A hole in the T cell repertoire specific for a pigeon cytochrome c related peptide associated with amino acid substitutions on I-Ab molecules.

When C57BL/10(B10) mice were immunized with a pigeon cytochrome c related peptide, 50V (AEGFSYTVANKNKGIT), two helper T cell populations with different specificity were activated. A major T cell population reacted with a 50V analog, 50V54A (AEGFSYTVANKAKGIT), more potently than with the immunogen, 50V, in a heteroclitic fashion, whereas the other minor T cell population responded only to 50V. By contrast, when bm12 mice were immunized with 50V, the minor T cell population responding only to 50V could hardly be demonstrated. The apparent deletion of the minor T cell population in bm12 mice seems to be attributable to negative selection under the influence of I-Abm12 molecules, since the minor T cell population was undetectable in both I-Ab and I-Abm12 restricted T cells from (B10 x bm12)F1 mice. Thus, three mutant points on the I-A molecule in bm12 mice appear to be involved in the seemingly negative selection of the certain T cell repertoire. The present finding demonstrates that a T cell repertoire generated under the influence of a MHC product (Ab) on one parental strain is eliminated by a different MHC product (Abm12) on the other parental strain of F1 cross. The mechanism underlying the apparent negative selection is discussed.     

Reactive lymphoid hyperplasia of the liver: literature review and 3 case reports

Reactive lymphoid hyperplasia (RLH) is a benign non-specific lesion having an unknown etiology and pathogenesis. The lesion is found in various organs but is rare in the liver. We report 3 cases of hepatic RLH associated with an extrahepatic malignant tumor. We also provide a literature review based on a search of the PubMed database from 1983 to 2009. The 3 cases showed radiological findings similar to those for malignant tumors and all cases were misdiagnosed as malignant tumors on the basis of these findings. It is difficult to distinguish RLH from malignant or metastatic tumors on the basis of imaging findings. Hepatic RLH is a rare entity and may cause a false diagnosis of malignancy. Because RLH occurs most commonly in middle-aged females, diagnosis of a hypervascular tumor of the liver requires particular care in these patients, especially if an extrahepatic malignancy is present.     

Incidence of the focal type of autoimmune pancreatitis in chronic pancreatitis suspected to be pancreatic carcinoma: experience of a single tertiary cancer center

Objective. With an increase in autoimmune pancreatitis (AIP) being reported, the focal type of AIP, which shows localized narrowing of the main pancreatic duct and focal swelling of the pancreas, has recently been recognized. Therefore, cases of focal-type AIP subjected to surgical intervention for presumptive malignancy might previously have been diagnosed as mass-forming chronic pancreatitis. The aim of this study was to elucidate the incidence of focal-type AIP in resected chronic pancreatitis at a single tertiary cancer center. The clinical and radiological features of focal-type AIP were also evaluated. Material and methods. We re-evaluated 15 patients who underwent pancreatic resection with a presumed diagnosis of pancreatic ductal adenocarcinoma, and who in the past had been diagnosed pathologically as having chronic pancreatitis. Results. Seven of 15 patients showed AIP, and the other 8 patients were diagnosed as having mass-forming chronic pancreatitis not otherwise specified by pathological retrospective examination. In other words, nearly half of the cases of resected chronic pancreatitis that were suspected to be pancreatic carcinoma preoperatively showed focal-type AIP. Regarding the characteristic findings of focal-type AIP, narrowing of the pancreatic duct on endoscopic retrograde pancreatography (ERP) might be diagnostic. Conclusions. Focal-type AIP is not a rare clinical entity and might be buried in previously resected pancreatic specimens that in the past were diagnosed simply as mass-forming pancreatitis.     

Risk Factors of Surgical Site Infection After Hepatectomy for Liver Cancers

Background  Risk factors of surgical site infection (SSI) after hepatectomy under the guideline of Centers for Disease Control and Prevention (CDC) are not well examined. Methods  Hospital records of consecutive patients who underwent hepatectomy without biliary reconstruction for liver cancers were reviewed retrospectively. Prophylactic antibiotics were given to patients just before skin incision and every 3 hours during the operations. Clinicopathological factors were compared between patients who developed SSI and those without it. Results  There were 405 patients identified, and the incidence of SSI was 23 cases (5.8%). In multivariate analysis, intraoperative bowel injury, blood loss >2000 ml, and age older than 65 years were significant risk factors of SSI after hepatectomy. Conclusions  Prophylactic antibiotics were necessary only during the operation for most patients who underwent hepatectomy without biliary reconstruction. However, patients with intraoperative bowel injury, blood loss >2000 ml, and age older than 65 years are at risk to develop SSI and might need additional administration of prophylactic antibiotics after surgery.     

Gallbladder agenesis with no other biliary tract abnormality: report of a case and review of the literature

We report a rare adult case of gallbladder agenesis with no other biliary tract abnormality. The patient was a 29-year-old man with pain in the right upper-quadrant of the abdomen, and vomiting. The gallbladder was not visualized by ultrasonography, computed tomography, or endoscopic retrograde cholangiography. The common bile duct was slightly dilated. No other abnormalities, including anomalous choledochopancreatic duct junction, were found. Based on these imaging findings and the patient's right hypochondrial pain, there was a high index of suspicion of chronic cholecystitis caused by incarcerated gallstones in the neck of the gallbladder. At operation, we carefully observed the gallbladder fossa, using laparoscopy, and found gallbladder to be absent. Although the operation involved only observation via a laparoscope, the patient has since remained well and asymptomatic. It is difficult to make a correct diagnosis of gallbladder agenesis preoperatively. We believe that, if the gallbladder is not visualized by imaging techniques, it may be better to perform laparoscopy for observation before performing laparotomy, in order to reduce surgical stress. Received for publication on Dec. 4, 1999; accepted on Feb. 6, 2000     

Effect of hypothermia on postmortem alterations in MAP2 immunostaining in the human hippocampus

Ischemic neuronal injury induce degradation of microtubule-associated protein 2 (MAP2). In addition to ischemia, postmortem brains show alterations in MAP2 immunoreactivity in the hippocampus, suggesting that the factors inducing cytoskeletal disruption in postmortem brain are similar to those in ischemic brains. Hypothermia reduces the severity of ischemic injury including disruption of MAP2 in the hippocampus. However, whether hypothermia reduces postmortem changes of MAP2 was not clear. In this study, we evaluated the effect of hypothermia on postmortem degradation of MAP2 in the human hippocampus at various postmortem intervals using immunohistochemistry. In postmortem brains without hypothermia (the normothermic group), the locus of MAP2 immunoreactivity moved from the dendrites to the cell bodies prior to becoming undetectable with increasing postmortem interval, particularly in the CA1-subiculum region. On the other hand, the change in MAP2 immunoreactivity was remarkably attenuated in brains of death from cold (the hypothermic group). The present study demonstrated that MAP2 disruption is remarkable in the CA1-subiculum region of autopsied brains and that hypothermia reduces the postmortem change of MAP2, as observed in ischemic brain. Therefore, immunostaining of MAP2 in the hippocampus could be used to diagnose hypothermia.     

Prevention of tissue factor generation in mononuclear cells by agents known to increase intracellular cyclic AMP.

Agents known to increase intracellular levels of cyclic 3', 5'-adenosine monophosphate (cyclic AMP) were examined for their effect on tissue factor generation by mononuclear cells cultured with E. coli endotoxin. Aminophylline, an inhibitor of phosphodiesterase, and epinephrine, a beta-adrenergic agent, showed an inhibitory effect, and these effects were reversible. Moreover, dibutyryl cyclic AMP also exhibited the effect. Dibutyryl cyclic GMP, however, did not enhance the tissue factor generation by mononuclear cells. On the basis of these observations, it was concluded that the phenomenon of tissue factor generation by mononuclear cells is a biological event, and that intracellular cyclic AMP has a possible role in modulating this phenomenon.