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Biomedical subjects

V Frýdl

Publications and source records attributed to V Frýdl.

16 recordsLinked to original sources
PubMed1992

[Annotation to the mitochondrial genome].

After a brief explanation of the mitochondrial function, especially in the relation to the inner-cell coordination, the study analyzed the mitochondrial hypertroph-dilatative cardiomyopathy, myopathy and scrapie which were recently tied to the "D-loop fragment" of the mtDNA. Any primary connection between viral unconventional slow infections and the mitochondrial genome seems unlikely. It is argued in the study that this category of diseases can be much better explained through the transfer of the so-called mobile retroelements.

Animals↗
PubMed1991

[The problem of aneurysma dissecans in an example of an aorta "pseudoduplex"].

Dissecting aneurysms of the aorta, taking a chronic course are rare. We describe a case of a female patient who died at the age of 75 years. The left intercostal and lumbar arteries and the left renal artery originated from the aneurysmatic cleft in the aortic wall whereas the corresponding right hand-side arteries originated from the proper aortic lumen. The proximal part of the left common carotid artery was compressed by the aneurysm. The dissecting aneurysm extended into the left common and external iliac arteries. It became obvious from the history of the patient and repeated x-rays of the chest, that the aneurysm had existed 35 months before death. Our case is similar to that published by Busse in 1906. No such cases have been published in recent years. This is an indication of the acute fatal outcome of most of the dissecting aneurysms of the aorta.

Aged↗
PubMed1991

[Creutzfeldt-Jakob disease and Gerstmann-Sträussler syndrome with reference to their differential diagnosis].

Differential diagnosis has quite often proved to be difficult between CREUTZFELDT-JAKOB disease (CJD) and GERSTMANN-STRAUSSLER syndrome. Clinical and morphological aspects as well as the pathological course and differential diagnosis of CJD and Gerstmann-Strüssler syndrome are discussed in some detail. Slow influence can be morphologically diagnosed with reference to the overall pattern of individual alterations with inclusion of scrapie-associated fibrils. This morphological diagnosis can be verified by experimental inoculation to susceptible animals.

Animals↗
PubMed1989

[The effect of formalin fixation on several properties of the brain].

Described in this paper are the effects on formalin fixation of 106 human brains autopsied at a large neuropsychiatric hospital. Mass and volume of the brains changed considerably during a 3-week fixation period. On average mass increased by 50 g, volume by 57 ml. Mean brain density decreased during the first week and attained its final value almost at the end of the third week. Most changes seem to happen during the first week. Male and female brains behaved differently. Formulas to predict at autopsy time mass and volume of the brain after 3-week fixation in formalin are presented. Possible interpretations of our findings are discussed and compared with results reported by previous workers on this subject.

Adolescent↗
PubMed1988

[Pathogenesis of elastofibroma].

On the occasion of a case report on histiocytoma associated with elastofibroma-like parts on the shoulder, the extreme rarity of elastofibroma was doubted. This thesis was confirmed by post-mortem reports from Turku and Prague as well as by clinical experiences from Japan. Its possible relationship to other subcutaneous tumors rich in collagen and elastin was mentioned, and the abundant production of elastin was discussed as a variation of a one-sided metabolic mistake of the cells producing parenchyma. The symmetric or multiple, but principally the extracutaneous localization of elastofibromas may also direct our attention to developing factors other than traumatic ones, especially those being hereditary or ethnical.

Collagen↗
PubMed1988

[Relation between slow virus infection of animals and man, their pathogenicity and resistance to therapy].

Besides conventional slow viruses, a category of pathogens exist, called "unconventional slow viruses". The latter evoke laughing death syndrome, Creutzfeldt-Jakob disease (resp. its special form of Gerstmann-Sträussler's syndrome) in man, in animal scrapie, infectious encephalopathy of the mink, and chronic wasting disease. They all are relatives, and their characteristics are longtime incubation, lacking immune reactions, high chemical and physical resistance, no proof of nucleic acids till now, a lacking proof in electron microscopy as well as a ceasing change of infectivity by immunologic manipulations. Of a special importance is the Creutzfeldt-Jakob disease as a iatrogenely contagious illness, be it in consequence of a surgical intervention or of a human growth hormone administered (resp. transplants).

Animals↗
PubMed1987

[Cerebrorenal oxalate formation--a metabolic abnormality following parenteral infusions of carbohydrate exchange substances].

A 46 years old male alcoholic was admitted with an assumed alcohol withdrawal syndrome accompanied by tonic-clonic seizures. Parenteral nutrition with fructose, sorbitol, xylitol, dextran, hydroxyethylstarch, electrolytes, vitamins and amino acids was undertaken. He died 20 d later due to renal insufficiency and bronchopneumonia. Calcium-oxalate-monohydrate (whewellite) was found in the central nervous system, the kidneys, the testes, the epididymis, the cardiac muscle cells and the lungs. The presence of urate crystals was suspected. The pathogenesis of secondary oxalosis is discussed.

Alcohol Withdrawal Delirium↗
PubMed1984

[Negative serologic and microscopic studies in vivo do not exclude malaria. Autopsy report with positive Plasmodium falciparum culture].

A 31-year old man, who had just flown in from the tropics collapsed certainly. Brain trauma and alcohol withdrawal were excluded. After serological and microscopical malaria tests had been negative, subarachnoidal bleeding or encephalomeningitis were considered as possible. Although repeated malaria tests were negative, antimalarial therapy was begun on the 8th day of illness. The patient died the next day on respiratory difficulties. Cultures from blood and spleen taken three days after death showed malaria rings, and also trophozoites were found in the spleen and the bone marrow etc. The brain contained schizonts. Malaria infection from older corpses is possible. Negative malaria test results should not delay malaria treatment or exclude malaria diagnosis. Plasmodium culture should be taken whenever malaria is suggested. The possibility of malaria should always be considered. To decide in dubio pro reo in doubtful cases, particularly in forensic medicine.

Adult↗
PubMed1983

[Giant brain-base aneurysm--manifested by psychotic symptoms].

An extensive aneurysm in two lobes simulated schizophrenic behavior for six months in a 55-year old man. Headaches, neurological symptoms, unconsciousness and computed tomography led to the diagnosis of a frontobasal tumor. The patient died several days later on hematocephalus internus and constriction of the cerebellum in the foramen occipitale magnum, followed by aneurysm wall dissection. This case shows the necessity of complementing computed tomography with angiography and all other possible tests for exogenous causes of psychotic symptoms.

Autopsy↗
PubMed1983

[Friedreich's spinal ataxia following measles? Overview of central nervous system diseases caused by measles - (preliminary report)].

A case of Friedreich's ataxia of the spine with intranuclear bodies in the cerebrum and stem was found in a 43-years old man. The disease is possibly the result of measles contracted when the patient was seven. This is the first observation of this type known to us; Friedreich's spinal ataxia has until now been believed to exist only hereditary ("hereditary spinal ataxia").

Adolescent↗
PubMedDate not supplied

[Changes in dendrites in disease and aging].

Just like in other organs, e.g. in the skin or in the supporting tissue, in the CNS too the reactions to diverse noxae or causes are always stereotyped. The mental or motor retardations are distinguished by a deterioration of the neuropils, especially by the recession of the dentritic branching and their spinae. Also during physiological aging the dendritic apparatus decreases. The neuropilic differences during physiological and pathological aging, however, are rather quantitative than qualitative ones. Dendritic proliferation as a compensation mechanism for neuron recession in old age is of particular importance.

Aged↗