Background Conventional open herniorrhaphy in children has been reported to have 0.3-3.8% recurrence and 5.6-30% postoperative contralateral hernia rates. We developed a unique technique to achieve completely extraperitoneal ligation of PPV without any skip areas under laparoscopic control. This report introduces our technique and results compared with the cut-down herniorrhaphy. Methods A consecutive series of 1,585 children with inguinal hernia/hydrocele (1996)(1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004)(2005)(2006) was analyzed. In laparoscopic patent processus vaginalis (PPV) closure (LPC), an orifice of PPV was encircled with a 2-0 suture extraperitoneally by a specially devised Endoneedle and tied up from outside of the body achieving completely extraperitoneal ligation of the ring. The round ligament was included in the ligation, whereas the spermatic cord and testicular vessels were excluded by advancing the needle across them behind the peritoneum. Cut-down herniorrhaphy (CD), with or without diagnostic laparoscopy, or LPC was selected according to parental preference under informed consent. Results Parents gave more preference to LPC (LPC in 1,257 children, CD in 308, and miscellaneous in 20). Age ranges were equal for both groups. Sex distribution showed female preponderance in the LPC group (44.8% vs. 26.6%, p \ 0.001) and umbilical hernia/cysts were predominantly included in the LPC group (11.9% vs. 2.9%, p \ 0.001). Mean operation times were equal for both groups for unilateral repair (28.2 ± 9.2 for LPC vs. 27.8 ± 13.5 for CD) and were shorter for bilateral repair in the LPC group (35.8 ± 11.6 vs. 46.7 ± 17.7). The incidence of postoperative hernia recurrence and contralateral hernia in the LPC group was 0.2% and 0.8%. Two children in the CD group had injuries to their reproductive system during the operation (0.6%). Conclusions The advantages of our technique include following: technically simple, short operation time, inspection of bilateral IIRs with simultaneous closure of cPPV, reproductive systems remain intact, routine addition of umbilicoplasty if desired, and essentially indiscernible wounds.

The malignant phenotype of chronic myeloid leukemia (CML) is due to the abnormal tyrosine kinase activity of the Bcr-Abl oncoprotein. We have previously reported that expression of the Bach2 transcription factor, which induces apoptosis in response to oxidative stress, is greatly reduced in CML cells. Because these cells are resistant to apoptosis, we tested whether Bach2 could also be regulated through posttranslational mechanisms that promote inhibition of the apoptotic response to mutagenic stimuli in CML. We found that Bach2 is phosphorylated on S521 via the phosphatidylinositol-3/S6 kinase pathway, and substitution of this site to alanine leads to nuclear accumulation of the protein, indicating that this phosphorylation is important for its subcellular localization. Ectopic expression of the S521 mutant imparts greater impairment to CML cell growth than the wildtype factor. Furthermore, we showed that Bach2 transcriptionally represses heme oxygenase-1, an antiapoptotic factor upregulated in CML. Because CML cells are known to produce high levels of intracellular reactive oxygen species, overexpression of heme oxygenase-1 resulting from inhibition of Bach2 activity may contribute to their genomic instability and leukemic phenotype. IntroductionChronic myeloid leukemia (CML) is a myeloproliferative disorder of the hematopoietic stem cell caused by a t(9;22)(q34;q11) translocation that generates the Philadelphia (Ph) chromosome. This genetic defect, also found in 20% to 30% of adult acute lymphoblastic leukemias, results in the expression of Bcr-Abl, a fusion oncoprotein with uncontrolled tyrosine kinase activity. Imatinib mesylate inhibits the Bcr-Abl tyrosine kinase, suppresses the proliferation of CML progenitor cells, and induces apoptosis of Ph-positive cell lines. It is a highly effective drug and has become the first-choice treatment of CML. However, resistance to the inhibitor emerges in some patients, especially in advanced phases of CML (reviewed by Yoshida and Melo 1 and Deininger et al 2 ).Bcr-Abl phosphorylates several substrates that activate multiple signaling pathways, including Ras, signal transducer and activator of transcription-5 (STAT-5), extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK), Janus kinase 2 (Jak-2), phosphatidylinositol-3 kinase (PI-3K), and others. 3 This abnormal signaling leads to the malignant cellular phenotype of CML, including increased proliferation, reduction of adhesion to the bone marrow stroma and extracellular matrix, and inhibition of the apoptotic response to mutagenic stimuli. 4 DNA damage can be caused by oxidative stress arising when reactive oxygen species (ROSs) are not adequately removed from cells. 5 Interestingly, it has been suggested that ROSs are increased in CML cells. [6][7][8] Because a persistent increase of ROSs can lead to accumulation of DNA mutations, it may induce genomic instability as a long-term consequence. 9,10 Thus, BCR-ABL-positive cells can survive under levels of oxidative stress that normally induc...

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Gastric teratomas are very rare and usually benign. Only a few cases of gastric teratomas with malignant components have been reported. This report describes recurrence of a yolk sac tumor following resection of a neonatal immature gastric teratoma. Gastric teratoma recurring as a malignant lesion has not been previously reported. Recurrence of immature gastric teratomas should be considered, and a periodic follow-up check with alpha-fetoprotein level should be mandatory.