation energy of (0.70 +/- 0.01) eV, which is independent of the ([Li]^{0}) content. The \textit{standard semiconducting} mechanism satisfactorily explains these results. Free holes are the main contribution to band conduction as they are trapped at or released from the ([Li]^{0})-acceptor centers. In as-grown MgO:Li crystals, electrical current increases dramatically with time due to the formation of ([Li]^{0}) centers. The activation energy values between 1.3 and 0.7 eV are likely a combination of the activation energy for the creation of ([Li]^{0}) centers and the activation energy of ionization of these centers. Destruction of ([Li]^{0}) centers can be induced in oxidized crystals by application of an electric field due to Joule heating up to temperatures at which ([Li]^{0}) centers are not stable.Comment: LaTeX, 20 pages, 9 Encapsulated Postscript Format Figures, use the version 4.0 of REVTEX 4 macro packag

    TWO CASES OF NON-ALCOHOLIC WERNICKE ENCEPHALOPATHY SUCCESSFULLY TREATED BY THIAMINE REPLACEMENT: DIAGNOSTIC AND THERAPEUTIC CONSIDERATIONS

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    Wernicke\u2019s encephalopathy (WE) is an acute neurologi- cal disorder, due to a lack of thiamin (vitamin B1) which is observed mainly in alcoholic patients. Unfortunately, the syn- drome is underestimated in clinical practice and most often recognized only on autopsy, especially among non-alcoholics. The common clinical picture include mental status changes, ocular dysfunction, and gait ataxia. Treatment consists of timely thiamine replacement through intravenous infusion. We describe the case of two patients who developed a non-alcoholic WE post-surgical, regressed completely after intravenous infusion of thiamine. These cases suggest intere- sting diagnostic and therapeutic implications

    BCR-ABL1 doubling-times and halving-times may predict CML response to tyrosine kinase inhibitors

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    In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found that the DTs of the former patients were significantly longer than those of patients developing IM resistance (57.80 vs. 41.45 days, p = 0.0114). Interestingly, the DT values of individuals failing second-generation (2G) TKIs after developing IM resistance were considerably shorter than those observed at the time of IM failure (27.20 vs. 41.45 days; p = 0.0035). We next wanted to establish if decreases in BCR-ABL1 transcripts would identify subjects likely to obtain deep molecular responses. We therefore analyzed the BCR-ABL1 halving-times (HTs) of a different cohort comprising 174 individuals receiving IM in first line and observed that, regardless of the time point selected for our analyses (6, 12, or 18 months), HTs were significantly shorter in subjects achieving superior molecular responses (p = 0.002 at 6 months; p < 0.001 at 12 months; p = 0.0099 at 18 months). Moreover, 50 patients receiving 2G TKIs as first line therapy and obtaining an MR3.0 (after 6 months; p = 0.003) or an MR4.0 (after 12 months; p = 0.019) displayed significantly shorter HTs than individuals lacking these molecular responses. Our findings suggest that BCR-ABL1 DTs and HTs are reliable tools to, respectively, identify subjects in MR3.0 that are failing their assigned TKI or to recognize patients likely to achieve deep molecular responses that should be considered for treatment discontinuation
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