[Value of intracavitary echography in the study of non-urologic pelvic pathology].
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Biomedical subjects
Publications and source records attributed to M Alonso.
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A total of 32 strains of Azospirillum mainly isolated from rhizosphere of grasses and soils of Argentina were examined for susceptibility to 9 antimicrobial agents (trimethoprim, ampicillin, carbenicillin, streptomycin, spectinomycin, chloramphenicol, kanamycin, nalidixic acid and tetracycline). Many of the strains were sensitive to tetracycline, kanamycin, chloramphenicol and nalidixic acid, and resistant to ampicillin (more than 50 mg/l) and carbenicillin (more than 200 mg/l). In spite of this general pattern, for most of the strains it was possible to obtain an antibiotype. Such antibiotype could be useful for identification of the strains in field experiments or in genetic transfer experiments.
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The authors study the greater incidence of testicle neoplasias in cryptorchidic patients and the convenience of hormone or surgical treatment before puberty. These follows a discussion of the therapy to be applied depending upon whether the cryptorchidia is unilateral or bilateral.
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Forty subjects were clinically examined using scales for cerebellar, pyramidal, parkinsonian, and mental status and by quantitative evaluation of neuroimages. The patients were classified into two groups: cerebellar-plus and "pure" cerebellar syndromes. Patients with "pure" cerebellar syndrome were diagnosed as autosomal dominant cerebellar ataxia III (ADCA III) or "pure idiopathic" late-onset cerebellar ataxia (ILOCA) in this series. Patients with cerebellar-plus syndrome were diagnosed as multiple system atrophy (MSA), subclassified as either ILOCA-plus, ADCA I, ADCA II or autosomal recessive LOCA. We have used visual (VEP), brainstem auditory (BAEP) and somatosensory (SEP) evoked potentials in order to establish their diagnostic validity. Cerebellar-plus syndrome and "pure" cerebellar syndrome showed overlapping VEP, BAEP and SEP abnormalities. VEP P100 latency, however, shows a certain ability to differentiate between the two groups (p = 0.08) and appears useful in distinguishing between sporadic cerebellar-plus syndromes (MSA or ILOCA-plus) and "pure" cerebellar syndromes (p < 0.02). The incidence of prolonged N9-N13 latency was significantly higher in the latter subgroup (p < 0.04) as well. Within cerebellar-plus syndromes, VEP, BAEP and SEP abnormalities were more frequent in inherited cases (ADCA I and II, along with autosomal recessive LOCA) than in sporadic ones. The most apparent differences were a higher incidence of abnormal BAEPs at brainstem level (p < 0.002), and of both peripheral and possible central SEP impairment in hereditary cerebellar-plus syndrome than in sporadic cerebellar-plus syndrome (p < 0.03). EP investigation is useful to a certain extent in differentiating between some variants of LOCA.
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The present investigation uses electrooculogram to evaluate multiple system atrophy (MSA) and late onset cerebellar atrophies (LOCAs), both idiopathic (ILOCA) and late onset autosomal dominant cerebellar ataxia (ADCA). Forty cases were clinically examined using scales for cerebellar, pyramidal, parkinsonian, mental status and neuroimaging quantitative evaluations. The patients were classified into three groups: olivopontocerebellar atrophy (OPCA), striatonigral degeneration (SND), Shy-Drager syndrome (SDS), and LOCA. We have used direct current electro-oculography in order to establish their validity in making the diagnosis. Cerebellar signs were significantly correlated with impaired VOR-fix gain and OKN, abnormalities of saccades, and reduced smooth pursuit gain (p < 0.05). Pons atrophy was significantly correlated with impaired VOR-fix gain (p < 0.01), abnormalities of saccades (p < 0.01), and reduced smooth pursuit gain (p < 0.05). Cerebellar hemisphere atrophy was significantly correlated only with impaired VOR-fix gain (p < 0.05), and medulla oblongata atrophy only with abnormalities of saccades (p < 0.05). Gaze-evoked nystagmus was found in 42.8% of patients with OPCA, and only in 14.2% with SND, but was not found in LOCA patients (t test, p < 0.05). In patients with OPCA, the combination of gaze-evoked nystagmus, abnormalities of sinusoidal VOR and reduced OKN gain measurements was very frequent, while infrequent in both LOCA (Fisher's exact test, p < 0.05) and SND subjects (p < 0.01). SDS also showed abnormalities of the oculomotor system.
The pathogenesis of gastrointestinal and alimentary atopy is an unclear problem. The reason of respiratory or gastrointestinal location of atopic symptoms is unknown. The density of intestinal IgG, IgM, IgA and IgE forming cells (Ig F.C.) was measured in 23 atopic and 16 non atopic children. The IgM F.C. was found to be increased in atopic children up to two years old (p less than 0.05). The IgE F.C. was increased in atopic patients (p less than 0.05), specially over two years old (p less than 0.001). The ratio IgA F.C./IgE F.C. was decreased (p less than 0.02) and we assume it is the more significant index. The same modifications were found in alimentary or gastrointestinal atopic patients and the location of allergic symptoms did not change the IgE F.C. density. We suggest the local increase of IgE F.C. does not play an important role on the type of clinical atopic disturbance. May be it only reflects the "atopic state" and the progressive systemic overstimulation by allergens.
The study was performed in 24 children aged 2 months to 6 years, without intestinal or immunological diseases. Intestinal biopsies were obtained by a Crosby's capsule, pediatric size. The number of immunoglobulin forming cells of lamina propria was measured by planimetry. Under 12 months of age there are increased levels of IgM forming cells and a low IgA forming cells/IgM forming cells quotient, but over 1 year the difference disappears. This suggests that the maturity process is very rapid. There are no correlation between serum IgA, IgM, and IgG levels and its respective forming cells number of lamina propria. It seems to support that the participation of intestinal lymphoid tissue in serum pool of immunoglobulin is very poor and that systemic and intestinal immunity maturation are completely independent.
BACKGROUND: GST pi (GSTPl) is overexpressed in bladder cancer and desquamation of the tumour may produce detectable levels of urinary GSTPl which could be used as a marker for the early diagnosis of bladder cancer. MATERIALS AND METHODS: A preliminary study in 27 transitional cell carcinoma (TCC) patients and 20 controls, using an ELISA methodl is presented here. RESULTS: 55.5% of TCC patients were positive for GSTP1, while all control samples were negative. Some of the GSTP1 positive cases also gave positive results for haematuria, which indicates that a limitation of this marker involves the contamination of the urine with erythocyte GSTP1. In 5 cases (18.5%) without haematuria detectable levels of GST pi were found. CONCLUSIONS: Further studies would be required to assess the advantages of this technique over clas sical cytology or as a complement to it, especially in patients in a phase of temporary negative haematuria.