Complications in Pediatric Surgery by Michael G. Caty

By Michael G. Caty

Addressing the necessity of pediatricians and pediatric surgeons for a one-stop, complete textual content on pediatric surgical procedure, issues in Pediatric surgical procedure covers every one case a doctor could stumble upon upon treating the pediatric surgical sufferer, from fetus to adolescent.

Complications in Pediatric surgical procedure offers separate and concise chapters, each one of which concentrates on a selected region of the physique. The chapters spotlight universal surgical mistakes and issues, in addition to the techniques and methods for use within the face of such issues.

Including key specialist critiques in every one part, this article explores following healing areas:

  • head and neck surgery
  • thoracic and chest wall surgery
  • extracorporeal lifestyles support
  • fetal surgery
  • abdominal wall and hernia surgery
  • intestinal and vascular access
  • esophageal surgery
  • stomach, duodenum, and small intestine
  • colon and anorectal surgery
  • appendicitis
  • hepatobiliary surgery
  • surgery of the spleen
  • oncologic surgery
  • laparoscopic and thorascopic surgery
  • pediatric trauma
  • transplantation
  • urologic surgery

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Extra resources for Complications in Pediatric Surgery

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It is not yet clear whether this multistep transformation occurs randomly in any somatic cell of the body or whether a special pool of progenitor cells within the organ (stem cells) harbor these genetic/ epigenetic alterations to produce cancer cells in a hierarchical fashion contributing to tumorigenesis. Stochastic theory explains that the mutations (or epigenetic changes) could take place in any cell of the body because of any physical/chemical mutagens from environmental factors or deregulation of the endogenous machinery of the cell.

Point mutations: Point mutations in the coding sequence of some oncogenes result in the substitution of one specific amino acid for another in the primary protein sequence. These alterations make the oncoprotein constitutively active. As in the case of ras, a point mutation in either codon 12, 13, or 61 of the gene encoding the Ras enzyme makes the enzyme constitutively active. Mutation of codon 12 results in glycine being substituted by valine (commonly designated as rasG12V), which is the most frequent gainof-function mutation in many cancers.

Secondly, it induces synthesis of tumor suppressor proteins p15INK4B and p21, which block cyclin, a cyclin dependent kinase complex responsible for pRb phosphorylation. The TGFb pathway is disrupted in many cancers in various ways. First, transcriptional downregulation and loss of function mutation of TGFb receptors are common in many cancers. Secondly, the downstream protein Smad4 is eliminated through loss of function mutation of its encoding gene. Thirdly, the genetic deletion or promoter hypermethylation causes downregulation of p15INK4.

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