[A case of fibrolamellar hepatocellular carcinoma mimicking a liver abscess].

A 23-year-old woman was presented with fever and epigastric pain. Contrast enhanced computed tomography revealed a 40mm mass in the lateral segment. Blood tests showed the elevation of WBC and CRP. With the diagnosis of liver abscess, the antibiotics were administered, and the clinical findings were promptly improved. One year later, she complained of the same symptoms, and the mass had increased to 50mm in diameter. Percutaneous liver biopsy led to the diagnosis of fibrolamellar hepatocellular carcinoma.

Intrahepatic subcapsular biloma after endoscopic retrograde cholangiopancreatography treated by endoscopic biliary drainage.

Several major complications from endoscopic retrograde cholangiopancreatography (ERCP), including pancreatitis, cholangitis, and hemorrhage have been discussed in detail; however, a few uncommon but severe complications have been reported. We encountered an unusual case of post-ERCP intrahepatic subcapsular biloma. An 89-year-old woman with a 25-mm mass located at the hepatic hilum, suggestive of cholangiocarcinoma, underwent ERCP which demonstrated complete stricture of the common hepatic duct. Subsequently, two plastic stents were placed from the common bile duct to the right and left intrahepatic branches. On day 3, serum inflammatory markers were elevated and computed tomography revealed a large subcapsular fusiform fluid collection in the right liver, consistent with biloma. On day 6, the biloma ruptured and 500 ml of biliary ascites were removed. On day 8, endoscopic nasobiliary drainage via the right intrahepatic branch was performed because of recurrence of biliary ascites. After the procedure, 150 ml of bile was collected through the drain every day and no ascites recurred. We believe that minor injury to the right intrahepatic bile duct due to guidewire manipulation caused the biloma. Biloma may become apparent several days after ERCP, and endoscopic biliary drainage placement adjacent to the bile duct rupture site can stop bile leakage.

A case of left subphrenic abscess caused by gastric ulcer penetration that was successfully treated with endoscopic transgastric drainage.

A 65-year-old male visited our hospital because of fever and difficulty in walking. He was suffering from left-sided hypochondrial pain for a month. Laboratory tests performed on admission revealed a white blood cell count of 1700/µl and C-reactive protein level of 9.51mg/dl, which were suggestive of severe inflammation. Contrast-enhanced computed tomography revealed a subphrenic abscess around the spleen, which we considered to be caused by gastric penetration into the gastrosplenic ligament. Upper esophagogastroduodenoscopy revealed a gastric ulcer together with a fistula that connected to the left subphrenic abscess. We thus performed endoscopic transgastric drainage through the fistula. Antibiotics and a proton pump inhibitor were administered, and drainage was continued. The patient's clinical and inflammatory symptoms subsequently improved. We thus consider that endoscopic transgastric drainage is an appropriate treatment option for subphrenic abscesses.

[A very elderly case of complete remission by chemotherapy in a patient of primary esophageal non-Hodgkin lymphoma].

A very elderly patient with primary non-Hodgkin lymphoma of the esophagus is reported. An 87-year-old woman presented with dysphagia. Endoscopy revealed an elevated lesion with ulceration in the middle and lower esophagus. Endoscopic biopsy demonstrated pathological diagnosis and immunochemistry typical of non-Hodgkin lymphoma (Ann Arbor stage IIIEA), diffuse large B-cell lymphoma on the WHO classification. Systemic chemotherapy with 6 courses of a 50% dose of R-CHOP followed by 8 courses of rituximab for maintenance, successfully resulted in complete remission. Complete remission has been maintained for 58 months.

Fasting and high-fat diet alter histone deacetylase expression in the medial hypothalamus.

Increasing attention is now being given to the epigenetic regulation of animal and human behaviors including the stress response and drug addiction. Epigenetic factors also influence feeding behavior and metabolic phenotypes, such as obesity and insulin sensitivity. In response to fasting and high-fat diets, the medial hypothalamus changes the expression of neuropeptides regulating feeding, metabolism, and reproductive behaviors. Histone deacetylases (HDACs) are involved in the epigenetic control of gene expression and alter behavior in response to a variety of environmental factors. Here, we examined the expression of HDAC family members in the medial hypothalamus of mice in response to either fasting or a high-fat diet. In response to fasting, HDAC3 and -4 expression levels increased while HDAC10 and -11 levels decreased. Four weeks on a high-fat diet resulted in the increased expression of HDAC5 and -8. Moreover, fasting decreased the number of acetylated histone H3- and acetylated histone H4-positive cells in the ventrolateral subdivision of the ventromedial hypothalamus. Therefore, HDACs may be implicated in altered gene expression profiles in the medial hypothalamus under different metabolic states.

Dopamine D5 receptor immunoreactivity is differentially distributed in GABAergic interneurons and pyramidal cells in the rat medial prefrontal cortex.

In the rodent neocortex, the dopamine D5 receptor (D5R) appears to be the predominant subtype of D1-like receptors that are generally considered to play important roles in cognitive functions subserved by the prefrontal cortex (PFC). In this study, to identify the precise localization of D5R in rat PFC, we used a receptor-specific antibody and observed the immunolabeled structures by light and confocal laser scanning microscopies. D5R immunolabeling was found in nearly all neurons, both excitatory and inhibitory neurons. Most of the excitatory neurons showing D5R immunolabeling appear to be pyramidal neurons. In these neurons, D5R immunolabeling was observed throughout somata and dendrites including dendritic spines. In neuropil, almost all of the fiber terminals, represented by synaptophysin immunopositivity, were devoid of D5R. Among inhibitory neuronal subpopulations, we examined parvalbumin-immunopositive neurons (PV neurons), because they form a major subpopulation of fast-spiking neurons. Because parvalbumin immunolabeling enables detection of somata and dendrites as well as axonal profiles, we analyzed the intracellular distribution pattern of D5R immunolabeling. As a result, we found that D5R immunolabeling was mainly in somata and proximal dendrites. The density of intradendritic D5R immunolabeling decreased toward the distal regions. Thus, the distribution pattern of D5R immunolabeling is markedly different between pyramidal neurons and PV neurons. D5R may underlie dopamine modulation of cognitive function in PFC.

A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein.

A 58-year-old man was admitted to our hospital because of anorexia and back pain. He had been previously diagnosed with chronic pancreatitis with blood thrombus of the splenic vein at another hospital. Abdominal ultrasonography and computed tomography revealed a large mass in the body and tail of the pancreas, which directly invaded the stomach and the spleen. Small nodular metastases in both lungs were also detected. Furthermore, tumor thrombus continuously involved the splenic and proximal superior mesenteric vein, main portal vein, and its right intrahepatic branch. A metastatic mass was disclosed in the adjacent liver. The specimens obtained from portal tumor thrombus were histologically compatible with acinar cell carcinoma. Portal tumor thrombus is a rare condition in pancreatic tumors; however, it seems to be important to differentiate tumor thrombus from blood thrombus of the portal vein in order to know the true clinical stage and provide a suitable treatment.

Synaptic characteristics between cortical cells in the rat prefrontal cortex and axon terminals from the ventral tegmental area that utilize different neurotransmitters.

Projections from the ventral tegmental area (VTA) have been demonstrated to terminate in the prefrontal cortex (PFC) and to be dopaminergic and/or gamma-aminobutyric acidergic (GABAergic), forming a neural circuit implicated in certain memory and cognitive processes. However, it has not been determined whether gamma-aminobutyric acid (GABA) and dopamine (DA) are localized in certain types of axon terminals from the VTA to the PFC. To determine the synaptic characteristics made by postsynaptic prefrontal cortical structures and mesoprefrontal fibers utilizing either GABA or DA, we performed a double-labeling method for electron microscopy, in which we combined peroxidase markers for anterograde tract-tracing with postembedding immunogold labeling for tyrosine hydroxylase, DA, and GABA in rats. The anterograde tract-tracing studies showed that tegmentocortical fibers from the VTA terminated as both symmetric and asymmetric axon terminals with the predominantly symmetric synaptic type in the prelimbic cortex of the rat. Furthermore, a study using the combination of anterograde tract-tracing and postembedding immunocytochemistry indicated that tegmentocortical axon terminals forming symmetric synapses were either GABAergic or dopaminergic, whereas a small fraction of tegmentocortical terminals ending as asymmetric synapses were not immunopositive for DA or GABA. These findings indicate that the mesocortical projections to the PFC exert an inhibitory effect on the spontaneous activity of PFC cells via symmetric synapses that use DA and GABA as neurotransmitters and that these projections also have as yet unknown effects via asymmetric synapses using other neurotransmitters.

Immunolocalization of muscarinic receptor subtypes in the reticular thalamic nucleus of rats.

In this study, to identify the precise localization of the muscarinic receptor subtypes m2, m3 and m4 in the rostral part of the rat reticular thalamic nucleus (rRt), namely, the limbic sector, we used receptor-subtype-specific antibodies and characterized the immunolabeled structures by light, confocal laser scanning, and electron microscopies. The m2-immunolabeling was preferentially distributed in the distal dendrite region where cholinergic afferent fibers tend to terminate and in the peripheral region of somata, whereas the m3-immunolabeling was more preferentially distributed in a large part of somata and in proximal dendrite shafts than in the distal dendrite region. Dual-immunofluorescence experiments demonstrated that majority of rRt neurons with parvalbumin immunoreactivity contain both m2 and m3. Neither m2 nor m3 was detected in presynaptic terminals or axonal elements. No m4-immunolabeling was detected in the rostral part of the thalamus including rRt. These results show the different distributions of m2 and m3 in rRt neurons, and strongly suggest that m2 is more closely associated with cholinergic afferents than m3.

Intraductal papillary mucinous tumor of the pancreas associated with autosomal dominant polycystic kidney disease.

A 43-year-old male with a history of autosomal dominant polycystic kidney disease (ADPKD) was admitted to our center with severe abdominal pain and was diagnosed with acute pancreatitis. CT showed multiple cysts in the liver and both kidneys along with ADPKD and a cystic mass, 4 cm in diameter, in the pancreatic head. The main pancreatic duct was dilated to 1 cm in diameter. The patient was diagnosed with acute pancreatitis due to intraductal papillary mucinous tumor (IPMT), and pancreatoduodenectomy was performed. Histologic examination revealed a multiloculated cystic tumor filled with mucin in the head of the pancreas. Microscopically, the tumor was diagnosed as adenocarcinoma and was found to have invaded the main pancreatic duct. Although, in addition to our case, only seven cases with association between ADPKD and malignant neoplasms have been reported, five of these cases had neoplasms arising from the pancreas. Therefore, we suggest that some genetic interactions may exist between ADPKD and pancreatic carcinogenesis.

Thalamocortical projection from the ventral posteromedial nucleus sends its collaterals to layer I of the primary somatosensory cortex in rat.

Here we examined quantitatively axonal projections originating from the ventral posteromedial thalamic nucleus (VPM) to layer I of the primary somatosensory cortex (SI) by extracellular and intracellular injections of biocytin as an anterograde tracer. Following the extracellular injections, two types of VPM afferents with different arborization patterns in SI were observed. The type I extended vertically, forming dense plexus in layers IV and VI, and projected collaterals to layer I. The type II rarely branched in SI, converged in the plexus formed by the type I, and projected no collaterals to the supragranular layers. The labeled fibers in layer I derived from the first type ran parallel to the brain surface, and their mean length was 339.7 +/- 87.5 microm. Intracellular injection into VPM neurons bearing both types of afferent demonstrated the full axonal arborization in both the reticular thalamic nucleus (Rt) and SI. The total length of the axon of a neuron bearing the type I was 86,968.8 microm, and the length of axonal collaterals in layer I of SI was 433.1 microm. The total axonal length of a neuron bearing the type II was very small. The present study is the first to demonstrate substantial projections from VPM to layer I of SI, and provide quantitative data on the entire extent of the axonal arborization of thalamocortical projections from single VPM neurons.

Microglial ecto-Ca(2+)-ATPase activity in a rat model of focal homologous blood clot embolic cerebral ischemia: an enzyme histochemical study.

Post-ischemic changes in ecto-Ca(2+)-ATPase activity in microglia and the infarcted tissue were studied in a rat model of focal embolic cerebral ischemia using an enzyme histochemical method. Ecto-Ca(2+)-ATPase activity was observed in whole brains in non-operated and sham-operated control animals. In addition, this enzyme activity was determined to be localized in ramified microglia. At 30 min after ischemia, non-microglial ecto-Ca(2+)-ATPase activity in the infarcted tissue slightly decreased and continued to decrease thereafter. The ecto-Ca(2+)-ATPase activity in microglia did not appear changed at this time. The decrease of enzyme activity in the infarcted tissue made it much easier to clearly observe ecto-Ca(2+)-ATPase-positive microglia. The enzyme activity of microglia in the ischemic area began to decrease 2 or 4h after embolization and remarkably decreased, except in the perinuclear cytoplasm, apical parts of the processes, and several parts along the processes, 8h after ischemia. By 12h after onset of embolization, the enzyme activity of microglia and infarcted tissue had almost completely disappeared. Ecto-Ca(2+)-ATPase of microglia is likely to play an important role in the metabolism of extracellular nucleotides in the ischemic area immediately after the onset of embolization by means of ecto-enzymes. Thus, the findings of the present study suggest that microglia might serve to protect the infarcted tissue in the ischemic brain.