The Physics of the B Factories

This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C

Recent and currently emerging medical treatment options for the treatment of alcoholic hepatitis

Patients with severe alcoholic hepatitis (AH) need to be treated with specific treatment for better outcome. Currently available specific treatment modalities are use of corticosteroids or pentoxifylline. However, the response rate to these drugs is only about 50%-60%. Hence, there is an urgent need for better and more effective treatment options. Tumor necrosis factor plays an important role in the pathogenesis of AH. However, agents blocking the action of tumor necrosis factor have not been found to be effective. Rather the randomized studies evaluating these agents showed an adverse effect and more infections in treated patients. Critical role of tumor necrosis factor in hepatic regeneration explaining this contrast is discussed. Oxidative stress and inflammation derived from gut bacteria ate two main components in the pathogenesis of AH laying foundation for the role of antioxidants, probiotics, and antibiotics in the management of AH. This article reviews the current data and status of these newer agents for the treatment of AH. Of the various options available, Vitamin E and N-acetylcysteine (NAC) have shown great promise for clinical use as adjunct to corticosteroids. With these encouraging data, future well designed studies are suggested to assess Vitamin E and NAC before their routine use in clinical practice in the management of AH

Novel Ex Vivo Model to Examine the Mechanism and Relationship of Esophageal Microbiota and Disease

Rates of esophageal cancer have increased over the last 40 years. Recent clinical research has identified correlations between the esophageal microbiome and disease. However, mechanisms of action have been difficult to elucidate performing human experimentation. We propose an ex vivo model, which mimics the esophagus and is ideal for mechanistic studies on the esophageal microbiome and resultant transcriptome. To determine the microbiome and transcriptome profile of the human distal esophagus, the microbiome was assessed in 74 patients and the transcriptome profile was assessed in 37 patients with and without Barrett’s esophagus. Thereafter, an ex vivo model of the esophagus was created using an air–liquid interfaced (ALI) design. This design created a sterile apical surface and a nutrient-rich basal surface. An epithelial layer was grown on the apical surface. A normal microbiome and Barrett’s microbiome was harvested and created from patients during endoscopic examination of the esophagus. There was a distinct microbiome in patients with Barrett’s esophagus. The ex vivo model was successfully created with a squamous epithelial layer on the apical surface of the ex vivo system. Using this ex vivo model, multiple normal esophageal and Barrett’s esophageal cell lines will be created and used for experimentation. Each microbiome will be inoculated onto the sterile apical surface of each cell line. The resultant microbiome and transcriptome profile on each surface will be measured and compared to results in the human esophagus to determine the mechanism of the microbiome interaction

The affective component of pain in rodents: Direct evidence for a contribution of the anterior cingulate cortex

Numerous human and animal studies indirectly implicate neurons in the anterior cingulate cortex (ACC) in the encoding of the affective consequences of nociceptor stimulation. No causal evidence, however, has been put forth linking the ACC specifically to this function. Using a rodent pain assay that combines the hind-paw formalin model with the place-conditioning paradigm, we measured a learned behavior that directly reflects the affective component of pain in the rat (formalin-induced conditioned place avoidance) concomitantly with “acute” formalin-induced nociceptive behaviors (paw lifting, licking, and flinching) that reflect the intensity and localization of the nociceptive stimulus. Destruction of neurons originating from the rostral, but not caudal, ACC reduced formalin-induced conditioned place avoidance without reducing acute pain-related behaviors. These results provide evidence indicating that neurons in the ACC are necessary for the “aversiveness” of nociceptor stimulation