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Biomedical subjects

R M Gómez

Publications and source records attributed to R M Gómez.

15 recordsLinked to original sources
PubMed2002

Androgen-secreting adrenal adenomas.

BACKGROUND: The androgen source in women with hirsutism and signs of virilism may be the ovary or adrenal gland. CASES: Three patients with androgen excess are reported. Two had hyperandrogenemia and Cushing syndrome with an adrenal mass greater than 5.5 cm; the third had a small adrenal adenoma secreting only testosterone and responsive to human chorionic gonadotropin. In all cases, the pathologic report from surgery and the long-term resolution of symptoms confirmed the benign nature of the tumors. CONCLUSION: Basal and dynamic hormonal tests cannot precisely differentiate ovarian from adrenal tumors. Adrenal adenomas must be considered as a cause of hyperandrogenic syndrome.

Adrenal Cortex Function Tests↗
PubMed2001

Host selenium status selectively influences susceptibility to experimental viral myocarditis.

The purpose of the present work was to determine whether dietary selenium (Se) deficiency could influence the injurious effect of human viruses other than Coxsackie virus B3 (CVB3) on mouse heart. Weanling C3H/HeN mice were fed a Se-deficient or Se-adequate diet for 4 wk and then were inoculated intraperitoneally with one of the following viruses: Coxsackie virus B1 (CVB1), echovirus 9 (EV9), Coxsackie virus A9 (CVA9), or herpes simplex 1 (HSV1). Polio virus 1 (PV1) was employed as a negative control. Prior to inoculation, mean serum Se levels were 430 versus 61 ng/mL in adequate versus deficient mice, respectively. Ten days later, hearts were removed and processed by routine histological procedures. Cardiac lesions were scored according to the number and size of myocarditic foci. Significantly greater heart damage resulting from CVB1 and EV9 was observed in Se-deficient than in Se-adequate mice, and the Se status had no influence on CVA9-induced myocarditis. In contrast, heart damage caused by HSV1 was significantly milder in Se-deficient than in Se-adequate mice. Therefore, it may be concluded that the Se status of the murine host selectively influences the degree of viral-induced myocarditic lesions.

Animals↗
PubMed2000

[Relationship between lung cancer and aflatoxin B1].

The relationship between aflatoxins and liver cancer is well established. In addition the inhalation exposure to carcinogen aflatoxin B1 (AFB 1) is considerable. Genotoxic chemical is known to react with DNA either directly or after metabolic activation to form adducts, a step thought to be relevant with respect to chemical carcinogenesis. The presence and the amount of specific DNA adducts provide a good indication of chemical exposure and genetic damage resulting the exposure to carcinogens and account for same of factors affecting individual susceptibility to cancer. Analysis of DNA adducts requires that the sensitivity of the methods to be sufficient high to allow detection of about 1 adduct/109 normal nucleotides. Most suitable method is based in physiochemical technique such as HPLC. Because circumstantial epidemiological evidence suggests that AFB1 inhalation may cause primary lung cancer. We investigate AFB1 by HPLC in three different tobacco sources, and in 39 patients with compatible lung cancer or chronic bronchitis. The patients were divided by clinical manifestations in lung cancer (n: 25) and chronic bronchitis (n: 14). Twenty-three of 25 patients presented epidermoid lung cancer within smoking habit, and 2 of 25 presented adenocarcinoma without smoking habit. In chronic bronchitis group 12 of 14 cases presented smoking habit. The control PBS liquid was negative to AFB1; the different tobacco sources, a) Virginia of Jujuy, b) Brasilero and c) black of Salta presented AFB1 positive determinations respectively. The bronchial tissues obtained by lung biopsies presented positive AFB1 in lung epidermoid cancer at 0.68 +/- 0.82 mg/L. The adenocarcinoma presented AFB1 negative determinations. In chronic bronchitis patients with smoking habit (n: 12) presented AFB1 positive with a level less than the epidermoid lung cancer group, 0.21 +/- 0.109 mg/L, p < .025.

Adenocarcinoma↗
PubMed1999

[Importance of the benzylpenicillin nucleus and the side chain of the beta-lactams. Demonstration by skin tests and RAST in penicillin allergic patients].

We studied 30 patients with beta-Lactams allergy demonstrated by clinical findings. The aim of this work was to determine the capacity of the beta-Lactams nucleus and the side chain in the induction of specific IgE to BPO, Ax, Amp, performed by intradermal skin test and RAST. The patients were divided by clinical manifestations in: 1-Accelerated reactions (n:19); and 2-Immediate reactions (n:11). The Prick tests were performed with BPO-PL, Ax-PL, Amp-PL, MDM-BP, MDM-Ax, MDM-Amp. The accelerated group presented BPO-PL (+) in 2 cases, Ax-PL & Amp-PL (+) in 4 cases, and all of the reactives were (+) in 13 out of 19 cases. The immediate group presented MDM-BP (+) in 10 out of 11 cases and MDM-Amp was (+) in 1 out of 11 cases. The RAST's were performed in all patients(n:30). In accelerated group were (+) to BPO-PL in 13 out of 19 cases, to Ax-PL in 3 out of 19 cases, to Amp-PL in 1 out 19 cases, to BPO-PL and Ax-PL on overlap in 1 out of 19 cases, and 1 case was negative to all reactives. The immediate group presented RAST's negatives in 11 out of 11 cases. The control group(n:20) presented Prick (+) to Ax-PL in 1 out of 20 cases, and the others reactives were negatives in all cases. The RAST's to all reactives were (-) in 20 out of 20 subjects. These results indicate that BPO was the most important determinant, and the side chain of the Ax or Amp were others determinants of the beta-Lactams drugs. These determinants induced specific IgE, and in rare occasions appears specific IgE for two different determinants on overlap in the same patient. The intradermal skin testing is the method of choice to study the penicillin allergies, because non satisfactory RAST's have yet been developed for minor determinant-specific IgE antibodies.

Adult↗
PubMed1997

Molecular determinants for virulence in coxsackievirus B1 infection.

Studies demonstrated that a strain derived from an infectious clone of coxsackievirus B1 (CVB1N) (N. Iizuka, H. Yonekawa, and A. Nomoto, J. Virol. 65:4867-4873, 1991) was 3 to 4 log10 less virulent than the myotropic Tucson strain of CVB1 (CVB1T) following intraperitoneal inoculation of newborn mice. Replacement of nucleotides (nt) 69 to 804 from the 5' untranslated region (5' UTR) and 1A coding region of CVB1N or nt 117 to 161 from the 5' UTR with the corresponding part from CVB1T restored greater than 90% of the virulence. Sequencing of the 5' UTR of CVB1T demonstrated areas with a greater similarity to particular echoviruses than to CVB1N, suggesting that recombination events might have occurred, perhaps influencing the virulence phenotype.

Animals↗
PubMed1996

Theiler's murine encephalomyelitis virus-induced cardiac and skeletal muscle disease.

The DA strain of Theiler's murine encephalomyelitis virus, a member of the cardiovirus genus of picornaviruses, induces a restricted and persistent infection associated with a demyelinating process following intracerebral inoculation of mice; both virus infection and the immune response are believed to contribute to the late white matter disease. We now report that intraperitoneal inoculation with DA produces an acute myositis that progresses to a chronic inflammatory muscle disease in CD-1 mice as well as several inbred mouse strains. Some mouse strains also develop central nervous system white matter disease and a focal myocarditis. Infectious virus in skeletal muscle falls to undetectable levels 3 weeks postinoculation (p.i.), although viral genome persists for at least 12 weeks p.i., the longest period of observation. Severe combined immunodeficient animals have evidence of muscle pathology as long as 5 weeks p.i., suggesting that DA virus is capable of inducing chronic muscle disease in the absence of an immune response. The presence in immunocompetent mice, however, of prominent muscle inflammation in the absence of infectious virus suggests that the immune system also contributes to the pathology. T lymphocytes are the predominant cell type infiltrating the skeletal muscle during the chronic disease. This murine model may further our understanding of virus-induced chronic myositis and help to clarify the pathogenesis of human inflammatory myopathies.

Animals↗
PubMed1993

Differential behaviour in pancreas and heart of two coxsackievirus B3 variants.

In order to characterize viral kinetics and pathogenic properties of two intratypic variants of coxsackievirus B type 3, Balb/c mice were intraperitoneally inoculated and serial samples harvested from days 2 to 28. Although both CB3o (amyocarditic) and CB3m (myocarditic) variants induced similar early infectivity titres in pancreas, only the latter led to severe acinar necrosis, followed in turn by patent viraemia and subsequent focal myocarditis. Nevertheless, when both variants were inoculated in cultured cardiac cells, neither infectivity nor cell death rate differed noticeable. Therefore, our findings indicate that overt myocarditis is not attributable to contrasting cardiomyocyte susceptibility to the tested variants but rather to prior viral events in pancreatic tissues.

Animals↗
PubMed1993

Ultrastructural study of cell injury induced by coxsackievirus B3 in pancreatic and cardiac tissues.

Balb/c weanling mice were intraperitoneally inoculated with a myocarditic variant of coxsackievirus B3, with the aim of characterizing more thoroughly the features of virus-induced cell injury in pancreas and heart, as well as to compare ultrastructural alterations with histological and virological findings. During the first week post-infection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. At electron microscopy, acinar cells showed patent distortion, including marked loss of organelles and zymogen granules, together with gross dilatation of rough endoplasmic reticulum. Cardiac cells presented severe cytoskeletal changes, as myofibrillar collapse with a haphazard arrangement, concomitant with a decrease in myofibril number; besides, irregular pattern of nuclear chromatin and increased presence of swollen mitochondria were often observed. As the few initially detected lymphocytes tended to disappear in necrotic foci, there was an increase in fibroblast number concurrent with progressive scarring. Ultrastructural changes in both pancreas and heart correlated with local viral replication, suggesting that cell damage is attributable to direct viral action.

Animals↗
PubMed1992

Extracellular matrix remodelling after coxsackievirus B3-induced murine myocarditis.

Weanling inbred Balb/c mice were intraperitoneally inoculated with a myocarditic variant of coxsackievirus B3. At days 1, 2, 4, 6, 8, 10, 14, 24 and 30 post-infection (p.i.), myocardial tissue was harvested for viral infectivity titrations and histological studies, including routine techniques (haematoxylin-eosin, Masson trichrome and von Kossa) and specialized procedures (silver impregnation for reticulin, picrosirius red stain for collagen and immunoperoxidase labelling for laminin). Virus was isolated as from day 2, reached maximal infectivity at days 6-8 and decreased gradually to become undetectable by day 14. Early histological findings during the 1st week consisted mainly of scattered foci of necrotic myocytes showing calcium deposits; slight mononuclear cell infiltration and fragmentation of both reticulin fibres and pericellular laminin were also present. From the 2nd up to 4th week p.i., inflammatory reaction abated concomitantly with the gradual development of fibrosis, as evidenced by reticulin fibre thickening, irregular laminin distribution and collagen fibre increase. Our results suggest that viral-induced necrosis is able to trigger marked extracellular matrix remodelling even in the case of minimal inflammation.

Animals↗
PubMed1991

Murine acinar pancreatitis preceding necrotizing myocarditis after Coxsackievirus B3 inoculation.

Balb/C weanling mice were inoculated intraperitoneally with a myocarditic variant of coxsackie-virus B3, with the aim of characterizing more fully the cell damage induced in the heart as well as in other organs. During the first week postinfection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. In accordance with the increasing infectivity titers, such progressive histopathological changes correlated with local viral replication. From day 4 pi, acinar degeneration accompanied by diffuse inflammatory exudate was observed in the pancreas, followed by fatty tissue replacement by day 8. In the heart, focal necrosis rather than inflammatory reaction first appeared at 4 days pi and became widespread by 6-8 days pi. Necrotic foci usually presented calcium deposits, with absence of myofibrils in the affected fibers. The fact that both periodic acid Schiff (PAS) and Best carmine staining remained positive even after diastase treatment ruled out basophilic necrosis. In summary, the pancreas appeared to be the site of primary viral replication leading to viremia.

Animals↗
PubMed1991

Long-term low-dose glucocorticoid therapy in hyperandrogenized women: utility and effects on bone mineral content and hypothalamic-pituitary-adrenocortical function.

The effect of chronic low-dose glucocorticoid administration on bone mineral content and corticotrope reserve was investigated in 12 hyperandrogenized women treated with 1-6 mg oral evening doses of 16 beta-methylprednisone for 12-58 months. The hypothalamic-pituitary-adrenal axis was evaluated in 9 patients by a standard metyrapone test after 45-75 days off steroid therapy. All the patients had a normal rise in serum 11-deoxycortisol after metyrapone. Bone densitometry was assessed at the end of therapy using dual photon absorptiometry. No significant differences between patients and age-matched hyperandrogenic controls were found either in spine (1.048 +/- 0.096 vs. 1.023 +/- 0.175 g/cm2) or femoral neck (0.863 +/- 0.115 vs. 0.899 +/- 0.216 g/cm2), respectively. In conclusion, absence of quantitative bone mass reduction and normal corticotrope reserve were observed even after 58 months of daily steroid administration.

Adolescent↗
PubMed1985

Nocturnal high-dose dexamethasone suppression test in the aetiological diagnosis of Cushing's syndrome.

Seventeen patients with well-proven Cushing's syndrome (13 with Cushing's disease, 3 with adrenal tumour and 1 presenting ectopic ACTH syndrome caused by bronchial carcinoid) were investigated by using a single-dose 8 mg dexamethasone nocturnal test. The results obtained were compared with those of the classical 8 mg Liddle's test, metyrapone stimulation, plasma ACTH concentration and with the final diagnosis reached through surgery, pathologic anatomy, and/or clinical and biochemical follow-up of the patients after treatment. The diagnostic efficacy or the predictive power of the test (defined as the ratio between the number of cases in which the diagnosis was correctly predicted and the total number of cases), was at least 82.4% vs 84.6% for the classical 8 mg Liddle's test. This percentage increased to 94.1% when the results of repeated tests on three patients with conflicting data were included. It is concluded that the nocturnal high-dose dexamethasone suppression test is a valuable tool in the aetiological diagnosis of Cushing's syndrome.

17-Hydroxycorticosteroids↗