4 results on '"Pereira AD"'
Search Results
2. Arthroscopic Pisiform Excision in Pisotriquetral Osteoarthritis Technique Using a Direct Pisotriquetral Portal.
- Author
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Carratalá Baixauli V, Pereira AD, Lucas García FJ, Guisasola Lerma E, and Martínez Andrade C
- Subjects
- Arthralgia surgery, Arthroscopy, Humans, Wrist Joint surgery, Carpal Joints surgery, Osteoarthritis surgery, Pisiform Bone surgery
- Abstract
Pisotriquetral (PT) joint arthritis is a common cause of ulnar-sided wrist pain. Open pisiform excision is a well-established procedure and is indicated when the conservative treatment fails. Although arthroscopic visualization of the PT joint is part of the routine examination in a patient with ulnar-sided wrist pain, therapeutic arthroscopy of the PT joint is limited to one case in the literature through the standard dorsal portals. Arthroscopic pisiform excision is a novel technique described by the authors. The first aim of this procedure is pain relief maintaining wrist stability and strength. With this minimally invasive approach we believe that preserving the flexor carpi ulnaris and the PT ligament complex we maintain their biomechanical function, while at the same time, reducing scar tenderness and postoperative discomfort with better esthetic results and less recovery time. In addition to standard dorsal portals, a direct PT portal was used to have access to the PT space and as a working portal to complete the pisiform excision., Competing Interests: Conflicts of interest and Source of Funding: The authors report no conflicts of interest and no source of funding., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)
- Published
- 2021
- Full Text
- View/download PDF
3. Is Barrett's esophagus the precursor of most adenocarcinomas of the esophagus and cardia? A biochemical study.
- Author
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Mendes de Almeida JC, Chaves P, Pereira AD, and Altorki NK
- Subjects
- Adenocarcinoma etiology, Adenocarcinoma pathology, Barrett Esophagus complications, Barrett Esophagus pathology, Cell Transformation, Neoplastic metabolism, Esophageal Neoplasms etiology, Esophageal Neoplasms pathology, Esophagitis, Peptic metabolism, Esophagitis, Peptic pathology, Fluorescent Antibody Technique, Indirect, Histocytochemistry, Humans, Mucous Membrane metabolism, Mucous Membrane pathology, Phenotype, Adenocarcinoma metabolism, Antigens, Neoplasm metabolism, Barrett Esophagus metabolism, Biomarkers, Tumor metabolism, Esophageal Neoplasms metabolism, Sucrase-Isomaltase Complex metabolism
- Abstract
Objective: To obtain biochemical evidence that Barrett's esophagus (BE) is the precursor of most adenocarcinomas (Adc) of the esophagus and cardia., Summary Background Data: Based on morphologic data, BE was previously proposed as the precursor of most Adc of the esophagus. This hypothesis would receive strong support if biochemical evidence were found to demonstrate a pattern common to BE and Adc of the esophagus and cardia., Methods: We studied the presence of intestinal-type proteins sucrase-isomaltase (SI) and crypt Cell Antigen (CCAg) in BE, Barrett's Adc, and esophageal-cardial Adc without BE. In each case specimens were collected from normal esophagus, stomach, tumor, and BE mucosa when present. To study related conditions, five specimens of peptic esophagitis and of squamous cell carcinoma were also analyzed. An indirect immunofluorescence technique was employed and sections were analyzed with laser confocal microscopy imaging., Results: Most Barrett's mucosa specimens stained positively for SI (93%) and CCAg (89%). These proteins were detected in BE independently of the type of metaplasia, the coexistence of dysplasia, or the presence of associated Adc. SI and CCAg were present in 25 (96%) and 24 (92%) of the cases of Adc respectively. No statistical difference was detected in SI and CCAg expression between Adc samples with and without BE, between BE and Adc samples with or without BE, and between tumors located in the esophagus versus the cardia. No staining for these proteins was detected in stomach or esophageal mucosa, in submucosal glands of the esophagus, in peptic esophagitis or squamous cell carcinoma., Conclusion: These data show that BE and Adc of the esophagus and cardia have a similar phenotype and support the hypothesis that most of these tumors probably originate from preexisting BE.
- Published
- 1997
- Full Text
- View/download PDF
4. DNA methylation as an intermediate biomarker in colorectal cancer: modulation by folic acid supplementation.
- Author
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Cravo M, Fidalgo P, Pereira AD, Gouveia-Oliveira A, Chaves P, Selhub J, Mason JB, Mira FC, and Leitao CN
- Subjects
- Adenoma metabolism, Adenoma prevention & control, Adult, Aged, Biomarkers, Tumor, Carcinoma metabolism, Carcinoma prevention & control, Colorectal Neoplasms metabolism, Colorectal Neoplasms prevention & control, Female, Humans, In Vitro Techniques, Intestinal Mucosa metabolism, Male, Methylation, Middle Aged, Prospective Studies, Adenoma diagnosis, Carcinoma diagnosis, Colorectal Neoplasms diagnosis, DNA metabolism, Folic Acid therapeutic use
- Abstract
Several studies have suggested that DNA hypomethylation is an early step in colorectal carcinogenesis. However, it is not clear at which stage in carcinogenesis this hypomethylation occurs, what promotes it, the extent to which it can be reversed and the consequences of such reversal in affecting tumour development. In an attempt to address some of these questions, we studied three groups of subjects with similar age and gender distributions: a group of 12 patients with colorectal carcinomas; a group of 12 patients with colorectal adenomas; and a group of eight healthy control subjects. Two experimental protocols were employed. In the first protocol, intrinsic DNA methylation was evaluated in neoplastic and in normal-appearing rectal mucosa of patients with colonic carcinomas or adenomas, compared with a group of healthy controls. In the second protocol, we examined, in a prospective and controlled fashion, the effect of folic acid supplementation (10 mg/day) on the degree of DNA methylation of rectal mucosa from those same patients after removal of the neoplasms. The degree of intrinsic DNA methylation was assessed on the basis of the capacity of the DNA isolates to serve as methyl acceptors in in vitro incubations that contained DNA methylase and [3H-methyl] S-adenosylmethionine. Intrinsic DNA methylation was significantly lower in carcinomas than in adenomas (P < 0.005). In addition, normal-appearing rectal mucosa from patients with carcinomas was significantly less methylated than in healthy controls (P < 0.005); the mean value found in the latter was also greater than the value observed in patients with adenomas, but not significantly so (P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
- Full Text
- View/download PDF
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