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A 55-year-old woman presented with persistent nausea, vomiting, and weight loss previously attributed to Ménétrier’s disease. On further workup, she was found to have metastatic lobular breast carcinoma causing gastric outlet obstruction, diagnosed by endoscopic ultrasound with fine needle aspiration after previous gastric mucosal biopsies were unremarkable. In most reported cases of gastric metastasis from breast cancer, a diagnosis was established by mucosal biopsy. This case is an important reminder that mucosal biopsies can be negative in about 20% of patients with gastric metastasis, which may lead to a delay in diagnosis and treatment. Gastroenterologists should be diligent in taking deeper biopsies if there is a suspicion for gastric metastasis.

A 71-year-old male presented to our institution with cholestatic hepatitis after having recently undergone upper endoscopy for treatment of gastrointestinal bleeding. Further investigation with endoscopic retrograde cholangiopancreatography revealed a hemostatic clip on the ampulla of Vater. After initial attempts at cannulation of the common bile duct were unsuccessful, biliary decompression was achieved by use of needle-knife fistulotomy. A common bile duct stent was placed and the liver function tests improved prior to discharge.

India has been one of the growing world economies over the last few decades, and one of the defining features of India's growth has been investment-led growth. India's sustained economic growth and increased competitiveness in manufacturing has been underpinned by a massive economic development due to various critical factors. In this context, an attempt has been made to focus on the role of these critical factors on the growth of GDP and the Indian economy. Although the paper examines these phenomena in the specific case of the Indian economy, the analysis has a much wider application, both for the economic policy and for the theories of growth and structural change.

Background Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. Methods Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions. Furthermore, we studied the effects of Wallerian degeneration blockage on clinical severity, inflammatory pathology, acute axonal damage, and long-term axonal loss in experimental autoimmune encephalomyelitis using Wallerian degeneration slow (Wld S ) mutant mice. Results The highest numbers of axons undergoing Wallerian degeneration were found in the perilesional white matter of multiple sclerosis patients early in the disease course and with actively demyelinating lesions. Furthermore, Wallerian degeneration was more abundant in patients harboring chronic active as compared to chronic inactive lesions. No co-localization of neuropeptide Y-Y1 receptor, a bona fide immunohistochemical marker of Wallerian degeneration, with amyloid precursor protein, frequently used as an indicator of acute axonal transport disturbance, was observed in human and mouse tissue, indicating distinct axon-degenerative processes. Experimentally, a delay of Wallerian degeneration, as observed in Wld S mice, did not result in a reduction of clinical disability or acute axonal damage in experimental autoimmune encephalomyelitis, further supporting that acute axonal damage as reflected by axonal transport disturbances does not share common molecular mechanisms with Wallerian degeneration. Furthermore, delaying Wallerian degeneration did not result in a net rescue of axons in late lesion stages of experimental autoimmune encephalomyelitis. Conclusions Our data indicate that in multiple sclerosis, ongoing demyelination in focal lesions is associated with axonal degeneration in the perilesional white matter, supporting a role for focal pathology in diffuse white matter damage. Also, our results suggest that interfering with Wallerian degeneration in inflammatory demyelination does not suffice to prevent acute axonal damage and finally axonal loss. peerReviewed

Elastofibroma is a benign tumor of the musculoskeletal system characterized by the abnormal accumulation of elastinophilic fibers. It has been classically described for subscapular region but has been reported in several musculoskeletal sites over the years and rarely even in the GI tract but never in pancreas. We therefore present the case of a 45-year-old female who presented with intermittent abdominal pain. CT of abdomen revealed 1.4 cm pancreatic neck lesion without peripancreatic lymphadenopathy. Endoscopic ultrasound (EUS) guided FNA was nondiagnostic. Surgical resection was performed with central pancreatectomy. Histopathology revealed well demarcated nodules of hypocellular collagen with abundant elastic fibers, characteristic of pancreatic elastofibroma. Treatment is not needed unless symptomatic and surgical resection is the preferred therapeutic option when indicated. This case adds another entity to the differential diagnosis of pancreatic mass lesions.

Journal of neuroinflammation 9, 156 (2012). doi:10.1186/1742-2094-9-156, Published by BioMed Central, London