Radiographic findings in esophageal atresia with proximal pouch fistula (type B)

1975 ◽  
Vol 3 (2) ◽  
pp. 70-74 ◽  
Author(s):  
Walter E. Berdon ◽  
David H. Baker
2009 ◽  
Vol 44 (12) ◽  
pp. 2433-2434
Author(s):  
Kenneth K.Y. Wong ◽  
Godfrey Lam

2019 ◽  
Vol 32 (Supplement_1) ◽  
Author(s):  
A Wiseman ◽  
J Krishnan ◽  
D Wanaguru ◽  
C Langusch ◽  
V Varjavandi ◽  
...  

Abstract Background Long-gap esophageal atresia (LGEA) has traditionally been managed by delayed anastamosis. However, over the last 10 years the Foker technique of esophageal growth elongation has been used. There is limited data evaluating outcomes using both techniques. Aims The aim of this study was to compare the outcomes in LGEA repair using the traditional delayed repair technique versus the Foker technique. Methods A retrospective chart review was done of LGEA patients at Sydney Children's Hospital between 1997 and 2016, comparing the Foker technique with the delayed repair technique. Results There were 9 children repaired using the Foker technique, and 10 by delayed repair. There were 7 patients with Type A, 1 with Type B, and 1 with Type C in the Foker group and in the delayed repair cohort, 5 were Type A, 2 Type B, 2 Type C, and 1 Type D esophageal atresia/tracheoesophageal fistula. There were 4 males in the Foker group and 5 in the non-Foker group. Median time to join was 59 days (15–117 days) for Foker repair and 173 days (16–433 days) for delayed repair. There was no significant difference in the incidence of post-operative leak, incidence of strictures needing dilation, presence of reflux symptoms, presence of reflux esophagitis on endoscopy, proton pump inhibitor use, need for fundoplication, incidence of cyanotic spells, occurrence of recurrent fistula, and symptoms of dysphagia when comparing both groups. Data on time to oral feeds and incidence of malnutrition was incomplete. Details are shown in Table 1. Conclusions Although the time to anastamosis was shorter in the Foker group and the incidence of post-operative leak, strictures needing dilation, need for fundoplication, and dysphagia were lower in the Foker group, the difference was not significant probably secondary to the small sample size. These results require validation in larger cohorts.


2018 ◽  
Vol 25 (4) ◽  
pp. 186-190
Author(s):  
Young Mi Han ◽  
Narae Lee ◽  
Shin Yun Byun ◽  
Soo-Hong Kim ◽  
Yong-Hoon Cho ◽  
...  

Author(s):  
S. Fujinaga ◽  
K. Maruyama ◽  
C.W. Williams ◽  
K. Sekhri ◽  
L. Dmochowski

Yumoto and Dmochowski (Cancer Res.27, 2098 (1967)) reported the presence of mature and immature type C leukemia virus particles in leukemic organs and tissues such as lymph nodes, spleen, thymus, liver, and kidneys of SJL/J strain mice with Hodgki's-like disease or reticulum cell neoplasm (type B). In an attempt to ascertain the possibility that this neoplasia may be of viral origin, experiments with induction and transmission of this neoplasm were carried out using cell-free extracts of leukemic organs from an SJL/J strain mouse with spontaneous disease.It has been possible to induce the disease in low-leukemia BALB/c and C3HZB strain mice and serially transfer the neoplasia by cell-free extracts of leukemic organs of these mice. Histological examination revealed the neoplasia to be of either reticulum cell-type A or type B. Serial transfer is now in its fifth passage. In addition leukemic spleen from another SJL/J strain mouse with spontaneous reticulum cell neoplasm (type A) was set up in tissue culture and is now in its 141st serial passage in vitro. Preliminary results indicate that cell-free material of 39th tissue culture passage can reproduce neoplasia in BALB/c mice.


Author(s):  
P. F. Flicker ◽  
V.S. Kulkarni ◽  
J. P. Robinson ◽  
G. Stubbs ◽  
B. R. DasGupta

Botulinum toxin is a potent neurotoxin produced by Clostridium botulinum. The toxin inhibits release of neurotransmitter, causing muscle paralysis. There are several serotypes, A to G, all of molecular weight about 150,000. The protein exists as a single chain or or as two chains, with two disulfide linkages. In a recent investigation on intracellular action of neurotoxins it was reported that type B neurotoxin can inhibit the release of Ca++-activated [3H] norepinephrine only if the disulfide bonds are reduced. In order to investigate possible structural changes in the toxin upon reduction of the disulfide bonds, we have prepared two-dimensional crystals of reduced type B neurotoxin. These two-dimensional crystals will be compared with those of the native (unreduced) type B toxin.


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