This article describes clinic, a type of medical facility. For information on the band of the same name, see Clinic (band).

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Pediatric Surgery International

Immunohistological evidence for Wnt-signaling activation in Peutz-Jeghers polyposis
Fri, 18 Dec 2009 07:06:10 -0000
Abstract Objective  Molecular pathogenesis of gastrointestinal polyposis in Peutz-Jegher’s syndrome (PJS) has been linked to the loss-of-function mutation of LKB1. Recent functional genetic studies have pointed out that LKB1 plays a physiological role in controlling the Wnt-signaling pathway and activation of the pathway as a consequence of LKB1 haploinsufficiency might be responsible for the development of harmatomatous polyps. This study aimed to look for immunohistochemical evidence of Wnt-signaling activation in PJS polyps. Method  Beta-catenin immunohistochemistry patterns were evaluated in gastrointestinal polyps from five cases of PJS. All patients were also evaluated for germline mutations of LKB1 and somatic mutations of beta-catenin in the polyps. Results  Four of the five cases had germline mutations of LKB1, including two novel mutations, a one-base insertion at codon 53 and a large deletion encompassing exon 3 (codon 136–155). PJS polyps from all patients showed generalized membrane and cytoplasmic localizations of beta-catenin along the mucosal endothelium. Polyps from two cases with LKB1 mutations revealed moderate-intensity nuclear staining in approximately 20 and 70% of the polyps. Conclusion  The study offers additional evidence of Wnt-signaling activation in PJS polyp development at the tissue level, although the degree of up-regulation was not as high as has been found in Wnt-associated neoplasms. Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00383-009-2547-zAuthors Walawee Chaiyapan, Prince of Songkla University Tumor Biology Research Unit, Faculty of Medicine Hat Yai Songkhla 90110 ThailandSurasak Sangkhathat, Prince of Songkla University Tumor Biology Research Unit, Faculty of Medicine Hat Yai Songkhla 90110 ThailandSamornmas Kanngurn, Prince of Songkla University Tumor Biology Research Unit, Faculty of Medicine Hat Yai Songkhla 90110 ThailandMonlika Phukaoloun, Prince of Songkla University Anatomical Pathology Unit, Faculty of Medicine Hat Yai Songkhla 90110 ThailandPiyawan Chiengkriwate, Prince of Songkla University Pediatric Surgery Unit, Faculty of Medicine Hat Yai Songkhla 90110 ThailandSakda Patrapinyokul, Prince of Songkla University Pediatric Surgery Unit, Faculty of Medicine Hat Yai Songkhla 90110 Thailand Journal Pediatric Surgery InternationalOnline ISSN 1437-9813Print ISSN 0179-0358
New experimental corrosive esophagitis model in rats
Fri, 11 Dec 2009 06:52:13 -0000
Abstract Purpose  Caustic esophagitis is a serious clinical problem and many agents are currently tried out in many experimental models. The model of Gehanno is the most commonly used invasive model, which is required general anesthesia and laparotomy. We aimed to form a new pratic and non-invasive model. Methods  Twenty rats were studied. The stomachs of the rats were reached through guidance catheter with ether anesthesia, Fogarty catheter was send in through, it was filled with pressure in the stomach. Then, Fogarty was pulled back and stomach entrance was closed. Control group was given; n = 10; 0.25 cc isotonic, injury group was given; n = 10; 0.25 cc, %40 NaOH and it was waited for 60 s. Their esophagi were examined after 28 days. Results  In the histopathologic evaluation of the control group, no pathology was discovered. Sub-mucosal collagen increase, muscularis mucosa and tunica muscularis damage have all been detected in the injury group p < 0.005; p < 0.003; p < 0.005). Conclusions  Corrosive esophagitis was formed without general anesthesia and laparotomy. Burn was formed in the total esophagus, unlike other models in which the burn is just formed at the below end. With our less invasive, more easily applied model; treatment agents can be given just as the corrosive esophagitis can be formed. Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00383-009-2546-0Authors Ekrem Senturk, Adnan Menderes University Thoracic Surgery Department, Medicine Faculty 09010 Aydin TurkeySerdar Sen, Adnan Menderes University Thoracic Surgery Department, Medicine Faculty 09010 Aydin TurkeyEngin Pabuccu, Adnan Menderes University Thoracic Surgery Department, Medicine Faculty 09010 Aydin TurkeyCengiz Unsal, Adnan Menderes University Physiology Department, Veterinary Faculty Aydin TurkeyIbrahim Meteoglu, Adnan Menderes University Pathology Department, Medicine Faculty Aydin Turkey Journal Pediatric Surgery InternationalOnline ISSN 1437-9813Print ISSN 0179-0358
Microecology, intestinal epithelial barrier and necrotizing enterocolitis
Sat, 05 Dec 2009 08:58:33 -0000
Abstract  Soon after birth, the neonatal intestine is confronted with a massive antigenic challenge of microbial colonization. Microbial signals are required for maturation of several physiological, anatomical, and biochemical functions of intestinal epithelial barrier (IEB) after birth. Commensal bacteria regulate intestinal innate and adaptive immunity and provide stimuli for ongoing repair and restitution of IEB. Colonization by pathogenic bacteria and/or dysmature response to microbial stimuli can result in flagrant inflammatory response as seen in necrotizing enterocolitis (NEC). Characterized by inflammation and hemorrhagic–ischemic necrosis, NEC is a devastating complication of prematurity. Although there is evidence that both prematurity and presence of bacteria, are proven contributing factors to the pathogenesis of NEC, the molecular mechanisms involved in IEB dysfunction associated with NEC have begun to emerge only recently. The metagenomic advances in the field of intestinal microecology are providing insight into the factors that are required for establishment of commensal bacteria that appear to provide protection against intestinal inflammation and NEC. Perturbations in achieving colonization by commensal bacteria such as premature birth or hospitalization in intensive care nursery can result in dysfunction of IEB and NEC. In this article, microbial modulation of functions of IEB and its relationship with barrier dysfunction and NEC are described. Content Type Journal ArticleCategory Review ArticleDOI 10.1007/s00383-009-2536-2Authors Renu Sharma, University of Florida at Jacksonville Division of Neonatology, Department of Pediatrics 655 West 8th Street Jacksonville FL 32209 USAJoseph J. Tepas, University of Florida at Jacksonville Department of Surgery Jacksonville USA Journal Pediatric Surgery InternationalOnline ISSN 1437-9813Print ISSN 0179-0358 Journal Volume Volume 26 Journal Issue Volume 26, Number 1 / January, 2010
Erratum to: The effect of non-steroidal anti-inflammatory drugs and Helicobacter pylori infection on the gastric mucosa in children with upper gastrointestinal bleeding
Thu, 03 Dec 2009 18:20:45 -0000
Erratum to: The effect of non-steroidal anti-inflammatory drugs and Helicobacter pylori infection on the gastric mucosa in children with upper gastrointestinal bleeding Content Type Journal ArticleCategory ErratumDOI 10.1007/s00383-009-2545-1Authors Samir Boukthir, Hôpital d’enfants Tunis TunisiaSonia M. Mazigh, Hôpital d’enfants Tunis TunisiaNicolas Kalach, Catholic University of Lille Department of Saint Vincent de Paul Hospital Lille FranceOlfa Bouyahya, Hôpital d’enfants Tunis TunisiaAzza Sammoud, Hôpital d’enfants Tunis Tunisia Journal Pediatric Surgery InternationalOnline ISSN 1437-9813Print ISSN 0179-0358
Therapeutic intussusception in necrotizing enterocolitis: a novel surgical strategy
Thu, 03 Dec 2009 12:49:20 -0000
Abstract  The optimal operative management of babies with necrotizing enterocolitis (NEC) remains uncertain. We report the case of a premature neonate with advanced NEC where areas of necrotic small bowel were successfully managed by intussusception into adjacent distal intestine and we discuss the merits of therapeutic intussusception as an option in the surgical management of advanced NEC. Content Type Journal ArticleCategory Case ReportDOI 10.1007/s00383-009-2544-2Authors Lynne Anne Holmes, Royal Aberdeen Children’s Hospital Aberdeen Scotland, UKGeorge G. Youngson, Royal Aberdeen Children’s Hospital Aberdeen Scotland, UK Journal Pediatric Surgery InternationalOnline ISSN 1437-9813Print ISSN 0179-0358
In vitro construction of scaffold-free cylindrical cartilage using cell sheet-based tissue engineering
Fri, 27 Nov 2009 07:02:54 -0000
Abstract Purpose  Tissue-engineered cartilage may offer a solution for the treatment of serious airway disease. This study developed a novel procedure to fabricate a scaffold-free cylindrical cartilage under in vitro conditions, while also evaluating the effect of a dynamic culture on the engineered construct. Methods  Auricular chondrocytes were harvested from New Zealand white rabbits and cultivated under high-density conditions to form a chondrocyte sheet. The sheet was looped around a silicon tube and cultivated for 6 weeks in dynamic or static conditions. The engineered cylindrical cartilages were evaluated macroscopically and histologically. The expression of collagen, glycosaminoglycan content and mechanical properties were determined. Results  The cylindrical cartilage was sufficiently elastic and stiff to maintain the structure without disruption. Histologically, the construct contained a Safranin-O positive cartilaginous matrix accompanied by the expression of type II collagen. The glycosaminoglycan content increased and reached 72% of the native tracheal cartilage after 6 weeks of cultivation. Conclusion  A novel procedure was developed for fabricating engineered cartilage, which maintained the shape and a proper level of rigidity and flexibility, under in vitro conditions using sheet-based tissue engineering techniques. This procedure may allow for the development of a tailor-made autograft and a functionally engineered trachea. Content Type Journal ArticleCategory Original ArticleDOI 10.1007/s00383-009-2543-3Authors Gakuto Tani, Osaka University Graduate School of Medicine Department of Pediatric Surgery 2-2 Yamadaoka, Suita Osaka 565-0871 JapanNoriaki Usui, Osaka University Graduate School of Medicine Department of Pediatric Surgery 2-2 Yamadaoka, Suita Osaka 565-0871 JapanMasafumi Kamiyama, Osaka University Graduate School of Medicine Department of Pediatric Surgery 2-2 Yamadaoka, Suita Osaka 565-0871 JapanTakaharu Oue, Osaka University Graduate School of Medicine Department of Pediatric Surgery 2-2 Yamadaoka, Suita Osaka 565-0871 JapanMasahiro Fukuzawa, Osaka University Graduate School of Medicine Department of Pediatric Surgery 2-2 Yamadaoka, Suita Osaka 565-0871 Japan Journal Pediatric Surgery InternationalOnline ISSN 1437-9813Print ISSN 0179-0358

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