The experiment shows that using bFGF, better mechanical strength was obtained but with poor cartilage growth.

Among 36 neonates with intestinal perforations (IP) between 1975 and 1996, 5 had necrotizing enterocolitis (NEC IP) and 10 had focal IPs (FIP). A histologic review of the bowel near the perforations was made to see if there was any difference between cases of NEC IP and FIP. In 1 case of NEC IP, a defect in the musculature was found in addition to disappearance of the mucosal villi and dilated vessels or hemorrhage in the submucosa. Thinning or absence of the intestinal musculature and short villi in the mucosa was observed in 3 cases of FIP, but the acute ischemic changes in FIP were much less than in NEC IP. Hypothesizing that the defective musculature in FIP may be acquired by a vascular accident either before or after birth, we examined the histology of the latest consecutive infants diagnosed as having meconium peritonitis (MP) due to in-utero volvulus and perforation. In the tissue near the perforation, there was an identical focus of thinning and interruption of the musculature while the acute ischemic changes were minimal. We speculate that thinning or absence of the intestinal musculature in FIP may be a result of a transient ischemic event occurring in-utero and that FIP may develop in the damaged intestine after birth when it is fully dilated.

Hepatocellular carcinoma (HCC) is one of the most common malignancies in areas with endemic hepatitis virus infections, 1,2 which strongly suggests that hepatitis virus-related damage to the hepatocytes could contribute to HCC development. We demonstrated that the activity of hepatitis in chronic liver disease closely correlated with the intrahepatic recurrence after the operation of HCC. 3 Although the immunological mechanism in chronic hepatitis virus infection has not been clearly defined, it has been assumed that T-cellmediated cytotoxicity is responsible for the hepatocyte injury. In fact, the messenger RNA of the inflammatory cytokines, such as interferon gamma (IFN-␥) and interleukin-2, was preferentially detected in patients with increased hepatitis activity using reverse-transcriptase polymerase chain reaction (RT-PCR) in liver tissue. 4 Because HCC develops in chronic liver disease in which the host immune responses take place to excess, the escape from T-cell-mediated cytotoxicity is thought to be an essential role in the development and outgrowth of HCC.IFN-␥ is produced by activated T lymphocytes and naturalkiller cells, and plays an important role in the host defense mechanism by exerting antiviral, antiproliferative, immunoregulatory, and proinflammatory activities. 5-7 IFN-␥ exerts its pleiotrophic biological effects by transcriptional regulation of the expression of numerous genes, such as major histocompatibility complex (MHC) class I, FcrRI, and Fas through interaction with a specific cell membrane receptor (IFN-␥ receptor [IFN-␥-R]). 6,[8][9][10][11][12][13][14] Although the hepatocytes in the normal liver express weak or no IFN-␥-R, those in acute and chronic liver diseases up-regulated the expression of IFN-␥-R, and this up-regulation might play a partial role in the immunoregulatory action of IFN-␥ during liver inflammation. 15 Kaplan et al. demonstrated that IFN-␥-R ␣-chain knock-out mice developed tumors more rapidly and frequently than did the wild-type controls when bred onto a background deficient in the p53 tumor-suppressor gene, as well as when treated with the chemical carcinogen, 3-methylcolanthrene. 16 They proposed the concept that the actions of IFN-␥ on the tumor cells serve an extrinsic tumor-suppressor mechanism in immunocompetent hosts. Accordingly, blocking the signal transduction of IFN-␥ in HCC might contribute to escape from host immune surveillance in chronic liver disease in which many infiltrating lymphocytes produce IFN-␥. However, it is unclear how HCC blocks the signal transduction of IFN-␥. We examined the degree of tumor infiltration of IFN-␥-positive lymphocytes and the expression of IFN-␥-R, and IFN-␥-inducible genes, such as MHC class I and Fas, in HCC and investigated whether the modulation of IFN-␥-R expression was one of the mechanisms blocking the signal transducAbbreviations: HCC, hepatocellular carcinoma; IFN-␥, interferon gamma; RT-PCR, reverse-transcriptase polymerase chain reaction; MHC, major histocompatibility complex; IFN-␥-R, IFN-␥ receptor; AFP,...

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Purpose: This article presents the extracorporeal ligation of inguinal hernia defects using an epidural needle and preperitoneal hydrodissection. Patients and Methods: Thirteen children underwent laparoscopic extracorporeal ligation of their hernia defect using an epidural needle and preperitoneal hydrodissection. A 5-mm trocar for an operative laparoscope was placed through an infraumbilical incision, a Veress needle for forceps was inserted halfway between the umbilicus and the anterior superior iliac spine on the contralateral side of the hernia, and a 17-gauge epidural needle was inserted at the point of the internal inguinal ring. The hernia defect was closed extracorporeally by a nonabsorbable suture, which was introduced into the abdomen through the epidural needle on the lower half of the hernia defect and withdrawn on the opposite side by a wire-loop through the epidural needle going along the upper half side of the hernia defect in a series of movements. When a contralateral hernia defect is present, laparoscopic-assisted extracorporeal ligation of the contralateral hernia defect is performed during the same operation. Results: All patients were discharged uneventfully from the hospital within 24 hours postoperatively. The mean follow-up period is 6.1 months (range 2-12 mos), and no recurrence has been observed to date. Conclusions: This article describes a unique technique of extracorporeal circuit suturing of inguinal hernia defects using a minimally invasive technique as afforded by an epidural needle.