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Biomedical subjects

C Rubio

Publications and source records attributed to C Rubio.

174 records · Page 10Linked to original sources
PubMedDate not supplied

[Resistance to penicillin and other antimicrobials in 301 clinical isolates of Streptococcus pneumoniae].

BACKGROUND: The aim of this study was to assess the susceptibility to penicillin of Streptococcus pneumoniae clinical strains and to analyze the association between penicillin resistance and cefotaxime and cefixime activity in S. pneumoniae isolates with decreased sensitivity to penicillin. METHODS: 301 S. pneumoniae clinical strains were isolated from patients during 1995-1996. Susceptibility to penicillin, cefotaxime, cefepime, erythromycin, chloramphenicol, tetracycline, cotrimoxazole and ciprofloxacin were studied. RESULTS: 38.2% isolates were penicillin-susceptible and 61.8% were penicillin-resistant; 20.6% showed high-level resistance. Resistance rates to erythromycin, chloramphenicol, tetracycline, cotrimoxazole and ciprofloxacin were, respectively, 30.9, 30.2, 40.9, 66.4, and 13.3% overall, and 54.8, 54.8, 61.3, and 93.5% in the 62 strains with high-level resistance to penicillin. Strains resistant to cefotaxime and cefepime were 13.9 and 14.9%, respectively. MIC50 and MIC90 for cefotaxime and cefepime in penicillin-resistant strains were 0.5 and 1 mg/ml. CONCLUSIONS: A high proportion of S. pneumoniae isolates showed resistance to penicillin, in agreement with other Spanish reports. Moreover, resistance to penicillin was significantly associated (p < 0.001) with resistance to erythromycin, chloramphenicol, tetracycline and cotrimoxazole, but not with ciprofloxacin. MIC50 and MIC90 for cefotaxime and cefepime were similar, and lower than those for penicillin in penicillin-resistant pneumococci strains.

Adolescent↗
PubMedDate not supplied

Colorectal cancer in colonic Crohn's disease--high frequency of DNA-aneuploidy.

BACKGROUND: The risk of colorectal cancer (CRC) in colonic Crohn's disease (CCD) seems to be of the same magnitude as in extensive, longstanding ulcerative colitis (UC) and colonoscopic surveillance has been advocated. Mucosal dysplasia and DNA-aneuploidy are early warning markers of malignant transformation in UC. Data concerning the occurrence of such premalignant lesions in CCD are scarce. AIMS: The objective of this study was to investigate the DNA ploidy pattern in CCD-patients with manifest CRC, both in the tumour, as well as in the adjacent and distant colorectal mucosa. The results from DNA-flow cytometry analyses (FCM) prior to the development of a CRC in CCD were also investigated. MATERIALS AND METHODS: Biopsies obtained at colonoscopy and surgical specimens from 43 patients with colonic or ileocolonic CD developing CRC between 1988 and 1998 were reviewed. The CRC histological phenotype, and the occurrence of dysplasia were registered. CRC-tissue and tissue from areas with dysplasia adjacent to and/or distant from the tumour were obtained from paraffin-embedded blocks and were analysed by FCM after preparation. RESULTS: Twenty-four CRCs in 21 patients (14 men) were suitable for FCM-analyses. The median age at CRC-diagnosis was 53 years (21-73) and the median CCD-duration was 14.5 years (1-50). A predominance of CRC was found either in the cecum (9124) or in the rectum (7/24). DNA-aneuploidy was found in 62.5% (15/24) of the tumours, in 25% (2/8) in adjacent and/or distant mucosa, and in 50% (2/4) of the patients that had been subjected to colonoscopic surveillance prior to the CRC-diagnosis. In 7patients (29%), definite dysplasia was detected adjacent to andlor distant from the tumour. Of the 6 patients undergoing colonoscopic surveillance, 3 (50%) displayed definite dysplasia prior to the colectomy. CONCLUSION: Since DNA- aneuploidy is a' common feature in CRCs in CCD and precede the development of invasive carcinoma, inclusion of FCM-analyses of colorectal biopsies may enhance the sensitivity of identifying high-risk CCD-patients prone to develop CRC within the frame of colonoscopic surveillance programs.

Adult↗
PubMedDate not supplied

The tumor-associated antigens BR55-2, GA73-3 and GICA 19-9 in normal and corresponding neoplastic human tissues, especially gastrointestinal tissues.

Immunohistochemical analysis with a monoclonal antibody, anti-BR55-2, was carried out on 163 tumors with their adjacent normal tissues and on 51 normal tissues from various organs by the ABC method. The expression of the antigen BR55-2 was compared with the expression of the colorectal carcinoma (CRC) associated antigens, GA73-3 and GICA19-9. BR55-2 was expressed in most normal epithelial tissues, whereas in the colon it seems to be exclusively a tumor-associated antigen. MAb55-2 might be of value in studying dysplastic lesions of the colon and in assessing the depth of invasion of CRC. In CRC, the expression of BR55-2 was complementary to that of GA73-3. MAb55-2 may therefore be of value in immunotherapy of CRC.

Antibodies, Monoclonal↗
PubMedDate not supplied

Image cytometry DNA analysis of invasive squamous cell carcinoma of the esophagus.

The Feulgen-DNA content of squamous carcinoma cell nuclei from the human esophagus was assessed in punch biopsies from 47 untreated patients. Forty-four of the 47 biopsies (93.6%) demonstrated aneuploid cell populations, and the remaining 3 (6.4%) were non-diploid. Previous studies have demonstrated that in esophageal dysplasias adjacent to invasive squamous cell carcinoma, DNA in single cells is substantially altered. Thus the process of esophageal carcinogenesis can be monitored not only by histological changes, but also by DNA aberrations in single cells. Quantitative DNA measurement appears, therefore, to be a complement to the histological evaluation of esophageal lesions with suspected, but not unequivocal, evidence of neoplastic growth.

Adult↗
PubMedDate not supplied

Comparative studies on the histogenesis of squamous carcinoma of esophagus in mice and in human subjects.

Histological changes occurring in the esophageal mucosa of 110 C57b1 mice, after protracted topical treatment with diethylnitrosamine, were compared to those present in human esophagus in three patients operated for early esophageal cancer. Both in mice and in human material, the histological changes were classified into slight, moderate or severe dysplasia, carcinoma in situ, questionable invasive carcinoma and invasive carcinoma. Starting from moderate dysplasia, the epithelial-stroma border became irregular with bud formation bulging into the stroma. The findings strongly suggest an association between the degree of cellular atypia, the formation of epithelial buds, and progression towards invasive carcinoma.

Animals↗
PubMedDate not supplied

Involvement of aberrant p53 expression and human papillomavirus in carcinoma of the head, neck and esophagus.

Biopsies from 34 patients with cancer of the head, neck or esophagus, 2 laryngeal papillomas, and 2 normal tonsils were analysed for human papillomavirus (HPV), Epstein Barr virus (EBV) genomes and mutated or elevated levels of p53. In 4 biopsies p53 was also analysed by DNA sequencing. HPV type 31 was found in one laryngeal cancer with normal p53 and HPV type 16 in two tonsil cancers with aberrant p53 expression. EBV was detected by PCR in 11 biopsies, but in situ hybridisation and immunohistochemistry, did not confirm this finding. Aberrant p53 expression was observed in approximately half of the tumours. These results support the involvement of both aberrant p53 expression and HPV in the aetiology of squamous cell carcinoma of the head and neck.

Base Sequence↗
PubMedDate not supplied

Further studies on the carcinogenic-free interval following exposure in experimental esophageal tumorigenesis.

247 C57B1 male mice were killed after Diethylnitrosamine (DEN) treatment at various time intervals ranging from one day to nine months. The number of esophageal tumors was divided by the length of the resected esophagus (i.e. Tumor Index = TI). Animals treated for up to 2 months had a TI of 0.1. Since the histological examination of the esophagi in those animals revealed only normal histology, the conclusion drawn was that the TI of 0.1 was a methodological error in assessing esophageal tumors by transillumination. Three months' treatment with DEN resulted in a 9-fold increased TI and 6 months' treatment in a 69-fold increased TI. Other groups of animals treated with DEN for the same period of time were allowed to survive 7, 9 or 12 months without further treatment. Animals treated with DEN for 1 day but followed without further treatment for 7 months demonstrated a 3.5-fold increased TI. For animals treated with DEN for only 14 days, (TI 0.1) and followed for 7 months with a carcinogenic-free diet, a 7-fold TI was observed. For the group of animals treated for 3 months (TI 0.9) but allowed to survive to complete 7 months on a carcinogen-free diet, a 5-fold higher TI was recorded. DEN animals treated for 6 months (TI 6.9) but allowed to survive 3 additional months had a TI of 9.6. A similar TI, namely 9.7, was found when the carcinogen-free interval was prolonged for 6 more months. These results suggest that clones of esophageal cells are "programmed" for tumor growth at an early stage of DEN treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Histologic differences between flat tubular colorectal neoplasias in Japan and Sweden.

A total of 231 flat colorectal neoplasias were investigated at two disparate geographical regions (Stockholm and Tokyo). Of the 141 flat neoplasias seen in Tokyo, 24.8% had HGD, 7.0% intramucosal carcinoma and 9.9% invasive carcinoma. On the other hand, of the 90 flat mucosal neoplasias seen in Stockholm, 13.3% had HGD, 1.1% intramucosal carcinoma and 1.1% invasive carcinoma. The differences between flat adenomas with HGD, intramucosal carcinomas and invasive carcinomas in Japanese patients were significantly higher (p < 0.001) than in Swedish patients. While the causes responsible for this geographic difference remains unclear, possible influences of ethnicity and/or of environmental factors were advanced.

Adenoma↗