Laparoscopic enucleation of a gastroenteric duplication cyst arising in a pancreatic tail that did not communicate with the pancreatic duct: Report of a case

Gastroenteric duplication rarely occurs in locations such as the pancreas. We report a case of gastroenteric duplication of the pancreatic tail, which was noncontiguous with the stomach and had no communication with the pancreatic duct, in a 3-year-old girl. The cyst was enucleated by laparoscopy, without the need for pancreatic resection. The optimal treatment procedures vary considerably, depending on where the gastroenteric duplication is located in the pancreas and, most importantly, whether there is communication with the pancreatic duct.     

C-Peptide/Creatinine Ratio in Early Morning Urine as an Indicator of Residual B-Cell Function in Insulin-Dependent Diabetes

The C-peptide/creatinine (Cr) ratio in early morning urine was evaluated to assess B-cell function. The subjects were 12 boys and 36 girls with insulin-dependent diabetes mellitus (IDDM). The controls were 130 boys and 137 girls aged 4–15 years. There was a significant inverse correlation of this ratio with the duration of insulin therapy (r = -0.5807, P<0.01). The daily insulin dose in U/kg was significantly different among the following groups: 1.22 ± 0.31 U/kg in group 1 with undetectable C-peptide, 0.94 ± 0.37 in group 2 with a decreased ratio and 0.45 ± 0.28 in group 3 with a normal ratio. HbAl levels were 11.3 ±1.6% in group 1 and 9.2 ± 1.1% in group 3. The difference was significant. The result shows that the C-peptide/ Cr ratio in early morning urine is useful for assessing B-cell function in diabetic children.     

Increased expression of mRNAs for microtubule disassembly molecules during nerve regeneration

The mRNA expression of the microtubule disassembly molecules (SCG10, stathmin, SCLIP and RB3) in response to nerve injury was examined using a rat hypoglossal nerve injury model. After nerve injury prominent increase in mRNA expression of SCG10, stathmin and RB3 was observed, while only slight increase in SCLIP mRNA was observed in injured motor neurons. The increase in SCG10 and RB3 mRNA expression was quicker than that of stathmin and SCLIP. All the elevated signals decreased gradually to control levels by 4 weeks after nerve injury.     

Immediate early genes and p21 regulation in liver of rats with acute hepatic failure

It has been observed that liver regeneration in acute hepatic failure (AHF) is suppressed [Eguchi et al. Hepatology 1996;24(6):1452-9]. The molecular mechanism regulating this inhibition is not known. We previously reported that in AHF rats, hepatocyte proliferation was significantly impaired with elevation in serum IL-6, TGF-beta1, and HGF [Kamohara et al. Biochem Biophys Res Commun 2000;273(1):129-35]. Following either 70% partial hepatectomy (PH) or liver injury, quiescent mature hepatocytes are "primed" to re-enter the cell cycle. The process of "priming" appears to be triggered by extracellular cytokines (IL-6 and TNF-alpha) and is characterized by expression of immediate early genes. Under the stimulation of growth factors such as HGF, "primed" hepatocytes exit the G1 phase of the cell cycle. G1-associated cyclins and their inhibitors play a pivotal role in G1/S cell cycle transition. Here, we demonstrate that immediate early gene (i.e. c-myc, c-fos) expression and AP-1 activity are preserved in AHF rat livers despite absence of hepatocyte proliferation. In contrast, p21 mRNA and protein are both over-expressed in AHF livers compared to livers from rats undergoing PH; this elevation leads to inhibition in Cdk2 activity, resulting in G1 cell cycle arrest and inhibition of regeneration.     

Membrane-associated Lymphotoxin Expression and Functional Analysis of Lymphokine-activated Killer Cells Derived from Tumor-infiltrating Lymphocytes

The expression of a membrane-associated lymphotoxin molecule (mLT) on lymphokine-activated killer (LAK) cells obtained from 18 patients with malignant tumors and its role in the tumor cell killing mechanisms were investigated. LAK cells from tumor-infiltrating lymphocytes (TIL-LAK cells) were mainly composed of CD3-positive cells, whereas LAK cells from peripheral blood lymphocytes (PBL-LAK cells) were mainly composed of CD16- and CD56-positive cells. However, mLT was found to be expressed on TIL-LAK cells as well as PBL-LAK cells. The degree of mLT expression correlated with the killing activity of LAK cells towards L929 cells (r=0.806, P <0.01, n = 15), but not with that towards Daudi or K562 cells. Although the degree of mLT expression correlated with the amount of secreted lymphotoxin (LT) in the supernatant of LAK cell culture, the secreted LT itself could not account for the tumor cell killing activity of LAK cells. Polyclonal rabbit anti-LT antibody partially inhibited the killing activities of LAK cells towards L929 cells and this inhibition was found in the combination of autologous tumor cells and PBL-LAK cells. These findings suggest the possibility that the mLT-related cytotoxicity is involved in the tumor cell killing mechanisms of TIL-LAK cells as well as PBL-LAK cells.     

An elder case of neurosarcoidosis associated with brain infarction]

A 75-year-old woman with sarcoidosis developed sudden weakness of the left upper and lower limbs. Neurological examination revealed left-sided hemiplegia, hyperreflexia with pathological reflexes and hypesthesia. She was disoriented and euphoric. Diffusion-weighted brain MRI showed high intensity lesions in the right parietooccipital lobes. Electroencephalogram showed diffuse slowing of the background activity. Serum lysozyme increased to 18.4 mg/ml, CSF protein to 51 mg/dl. After admission, she presented psychotic manifestation followed by a progressive disturbance of consciousness. Epithelioid granulomas without caseous necrosis were present in the biopsied lymph node and specimens from the occipital cortex, indicating neurosarcoidosis. Necrosis was also present in the sampled brain tissue. The psychotic symptoms and consciousness disturbance rapidly ameliorated after the treatment with oral prednisolone, 40 mg/day. Neurosarcoidosis should be considered even in an elder case of sarcoidosis complicated with a stroke.     

Effects of immunosuppressants on induction of regulatory cells after intratracheal delivery of alloantigen

BACKGROUND: We previously reported that intratracheal delivery (ITD) of alloantigen generated regulatory cells in mice. Here, we examined the effect of various doses of conventional immunosuppressants (FK506, cyclosporine A, azathioprine, mycophenolate mofetil, and rapamycin) on inducing regulatory cells in our model. METHODS: CBA mice (primary recipients) were given C57BL/6 splenocytes by ITD and either no additional treatment or various doses of an immunosuppressant. Seven days later, splenocytes from these mice were adoptively transferred into naive secondary CBA recipients that underwent C57BL/6 cardiac grafting the same day. RESULTS: Adoptive transfer from primary recipients given ITD of splenocytes alone induced prolonged allograft survival in secondary recipients (median survival time [MST], 50 days), suggesting that regulatory cells were generated. When ITD of alloantigen was combined with daily administration of 0.1 mg/kg FK506 or 0.2 mg/kg rapamycin, graft survival was similarly prolonged (MST 55 and 50 days, respectively). When combined with 20 or 40 mg/kg MMF or 0.4 mg/kg rapamycin, the majority of recipients demonstrated indefinite survival (MST, >100 days in all groups). When ITD of alloantigen was combined with 0.3, 0.5, or 1.0 mg/kg FK506; 5, 10, or 25 mg/kg cyclosporine A; or 1.0 or 2.0 mg/kg azathioprine, allografts were rejected acutely (MST 7-13 days). CONCLUSION: Generation of regulatory cells by ITD of alloantigen was facilitated by mycophenolate mofetil and high doses of rapamycin but abrogated by cyclosporine A, azathioprine, and high doses of FK506. Low doses of rapamycin and of FK506 did not interfere with generation of regulatory cells.