Papillary and solid epithelial neoplasm of the pancreas from five patients were studied using immunohistochemistry and electron microscopy to define the cellular origin of this type of tumor. The tumors ranged in diameter form 5.5 to 15 cm Grossly, these were well circumscribed by a firm, gray-white, fibrous capsule and their cut-surface showed mainly area containing mucinous substance with necrotic and hemorrhagic material, with some solid portion. Microscopically, there was a solid and papillary pattern, with uniform cells typically having round to ovoid nuclei containing indistinct nucleoli and eosinophilic, granular cytoplasm. Within the cytoplasm of the tumor cells, numerous PAS-positive granules were found. Immunostaining was positive for neuron-specific enolase(three of five cases), alpha1-antitrypsin and alpha1-antichymotrypsin(three of five cases) in the solid and papillary portion of the tumor. But no polypeptide hormone immunoreactive cells were present in all cases except for gastrin which showed focally weak positivity in the papillary area. Ultrastructurally, the papillary and solid epithelial neopasm of the pancreas showed evidence of acinar cell differentiation, because in the cell of one observed some zymogen-like granules and presence of annulate lamellae. But also, abundant typical neurosecretory granules were detected in the tumor cells ultrastructurally. Both facts suggested acinar and islet cell differentiation of the tumor. From the these findings, it concluded that papillary and solid epithelial neoplasm of the pancreas may be originated from a primordial cell which will be able to render both endocrine and exocine component.

Over 80% of patients with pancreatic ductal adenocarcinomas (PDAs) present with symptomatic, surgically unresectable disease. If a “stage shift” from the current 20% proportion of resectability to early detection could be achieved, this would greatly improve the survival of patients with this generally dismal disease. Although the goal of early detection is laudable, the relatively low prevalence of PDA renders general population screening unfeasible. To avoid the perils of overdiagnosis and to focus early detection efforts on individuals deemed to be at higher-than-average risk, we need to define such subsets of individuals, such as kindred of existing patients and those with precursor cystic lesions, chronic pancreatitis, and new-onset diabetes. The next step is to determine when and how often to monitor at-risk individuals and the diagnostic modalities that will be employed in the surveillance.Enormous challenges remain in terms of validated blood-based biomarkers, imaging modalities, and when and how often surveillance.

Pancreatic cancer can arise in the background of chronic pancreatitis (CP). The relative risks for pancreatic cancer in CP vary considerably according to other contributing factors such as disease duration, excess alcohol consumption, tobacco consumption, eating habits, physical activity, and late-onset diabetes. The incidence of pancreatic cancer is estimated to be about 10 per 105 per year, and the incidence and prevalence of CP are estimated to be 5-12 per 105 and 50 per 105 per year, respectively. The pooled relative risk estimates for pancreatic cancer in CP patients range from 2.7 to 13.3. Subsets of CP subjects with a family history of pancreatic cancer or those with newly developed diabetes over the age of 50 have a higher risk for pancreatic cancer. However, the prevalence of pancreatic cancer is not high enough to justify general screening of the adult CP population. Thus, it is necessary to select subsets of CP cohorts with a significantly high risk of pancreatic cancer. We need a better overall disease model that can define the interaction of multiple risk factors and their cumulative or potential effects on pancreatic cancer.

More than 80% of patients with pancreatic ductal adenocarcinoma (PDA) present with symptomatic, surgically unresectable disease. If a “stage shift” from the current 20% resectable proportion to greater by early detection can be achieved, it will unequivocally lead to improved survival in this otherwise dismal disease. Although the goal of early detection of PDA is laudable, the relatively low prevalence PDA renders general population screening infeasible. To avoid the perils of overdiagnosis and to focus early detection efforts on individuals deemed to be at higher-than-average risk, we need to define those subsets of individuals, such as familial kindred and patients with precursor cystic lesions, chronic pancreatitis, and new-onset diabetes. The next step is to determine when and how often to conduct surveillance in the atrisk individuals and the modalities (biomarkers and imaging) that will be used in the surveillance and diagnostic settings, respectively. Nonetheless, vast challenges still remain in terms of validated blood-based biomarkers, imaging modality, and when and how often the surveillance.

Over 80% of patients with pancreatic ductal adenocarcinomas (PDAs) present with symptomatic, surgically unresectable disease. If a “stage shift” from the current 20% proportion of resectability to early detection could be achieved, this would greatly improve the survival of patients with this generally dismal disease. Although the goal of early detection is laudable, the relatively low prevalence of PDA renders general population screening unfeasible. To avoid the perils of overdiagnosis and to focus early detection efforts on individuals deemed to be at higher-than-average risk, we need to define such subsets of individuals, such as kindred of existing patients and those with precursor cystic lesions, chronic pancreatitis, and new-onset diabetes. The next step is to determine when and how often to monitor at-risk individuals and the diagnostic modalities that will be employed in the surveillance.Enormous challenges remain in terms of validated blood-based biomarkers, imaging modalities, and when and how often surveillance.

No abstract available.
Aged ; Common Bile Duct/*pathology ; Common Bile Duct Diseases/*diagnosis/pathology/ultrasonography ; Diagnosis, Differential ; Female ; Humans ; Hyperplasia ; Magnetic Resonance Imaging ; Polyps/*pathology ; Positron-Emission Tomography ; Tomography, X-Ray Computed

Pancreatic Fluid Collection (PFC) develops as a result of acute pancreatitis, chronic pancreatitis, trauma, and postoperation. Although percutaneous drainage, surgery and Endoscopic Retrograde Panceatogram are used as conventional treatments in complicated PFC, the clinical course of PFC is unsatisfactory due to its clinical success rate and the risk of procedure-related complications. Endoscopic ultrasonography-guided transmural drainage of PFC is a safe and effective modality for the management of PFC, particularly in patients with pancreas necrosis. A range of techniques and stents have been introduced and a newly designed metal stent is now available.
Drainage ; Endosonography ; Humans ; Necrosis ; Pancreas ; Pancreatic Pseudocyst ; Pancreatitis ; Pancreatitis, Chronic ; Stents

Crossed aphasia refers to language disturbance induced by unilateral right hemisphere (non-language dominant) injury in right-handed people who had no previous history of brain damage. Crossed aphasia occurs in less than 2 percent who developed a aphasia. We report a case of a 49-year-old right handed man with language disturbance after right middle cerebral infarction. He showed nonfluent crossed aphasia with Gerstman syndrome such as right-left disorientation, finger agnosia, acalculia and agraphia, but not with apraxia and neglect. At 7 weeks after onset, language function indicated improvement in spontaneous speech and at 19 weeks after onset, improvement in spontaneous speech, comprehension, repetition, naming and reading.
Agnosia ; Agraphia ; Aphasia* ; Apraxias ; Brain ; Cerebral Infarction ; Comprehension ; Dyscalculia ; Hand ; Humans ; Infarction, Middle Cerebral Artery* ; Middle Aged

OBJECTIVES: The antimicrobial activity of silver nanoparticles has resulted in their widespread use in many consumer products. Yet, despite their many advantages, it is also important to determine whether silver nanoparticles may represent a hazard to the environment and human health. METHODS: Thus, to evaluate the genotoxic potential of silver nanoparticles, in vivo genotoxicity testing (OECD 474, in vivo micronuclei test) was conducted after exposing male and female Sprague-Dawley rats to silver nanoparticles by inhalation for 90 days according to OECD test guideline 413 (Subchronic Inhalation Toxicity: 90 Day Study) with a good laboratory practice system. The rats were exposed to silver nanoparticles (18 nm diameter) at concentrations of 0.7 x 10(6) particles/cm3 (low dose), 1.4 x 10(6) particles/cm3 (middle dose), and 2.9 x 10(6) particles/cm3 (high dose) for 6 hr/day in an inhalation chamber for 90 days. The rats were killed 24 hr after the last administration, then the femurs were removed and the bone marrow collected and evaluated for micronucleus induction. RESULTS: There were no statistically significant differences in the micronucleated polychromatic erythrocytes or in the ratio of polychromatic erythrocytes among the total erythrocytes after silver nanoparticle exposure when compared with the control. CONCLUSION: The present results suggest that exposure to silver nanoparticles by inhalation for 90 days does not induce genetic toxicity in male and female rat bone marrow in vivo.
Animals ; Bone Marrow ; Erythrocytes ; Female ; Femur ; Humans ; Inhalation ; Inhalation Exposure ; Male ; Mutagenicity Tests ; Nanoparticles ; Rats ; Rats, Sprague-Dawley ; Silver

HHE syndrome is characterized by hemiconvulsive seizure, hemiplegia and epilepsy occurring in sequence. Recently, cytotoxic edematous swelling of one hemisphere was presented as the pathogenesis because high signal intensity was shown in the diffusion image but no remarkable findings were noticed in the FLAIR image and T2WI in two cases presented by Freeman etc. The clinical course and the radiologic findings in our patient was the same as the above description other than sparing paracentral lobule. This reinforces the assumption that the brain damage in HHE syndrome is not induced by vascular hypoxic damage but by selectively cytotoxic damage through immunologic pathogenesis. Therefore, diffusion image is needed for the diagnosis of HHE syndrome in a febrile convulsive child. Also, early adequate treatment is required such as immunosuppressive treatment with high dose steroid and intravenous immunoglobulin. Furthermore, a proper measure to reduce cerebral edema is essential for the prevention of neurologic sequalae and deterioration to epilepsy.
Brain ; Brain Edema ; Child ; Diffusion ; Epilepsy ; Follow-Up Studies ; Hemiplegia ; Humans ; Immunoglobulins ; Magnetic Resonance Imaging ; Magnetic Resonance Spectroscopy ; Magnetics ; Magnets ; Seizures