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.

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.

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.

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

In order to study the implantation mechanism various methods for culture of endometrial cells in vitro have been attempted. However, a disadvantage is that primary cultures of stromal and epithelial cells do not have the ability to differentiate, and therefore cannot be reproduced in the same manner as in vivo endometrium. The object of this study is to establish a three dimensional culture of endometrial cells which are both morphologically and functionally identical to in vivo endometrium. Endometrial tissues obtained after hysterectomies were cut into thin slices and treated with collagenase and trypsin-EDTA. The stromal cells and the epithelial cells were separated by centrifugation and cultured for 24 hours in DMEM media containing 10% FCS, 100 nM progesterone, and 1 nM estradiol. The cultured stromal cells were mixed with collagen gel and solidified, after which it was covered with matrigel. Epithelial cells were inoculated on the top and then cultured for 3 days. The three dimensionally cultured endometrial cells were stained for integrin alphal, alpha4, beta3, and cyclooxygenase-1, -2 by immunohistochemistry, which all showed strong expression. The cultured epithelial cells showed the formation of microvilli, tight junctions and pinopodes by electron microscopy. Studies are currently under way utilizing this three dimensional culture model to ascertain the interaction between the embryo and human endometrial cells at the time of implantation, and it is thought that further studied into a new culture environment which would allow longer periods of culture will be necessary.
Antigens, CD11a ; Centrifugation ; Collagen ; Collagenases ; Cyclooxygenase 1 ; Embryonic Structures ; Endometrium ; Epithelial Cells ; Estradiol ; Female ; Humans* ; Hysterectomy ; Immunohistochemistry ; Microscopy, Electron ; Microvilli ; Progesterone ; Stromal Cells ; Tight Junctions

PURPOSE: Radiotracers that bind to the central benzodiazepine receptor are useful for the investigation of various neurological and psychiatric diseases. [C-11]Flumazenil, a benzodiazepine antagonist, is the most widely used radioligand for central benzodiazepine receptor imaging by PET. We synthesized 3-(2-[F- 18]fluoro)flumazenil, a new fluorine-18 (t1/2=110 min) labeled analogue of benzodiazepine receptor imaging agent, and evaluated in vivo for biodistribution in mice. MATERIALS AND METHODS: Flumazenil (Ro 15-1788) was synthesized by a modification of the reported method. Precursor of 3-(2-[F-18]fluoro)flumazenil, the tosylated flumazenil derivative was prepared by the tosylation of the ethyl ester by ditosylethane. [F-18] labeling of tosyl substitued flumazenil precursor was performed by adding F-18 ion at 85 degree C in the hot cell for 20 min. The reaction mixture was trapped by C18 cartridge, washed with 10% ethanol, and eluted by 40% ethanol. Bidistribution in mice was determined after intravenous injection. RESULTS: The total chemical yield of tosylated flumazenil derivative was ~40%. The efficiency of labeling 3-(2-[F-18]fluoro)flumazenil was 66% with a total synthesis time of 50 min. Brain uptakes of 3-(2-[F-18]fluoro)flumazenil at 10, 30, 60 min after injection, were 2.5+/-0.37, 2.2+/-0.26, 2.1+/-0.11 and blood activities were 3.7+/-0.43, 3.3+/-0.07, 3.3+/-0.09%ID/g, respectively. CONCLUSION: We synthesized a tosylated flumazenil derivative which was successfully labeled with no-carrier-added F-18 by nucleophilic substitution.
Animals ; Benzodiazepines* ; Brain ; Ethanol ; Flumazenil* ; Injections, Intravenous ; Mice ; Receptors, GABA-A*