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Biomedical subjects

G Di Perri

Publications and source records attributed to G Di Perri.

At least 91 records · Page 5Linked to original sources
PubMed1990

In vitro antibacterial activity of cefotaxime and desacetylcefotaxime, alone or in combination, against gram-positive cocci.

The in vitro activity of cefotaxime and desacetylcefotaxime against Staphylococcus aureus, Staph. epidermidis and Streptococcus pyogenes was investigated. Synergy studies were performed using time-kill curves and the chequerboard test. The time-kill curves were performed on five strains each of Staph. aureus, Staph. epidermidis and Strep. pyogenes; cefotaxime and desacetylcefotaxime were tested alone or in combination at MIC and sub-MIC values. The chequerboard test was performed in microtitre plates on ten strains each of Staph. aureus, Staph. epidermidis and Strep. pyogenes: the results were interpreted by the fractional inhibitory concentration index. In some cases both methods showed synergistic interaction against the staphylococci tested. Indifference was observed against Strep. pyogenes.

Cefotaxime↗
PubMed1990

AIDS--associated predominantly sensory neuropathy. The role of herpes viruses.

Three patients with predominantly sensory neuropathy in course of HIV-1 infection are reported. In all cases ultrastructural examination showed herpes virus-like particles in the axoplasmic matrix of myelinated fibers and in endoneurial macrophages. In 2 cases clinical patterns of posterior column involvement were observed.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Therapy of entamebiasis.

Therapy of entamebiasis is critical in that, if untreated, the disease can be fatal. Recently, a new method for differentiating pathogenic and non-pathogenic amebae has been standardized. This method relies upon the electrophoretic analysis of 4 isoenzymes which allow the identification of 20 different zymodemes. It is now widely accepted that non-pathogenic strains of Entamoeba histolytica are not a hazard for humans and therefore don't need therapy. As a consequence, treatment must be addressed only toward infections caused by pathogenic strains. As there are different drugs available for treating amebiasis, from a therapeutical point of view the disease must be divided into two forms: intestinal and extraintestinal. For the former, drugs which reach therapeutical levels in the gut are required. The mainstay for the treatment of asymptomatic carriage of pathogenic strains is DILOXANIDE FUROATE, a very well tolerated luminal amebicide. METRONIDAZOLE and other 5-nitroimidazole compounds such as ORNIDAZOLE are indicated for the treatment of symptomatic intestinal infections as they reach good concentrations in tissues, including the bowel where ulcerations develop. In order to ensure the clearance of amebae from the gut, a subsequent cycle with diloxanide furoate is advisable. Extraintestinal forms include amebic abscesses which can develop in many sites, but most commonly in the liver. Metronidazole and related compounds are the drugs of choice; in case of liver abscess, the addition of CHLOROQUINE is indicated because of its good concentration in tissues. A subsequent cycle with diloxanide furoate is also indicated.(ABSTRACT TRUNCATED AT 250 WORDS)

Amebiasis↗
PubMed1989

Usefulness of computerized electroencephalography in diagnosing, staging and monitoring AIDS-dementia complex.

One hundred and one subjects, with various degrees of HIV infection, were enrolled in a longitudinal study aimed at evaluating the correlation between clinical and instrumental findings in the development of HIV-related subacute encephalitis. The method used was electroencephalography coupled with computerized spectral analysis (EEG-CSA) and mapping. The findings recorded by this method were compared with those obtained by computed tomography (CT) scan and neurological examination. The EEG-CSA findings were divided into four categories according to their severity. EEG-CSA was shown to be very sensitive in detecting the first signs of a forthcoming neurological disease. Following 11 months of observation, 22 out of 40 (55%) neurologically asymptomatic individuals who, at the beginning of the study showed some EEG-CSA abnormalities, had clinical evidence of a subacute encephalitis whereas only two out of 37 (5.4%) subjects who were previously free of EEG-CSA abnormalities had some signs of neurological disease (P less than 0.001) after the same period. Of those remaining who were already symptomatic when the study started, the neurological progression of HIV infection was also monitored by EEG-CSA.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Electroencephalography in the early diagnosis of HIV-related subacute encephalitis: analysis of 185 patients.

Of subjects with asymptomatic HIV infection or Lymphoadenopathy Syndrome, 185 were studied by means of electroencephalography coupled with computerized spectral analysis and mapping (EEG-CSA). Abnormal EEGs were found in 30 of 118 (25.4%) patients with asymptomatic infection (CDC Group II) and in 20 of 67 (29.9%) patients with Lymphoadenopathy Syndrome (CDC Group III). The most common EEG abnormalities were represented by theta slowing on the frontal and fronto-temporal lobes and, in some cases, by delta slowing and paroxysmal sharp activity on the forebrain. Among 50 patients with abnormal EEGs, 16 showed some abnormalities on neuropsychological testing, whereas mild signs of cerebral atrophy were evident on CT scan in only 12 patients. These findings suggest that EEG-CSA could be a useful and sensitive method in the early detection and monitoring of HIV-related subacute encephalitis.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Detection of HTLV-III-specific IgG bands in the CSF from a patient with AIDS and encephalitis.

Recent evidence would suggest that HTLV-III may be neurotropic. We have found oligoclonal IgG bands by isoelectric focusing in the CSF of a homosexual man with AIDS and encephalitis. Subsequent analysis revealed that such bands contained anti-HTLV-III activity, suggesting that neurologic symptoms in AIDS patients may be caused by replication of HTLV-III inside the CNS.

Acquired Immunodeficiency Syndrome↗