Human immunodeficiency virus in vacuolar myelopathy of the acquired immunodeficiency syndrome.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
H Maier
Publications and source records attributed to H Maier.
Studies on the activity of a protease associated with cells at the advancing edge of human tumour masses in frozen sections.
A fluorescent probe has been employed to study the status of a tumour associated protease, guanidinobenzoatase, in frozen sections of human tumours obtained from the head and neck regions. The results indicate that in vivo a naturally occurring inhibitor of guanidinobenzoatase effectively controls the activity of this enzyme on the majority of cells in a tumour mass. This inhibitor can be artificially displaced by formaldehyde treatment of the frozen sections and this treatment reveals the extent of latent enzyme in the section. In the frozen sections it was noticed that at the advancing edges of the tumour mass, the tumour cells possessed uninhibited guanidinobenzoatase, an enzyme known to degrade the link peptide between cells and fibronectin. It was shown that a synthetic inhibitor of guanidinobenzoatase selectively inhibited the guanidinobenzoatase of the tumour cells at the advancing edge of the tumour mass. It is suggested that the guanidinobenzoatase on cells at the leading edge of the tumour mass plays an important role in the invasion of adjacent host tissue. This synthetic inhibitor of guanidinobenzoatase has no inhibitory action on other trypsin-like enzymes and might therefore be of value in limiting the growth of the tumour mass in vivo.
Aminoacridines↗
Inhibition of guanidinobenzoatase by a substrate for trypsin-like enzymes.
Guanidinobenzoatase is a proteolytic enzyme capable of degrading fibronectin and is a tumour associated enzyme. Guanidinobenzoatase has been shown to be an arginine selective protease and is distinct from trypsin, plasmin and thrombin, the latter enzymes can be assayed with bis(carbobenzyloxycarbonyl-L-argininamido)-Rhodamine or BZAR. Guanidinobenzoatase is inhibited by BZAR when the enzyme is assayed in free solution and when the enzyme is cell-bound in frozen sections of tumour containing tissues. It is proposed that BZAR and its analogues may be of value in inhibiting tumour cell invasion in vivo and also that the selectivity of BZAR may be used to direct cytotoxic drugs to tumour cells possessing active guanidinobenzoatase.
Animals↗
[Coexpression of keratin and vimentin in squamous cell carcinoma as evidence of pseudosarcomatous differentiation].
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Carcinoma, Squamous Cell↗
Reduction of cytochrome c by oral mucosa of patients with oropharyngeal cancer.
Superoxide radicals and other reactive oxygen products are likely to play a role in the development of mouth cancer since they are able to convert penultimate carcinogens present in cigarette smoke into ultimate carcinogens. Those radicals can be generated, e.g., by phagocytes infiltrating inflamed mucosa or by semiquinone radicals present in cigarette tar. We therefore measured the ability of oral mucosa of patients with oropharyngeal tumors to reduce cytochrome c. All patients were heavy smokers and drinkers. It was found that patient mucosa had by far more reducing power than control mucosa. Within the control group, smokers' mucosa was most active. When tested, the cytochrome c reduction was not inhibitable by superoxide dismutase or copper(II)3,5-diisopropylsalicylate. We hypothesize that reduction of cytochrome c by oral mucosa of smokers and patients with mouth cancer is primarily due to residues of cigarette tar containing conjugated quinones of mixed oxidative states which are strong reductants as well as producers of oxygen-centered radicals.
Cytochrome c Group↗
Effect of chronic ethanol and nicotine consumption on the function and morphology of the salivary glands.
The effect of chronic ethanol and nicotine consumption on the function and the morphology of the salivary glands was studied. In smokers and drinkers there was a significantly reduced flow rate of parotid and submandibular saliva. The protein excretion in both secretions was significantly lowered. A reduced salivary flow rate and a lowered protein output also were found in rats that has been fed a liquid diet containing 36% of total calories as ethanol for 90 days. The parotid glands in these animals showed an impressive fatty degeneration. Additionally there was atrophy of the acinar cells. Rats in which nicotine was administrated orally via the drinking water (100 ml/l) did not show a reduction of salivary flow rate. However, salivary protein excretion was significantly lowered. The parotid glands of these animals showed a swelling of the acinar cells and an increase in the total number of intraacinar secretory granula. Most of these granula were immature light ones containing only small concentrations of glycoprotein, while the number of mature dark granula which contain high concentrations of glycoprotein was drastically reduced. The observed functional and morphological alterations reflect an exhaustion of salivary glands due to a nicotine-mediated chronic secretory stimulation. The results of this study indicate that mainly ethanol and to a lesser extent nicotine after chronic consumption cause severe morphological and functional alterations.
Alcoholism↗
[Clinical picture and possible causes of functional disorders of the parotid gland in radioiodine therapy of differentiated thyroid cancer].
The parotid gland function was examined in 31 patients with thyroid carcinoma treated with radio-iodine. Beside enhanced values of sodium concentration, protein concentration and alpha-amylase activity following each therapy, a continuous reduction of flow rate and alpha-amylase activity is found according to the cumulative total dose. The importance of glandular kallikrein und phosphohexoseisomerase (PHI) are discussed with regard to their possible role in glandular damage. A comparison is made with chronic recurrent parotitis, and therapeutical aspects are considered. On the whole the present investigation shows that radio-iodine therapy causes damage to the parotid gland, which normally leads to measurable effects after cumulative doses of 470 mCi.
Combined Modality Therapy↗
[Role of hyphomycosis of the maxillary sinus area].
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Adult↗
[Peripheral neurinoma of the hypoglossal nerve].
Neurinomas of the hypoglossal nerve are rarely reported. In most cases these tumors are intracranial or sited at the skull base. Only a few solitary neurinomas of the twelfth cranial nerve have been reported. In most of these cases the tumors arose from the descending part of the nerve in the parapharyngeal space. We report the first neurinoma recorded arising from the submandibular course of the hypoglossal nerve.
Aged↗
Binding sites of Ulex europaeus-lectin I in human parotid gland. A light-microscopic and ultrastructural study using the immunoperoxidase technique and immunocryoultramicrotomy.
Twenty non-neoplastic parotid glands (removed during neck dissection for regional tumours) were examined for cellular and subcellular binding sites of Ulex europaeus-lectin I (UEA-I), a lectin reported to be specific for alpha-L-fucose. For light microscopy, an extended peroxidase-antiperoxidase method was applied; for the evaluation of the subcellular localization of bound lectin, three of these glands were examined following immunocryoultramicrotomy and staining by the protein A-gold technique. In addition to the known cytoplasmic affinity of UEA-I for capillary endothelium, acinar cells bound the lectin within the cytoplasmic compartment; the number and distribution of stained acinar cells varied among individuals. Furthermore, cytomembrane-bound labelling that occurred most markedly at the luminar surface was observed in striated-duct epithelium. Using the electron microscope, protein A-gold particles were seen in zymogen granules and in Golgi cisternae of serous acinar cells; primary saliva secreted in the lumina exhibited strong labelling; serous acinar cells had binding sites on their cell membranes, striated-duct epithelium had binding sites on its surface membrane and in the vicinity of apical vesicles. Our results show that UEA-I is a useful tool for the study of the structure and functional states of the parotid gland epithelium and its associated pathological alterations.
Head and Neck Neoplasms↗
Cytokeratin expression in normal salivary glands and in cystadenolymphomas demonstrated by monoclonal antibodies against selective cytokeratin polypeptides.
The distribution of selective cytokeratin polypeptides, vimentin, and glial fibrillary protein (GFP) in 5 human cystadenolymphomas of the parotid gland was compared with normal human parotid (n = 5) and submandibular (n = 4) glands using a panel of monoclonal antibodies against diverse and selective cytokeratin polypeptides, vimentin and glial fibrillary protein (GFP). A biotinstreptavidin method was used on cryostat sections. The immunocytochemical finding of identical cytokeratin polypeptides Nos. 7, 8, 18 and 19 and basal cells selectively labeled by the monoclonal antibody KS 8.58, in both the epithelial part of the cystadenolymphomas and in the duct epithelium of the parotid gland, confirms the hypothesis that the epithelial compartment of cystadenolymphomas is derived from the duct system. The triple expression of cytokeratin, vimentin and GFP in myoepithelial cells of the parotid gland is discussed.
Adenolymphoma↗
Unilateral gallium-67 uptake in primary tuberculosis of the major salivary glands.
Unilateral radionuclide accumulation in salivary glands is an uncommon finding on gallium scintigraphy. The differential diagnosis includes malignant tumors and inflammatory processes of these organs. Two cases of unilateral gallium uptake of the parotid and submandibular gland respectively, verified as solitary tuberculosis, are presented, together with the correlative findings of Tc-99m pertechnetate scintigraphy, sialography, and sonography. None of these imaging modalities is specific enough to provide pathognomonic signs for tuberculosis. When assessing unilateral gallium uptake of the salivary glands, one should be aware of the possibility of tuberculosis.
Adult↗
[Accumulation of 67Ga in diseases of the large salivary glands].
In a prospective study (59 patients) the pattern of 67Ga-uptake of the large salivary glands (LSG) in the course of typical disorders of the glands was investigated. Inflammatory and granulomatous disorders revealed--dependent on their acuity--an identical pattern of Ga-uptake. Extraglandular uptake was found in some instances of tuberculosis, sarcoidosis and myoepithelial sialadenitis. Among the benign LSG tumors all cystadenolymphomas showed intensive uptake while all pleomorphic adenomas did not. In 75% of the malignant LSG tumors Ga-uptake was pathologically increased, particularly in all adenocarcinomas of the series. 67Ga scintigraphy seems to be useful in the follow-up of inflammatory and granulomatous LSG disorders and in the differential diagnosis of pleomorphic adenoma versus cystadenolymphoma. Extraglandular uptake may give valuable hints for diagnostic work-up.
Adult↗
Penetration of ciprofloxacin into parotid gland tissue and parotid saliva.
The penetration of 1-cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-7-(1-piperazinyl)-3-quinoline carboxylic acid (ciprofloxacin, Bay o 9867, Ciprobay) into parotid gland tissue and parotid saliva of the rat after intravenous administration (6 mg/kg body weight) was studied. 2 h after bolus injection ciprofloxacin mean levels in parotid gland tissue (0.60 mg/l) nearly reached 2-fold mean blood levels (0.36 mg/l). In parotid saliva the mean concentration of the gyrase inhibitor (0.20 mg/l) was lower than in blood, however, still high enough to be effective against the pathogens which most often cause inflammation of the parotid gland.
Animals↗
Influence of sex and age on kallikrein excretion in stimulated human parotid saliva.
We determined the activity of parotid salivary kallikrein in 65 healthy males and females. We then formed two groups of probands by age. The mean age in the first group (n = 35) was 24.5 +/- 1.7 years, whereas the mean age in the second group (n = 30) was 58.1 +/- 10.5 years. The activity of the glandular kallikrein was measured with a chromogenic substrate. The salivary kallikrein excretion in the younger females was higher when compared with that in the younger males. No sex differences concerning salivary kallikrein activity could be observed in the second group. A possible influence of female sex hormone on salivary kallikrein excretion is discussed.
Adult↗
The effect of chronic ethanol consumption on salivary gland morphology and function in the rat.
Chronic ethanol consumption in rats resulted in a striking fat accumulation in the acinar cells of the parotid gland demonstrated by light microscopy. In addition, a significant decrease in parotid wet weight (p greater than 0.02) and in protein content of the gland (p greater than 0.02) was observed following alcohol feeding. Wet weight, protein content, and morphology of the submaxillar gland were not affected by ethanol feeding. Alcohol metabolism, similar to that found in the pancreas, via a cytosolic alcohol dehydrogenase could be demonstrated in both the parotid and the submaxillar gland. However, the activity of this enzyme was not affected by chronic ethanol ingestion. Subsequently, chronic ethanol consumption significantly decreased salivary flow rate stimulated by pilocarpine hydrochloride (p greater than 0.02), salivary alpha-amylase activity (p greater than 0.02), and salivary sodium concentration (p greater than 0.01), whereas potassium concentration of the saliva was increased (p greater than 0.05). In contrast salivary total protein concentration was not affected by alcohol ingestion. The changes of salivary electrolyte composition observed after chronic ethanol feeding could be due to an altered aldosterone metabolism or to a change in aldosterone receptors of the parotid gland caused by ethanol administration. The reduced salivary flow could play a role in the pathogenesis of oropharyngeal cancer in the alcoholic.
Alcoholism↗
[Treatment of chronic recurring parotitis with the protease inhibitor aprotinin (trasylol)].
Excessive release of glandular kallikrein into the interstitial space around the salivary gland ducts plays a significant role in chronic recurrent parotitis. In the present study 26 patients suffering from acute exacerbated chronic recurrent parotitis were subjected to treatment with the kallikrein inhibitor aprotinin (Trasylol, Bayer AG). During the first hour of treatment 1 mio KIU Aprotinin were infused intravenously, followed by 250 000 KIU/h for another 35 h. Within 12 h after initiation of therapy in all patients we observed remission of pain. Salivary gland function which had been seriously impaired prior to therapy was found to be largely normalized within 48 h in most patients treated in this way. The success of this therapy schedule underlines the suggestion that glandular kallikrein is a trigger enzyme in the pathogenesis of chronic recurrent parotitis.
Aprotinin↗
[Immunohistologic analysis of chronic obstructive sialadenitis. I. Changes in the expression of antigens of the major histocompatibility complex].
In the course of electrolyte sialadenitis progressing towards obstructive sialadenitis, changes in the epithelial expression of antigens of the major histocompatibility complex (MHC) occur even before morphological alterations and inflammatory cells can be detected. Class I antigens are enhanced and induced, and Class II antigens are induced. These changes begin focally. Only the expression of HLA-A,B,C and -DR in acinar epithelium is linked to the close vicinity of lymphohistiocytic infiltrates. In later stages of the disease the foci tend to fuse and antigenic changes are pronounced in areas of fibrosclerosis and parenchymal atrophy. The altered MHC antigen expression induced by chronical saliva congestion probably represents an important part of the postulated "immunoreaction in the duct epithelium" supposedly giving rise to this type of immunosialadenitis.
Adult↗