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M Sanguineti

Publications and source records attributed to M Sanguineti.

At least 19 recordsLinked to original sources
PubMed2002

Mouse-isolated plexus differentiates neural crest precursors into enteric neuroblasts.

Aim of this study was to investigate, for the first time, whether isolated newborn mouse enteric plexus could induce in vitro differentiation of the vagal neural crest-derived cells into enteric neuroblasts. Fragments of the myenteric plexus were isolated from the small intestine of 6-day-old Swiss mice and were collected and stored in DMEM-F12 medium, then cultured on polymerized human fibronectin layer. The vagal portion of the neural tube, isolated from a 9.5-day-old Swiss mouse embryo, was put in the same chamber slides where the isolated myenteric plexus had been cultured for 3 days. The vagal neural crest-derived cells migrated onto the polymerized human fibronectin layer and formed a crown of cells around the neural tube. After 6 days, the cultures were stopped and studied immunohistochemically for anti-NF160 KD, anti-TH, and RetR5 antibodies to analyse the differentiation stage of the cultured cells. Analysis of results included the comparison of two culture groups: Group 1, used as control, in which vagal neural crest-derived cells were put in DMEM-F12, supplemented only with 10 % of FCS; Group 2, in which vagal neural crest-derived cells were put in the same medium as Group 1, with the addition of myenteric plexus fragments isolated from newborn mice to form the co-culture. The following results were obtained: in Group 1 the neural tubes originated a cell population strongly positive for anti-NF160 and anti-TH Ab, but negative for RetR5 Ab. This positivity was found both in the cells adjacent to the neural tube and in those migrating from it distally. The Group 2 originated cells, which after migration were positive for anti-NF160 and for anti-TH antibodies. In addition, in this culture group, the cells which migrated from the neural tube were positive for anti-RetR5 antibody. The co-culture used in this study induces the differentiation of vagal stem cells into enteric neuroblasts, cells TH+ and RetR5+. These cells, after reaching the embryonic intestine, migrate to colonize the hindgut and form the ENS. Therefore this biotechnology seems a good method to obtain in vitro enteric precursors of ENS.

Animals↗
PubMed2000

[Experimental microsurgical gastrocystoplasty] .

BACKGROUND: Stomach tract used for bladder augmentation decreases urinary pH and produces the syndrome of dysuria and hematuria; gastric mucosa in contact with urine may develop prominent histopathological changes including proliferative lesions. The aim of this study was to investigate in an experimental model the possibility of detecting the factors involved in the mucosal damage. METHODS: Thirty-five Sprague Dawley rats randomly underwent microsurgical gastrocystoplasty or sham operation (5 controls). During operation elliptical gastric patch was isolated with its gastroepiploic vascular pedicle, bladder was opened with midline incision and anastomosis performed. Urine was aspirated from the bladder for culture, pH and electrolytes evaluation; venous blood was samples for electrolytes, BUN and creatinine. Mean follow-up time was 6 months. RESULTS: Of the 30 rats subjected to gastrocystoplasty 23 survived (77%). All of cultures were negative, the urinary pH decreased after operation and increased gradually two months later. Urinary sodium and potassium ions concentrations increased significantly in gastrocystoplasty (p < 0.05). There were no significant changes in serum electrolytes or renal function. CONCLUSIONS: This experimental model was useful to investigate the effects related to the presence of gastric mucosa in the urinary tract.

Animals↗
PubMed1999

Anorectal malformations associated with enteric dysganglionosis in Danforth's short tail (Sd) mice.

BACKGROUND: The spontaneous mutant Danforth's short tail (Sd) mouse has been studied over the last 60 years from the morphological, embryological, and genetic point of view. The Sd mutation affects a gene essential to notochordal development, and the Sd mouse phenotype represents an analogue of human caudal regression syndrome. The Sd/Sd mouse presents different types of anorectal malformations (ARM) and was suggested as a simple and cheap model of investigation of ARM morphology and embryology. In the current study, the Sd mouse enteric nervous system (ENS) was thoroughly investigated with specific immunohistochemical markers. METHODS: Macroscopic analysis, normal histology, and immunohistochemical techniques for detecting neurofilaments (NF) and NOS1 were used to study ENS of 138 Sd mice and 25 controls. RESULTS: The surprising results of this study showed that Sd mutation is associated with different degrees of hypoganglionosis and aganglionosis. In 41% of Sd/SD-affected mice, the rectal pouch was aganglionic and in the remaining 58% was severely hypoganglionic. In addition, 4.1% of heterozygous mice presented a distal aganglionosis and 8.3% hypoganglionosis. CONCLUSIONS: These results suggest that Sd mutation independently affects distinct cell lines during early organogenesis, as notochord cells, ventral hingut endoderm, and neuroblasts migrating from neural crest cells. Comparing the Sd murine model with human pathology, this study confirms that the association between ARM and intestinal dysganglionosis is not rare and underlines the importance of detecting in every ARM patient the innervation abnormalities of rectal pouch and fistulas.

Anal Canal↗
PubMed1989

DNA damage induced by some bile acids, evaluated with alkaline elution technique.

Bile acids are promoting agents in colon carcinogenesis. In this work we have tried to characterize the DNA alteration induced by bile acids in Sprague-Dawley male rats. Confirming previous findings, a clear increase in elution rate was observed at alkaline pH. No effect could be observed when the nuclei were washed before the elution, in condition totally unsuitable for the repair of the type of DNA damage induced by typical genotoxic agents. We advanced the hypothesis that the increased alkaline elution rate observed with bile acids could be independent of DNA fragmentation and related to changes in chromatin structure.

Animals↗
PubMed1987

Considerations on 131I-metaiodobenzylguanidine therapy of six children with neuroblastoma.

Six children affected by neuroblastoma at stages III and IV were treated with high-specific-activity 131I-metaiodobenzylguanidine (MIBG). After 131I-MIBG treatment three patients died at 12, 10, and 12 weeks, respectively; the other three were still living at 21, 16, and 24 weeks, respectively. Although the assumptions for this therapy were propitious, the results obtained do not correspond to those expected. It is supposed that large tumor volume and previous chemotherapy and/or radiotherapy may impair the effectiveness of 131I-MIBG therapy. Consequently, 131I-MIBG therapy is recommended even if the spread of disease is not proved-only, however, when the tumor is small.

3-Iodobenzylguanidine↗
PubMed1985

Effects of tamoxifen, estradiol benzoate and medroxyprogesterone acetate on the growth of DMBA-induced rat mammary carcinoma.

The potential synergism of sequential combinations of tamoxifen (TMX) or estradiol benzoate (E2B) with medroxyprogesterone acetate (MPA) in inhibiting the growth of 7.12-dimethylbenz(a)anthracene(DMBA) - induced rat mammary tumors has been investigated. In addition, the effect of TMX and E2B on estrogen and progesterone receptors' (ERs and PgRs) synthesis has been evaluated in the attempt to elucidate possible mechanisms involved. Previous treatment both with TMX and E2B has been shown to strongly enhance the antitumor activity of MPA. A priming on PgR synthesis has been observed only after E2B administration, TMX producing a sharp decrease in PgR levels. It is concluded that, while the priming action exerted by E2B on PgRs might explain the potentiating effect shown by E2B on MPA activity, the synergism observed between TMX and MPA should be explained on an extrareceptorial basis, an induction on PgR synthesis by TMX not being evident at the dosage and priming time employed in this study.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

[Evaluation of left ventricular ejection fraction in coronary disease patients by the gated blood pool method and cineangiography. Critical analysis of divergences between the 2 methods].

In order to assess the reliability of left ventricular ejection fraction as estimated by gated blood pool method, radionuclide angiography (LAO) and single plane (RAO) contrast cineangiocardiography were performed within 14 days in 60 patients with coronary artery disease. The mean value of radionuclide ejection fraction was found to be 55 +/- 16%; contrast cineangiographic ejection fraction was 57 +/- 15%; r = 0.92. In 23 patients with previous anterior myocardial infarction gated blood pool method was found to underestimate left ventricular ejection fraction when compared with contrast cineangiography. The observed underestimation was wide significant in 11 patients with previous anterior infarction, low (less than 50%) radioisotopic ejection fraction and septal akinesia and/or apical dyskinesia; radionuclide ejection fraction = 33 +/- 8%; contrast cineangiographic ejection fraction = 42 +/- 9%; r = 0,76. This study confirms that the values of left ventricular ejection fraction as estimated by gated blood pool method in coronary patients are quite reliable; moreover, the intrinsic variability of the data is low. This may be not true in patients with previous anterior myocardial infarction. The Authors discuss the possible causes of disagreement between radioisotopic and contrastographic ejection fraction in patients with previous anterior infarction and poor left ventricular function: physical problems of measuring ejection fraction by gated blood pool in dilated ventricles; possible mistakes in evaluating blood pool due to the low mobility of the blood mass nearest to the scintillation camera; inhability of contrast cineangiography in RAO to recognize the interventricular septum and evaluate its kinetic abnormalities; unreliability of the geometrical model of revolution elypsoid in calculating end-systolic volumes in ventricles with abnormal wall-kinesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Cineangiography↗
PubMed1983

Carcinogenic activity of benzo[a]pyrene and some of its synthetic derivatives by direct injection into the mouse fetus.

We have studied the carcinogenic effects of direct injection of benzo[a]pyrene (BP) and 6-methylbenzo[a]pyrene (BP6M) into fetal Swiss mice at 15 days of intrauterine growth. To determine the sensitivity of mouse fetuses to the action of ultimate carcinogens, benzo[a]pyrene-4,5-oxide (BPO) and a racemic mixture of 7 beta,8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9, 10-tetrahydrobenzo[a]pyrene (BPDE), respectively, a proximal metabolite and an ultimate carcinogenic metabolite of BP, were also investigated in our system. The compounds were dissolved in acetone and trioctanoin (1:1) and injected at doses ranging from a minimum of 0.4 to a maximum of 19.8 nmol/fetus. Controls received 1 microliter/fetus of solvent. The experiment was terminated when the animals were 12-15 weeks old. On the basis of the percentages of lung adenomas and the average number of nodules/mouse, BPDE appears to be the most potent carcinogen of this group, causing 55% of tumors at a dose of 0.4 nmol and 73% at a dose of 4.0 nmol/fetus. At the dose of 0.4 nmol/fetus, neither BP nor BP6M induced tumors; injection of 4.0 or 19.8 nmol/fetus, caused incidences of 53% and 92%, respectively, in the case of BP6M and 24% and 39%, respectively, in the case of BP. BPO was not tumorigenic in this system, even at doses as high as 15.7 nmol/fetus. Eleven percent of the control animals had lung adenomas. The average number of nodules/mouse varied with the compound and the dose injected and closely followed the pattern of tumor incidence.

Animals↗
PubMed1983

Carcinogenicity study with technical-grade dichlorodiphenyltrichloroethane and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene in hamsters.

Studies conducted by others have revealed that 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), a proximal metabolite of dichlorodiphenyltrichloroethane (DDT), is a strong hepatocellular carcinogen in mice. Since hamsters appear to be resistant to tumor induction by DDT, we wanted to investigate whether DDE has any neoplastic effect in this species. DDE (99% pure) was mixed into the diet at doses of 500 or 1000 ppm and given to groups of male and female Syrian golden hamsters for life. Another group of animals received a diet containing 1000 ppm technical-grade DDT, and a further group served as control. Groups contained a minimum of 40 hamsters per sex. The tested compounds had no effect on the incidence of tumors at all sites, compared to controls. A specific finding in animals exposed to DDE was the appearance of hepatocellular tumors late in life. They were classified as neoplastic nodules, and the incidence was 15% in females and 47% in males of the 500-ppm DDE dose groups and 21% in females and 33% in males of the 1000-ppm DDE dose groups. None of the untreated or DDT-treated animals had these tumors. Eight animals treated with 1000 ppm DDE and four of those treated with DDT had hyperplastic foci of the liver. In addition, adrenocortical adenomas, spontaneous to Syrian golden hamsters, were more frequent in DDE- and DDT-treated animals than in control animals. These results showing that DDE, but not its parental compound, induces liver cell tumors in hamsters emphasize the importance of this metabolite as a proximal carcinogen of DDT.

Animals↗
PubMed1975

Pure red cell aplasia (PRCA): Response of three patients of cyclophosphamide and/or antilymphocyte globulin (ALG) and demonstration of two types of serum IgG inhibitors to erythropoiesis.

Three cases of adult pure red cell aplasia (PRCA) ARE REPORTED. All patients proved refractory to various combinations of androgens and corticosteroids. The first case, harboring a thymoma, showed a complete clinical remission following cyclophosphamide therapy. The second and third responded similarly to either a combined cyclophosphamide + antilymphocyte globulin (ALG) treatment or to ALG administration preceded by a small dosage of cyclophosphamide, which had proved ineffective when administered alone. Serum IgG inhibitors to erythropoiesis were demonstrated in all cases by means of in vivo and/or in vitro techniques. The inhibitor(s), although directed against the erythroid marrow in both the first and third patients (PRCA type A), apparently functioned as an antibody to circulating erythropoientin (Ep) in the second case (PRCA type B). The inhibitor(s) was always absent in postremission samples. Additionally, experimental models for both types of human PRCA were established in normal rodents. The present studies support the contention that adult PRCA is an autoimmune disease. The therapeutic role of cytotoxic-immunodepressive agents in PRCA patients is confirmed. It is emphasized that ALG may represent an additional therapeutic tool in cases resistant to cyclophosphamide and/or steroids. In addition, cyclophosphamide proved effective in a patient harboring a thymoma not amenable to surgery. Finally, it is postulated that IgG serum autoantibodies, directed against either an early erythroid precursor (PRCA type A) or, more rarely, circulating Ep (PRCA type B), play a major role in the pathogenesis of the disease.

Aged↗