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Biomedical subjects

C A Rubio

Publications and source records attributed to C A Rubio.

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

Quantification of the sulphomucin-producing cell population of the colonic mucosa during protracted stress in rats.

The sulphomucins contained in goblet cells of the descending colon of 55 Sprague-Dawley rats were histochemically labelled by High Iron Diamine (HID) and quantified in an image analyzer (Cortex controller). After transportation to the stress laboratory, 25 rats were compelled to swim for two consecutive hours/day either only once (5 rats), for one week (5 rats), two weeks (5 rats), four weeks (5 rats) or eight weeks (5 rats). 25 additional rats were only transported to the stress laboratory (i.e. "sham-handled" control), either once (5 rats), for one week (5 rats), two weeks (5 rats), four weeks (5 rats) or eight weeks (5 rats). The remaining 5 rats were "untransported", resting control rats (i.e. day zero). The results were expressed in percent of HID-staining/total mucosa analyzed. When various time intervals were compared with those of day zero (i.e. horizontal study), it was found that one day swimming rats had a significantly lower percentage (p less than 0.001) of HID stained material. The fluctuations at other time intervals were non-significant. On the other hand, for transported rats, a significant increase (p less than 0.001) in the percentage of HID positive areas was found for rats swimming for eight weeks. When compared to day one, the percentage of HID positive areas increased from day one to one-eight weeks, the differences being significant (p less than 0.001) at four and (p less than 0.01) eight weeks. Similar results were found for transported rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Neoplasias of the colorectal crypts.

Colorectal cancers are often preceded by noninvasive neoplasias arising in the surface epithelium, namely tubular, tubulovillous and villous adenomas. That neoplasias may also arise in the colorectal crypts is less well known. Between 1998 and 2002, colonoscopies, rectoscopies and colorectal surgical specimens from 8647 patients were received at this Department for histological diagnosis. The material included 502 adenomas, 865 invasive tumours and 221 cases of ulcerative colitis (UC). The following cryptal lesions were investigated: (a) neoplasias arising in the crypts, (b) neoplasias possibly arising in the crypts and (c) cryptal lesions alleged to be premalignant. Over the 5-year period, the most frequent phenotype encountered was single crypt dysplasia (in all 5 colectomies from familial adenomatous polyposis patients), followed by serrated adenomas (11.2%), hyperplastic polyps (8.4%), dysplasia in UC (6.3%), pure carcinoid tumours (1.7%), signet ring cell carcinoma (1.1%), adenocarcinoid tumours (0.2%) and de novo carcinomas (0.1%). In this survey, no case of Paneth cell adenoma or of cryptal neoplasia in lymphoid-associated mucosa (also known to originate from the crypts) was found. Hence, it was demonstrated that several neoplasia phenotypes actually arise in the colorectal crypts. The awareness that colorectal neoplasias may evolve from that particular cellular domain may cast more light on the understanding of the complex mechanisms of colorectal carcinogenesis.

Adenoma↗
PubMedDate not supplied

Apoptosis versus polemosis. Different mechanisms leading to non-necrotic cell death.

Apoptosis is a physiological auto-suicidal, genetically-induced cell deletion process of senescent effete normal cells. Apoptosis guarantees genetic fidelity, minimizes phenotypic variation and eliminates genotypic alteration. The auto-destruction-induced by a cascade of caspases--results in the breakdown of normal cells and the formation of apoptotic bodies. Those bodies are rapidly phagocytized by macrophages and internalized by cells of the same type. On the other hand, polemosis (from Greek polemos: war) is a more dynamic mechanism of cell destruction between two different cell systems. Polemosis is focal, haphazardly distributed at the time of observation, probably erratic and influenced by the chemotactical attraction of committed lymphocytes by neoplastic cells. Polemosis is implemented by the interaction of the Fas-Fas ligand compulsory cellular system of self-defence. The end result of that struggle is manifested by the destruction of committed lymphocytes and the appearance of polemotic bodies (nuclear fragmentation with or without cytoplasmic remnants). The question arises as to whether polemotic bodies are also engulfed by macrophages, as is the case with apoptotic granules. In this work, the possible association between CD68-positive macrophages and intraepithelial polemotic bodies was investigated in sections from 50 colorectal adenomas. Polemotic bodies were found in groups of dysplastic cells in 84% (n=42) of the 50 adenomas, but none of them showed an accumulation of CD68 macrophages around the polemotic bodies. As polemotic bodies (autologous T-cells DNA) are not engulfed by macrophages it is hypothesized that the DNA of these bodies might be incorporated into the nuclei of dysplastic cells. This would satisfy the avidity of the DNA of rapidly proliferating dysplastic cells, a process that takes place, unremittingly, at any given time.

Adenoma↗
PubMedDate not supplied

Cell proliferation at the leading invasive front of colonic carcinomas. Preliminary observations.

Dilated neoplastic glands, some with a layer of flat tumour cells and others lacking a group of consecutive lining tumour cells (i.e., glandular gaps called pores), were previously found at the leading invading tumour edge of colorectal carcinomas. Through the glandular pores, the retained intraglandular material was siphoned off directly into the juxtaposed extracellular matrix (ECM). The tumour cell fabricates, rich in proteolytic enzymes, disrupted the paratumoral anatomy of the ECM and encouraged further tumour penetration. In this work, cell proliferation in the neoplastic glands of the outermost advancing front of seven colonic carcinomas was studied with the proliferation marker Ki67. A total of 105 neoplastic glands were investigated in the seven tumours. In 33 of the 35 neoplastic glands with flat tumour cells, no Ki67 expression could be recorded in the flat cells. In the other two neoplastic glands, only occasional flat tumour cells showed Ki67 expression. The remaining (non-flat) neoplastic cells in the lateral and proximal aspects in the same 35 glands showed Ki67 expression. In 19 out of the 35 neoplastic glands with pores, the tumour cells at the tip of the pores (non-flat) showed Ki67 expression. In the remaining 16 neoplastic glands with pores, the tumour cells at the tip of the pores showed no Ki67 expression. In 15 out of the 35 neoplastic complete glands (i.e., having neither flat tumour cells nor epithelial pores) variable amounts of tumour cells lacking Ki67 expression were seen at the leading invading front. In the remaining 20 complete glands, all tumour cells showed Ki67 expression at the leading invading front. These preliminary results showed, for the first time, that human colonic flat neoplastic cells arrest their proliferation at the invading tumour front. The possibility that these Ki67-negative tumour cells were arrested in G1-phase was entertained. It is not inconceivable that this unexpected paradoxical biological behaviour of flat tumour cells might be connected with the formation of glandular pores at the level of advancing invasion in colonic carcinomas.

Adenocarcinoma↗
PubMedDate not supplied

An improved method to visualize eosinophils in eosinophilic esophagitis.

We previously found in Giemsa-stained colorectal sections from IBD patients that eosinophilic granulocytes turned fluorescent when excited with indirect fluorescent light, while other inflammatory cells were non-fluorescent. We now studied with that method, the frequency of eosinophilic granulocytes in sections from patients with eosinophilic esophagitis (EE). Cell counting was done in consecutive sections stained with Giemsa stain using indirect fluorescence light (G-IFL setting) and with hematoxylin-eosin using transmitted light (HE-TL setting) in 5 cases of EE and in 10 consecutive cases of reflux esophagitis (RE) grade 2. In EE 45.0 eosinophils/case (range 39-51) were recorded with the G-IFL setting but only 33.4 eosinophils/case (range 28-39) with the HE-TL setting (p < 0.05). In RE cases, 3 eosinophils/case (range 2-4) were found with the G-IFL setting and 2 eosinophil/case (range 1-3) with the HE-TL setting. The G-IFL method is not only more sensitive in detecting eosinophils than the conventional HE-TL method but also quicker, since a differential cell counting is not necessary.

Adolescent↗
PubMedDate not supplied

Kinetics of cell replication in the uterine cervix. VIII. Quantitation of chronologic events in proliferating loci.

The frequency and the topographic distribution of DNA replicating cervical basal squamous cells (as deduced by 3H-thymidine in vivo administration up to 8 hours before sacrifice) was studied in 70,000 basal cells in 70 C57B1 mice. While the number of labelled basal cells/animal was similar in those injected only once, a significantly higher number of labelled basal cells was recorded in animals injected twice or three times. Following one single injection, 30% (8 h previously) and 31% (1 h previously) of the DNA replicating basal cells occurred in pairs or in loci of three, four or more labelled cells. After repeated injections, the rates were 49% for those animals injected twice before sacrifice and 47% for those injected three times. Thus repeated injections resulted in a significantly increased number of loci of three, four or more DNA replicating basal cells when compared to those injected only once. The present results suggest that there is a chronological asynchrony in the DNA replication of proliferating basal cells-loci of the uterine cervix.

Animals↗
PubMedDate not supplied

Kinetics of cell replication of the uterine cervix. I. Normal epithelium.

The rate of cell production in the squamous cervical epithelium, as deduced from the number of arrested mitoses at various time intervals after a single injection of vincristine, was investigated in 83 C57B1 mice. In the basal cell layer several peaks of arrested mitoses were registered: the first major peak was found at 9 hours, the second at 12 hours, the third at 16 hours and the fourth at 20 hours. Distinct peaks of arrested mitosis were also found in the nonbasal (parabasal) cell layers. Each mitotic peak may correspond to a number of cells that had entered the proliferative pool from the "resting" compartment. The stathmokinetic effect of vincristine on the squamous cervical epithelium had ceased after 20 hours.

Animals↗
PubMedDate not supplied

The induction of esophageal tumors in mice: dose and time dependency.

Three hundred and forty eight C57Bl mice were killed after diethyl-nitrosamine (DEN) treatment at various time intervals ranging from one day to six months. No esophageal tumors occurred in the first three months after DEN treatment; They occurred, however, at four months and increased in number at six months of DEN treatment. Other groups of animals under the same initial DEN treatment were allowed to survive seven or nine months without treatment. One esophageal tumor was recorded at observations made seven months after one single day of DEN administration. A significant increase in the number of esophageal tumors occurred at seven months in mice treated with DEN for two weeks, and for one, two, three or four months; the highest tumor frequency was found in mice treated for six months and surviving three additional months on a carcinogen-free diet. These results suggest that clones of esophageal cells had been "programmed" for tumor growth at an early stage of DEN treatment. The tumors had, however, remained undetected at macroscopical and microscopical examination several months previously. It is apparent that not only the dose administered, but also the post-carcinogen interval is an important factor in esophageal carcinogenesis in the mouse.

Animals↗
PubMedDate not supplied

Lymphoid tissue-associated colonic adenocarcinomas in rats.

Eight months after a single s.c. injection of 1,2-dimethylhydrazine (21 mg/kg b.w.) to male Sprague-Dawley rats, seven colonic tumors (i.e. 17.5%) were found at autopsy. Histological examination revealed invasive adenocarcinomas in all seven tumors. All tumors were seen to originate in pre-existing discrete lymphoid aggregates. Adenomas or adenocarcinomas arising from pre-existing adenomas were not found. Previous experiments, using the same strain of rats, demonstrated the occurrence of adenomas with or without invasive adenocarcinomas after multiple doses of DMH. The causes responsible for the dose-dependent specificity in the histogenesis of colonic tumors in our model remains to be elucidated.

1,2-Dimethylhydrazine↗
PubMedDate not supplied

Autografting colonic adenocarcinomas into the colonic submucosa in rats.

After inducing colonic tumors in 47 rats by weekly subcutaneous injections of 1,2-dimethylhydrazine, all rats were laparotomized and tumors were autotransplanted to tumor-free areas of the transverse colon. True autotransplants were considered to be tumors occurring in the grafted areas, which were covered by normal colonic mucosa. The frequency of auto-grafted tumors was 35.5%. In a previous work, a low incidence of 1,2-dimethylhydrazine-induced tumors was found in the transverse colon of the rat. The present results suggest that the failure of tumor growth in the transverse colon may be unrelated to an intrinsic natural "resistance" of that segment of the colon to tumor growth.

1,2-Dimethylhydrazine↗
PubMedDate not supplied

DNA synthesis in the gastroduodenal mucosa during acute and chronic stress in the rat.

We investigated the effects of acute and chronic stress on the DNA synthesis of the gastroduodenal mucosa of the rat using two different methods of physical stress at various time intervals. Acute stress was produced in the rats being briefly plunged or swimming for two hours (water temperature 37 degrees C). "Sham - transported" rats were used as controls. The results indicate that in the stomach the DNA synthesis was substantially reduced during acute stress in both groups tested (when compared to controls). The DNA synthesis was also reduced in experimental rats after one and two weeks of stress (as compared to day one). By four and eight weeks, the rate of DNA synthesis in the gastric mucosa had significantly increased in the stressed animals. Controls demonstrated significantly lower DNA values following two to eight weeks of stress (as compared to day one). From the outset, the DNA replication values were 2.5 to 3 times higher in the duodenal mucosa than in the gastric mucosa. Following two weeks of stress, the duodenal mucosa of both test groups showed significantly lower DNA values than controls, but significantly higher values after four weeks of stress. By eight weeks, the duodenal mucosa in all rats had reached the same values as that of day one. This was considered a sign of "adaptation to stress" in the duodenal mucosa. The above results suggest that the fluctuations of DNA replication may be connected to compensatory mechanisms aimed at adjusting the gastroduodenal mucosa to protracted stress situations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMedDate not supplied

The detection of dysplasias in ulcerative colitis by a monoclonal antibody: preliminary report.

The reactivity of dysplasia and of adenocarcinoma tissues with the monoclonal antibody 52-2 was tested in 40 specimens from colitic and non-colitic patients. These included specimens from colitic patients having abnormal glands with nuclear stratification and hyperchromasia, surrounded by severe inflammation. While the normal colonic mucosa demonstrated a positive reaction only at the base of the crypts (germinal epithelium), dysplasia in colitic patients demonstrated reactivity in the full length of the dysplastic glands: at the apical aspect of dysplastic cells, at the glycocalix, in the entire cytoplasm and the level of the cell membrane (between two contiguous dysplastic cells and at the stromal aspect of the cells). A similar reaction was found in dysplastic glands from colorectal adenomas in non-colitic patients. Invasive adenocarcinomas in colitis and in non-colitics showed strong positive reaction. In colitics, no reactivity was found in abnormal glands with nuclear stratification with hyperchromasia, surrounded by severe chronic inflammation. The possibility of differentiating dysplasias from reactive reparative cellular changes in patients with ulcerative colitis is discussed.

Adenocarcinoma↗
PubMedDate not supplied

Kinetics of cell replication in the uterine cervix. VII. Loci of mitotic basal cells during cervical carcinogenesis.

The frequency and the topographic occurrence (i.e., loci) of vincristine-arrested mitosis in the basal-cell layer was studied during the process of cervical carcinogenesis in C57B1 mice. The total frequency of mitosis decreased (by comparison to controls) not only in cervical intraepithelial neoplasias of grades I, II and III and in invasive carcinomas, but also in the normal epithelium of carcinogen-treated animals. This confirms earlier results and suggests that the pace of replication of cells in contact with the stroma is decreased during carcinogenesis. On the other hand, the proportion of the number of mitotic basal cells occurring singly or in groups of 2, 3 or greater than or equal to 4, as well as the proportion of loci with 1, 2, 3 or greater than or equal to 4 mitoses, were similar during cervical carcinogenesis (when compared to controls). It would thus appear that the proliferation of the cervical epithelium during carcinogenesis is regulated by two factors: one that seems to diminish the total number of mitotic basal cells during carcinogenesis, and another that seems to maintain as constant the proportion of mitotic loci, both under normal conditions and throughout the development of intraepithelial neoplasias, in the uterine cervix.

Animals↗
PubMedDate not supplied

Intestinal metaplasia of the stomach. I: Quantitative analysis in gastric peptic ulcer and in incipient adenocarcinoma in Japanese subjects.

A novel method of quantitation of the extent of intestinal metaplasia (IM) was applied to 50 resected stomachs from Japanese subjects; 25 with peptic gastric ulcer, 25 with incipient adenocarcinoma. The total length of the IM was significantly larger (p less than 0.05) in incipient adenocarcinomas than in peptic ulcers; the total length of the gastric mucosa analyzed being similar in the two groups. The intestinal metaplasia index (IMI; i.e. the ratio between IM and the length of the gastric mucosa analyzed) in incipient adenocarcinomas was significantly higher (p less than 0.05) than in gastric ulcers. In incipient adenocarcinomas, the IMI decreased significantly (p. less than 0.001) from lesser towards greater curvature. In peptic ulcers, the decrease was less abrupt. In 12 of the 25 specimens, the incipient adenocarcinoma was classified as intestinal type, and in the remaining 13 specimens as diffuse type. The total length of the IM was significantly larger (p less than 0.01) in specimens with intestinal type adenocarcinoma than in specimens with diffuse type; the total length of the gastric mucosa investigated being similar in the two groups. The IMI was significantly higher (p less than 0.01) in specimens containing intestinal type adenocarcinoma as compared to those with diffuse type adenocarcinoma. This was valid for the lesser curvature, for the mucosa adjacent to the lesser curvature, and for the mucosa by the greater curvature. From the results, it is apparent that intestinal metaplasia is a widely occurring phenomenon not only in specimens with intestinal type incipient adenocarcinoma or with diffuse type incipient adenocarcinoma, but also with benign peptic ulcer. The difference resides in that the metaplastic mucosa is more universally distributed in specimens with incipient intestinal adenocarcinomas (provided that longitudinal mucosal areas are considered in the comparison). The quantitative method herein reported will be applied in the future to compare the extent and distribution of intestinal metaplasia in gastric specimens from various geographical regions having disparate incidences of gastric ulcers and carcinomas.

Adenocarcinoma↗