Peripartum patient with epigastric pain

A 44-year-old female, gravida 2, para 1, abortus 1, presented to the emergency department with epigastric pain, vomiting and nosebleed at 36 weeks gestation. She had right upper quadrant tenderness and was hypertensive at 138/90 mmHg. Laboratory studies demonstrated decreased platelets of 122 k/mcL, Hb of 11.2 g/dL and RBC of 3.48 M/mcL, elevated AST of 371 U/L and ALT of 522 U/L, and proteinuria of 13 mg/dL

Three-Prong Distribution of Massive Narrow QCD Jets

We study the planar-flow distributions of narrow, highly boosted, massive QCD jets. Using the factorization properties of QCD in the collinear limit, we compute the planar-flow jet function from the one-to-three splitting function at tree-level. We derive the leading-log behavior of the jet function analytically. We also compare our semi-analytic jet function with parton-shower predictions using various generators.Comment: 59 pages, 9 figure

Pancreatic cancer lecture

Department of Radiology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA, The IVth Congress of Radiology and Medical Imaging of the Republic of Moldova with international participation, Chisinau, May 31 – June 2, 2018Background: Pancreatic cancer staging is performed by imaging, with CT being the warhorse for T and M staging. MRI and ultrasound are routinely used to address specific clinical questions. Positron emission tomography has a role in post treatment assessment. The lecture aims to discuss the role of common imaging techniques (CT, MRI, ultrasound, and PET) in pancreatic cancer staging and post treatment evaluation. Content: Available literature on pancreatic cancer staging will be reviewed and several cases will be used as examples to illustrate the imaging approach to pancreatic cancer staging and post treatment follow-up. Interactive questions/answers with audience will be used to assess the proper delivery of the objectives. In particular the audience will be asked an opinion on multiple cases and the different answers will be discussed during the lecture. Conclusions: Attendees will be familiar with standardized reporting of pancreatic cancer staging and the use of the different imaging modalities. The attendees will also learn how to assess post treatment response and the pitfalls of pancreatic staging by imaging

Liver imaging in oncologic patients lecture

Department of Radiology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA, The IVth Congress of Radiology and Medical Imaging of the Republic of Moldova with international participation, Chisinau, May 31 – June 2, 2018Background: Multiple cancers have potential for metastasizing to the liver. Cancer treatment very often affects liver parenchyma causing for example steatosis or cirrhosis. The lecture aims to discuss imaging techniques (CT, MRI, ultrasound, and PET) in hepatic imaging in oncologic patients as well as the pitfalls of hepatic imaging in an oncologic population. Content: Available literature on liver imaging in oncologic patients will be reviewed and several cases will be used as examples to illustrate the imaging approach to liver imaging in an oncologic center. Interactive questions/answers with audience will be used to assess the proper delivery of the objectives. In particular the audience will be asked an opinion on multiple cases and the different answers will be discussed during the lecture. Conclusions: Attendees will be familiar with standardized approach to liver imaging and different imaging modalities in an oncologic population. The attendees will also learn how to assess post treatment response and the pitfalls of hepatic imaging in oncologic patients

Analgesic and Antineuropathic Drugs Acting Through Central Cholinergic Mechanisms

The role of muscarinic and nicotinic cholinergic receptors in analgesia and neuropathic pain relief is relatively unknown. This review describes how such drugs induce analgesia or alleviate neuropathic pain by acting on the central cholinergic system. Several pharmacological strategies are discussed which increase synthesis and release of acetylcholine (ACh) from cholinergic neurons. The effects of their acute and chronic administration are described. The pharmacological strategies which facilitate the physiological functions of the cholinergic system without altering the normal modulation of cholinergic signals are highlighted. It is proposed that full agonists of muscarinic or nicotinic receptors should be avoided. Their activation is too intense and un-physiological because neuronal signals are distorted when these receptors are constantly activated. Good results can be achieved by using agents that are able to a) increase ACh synthesis, b) partially inhibit cholinesterase activity c) selectively block the autoreceptor or heteroreceptor feedback mechanisms

Oxaliplatin Neurotoxicity Involves Peroxisome Alterations. PPARc Agonism as Preventive Pharmacological Approach

The development of neuropathic syndromes is an important, dose limiting side effect of anticancer agents like platinum derivates, taxanes and vinca alkaloids. The causes of neurotoxicity are still unclear but the impairment of the oxidative equilibrium is strictly related to pain. Two intracellular organelles, mitochondria and peroxisomes cooperate to the maintaining of the redox cellular state. Whereas a relationship between chemotherapy-dependent mitochondrial alteration and neuropathy has been established, the role of peroxisome is poor explored. In order to study the mechanisms of oxaliplatin-induced neurotoxicity, peroxisomal involvement was evaluated in vitro and in vivo. In primary rat astrocyte cell culture, oxaliplatin (10 µM for 48 h or 1 µM for 5 days) increased the number of peroxisomes, nevertheless expression and functionality of catalase, the most important antioxidant defense enzyme in mammalian peroxisomes, were significantly reduced. Five day incubation with the selective Peroxisome Proliferator Activated Receptor-γ (PPAR-γ) antagonist G3335 (30 µM) induced a similar peroxisomal impairment suggesting a relationship between PPARγ signaling and oxaliplatin neurotoxicity. The PPARγ agonist rosiglitazone (10 µM) reduced the harmful effects induced both by G3335 and oxaliplatin. In vivo, in a rat model of oxaliplatin induced neuropathy, a repeated treatment with rosiglitazone (3 and 10 mg kg(-1) per os) significantly reduced neuropathic pain evoked by noxious (Paw pressure test) and non-noxious (Cold plate test) stimuli. The behavioral effect paralleled with the prevention of catalase impairment induced by oxaliplatin in dorsal root ganglia. In the spinal cord, catalase protection was showed by the lower rosiglitazone dosage without effect on the astrocyte density increase induced by oxaliplatin. Rosiglitazone did not alter the oxaliplatin-induced mortality of the human colon cancer cell line HT-29. These results highlight the role of peroxisomes in oxaliplatin-dependent nervous damage and suggest PPARγ stimulation as a candidate to counteract oxaliplatin neurotoxicity