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Retina ◽  
2013 ◽  
Vol 33 (10) ◽  
pp. 2162-2169 ◽  
Author(s):  
Kai B. Kang ◽  
Anton Orlin ◽  
Thomas C. Lee ◽  
Michael F. Chiang ◽  
R. V. Paul Chan

Retina ◽  
2003 ◽  
Vol 23 (1) ◽  
pp. 128-131 ◽  
Author(s):  
SAAD SHAIKH ◽  
ANTONIO CAPONE ◽  
STEVEN D. SCHWARTZ ◽  
CHRISTINE GONZALES ◽  
MICHAEL T. TRESE

1995 ◽  
Vol 15 (1) ◽  
pp. 23-37 ◽  
Author(s):  
Raj P. Kapur ◽  
Derek J. deSa ◽  
Mark Luquette ◽  
Ronald Jaffe

1993 ◽  
Vol 14 (12) ◽  
pp. 475-480
Author(s):  
Molly O'Gorman ◽  
Alan M. Lake

Definition Chronic inflammatory bowel disease (IBD) of childhood is generally defined as either ulcerative colitis (UC) or Crohn disease (CD). The inflammation of UC is restricted to the mucosal lining of the colon, with the colonic involvement beginning universally in the rectum and extending proximally continuously. Although proctitis, persistent isolated involvement of the rectum, is common in adults (40%), it is rare in children (<10%). In contrast, the enteric inflammation of CD is transmural and involves any level of the intestinal tract discontinuously. The intervals of relatively normal bowel are termed "skip areas." In CD, characteristic lesions range from oral ulcerations to perianal lesions, although the most frequently involved area is the terminal ileum of the small bowel, a process termed ileitis. Recognition of these conditions by pediatricians is important because the peak incidence of IBD is in the second decade. Fewer than 5% of patients are diagnosed prior to age 5 years. In many children presenting with isolated colitis, the diagnosis of the chronic inflammation of IBD is established by biopsy before a clinical distinction between UC and CD can be established. These children carry the diagnosis of chronic nonspecific colitis or colitis type indeterminant. In our experience, the disease in approximately 50% of these children evolves within 5 years into more classic cases of UC or CD.


1986 ◽  
Vol 11 (1) ◽  
pp. 151-157 ◽  
Author(s):  
G. Marchal ◽  
E. Tshibwabwa-Tumba ◽  
E. Verbeken ◽  
W. Roost ◽  
W. Steenbergen ◽  
...  

1983 ◽  
Vol 101 (3) ◽  
pp. 388-391 ◽  
Author(s):  
S. Brownstein ◽  
D. A. Nicolle ◽  
F. Codere

1976 ◽  
Vol 94 (12) ◽  
pp. 2072-2077 ◽  
Author(s):  
D. M. Albert ◽  
M. C. Ruchman ◽  
J. L. Keltner

1974 ◽  
Vol 83 (4) ◽  
pp. 481-486 ◽  
Author(s):  
Max L. Som

Of 84 surgically treated cases of postcricoid carcinoma, 23 had a pharynxesophageal reconstruction by use of a laryngotracheal autograft. This procedure is most suitable in females with manifestations of the Paterson-Broun-Kelly syndrome. The distal esophagus is not “at risk” because of skip areas or second primary lesions. Failures are due predominantly to inability to control the lymphatic metastasis. Stomal recurrence may be due to ascending metastasis from the tracheoesophageal groove and mediastinum. A routine combined neck dissection is urged in all instances. Mediastinal node extirpation with or without resection of the manubrium may increase survival rate. Adequate surgical exposure with visualization, palpation, and exploration of the extent of the cancer is suggested prior to determination of the method of reconsruction of the pharyngoesophagus. In selected cases without previous radiotherapy the laryngotracheal autograft has proved satisfactory.


1964 ◽  
Vol 120 (4) ◽  
pp. 561-568 ◽  
Author(s):  
Sherwyn E. Warren ◽  
Myron Jacobson ◽  
Jafar Mirany ◽  
John Van Prohaska

1. Dogs develop severe gastrointestinal symptoms in response to intraintestinal administration of staphylococcal enterotoxin. These symptoms are salivation, vomiting, and diarrhea. 2. Staphylococcal enterotoxin induces acute enteritis marked by edema, hyperemia, round cell infiltration, mucosal exudation, and destruction of intestinal villi. 3. Prolonged administration of enterotoxin into the lumen of the intestine produced thickening of the entire bowel wall, edema, dilatation of the lymphatics, and exaggeration of submucous lymphoid nodules. The hypertrophy of the lymphoid nodules is visible, in the gross, as enlarged longitudinal mucosal ridges. This abnormality is arranged in skip areas, not dissimilar to those observed in human regional enteritis. 4. Chronic enterotoxin enteritis is associated with mesenteric lymph node hypertrophy. 5. The intestinal mucosa shows minute ulcerations, loss of villi, submucous fibrosis, and evidence of chronic inflammation.


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