Scalar and Pseudo-Scalar Higgs Production at Hadron Colliders

The evaluation of the NNLO QCD corrections to the production of a scalar and a pseudo-scalar Higgs boson is described.Comment: 5+2 pages, 4 figures (9 ps-files). Talk given at RADCOR/Loops and Legs 2002, September 8-13, 2002, Kloster Banz, German

Effects of SUSY-QCD in hadronic Higgs production at next-to-next-to-leading order

An estimate of the NNLO supersymmetric QCD effects for Higgs production at hadron colliders is given. Assuming an effective gluon-Higgs interaction, these corrections enter only in terms of process-independent, factorizable terms. We argue that the current knowledge of these terms up to NLO is sufficient to derive the NNLO hadronic cross section within the limitations of the standard theoretical uncertainties arising mainly from renormalization and factorization scale variations. The SUSY contributions are small with respect to the QCD effects, which means that the NNLO corrections to Higgs production are very similar in the Standard Model and the MSSM.Comment: LaTeX, 5 pages, 3 embedded PostScript figure

Thrombotic Thrombocytopenic Purpura Induced by Acute Pancreatitis

Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder characterized by clotting in small blood vessels of the body (microthrombi), resulting in a low platelet count. The disease consists of the pentad of microangiopathic hemolytic anemia, thrombocytopenic purpura, neurologic abnormalities, fever and renal disease. Many symptoms could develop with acute pancreatitis but being able to differentiate when it is associated with any hematological conditions such as TTP is crucial to initiate a proper medical treatment. We present a rare case of a thirty-eight years old African American female, who presented to the Emergency department with an abdominal pain associated with a pancreatic condition. A vital piece in medical practice is recognizing lifesaving decisions in critical conditions cases. Acute Pancreatitis (AP) is a well-described consequence of TTP but acute pancreatitis triggering TTP is still not as frequent

Cecal Bascule after Colonoscopy - Case Report and Review of Literature

Cecal bascule is a rare disease variant of a cecal volvulus. It consists of upward and anterior folding of the ascending colon, forming a flap valve, and occluding the bowel lumen resulting in proximal cecal dilatation. Herein, we present a case of a patient who developed persistent abdominal pain few hours after a colonoscopy. CT scan of the abdomen revealed an upward and anterior folding of the cecum. Subsequently the patient was taken to the operating room for a right hemi-colectomy. This case emphasizes the importance to consider cecal bascule as a differential diagnosis in patients with persistent abdominal pain after colonoscopy, considering the ease of diagnosis with imaging studies and emergent surgical correction

Higgs production and decay: Analytic results at next-to-leading order QCD

The virtual two-loop corrections for Higgs production in gluon fusion are calculated analytically in QCD for arbitrary Higgs and quark masses. Both scalar and pseudo-scalar Higgs bosons are considered. The results are obtained by expanding the known one-dimensional integral representation in terms of m_H/m_q, and matching it with a suitably chosen ansatz of Harmonic Polylogarithms. This ansatz is motivated by the known analytic result for the Higgs decay rate into two photons. The method also allows us to check this result and to extend it to the pseudo-scalar decay rate.Comment: LaTeX, 16 pages, 5 figures (8 eps-files

Isolated angioedema of the bowel due to C1 esterase inhibitor deficiency: a case report and review of literature

<p>Abstract</p> <p>Introduction</p> <p>We report a rare, classic case of isolated angioedema of the bowel due to C1-esterase inhibitor deficiency. It is a rare presentation and very few cases have been reported worldwide. Angioedema has been classified into three categories.</p> <p>Case presentation</p> <p>A 66-year-old Caucasian man presented with a ten-month history of episodic severe cramping abdominal pain, associated with loose stools. A colonoscopy performed during an acute attack revealed nonspecific colitis. Computed tomography of the abdomen performed at the same time showed a thickened small bowel and ascending colon with a moderate amount of free fluid in the abdomen. Levels of C4 (< 8 mg/dL; reference range 15 to 50 mg/dL), CH50 (< 10 U/mL; reference range 29 to 45 U/ml) and C1 inhibitor (< 4 mg/dL; reference range 14 to 30 mg/dL) were all low, supporting a diagnosis of acquired angioedema with isolated bowel involvement. Our patient's symptoms improved with antihistamine and supportive treatment.</p> <p>Conclusion</p> <p>In addition to a detailed comprehensive medical history, laboratory data and imaging studies are required to confirm a diagnosis of angioedema due to C1 esterase inhibitor deficiency.</p

Selective inhibition of FLT3 by gilteritinib in relapsed or refractory acute myeloid leukaemia: a multicentre, first-in-human, open-label, phase 1-2 study.

BackgroundInternal tandem duplication mutations in FLT3 are common in acute myeloid leukaemia and are associated with rapid relapse and short overall survival. The clinical benefit of FLT3 inhibitors in patients with acute myeloid leukaemia has been limited by rapid generation of resistance mutations, particularly in codon Asp835 (D835). We aimed to assess the highly selective oral FLT3 inhibitor gilteritinib in patients with relapsed or refractory acute myeloid leukaemia.MethodsIn this phase 1-2 trial, we enrolled patients aged 18 years or older with acute myeloid leukaemia who either were refractory to induction therapy or had relapsed after achieving remission with previous treatment. Patients were enrolled into one of seven dose-escalation or dose-expansion cohorts assigned to receive once-daily doses of oral gilteritinib (20 mg, 40 mg, 80 mg, 120 mg, 200 mg, 300 mg, or 450 mg). Cohort expansion was based on safety and tolerability, FLT3 inhibition in correlative assays, and antileukaemic activity. Although the presence of an FLT3 mutation was not an inclusion criterion, we required ten or more patients with locally confirmed FLT3 mutations (FLT3mut+) to be enrolled in expansion cohorts at each dose level. On the basis of emerging findings, we further expanded the 120 mg and 200 mg dose cohorts to include FLT3mut+ patients only. The primary endpoints were the safety, tolerability, and pharmacokinetics of gilteritinib. Safety and tolerability were assessed in the safety analysis set (all patients who received at least one dose of gilteritinib). Responses were assessed in the full analysis set (all patients who received at least one dose of study drug and who had at least one datapoint post-treatment). Pharmacokinetics were assessed in a subset of the safety analysis set for which sufficient data for concentrations of gilteritinib in plasma were available to enable derivation of one or more pharmacokinetic variables. This study is registered with ClinicalTrials.gov, number NCT02014558, and is ongoing.FindingsBetween Oct 15, 2013, and Aug 27, 2015, 252 adults with relapsed or refractory acute myeloid leukaemia received oral gilteritinib once daily in one of seven dose-escalation (n=23) or dose-expansion (n=229) cohorts. Gilteritinib was well tolerated; the maximum tolerated dose was established as 300 mg/day when two of three patients enrolled in the 450 mg dose-escalation cohort had two dose-limiting toxicities (grade 3 diarrhoea and grade 3 elevated aspartate aminotransferase). The most common grade 3-4 adverse events irrespective of relation to treatment were febrile neutropenia (97 [39%] of 252), anaemia (61 [24%]), thrombocytopenia (33 [13%]), sepsis (28 [11%]), and pneumonia (27 [11%]). Commonly reported treatment-related adverse events were diarrhoea (92 [37%] of 252]), anaemia (86 [34%]), fatigue (83 [33%]), elevated aspartate aminotransferase (65 [26%]), and increased alanine aminotransferase (47 [19%]). Serious adverse events occurring in 5% or more of patients were febrile neutropenia (98 [39%] of 252; five related to treatment), progressive disease (43 [17%]), sepsis (36 [14%]; two related to treatment), pneumonia (27 [11%]), acute renal failure (25 [10%]; five related to treatment), pyrexia (21 [8%]; three related to treatment), bacteraemia (14 [6%]; one related to treatment), and respiratory failure (14 [6%]). 95 people died in the safety analysis set, of which seven deaths were judged possibly or probably related to treatment (pulmonary embolism [200 mg/day], respiratory failure [120 mg/day], haemoptysis [80 mg/day], intracranial haemorrhage [20 mg/day], ventricular fibrillation [120 mg/day], septic shock [80 mg/day], and neutropenia [120 mg/day]). An exposure-related increase in inhibition of FLT3 phosphorylation was noted with increasing concentrations in plasma of gilteritinib. In-vivo inhibition of FLT3 phosphorylation occurred at all dose levels. At least 90% of FLT3 phosphorylation inhibition was seen by day 8 in most patients receiving a daily dose of 80 mg or higher. 100 (40%) of 249 patients in the full analysis set achieved a response, with 19 (8%) achieving complete remission, ten (4%) complete remission with incomplete platelet recovery, 46 (18%) complete remission with incomplete haematological recovery, and 25 (10%) partial remission INTERPRETATION: Gilteritinib had a favourable safety profile and showed consistent FLT3 inhibition in patients with relapsed or refractory acute myeloid leukaemia. These findings confirm that FLT3 is a high-value target for treatment of relapsed or refractory acute myeloid leukaemia; based on activity data, gilteritinib at 120 mg/day is being tested in phase 3 trials.FundingAstellas Pharma, National Cancer Institute (Leukemia Specialized Program of Research Excellence grant), Associazione Italiana Ricerca sul Cancro

Higgs production in gluon fusion at next-to-next-to-leading order QCD for finite top mass

The inclusive Higgs production cross section from gluon fusion is calculated through NNLO QCD, including its top quark mass dependence. This is achieved through a matching of the 1/mtop expansion of the partonic cross sections to the exact large s-hat limits which are derived from k_T-factorization. The accuracy of this procedure is estimated to be better than 1% for the hadronic cross section. The final result is shown to be within 1% of the commonly used effective theory approach, thus confirming earlier findings.Comment: 28 pages, 14 figure