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Biomedical subjects

L Nagy

Publications and source records attributed to L Nagy.

At least 127 records · Page 7Linked to original sources
PubMed1993

Static external fixation of finger fractures.

In spite of its similar design constructs, external fixation of finger fractures differs greatly from that of long bones. Besides its common indications in massive, high-energy trauma, and contaminated fractures, it offers true alternatives to open reduction and internal fixation and represents a superior treatment modality in well-selected cases of extensive comminution. Further pending improvement in design will increase its application, although it apparently does not yet resolve long-standing controversies in elective fracture care.

Clinical Protocols↗
PubMed1993

[Use of preserved homograft for covering burn injuries].

Authors describe the considerations supporting the use of cadaveric skin homografts. The surgical relations of the burns, the site and advantages of the application of the homografts in the treatment of the burned patients are summarized.

Adult↗
PubMed1993

[Structural and equilibrium studies of the proton and copper(II) complexes of N-D-gluconylglycine].

N-D-Gluconylglycine, a pseudopeptide derivative glucono-delta-lactone and glycine, was prepared and the equilibrium constants of its protonation and copper(II) coordination and the structures of the copper complexes formed were studied in aqueous solution by potentiometry, spectrophotometry, CD, EPR and 13C-NMR relaxation. The parent complexes formed in acidic medium have low stabilities, characteristic of carboxylate coordination. In the pH range 5-9, the amide group and the 2-OH group of the ligand undergo deprotonation. In parallel with these processes, one ligand is replaced from the copper(II) coordination sphere. For the species MLH-2' we propose (30, 1N) coordination in the equatorial plane around the copper(II). EPR measurements indicate that dimeric species are also formed. At pH > 9, further base-consuming processes start as an indication of the deprotonation of other alcoholic hydroxy groups of the sugar moiety or the formation of mixed hydroxy complexes.

Circular Dichroism↗
PubMed1992

Glutathione, protein sulfhydryls and cysteine proteases in gastric mucosal injury and protection.

Glutathione is one of the endogenous protective chemicals, like prostaglandins, in the gastric mucosa. Depletion of these agents aggravate the chemical- or stress-induced gastric erosions and ulcers. However, gastroprotection can be achieved even in the presence of low mucosal concentration of glutathione and prostaglandins, indicating the presence of other protective chemicals (e.g. polyamines, growth factors, neurotransmitters, steroids) in the stomach. Protein sulfhydryls were also implicated in the mechanism of action of gastroprotective drugs. We recently tested the hypothesis that cysteine proteases might be a target of gastroprotective and antiulcer agents, and decided to look for the presence of proteases and protease inhibitors (PI) in the gastric mucosa and juice. Protease activity and PI were measured with general substrates hemoglobin, azocasein and albumin at optimal pH (2.0, 5.6, 7.4) of aspartic, cysteine and serine proteases. Homogenates of glandular stomach mucosa and gastric juice from fasted rats were incubated in the presence or absence of specific inhibitors and gastroprotective SH alkylators such as NEM or iodoacetate. PI was measured after acid and heat inactivation of endogenous proteinases and addition of pepsin, cysteine proteinase papain, or trypsin. Our results indicate that of the proteases found in the stomach 98% was pepsin at pH 2.0, and up to 56% or 24% was SH-sensitive at pH 5.6 or 7.4, respectively. Intragastric administration of SH alkylators such as NEM or iodoacetate exerted a dose- and time-dependent gastroprotection against chemically induced acute erosions and ulcers. Thus, in addition to glutathione, proteinases and their specific endogenous inhibitors may also be involved in gastric mucosal injury and protection.

Animals↗
PubMed1992

Mechanisms of vagal nerve in gastric mucosal defense: unchanged gastric emptying and increased vascular permeability.

Gastric cytoprotection in response to different agents (prostaglandins, carotenoids, etc.) failed to occur after surgical vagotomy. Decreased gastric emptying and the increased vascular permeability were tested in ethanol-treated rats without and with bilateral surgical vagotomy. The experiments were carried out on Sprague-Dawley rats. The animals were fasted for 24 h before experiments. Bilateral surgical vagotomy or only laparatomy were carried out at 30 min before administration of ethanol (96%, 1 ml). The animals were killed at 0, 1, 5, 15, and 60 min after ethanol administration, when the number and severity of gastric mucosal lesions were noted. In another series of experiments, the animal received Evans blue (1 mg/100 g) i.v. 15 min before killing. The gastric contents were collected and the glandular mucosa was scraped. Evans blue was extracted in chloroform, and its concentration was spectrophotometrically measured. It has been found that (a) both number of lesions and severity of ethanol-induced gastric mucosal damage were larger at each time period in surgically vagotomized rats than in rats with intact vagal nerves; (b) the increased vascular permeability was significantly higher in gastric mucosa at an early period in surgically vagotomized rats compared to rats with intact vagal nerve; (c) the increased vascular events preceded the development of macroscopic appearance of gastric mucosa damage in both groups of animals; and (d) the time-related responses were the same in both groups of animals. It is concluded that increased vascular permeability, but not gastric emptying, probably has some role in the failure of the development of gastric cytoprotection in surgically vagotomized rats.

Animals↗
PubMed1992

Measurement of non-steroid antiinflammatory drugs induced gastric microbleeding.

The damage of the mucous membranes in the gastrointestinal tract caused by non-steroid antiinflammatory drugs are well known. The gastrointestinal microbleeding was measured by the method of Fischer and Hunt before and after the intake of indomethacin (4 x 25 mg), naproxen-sodium (4 x 275 mg), diclofenac (3 x 50 mg) and azapropazone (2 x 600 mg). In the indomethacin group microbleeding increased from 0.91 +/- 0.12 ml/24 h to 7.30 +/- 1.20 ml/h. In the naproxen-sodium group from 1.22 +/- 0.16 ml/24 h to 3.56 +/- 0.40 ml/24 h, in the diclofenac group from 0.86 +/- 0.14 ml/24 h to 3.18 +/- 0.28 ml/24 h, in azapropazone group from 0.92 +/- 0.18 ml/24 h to 2.50 +/- 0.20 ml/24 h, respectively. All non-steroid antiinflammatory drugs increased the gastric microbleeding, however, there were considerable differences in the degree of enhancement. This can be explained by the different inhibitory activities of the drugs on the cyclooxygenase enzyme activity.

Adult↗
PubMed1992

Pathways, mediators and mechanisms of gastroduodenal mucosal injury.

This review provides evidence that gastroduodenal mucosal injury is a complex process because of the heterogeneous structure and multiple functions of the gut. The action of exogenous etiologic agents is usually mediated in part, or amplified by endogenous mediators which very often exert biphasic, i.e., damaging and protective effects. The pathogenetic pathways involve direct/indirect chemical injury, vascular damage and its consequences, and acute or chronic inflammatory processes following infectious, chemical or ischemic injury. The role of oxygen, free radicals, calcium and proteases as well as the components and forms of gastroduodenal injury, e.g., reversible and irreversible cell injury, tissue necrosis, acute and chronic inflammation are also briefly discussed. Only a slight or moderate direct cytoprotection was demonstrated in vitro using isolated, mixed rat gastric mucosal cells by the known gastroprotective drugs including PG and SH compounds. Thus, the terms of organo or gastroprotection are more descriptive then the misleading "gastric cytoprotection".

Animals↗
PubMed1991

Retinoic acid receptor transcripts in human umbilical vein endothelial cells.

Human umbilical vein endothelial cells contain high levels of mRNA for the beta-retinoic acid receptor, and very low levels of alpha-retinoic acid receptor transcripts. The cells responded to retinoic acid with a significant induction of tissue transglutaminase expression but no alterations in the expression of beta-retinoic acid receptor transcripts. The physiological implications of the constitutive expression of this receptor in endothelial cells is discussed.

Blotting, Northern↗
PubMed1991

Failure of prostacyclin, beta-carotene, atropine and cimetidine to produce gastric cyto- and general mucosal protection in surgically vagotomized rats.

Different chemicals (such as ethanol, HCl, drugs) produce gastric mucosal injury. A special type of gastric mucosal defense, which differed from the inhibition of gastric acid secretion, was discovered in response to small doses of prostaglandins. This phenomenon was termed "gastric cytoprotection". Later, the existence of gastric cytoprotection was proved using different compounds, such as vitamin A and other carotenoids, prostacyclin, small doses of anticholinergic and H2-blocking agents. These compounds produce cyto-protection by different mechanisms. In this study we tested the role of vagus nerve on the development of these different types of gastric cytoprotection. These compounds prevent ethanol-induced gastric mucosal injury in rats with intact vagus nerve, but their cyto- and mucosal protective effects disappear in surgically vagotomized rats. These results indicate that the intact vagus nerve is basically necessary for the overproduction of HCl and pepsin secretion, and for the development of gastric cytoprotection, produced by different compounds (e.g. prostacyclin, beta-carotene, small doses of atropine and cimetidine) acting without the presence of inhibition of gastric acid secretion.

Animals↗
PubMed1991

The role of adenosine and adenosine transport in ethanol-induced cellular tolerance and dependence. Possible biologic and genetic markers of alcoholism.

Acute exposure to ethanol in culture inhibits adenosine uptake into cells, thereby increasing the concentration of extracellular adenosine. Extracellular adenosine then reacts with adenosine A2 receptors to stimulate intracellular cAMP production. During prolonged exposure to ethanol, the increase in cAMP is followed by the development of heterologous desensitization of receptors coupled to adenylyl cyclase via Gs, the stimulatory GTP-binding protein. Ethanol-induced heterologous desensitization appears to be due to a reduction in mRNA and protein for G alpha s, a subunit of Gs. This is an example of cellular dependence on ethanol. The important implication of these findings is that a selective inhibitory effect of ethanol on adenosine uptake can lead to desensitization of diverse receptors coupled to cAMP production. Such changes could contribute to the pleiotropic effects of ethanol in the brain and other organs. Prolonged exposure to ethanol also alters the nucleoside transport system. While ethanol inhibits adenosine uptake into naive cells, ethanol no longer inhibits adenosine uptake into cells that have adapted to ethanol. This resistance to ethanol inhibition appears to be a form of cellular tolerance to ethanol. Thus, there appears to be a synergism between ethanol-induced heterologous desensitization of receptor-stimulated cAMP production (cellular dependence) and resistance to ethanol inhibition of adenosine uptake (cellular tolerance), because both lead to reduced intracellular levels of cAMP. Our studies on cAMP signal transduction in cell culture are directly relevant to the pathophysiology of human alcoholism. Heterologous desensitization of cAMP production is demonstrable in lymphocytes taken from actively drinking alcoholics; this measurement appears to be a biologic marker of active alcohol consumption. In addition, regulation of adenosine receptor-dependent cAMP production may be altered in patients at risk to develop alcoholism because of genetic factors. Thus, lymphocytes from alcoholics cultured many generations in the absence of ethanol show increased adenosine receptor-dependent cAMP production and increased sensitivity to ethanol-induced heterologous desensitization. These persistent phenotypic abnormalities in cell culture could be used as genetic markers for alcoholism. Studies are under way to test this possibility.

Adenosine↗
PubMed1991

Cultured peripheral blood mononuclear cells derived from patients with acute severe asthma ("status asthmaticus") spontaneously elaborate a neutrophil chemotactic activity distinct from interleukin-8.

Peripheral blood mononuclear cells (PBMC) isolated from patients with acute severe asthma on the day of admission to hospital were cultured in vitro in serum-free medium in the absence of mitogenic stimulants for as long as 72 h. PBMC isolated from control groups (mild asthma, chronic obstructive airway disease, normal subjects) were cultured in a similar fashion. After incubation, the culture supernatants were tested for neutrophil chemotactic activity (NCA) using a modified Boyden chamber technique. PBMC from patients with acute severe asthma elaborated significantly greater amounts of NCA into the culture supernatants as compared with all three control groups (p less than 0.01). The amounts of PBMC-derived NCA from the same patients after 7 days of hospital therapy and clinical improvement were reduced (p less than 0.01). A correlation was observed between the extent of reduction in spontaneous release of NCA by PBMC derived from patients with acute severe asthma and the degree of clinical improvement of their asthma (p less than 0.02). Both monocytes and lymphocytes, when cultured separately, released NCA in amounts sufficient to account for the total activity released by unfractionated PBMC. NCA in PBMC culture supernatants accumulated progressively with time, a process inhibited in a dose-dependent fashion by cycloheximide. The amounts of NCA in culture supernatants did not correlate with the concentrations of histamine in lysates of the PBMC prepared just prior to culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Parenteral and enteral nutrition and the enterocutaneous fistula treatment. I. Investigations on fistula output, nutritional status complications.

Prospective evaluation were made of 45 patients with postoperative small bowel fistulas treated with total parenteral nutrition (TPN) and enteral nutrition (EN) between 1971-1988. The administration of TPN in the early treatment of enteric fistulas decreased the mean fistula output significantly (p < 0.05-0.001) and provided an effective tool in the control of high-output fistulas. The electrolyte contents of different fistula secretions were unchanged and the losses through the fistulas depended on the daily output. In patients with high-output fistulas acid-base balance disturbances had to be corrected. When comparing two parenteral nutrition regimens (carbohydrate+amino acids /CH + AA/ versus carbohydrate + amino acids + fat /CH + AA + F/) both facilitated the reduction of fistula secretion (in high-output fistulas. CH + AA = -50.2%; CH + AA + F = -49%). Positive nitrogen balance was achieved in non septic patients after 13 days of treatment. Improvement of serum protein and albumin occurred by the time of fistula healing. In non surviving patients significant decrease in protein synthesis was observed. Out 7 of 75 central venous catheters yielded positive bacterial cultures (9.3%). In 5 patients autopsy proved generalized sepsis. The use of parenteral and enteral nutrition proved to be a powerful method for controlling the enterocutaneous fistulas and maintaining the nutritional integrity of patients.

Adult↗
PubMed1991

Parenteral and enteral nutrition and the enterocutaneous fistula treatment. II. Factors influencing the outcome of treatment.

An 18-year review of 64 patients treated with 71 postoperative enterocutaneous fistulas of the stomach /4/, duodenum /21/, jejunum /9/ and ileum /37/ was carried out to identify the factors affecting morbidity and mortality. Age, localization, output, inflammatory or malignant bowel disease, nutritional status and associated sepsis were analysed. The administration of total parenteral nutrition (TPN) or/and enteral nutrition (EN) as adjuvant therapy in the management of gastrointestinal fistulas increased the fistula closure rate (64%) and decreased mortality (33%). In patients over 65 years a rise in mortality rate (69%) was found. TPN and EN support yielded the best results in duodenal and jejunal fistula patients (closure rate 83% and 71%; respectively). In patients with high-output fistulas, inflammatory bowel disease and malignancy good results could be achieved with nutritional treatment. The presence of malnutrition had an adverse effect on the outcome in the non-TPN group with a mortality rate of 49%. In 43 patients severe septic complications occurred and 21 died due to septic multiple organ failure proved by autopsy. The overall mortality rate was 39%. Timing of fistula surgery had little impact on the fistula closure rate, but better results were obtained when reconstructive surgery was deferred beyond 6 weeks from fistula onset. Mortality has decreased since 1980. While many factors influence the outcome of fistula disease, adequate antiseptic treatment is assumed of primary importance. The nutritional therapy facilitated the spontaneous fistula healing and allowed the elective intestinal reconstruction to be scheduled at an optimal time.

Adolescent↗
PubMed1991

Acute acalculous cholecystitis.

In 1884 Duncan was the first to report on acute postoperative acalculous cholecystitis (ref.: 14). Initial publications reported a small number of cases. Literary data have shown a change of the situation for the past few decades /16/. It was most frequently observed following surgical intervention, trauma, delivery or parenteral nutrition /1, 13, 16/. The number of new acalculous cholecystitis cases often requiring surgical intervention and causing death in elderly male patients has increased /5, 16/. Therefore we decided to undertake a clinical study. In Hungary the authors who deal with this theme are: Csengódy /2/, Sándor /17/, Lukács /12/ and Ezer et al. /3/.

Acute Disease↗