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Biomedical subjects

F Gullotta

Publications and source records attributed to F Gullotta.

At least 91 records · Page 5Linked to original sources
PubMed1989

Purple acid phosphatase of human brain macrophages in AIDS encephalopathy.

Brains from AIDS patients with an HIV-induced encephalopathy but without opportunistic infections or indications for an inflammation were studied by immuno- and enzyme-histochemical methods. It was found that the macrophages of these brains expressed a lysosomal tartrate-resistant acid phosphatase which gave a good immunological cross-reaction with an antibody to the well-characterized iron-containing bovine spleen purple acid phosphatase, belonging to the group of purple phosphatases, which are regarded as a marker for a special phenotype of activated macrophages. It was discussed that the numerous brain macrophages found in AIDS encephalopathy derive from latently infected monocytes which are believed to be drawn to the brain from the bloodstream.

AIDS Dementia Complex↗
PubMed1989

Cerebral listeriosis in adults. Three cases report.

The Authors describe three autoptic cases of meningoencephalitis in adults due to an emerging pathogen, the Gram-positive bacillus Listeria monocytogenes. Only one of these was an immunosuppressed patient (recurrent carcinoma of the larynx and bladder papillomas), while no severe cause of debilitation was detected in the other two cases, excluding colonic diverticulosis in both. The post-mortem examination revealed leptomeningitis and encephalitis. Lympho-monocytic tissue reaction with perivascular cuffing was present in all the cases. The etiologic agent, L. monocytogenes, was identified by cultures from clinical or autoptic specimens.

Aged↗
PubMed1989

[The morphology of HIV encephalopathy].

Reported in this paper are postmortem findings recorded from the central nervous system of 51 HIV carriers, among them 43 with clinically manifest AIDS. Opportunistic infections and tumours were established in 24 cases, including toxoplasmosis, cytomegaly, progressive multifocal leucoencephalopathy, and lymphomas. Findings obtained from 5 patients were restricted to unspecific alterations. No pathological findings at all were recordable from 8 HIV carriers without AIDS. So-called subacute microglial encephalitis (SME) was detected in 26 cases. SME was found to provide for the morphological substrate of genuine HIV encephalopathy. It was characterised by occurrence of mononuclear and even multinucleated cells which were macrophages and obviously served as virus carriers. Multinucleated cells are pathognomonic of HIV encephalopathy. No unambiguous evidence has so far been produced to primary invasion of neurons or glial cells by HI viruses.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Cryptic gliomas.

Explore the source record for details and available documents.

Brain Diseases↗
PubMed1988

Chronic trichinosis. Clinical, bioptic, serological and electromyographic observations.

Acute trichinosis can be followed by a chronic stage. Myalgia is the main clinical symptom in the chronic course of the disease. From 19 patients with a history of acute trichinosis 2-42 years ago, 15 patients suffered from chronic myalgia. Other typical complaints of our patients in the chronic stage were opthalmodynia, burning of the eyes, headache and early fatigability.

Adult↗
PubMed1988

[Concordance of Kearns-Sayre syndrome and Klinefelter syndrome].

In the last years the Kearns-Sayre-Syndrome has been defined with the typical trias of chronic external ophthalmoplegia, pigmentary retinal dystrophy and cardiac conduction defects. Today it is no longer believed to present an entity but a variant of the multiple plussymptoms of the ophthalmoplegia-plus group. In pediatrics the existence of this clinical disorder is not yet well acknowledged. The case of a 16-year-old patient is used as an example for the impressive clinical symptoms and the involvement of several organs in this clinical disorder. The combination with a Klinefelter-Syndrome has not previously been reported.

Adolescent↗
PubMed1987

Arachnoid cyst of the middle cranial fossa--aplasia of temporal lobe?

In 11 cases of intracranial, temporal arachnoid cysts the etiology, clinical and radiographic findings, surgical treatment, and outcome are reviewed in respect of post-traumatic subdural hematoma. Cysts of the middle cranial fossa are susceptible to trauma, which may cause bleeding either into the cyst or into the subdural space. Signs and symptoms of increasing intracranial pressure (ICP), local neurological deficits, and sometimes epileptic seizures may lead to hospitalization. CT or MRI scans are diagnostic in these cases. In cases of intracranial mass lesion with displacement of the midline structures and increasing ICP, osteoplastic craniotomy is performed and the lateral wall of the cyst is resected down to the tentorial notch by a microsurgical procedure, with opening into the basal cisterns. There were no operative or postoperative complications in 11 consecutive cases. However, one boy required a cystoperitoneal shunt 3 months later as a result of hydrocephalus following subdural hematoma. Asymptomatic arachnoid cysts are discussed with respect to brain function and social behavior.

Arachnoid↗
PubMed1987

Prevention of neuroma formation by Neodym Yag laser--experimental observations.

The influence of Laser radiation on neuroma formation was investigated in rat sciatic nerves. Peripheral nerve trunks were divided by focused Neodym Yag Laser and compared with those transected by microscissors. The nerves were re-exposed at different time intervals up to 240 days after initial operation. True neuroma formation could not be observed after laser transection. Sharp division resulted in widespread amputation neuromas consisting of regenerating axons and connective tissue. Neodym Yag laser radiation by its scattering effect may cause deep coagulation necrosis and thrombosis of vasa nervorum thus sealing the dome of the divided nerve trunk. The formation of amputation neuromas may be suppressed by laser application.

Amputation Stumps↗
PubMed1987

Granular cell tumors: evidence for heterogeneous tumor cell differentiation. An immunocytochemical study.

Eighteen granular cell tumors from various sites were examined with antisera directed against protein S-100, neuron specific enolase (NSE), alpha-1-antichymotrypsin, and alpha-1-antitrypsin, glial fibrillary acidic protein (GFAP), lysozyme, factor VIII-related antigen, myoglobin and vimentin, as well as with a monoclonal antibody (lu-5) directed against a panepithelial marker. The immunocytochemical reaction pattern of the tumors was heterogeneous. The brain and pituitary tumors and one thyroid tumor reacted for alpha-1-antichymotrypsin and alpha-1-antitrypsin, but not for S-100 protein and NSE. However, tumors from other sites showed immunoreactions for S-100 protein and NSE and some also for vimentin. Reactions for alpha-1-antichymotrypsin and alpha-1-antitrypsin were not observed. All other reactions were similarly negative. We conclude that the morphologically homogeneous group of granular cell tumors is biologically heterogeneous.

Cell Differentiation↗
PubMed1987

Development of a subacute tetraparesis after disulfiram intoxication. Case report.

A chronic alcoholic was intoxicated with the excessive dose of 25 g of disulfiram and developed a subacute flaccid tetraparesis and an associated encephalopathy. The severity of the clinical picture is partly explained by malnourishment including folate and vitamin B12 deficiency. The clinical, electrophysiological and pathological examinations are in accordance with the concept of a central-peripheral distal axonopathy.

Alcoholism↗
PubMed1986

Hydrocephalus, lissencephaly, ocular abnormalities and congenital muscular dystrophy. A Warburg syndrome variant?

The authors report a family in whom three members suffered from congenital hydrocephalus and ocular abnormalities. One of these patients showed along with these symptoms congenital muscular dystrophy. In this child, autopsy disclosed severe cerebral malformations consisting of lissencephaly, arhinencephaly, stenosis of aqueduct, Dandy-Walker cyst and cerebellar micropolygyria. The mode of transmission, the eyes abnormalities and the neuropathological findings of this family resemble the clinical and pathological aspects of Warburg syndrome. However, the presence of congenital muscle dystrophy in one of these children suggests some links with Fukuyama's congenital muscular dystrophy and/or with so-called brain-eye-muscle disease of Santavuori. These three syndromes are shortly discussed. The present case and few others reported in the literature obviously represent a severe and lethal form of a congenital disease involving brain, muscle and eyes.

Abnormalities, Multiple↗
PubMed1986

[Clinical follow-up in the adult (myopathic) form of glycogenosis type II].

Adult acid maltase deficiency (AMD, glycogen storage disease type II) may involve respiratory muscles leading to severe respiratory failure even before the affection of pelvic girdle muscles has turned the patient non-ambulatory. The case of a 29-year-old woman is presented to demonstrate that long-term survival is possible even after acute respiratory failure has occurred. The examination of the patient's family revealed the diagnosis of AMD in her 24-year-old sister, so far without clinical symptoms. The comparison between the two patients of serum enzyme elevations (CK, LDH, GOT, GPT, aldolase) suggested that both physical activity and the stage of the disease may be correlated with the degree of enzyme level elevation.

Adult↗
PubMed1985

Remarks on the follow-up of cerebellar astrocytomas.

A retrograde study was performed in 105 patients operated upon between 1950 and 1972 for a cerebellar astrocytoma. Complete histories were available for 89 patients. Forty-five patients died within the first 3 months after operation. Of the 32 patients who were still alive, 14 patients had been operated upon 20-30 years previously and 18 patients 10-19 years previously. Twelve patients died over 3 months after the operation; in 6 cases, recurrence of tumour was the cause of death. Of the 7 patients who were irradiated post-operatively, 5 died. In 26 patients the tumor had infiltrated the brain-stem and only 7 patients survived the operation. However, 2 patients are still alive after 25 and 10 years, respectively. The findings indicate that patients operated upon for a localized cerebellar astrocytoms can be considered cured and irradiation and chemotherapy are not warranted. When the tumour has infiltrated the brain-stem, a survival period of more than 20 years is possible after partial resection.

Adolescent↗
PubMed1985

Metabolic myopathies.

The most frequent metabolic myopathies of children and adults (glycogenoses; neutral fat myopathies; "mitochondrial" myopathies) are reviewed. In glycogenoses and neutral fat myopathies the most prominent histological feature is represented by a vacuolation of muscle fibres, vacuoles being filled with glycogen or neutral fat. Enzyme defects of glycogenoses are known. In some neutral fat myopathies, an involvement of carnitine metabolism can be found; in many other cases, biochemical investigations have failed to identify the enzyme defect(s), or have demonstrated the contemporaneous involvement of mitochondria ("mitochondrial" myopathy). The large group of "mitochondrial" myopathies is built up of many heterogeneous polygenetic syndromes, the appearance of which signalises only an impaired mitochondrial function due to underlying biochemical defect(s). In these cases, accumulations of mitochondria in muscle fibres, easily recognisable with trichrome stain ("ragged-red fibres") may be found. These mitochondria usually present very peculiar ultrastructural changes ("paracrystalline inclusions"). One of the leading clinical symptoms of metabolic myopathies is represented by myoglobinuria. In every case of "idiopathic" rhabdomyolysis, a metabolic myopathy should hence be suspected. The negative result of histological and enzymehistochemical investigations, does not exclude the presence of a metabolic disorder, however. Research in this field requires a very strong cooperation between morphologists and biochemists. Future therapeutical approaches can in fact only come from and through biochemistry.

Adult↗
PubMed1985

GFAP in brain tumor diagnosis: possibilities and limitations.

Investigation of GFAP (Glial Fibrillary Acidic Protein) in 175 brain tumours showed varying amounts of fibrillary acidic protein in every glioma. In ependymal and oligodendroglial tumours a high number of positive neoplastic elements were detected, GFAP positive were also the peri-vascular cells of a so-called astroblastoma. In pilocytic astrocytomas, Rosenthal fibers were in part GFAP positive, in part negative. In giant cells gliomas, giant cells were GFAP negative or weakly positive. Intraleptomeningeal growing tumour cells presented usually a very strong positivity. In 8 recurring oligodendrogliomas, the number of GFAP positive tumour cells was the same in the primary tumour and in its recurrence. These results demonstrate that GFAP is not a specific astrocytic, but a glial-specific protein. Although GFAP is usually present in greater concentration in differentiated, slow growing gliomas, absolute reliable predictions on biological behaviour of the individual tumour are not possible, because a high GFAP content can be detected also in malignant tumours. GFAP investigation does not seem reliable for solving the pathogenetic problems of undifferentiated tumours: the results obtained in 50 medulloblastomas showed that the investigation of small tumour samples or the positivity of a single cell are inadequate data for a correct evaluation of the findings, especially bearing in mind that GFAP of degenerated astrocytes can be phagocytised by other cells, these findings giving rise to misinterpretations.

Arachnoid↗
PubMed1985

[Sonographic diagnosis of holoprosencephaly in the 2d trimester].

Data on the sonographic diagnosis of holoprosencephaly in the second trimester are presented. Polyhydramnions was detected during outside ultrasound screening, and the lacking midline echo in association with hypotelorism and central face clefting allowed early diagnosis. The autopsy of the fetus confirmed the prenatal diagnosis, the parents subsequently had genetic counseling. The recurrence risk of holoprosencephaly depends on the specific etiology. Special ultrasound examination should be offered in subsequent pregnancies.

Adult↗