Acute pancreatitis caused by impaction of hydatid membranes in the papilla of Vater: a case report

Acute pancreatitis is a rare complication of hydatidosis and the successful use of endoscopic sphincterotomy associated with extraction of hydatid membranes has been rarely reported. We describe a young man who developed acute pancreatitis after rupture of an echinococcus cyst, located at the left hepatic lobe, into the biliary tract. The cause of pancreatitis was confirmed by endoscopic retrograde cholangiopancreatography, which revealed the presence of a daughter cyst impacted in the major papilla. After sphincterotomy and removal of hydatid membranes from the biliary tract, the patient presented rapid resolution of pancreatitis and made an uneventful recovery

Severe dysphagia due to a huge epiphrenic diverticulum: long-term treatment with balloon dilation and botulinum toxin injection: a case report

We herein describe the first case of a high elderly patient with severe dysphagia in solids and liquids, caused by a huge epiphrenic diverticulum, who was treated with combined therapy of balloon dilation and botulinum toxin injection. Due to comorbid associated diseases the patient was unsuitable to withstand surgical or laparoscopic intervention. Treatment with botulinum toxin injection at the region of lower esophageal sphincter was unsuccessful. Combined therapy with balloon dilatation and botulinum toxin injection at the compressed part of esophageal lumen by the diverticulum resulted in improvement in dysphagia and malnutrition. During the long-term follow-up the patient developed symptomatic relapses, successfully treated by subsequent combined therapy resulting in longer-lasting symptom relief

Identification of cis-acting determinants mediating the unconventional secretion of tau.

The deposition of tau aggregates throughout the brain is a pathological characteristic within a group of neurodegenerative diseases collectively termed tauopathies, which includes Alzheimer's disease. While recent findings suggest the involvement of unconventional secretory pathways driving tau into the extracellular space and mediating the propagation of the disease-associated pathology, many of the mechanistic details governing this process remain elusive. In the current study, we provide an in-depth characterization of the unconventional secretory pathway of tau and identify novel molecular determinants that are required for this process. Here, using Drosophila models of tauopathy, we correlate the hyperphosphorylation and aggregation state of tau with the disease-related neurotoxicity. These newly established systems recapitulate all the previously identified hallmarks of tau secretion, including the contribution of tau hyperphosphorylation as well as the requirement for PI(4,5)P2 triggering the direct translocation of tau. Using a series of cellular assays, we demonstrate that both the sulfated proteoglycans on the cell surface and the correct orientation of the protein at the inner plasma membrane leaflet are critical determinants of this process. Finally, we identify two cysteine residues within the microtubule binding repeat domain as novel cis-elements that are important for both unconventional secretion and trans-cellular propagation of tau

Benign retropneumoperitoneum developed after endoscopic sphincterotomy and large balloon dilation of biliary sphincter for removal of large biliary stones: a case report

Biliary endoscopic sphincterotomy (ES) followed by biliary orifice dilation (BOD) with large-diameter balloons (> 12 mm) is a relative new technique for extraction of large biliary stones. However, the safety and the potential complications of this combined technique are not known yet. We present a patient who developed benign retroperitoneum after ES plus BOD with large-diameter balloon for removal of a large biliary stone, which was successfully treated conservatively. To the best of our knowledge this is the first report of such a complication after introduction of this method to clinical practice

Idiopathic portal hypertension in an "inactive" HBV carrier: a case report

Idiopathic portal hypertension belongs to the group of non-cirrhotic portal hypertension, its etiology is still unknown but its prognosis is excellent. We report a case of 45 year old female with inactive hepatitis B virus (HBV) carrier status and persistently elevated alpha-fetoprotein (AFP), presented with features of portal hypertension and without evidence of cirrhosis or fibrosis on liver biopsy

Microglia become hypofunctional and release metalloproteases and tau seeds when phagocytosing live neurons with P301S tau aggregates.

[Figure: see text]

A variant of the double gallbladder. A possible cause of cholelithiasis?

Congenital duplication of the gallbladder is a rare anatomical malformation, which is usually discovered as an incidental finding during cholecystectomy. We report a case of a double gallbladder in a 45-year-old woman, which was discovered during laparoscopic cholecystectomy for symptomatic cholelithiasis. As it was not possible to identify the anatomical structures safely, the procedure was converted to open cholecystectomy. Inspection of the resected gallbladder showed that it consisted of 2 chambers with separate cystic ducts, which communicated through an ostium. Both chambers contained multiple gallstones. The inadequate drainage of the second chamber could be considered as a predisposing factor for the development of cholelithiasis in this case

Traumatic Neuroma around the Celiac Trunk after Gastrectomy Mimicking a Nodal Metastasis: A Case Report

Traumatic neuroma is a well-known disorder that occurs after trauma or surgery involving the peripheral nerve and develops from a nonneoplastic proliferation of the proximal end of a severed, partially transected, or injured nerve. We present a case of traumatic neuroma around the celiac trunk after gastrectomy in a 56-year-old man, which was confirmed by pathology. CT demonstrated the presence of a lobulated, homogeneous, hypoattenuating mass around the celiac trunk, mimicking a nodal metastasis

The Role of Antibodies and Their Receptors in Protection Against Ordered Protein Assembly in Neurodegeneration.

Ordered assemblies of proteins are found in the postmortem brains of sufferers of several neurodegenerative diseases. The cytoplasmic microtubule associated protein tau and alpha-synuclein (αS) are found in an assembled state in Alzheimer's disease and Parkinson's disease, respectively. An accumulating body of evidence suggests a "prion-like" mechanism of spread of these assemblies through the diseased brain. Under this hypothesis, assembled variants of these proteins promote the conversion of native proteins to the assembled state. This likely inflicts pathology on cells of the brain through a toxic gain-of-function mechanism. Experiments in animal models of tau and αS pathology have demonstrated that the passive transfer of anti-tau or anti-αS antibodies induces a reduction in the levels of assembled proteins. This is further accompanied by improvements in neurological function and preservation of brain volume. Immunotherapy is therefore considered one of the brightest hopes as a therapeutic avenue in an area currently without disease-modifying therapy. Following a series of disappointing clinical trials targeting beta-amyloid, a peptide that accumulates in the extracellular spaces of the AD brain, attention is turning to active and passive immunotherapies that target tau and αS. However, there are several remaining uncertainties concerning the mechanism by which antibodies afford protection against self-propagating protein conformations. This review will discuss current understanding of how antibodies and their receptors can be brought to bear on proteins involved in neurodegeneration. Parallels will be made to antibody-mediated protection against classical viral infections. Common mechanisms that may contribute to protection against self-propagating protein conformations include blocking the entry of protein "seeds" to cells, clearance of immune complexes by microglia, and the intracellular protein degradation pathway initiated by cytoplasmic antibodies via the Fc receptor TRIM21. As with anti-viral immunity, protective mechanisms may be accompanied by the activation of immune signaling pathways and we will discuss the suitability of such activation in the neurological setting