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At least 505 records · Page 28Linked to original sources
PubMed1986

Platelet-activating factor-induced ischemic bowel necrosis. An investigation of secondary mediators in its pathogenesis.

The authors have previously reported a model of ischemic bowel necrosis produced in the rat by synthetic platelet-activating factor (PAF) or a combination of PAF and bacterial endotoxin. Because rat platelets are refractory to PAF and thromboemboli were not found in the mesenteric or intestinal microvasculature, they suspected that secondary mediators were involved in the pathogenesis of bowel necrosis. They have found the following lipoxygenase products of arachidonic acid, especially leukotrienes (LT), probably played an important role in the pathogenesis of bowel necrosis, because diethylcarbamazine (an inhibitor for LTA synthesis) and FPL55712 (LT antagonist) ameliorated, and at times completely prevented, the lesions. NDGA (a nonspecific lipoxygenase inhibitor) was less effective, probably because of its additional effect on cyclooxygenase inhibition. Verapamil, a calcium channel blocker, ameliorated the disease. Thromboxane A2, a potent vasoconstrictor, was probably not responsible for the ischemia of the gastrointestinal tract. This is suggested by the ineffectiveness of OKY-046 in preventing bowel necrosis. Prostaglandin (PG) E1 infusion often prevented the bowel necrosis, which suggested beneficial effects of vasodilating PGs, probably released as a defense mechanisms. Indomethacin aggravated the disease, probably by inhibiting PG release and shifting the metabolic pathway toward the lipoxygenase pathway. Antihistamine and antiserotonin had no effect, which suggested that these mediators were not involved in the pathogenesis of bowel necrosis. Shock produced by PAF was probably not the only cause of bowel necrosis, because reversal of the hypotension did not always prevent the development of bowel necrosis. Hemoconcentration (increased vasopermeability) and leukopenia induced by PAF did not correlate with the development or severity of bowel necrosis.

Alprostadil↗
PubMed1987

Czechoslovak contribution to current concepts in impotence, its pathogenesis, diagnosis and treatment.

Czechoslovak contribution to the current concepts in impotence, its pathogenesis, diagnosis and treatment, consists especially in: the recognition of the haemodynamics of erection. The process involves two stages; in the first one, the arterial bed must deliver to the corpora cavernosa (CC) threshold values of volume and pressure needed for filling and distention of the CC, in the second period, the CC function as a closed system on the hydraulic principle, and contractions of the ischiocavernous muscles increase intracavernous pressure to suprasystolic values, the observation that it is just failure of the haemodynamics of erection that plays an important role in the pathogenesis of impotence in a majority of patients. The development of artificial erection into a real functional examination of the CC enables to differentiate: disorders with normal haemodynamics of erection, those due to insufficient arterial supply, insufficient blockage of venous return, or insufficient and ineffective contractions of the ischiocavernous muscles. the development of the phalloarteriographic technique which allows a precise anatomical diagnosis of the lesions in the afferent arterial bed, providing the basis for the development and indication of a number of reconstructive procedures in the arterial bed supplying the CC. In addition, the examination has also helped to clarify the relationship between erectile disorders, arterial disease and their risk factors. In retrospect, Czechoslovak research into impotence has substantially contributed to the recognition of vasculogenic impotence, to the therapy of arteriogenic erectile disorders and to a basic change in the concepts of the aetiology and pathogenesis of impotence.

Arterial Occlusive Diseases↗
PubMed1987

Molecular and genetic aspects of the pathogenesis of viral infections of the central nervous system.

Viral pathogenesis can be defined in terms of a series of successive interactions between a virus and its target host. In order for a virus to injure a target organ such as the central nervous system (CNS), it must first enter the host animal, replicate in some primary site near its place of entry, spread from this site to the CNS and infect and injure specific populations of cells within the CNS. At each of these steps, the virus must avoid or overcome a variety of immunological and nonimmunological host defenses. It has recently become possible to begin to identify the role of specific viral genes and the proteins they encode at specific steps in the pathogenesis cycle. This review focuses on current knowledge concerning the molecular and genetic basis for the pathogenesis of viral infections of the CNS. Emphasis is placed on recent research with a wide variety of neurotropic viruses including reoviruses, bunyaviruses, lymphocytic choriomeningitis virus, rabies virus, polio virus, herpes viruses, lentiviruses, and the unconventional agents responsible for disease such as scrapie.

Humans↗
PubMed1987

[An experimental study on the pathogenesis of congenital hand malformations--with reference to local disturbance in the limb bud and polydactyly].

Pathogenetic conditions for polydactyly and its pathogenesis were studied by inducing the condition at a high incidence by incubating fertilized ova of white leghorns and locally cauterizing the limb bud with a bipolar microcoagulator. Polydactyly commonly occurred in about 12 hours of the latter half of the third day after cauterization (5 watts) of the preaxial area of the limb bud. This suggests the involvement of space- and time-specificity under the appropriate strength of such stimulation in the pathogenesis of polydactyly. Most polydactyly involved the first toe. Disturbance in the primordium of the metatarsal bone was believed to be related to the pathogenesis. Many reductive complex malformations resembling polydactyly were seen, and the repairing mechanism of these malformations was similar to that of polydactyly. Thus, it seems that the repairing mechanism is oriented to acquiring the proper number of toes and that acquisition of the first toe becomes particularly dominant, resulting in a tendency for polydactyly in the first toe.

Animals↗
PubMed1985

[Clinical picture and pathogenesis of extrafocal symptoms in stroke].

The clinical picture and pathogenesis of the extrafocal symptoms were examined on the basis of 254 cases of hemorrhagic and 175 cases of ischemic strokes. The significance of these symptoms in the correct assessment of the site of the process is demonstrated. The following variants of the pathogenesis of the extrafocal symptoms in acute disorders of the cerebral circulation were identified: edema and swelling (cranio-basal compression and stem compression in the presence of a cerebellar hemorrhage); compression and dislocation (temporo-tentorial wedging and wedging of the cerebellar tonsils); secondary foci (at a distance and symmetrical); impairment of compensation in the earlier damaged structures; involvement of the functional systems (tonogenic and motor). The pathogenesis of the extrafocal symptoms was attributed to hemorrhagic and ischemic foci, death of neurons, focal histiolysis at a distance, etc.

Aged↗
PubMed1979

The role of the gallbladder in the pathogenesis of cholesterol gallstones.

During the past century, a variety of explanations have been proposed to explain the pathogenesis of cholesterol gallstones. Early attempts to account for the phenomenon of cholelithiasis focused on events in the gallbladder and stressed mucosal inflammatory changes, gallbladder stasis, stratification of bile, and absorption of bile salts from a damaged mucosa. The advent of the concept of "lithogenic bile" redirected attention to the liver and led to the proposal that an enzyme-mediated genetic and/or metabolic defect is the initiator of cholesterol cholelithiasis. While recognizing that the pathogenesis of gallstones is probably multifactorial, alterations in gallbladder and biliary ductal motor function constitute a plausible, but as yet unexplored, mechanism for alterations in enterohepatic circulation dynamics and subsequent cholesterol cholelithiasis. Gallbladder motor function is a complex phenomenon influenced by dynamic compliance, autonomic pharmacology, hormonal responses, and sphincter dynamics. Attempts to describe these aspects of biliary physiology may characterize the next phase in our understanding of the pathogenesis of cholesterol cholelithiasis.

Bile Acids and Salts↗
PubMedDate not supplied

[Phacomatoses. Pathogenesis - Classification - Vascular aspects].

The pathogenesis of the phacomatoses, developmental diseases of the embryonic plates, permits an understanding of the different manifestations which characterize these disorders. This pathogenesis also constitutes the best basis for a rational classification. The author sets out the main features of this pathogenesis and its practical applications, and then considers the principal vascular aspects of the phacomatoses, especially in Osler-Rendu disease, Blue Rubber Bleb Naevi, Mafussi's syndrome, the haemangioblastomatoses, Bailey's glomangiomatosis, the Louis-Bar syndrome, Struge-Weber angiomatosis, the syndrome of Bonnet-Dechaume and Blanc, Cobb's syndrome, the angio-osteo-hypertrophic syndromes, von Recklinghausen's neurofibromatosis, Bourneville's tuberous sclerosis, and the melanic phacomatoses.

Adolescent↗
PubMedDate not supplied

[The pathogenesis and prevention of urinary tract infection in women].

Urinary tract infection (UTI) in females occurs significantly more frequently than in males because of specific anatomical and functional features of female urinary system, sequelae of pregnancy, delivery, gynecological diseases. Much controversy still exists as to pathogenesis of UTI and UTI-induced urinary inflammation. We have examined 233 females of different age with UTI and obtained evidence which shows participation of such factors as early and intensive sex, ignorance of sex hygiene, multiple pregnancies, deliveries, abortions, inflammatory gynecological diseases, anogenital infection in its pathogenesis. These factors were registered 2-4 times more frequently in UTI females than in controls without UTI. Bacteriological urinary and genital findings coincide in 80% of cases in terms of an infective agent. This suggests that it is essential to detect urogenital infection in girls and females as early as possible and to treat it adequately with antibacterial and other drugs. The leading role of an ascending urinogenic route in urinary tract infection from local sources in anogenital zone, sexual factor and the absence of relevant hygienic habits proved most contributing to UTI pathogenesis. This concept serves the basis for UTI prevention in females.

Bacteria↗
PubMed1994

Histogenesis and pathogenesis of follicular small cleaved cell lymphoma (FSCCL), diffuse small cleaved cell lymphoma (DSCCL) and intermediate lymphocytic lymphoma/lymphocytic lymphoma of intermediate differentiation (ILL/IDL).

We have investigated the cellular origin and/or pathogenesis of follicular small cleaved cell lymphoma (FSCCL), diffuse small cleaved cell lymphoma (DSCCL) and intermediate lymphocytic lymphoma/lymphocytic lymphoma of intermediate differentiation (ILL/IDL) based on a series of immunologic and molecular genetic (bcl-1, bcl-2 and bcl-3 genes) studies. These studies have led to the conclusion that the cellular origin or pathogenesis of ILL/IDL and DSCCL is distinctly different from that of FSCCL: (1) FSCCL is a neoplastic counterpart of follicular center cells (FCC) of secondary follicles because of the presence of CD10 and bcl-2 gene rearrangement and the absence of CD5 and bcl-1 gene rearrangement; (2) DSCCL and ILL/IDL are a neoplastic counterpart of mantle zone (MZ) B lymphocytes because of the presence of CD5 and bcl-1 gene rearrangement and absence of CD10 and bcl-2 gene rearrangement; and (3) FSCCL scarcely develops into DSCCL, and the previously proposed concept that DSCCL represents a diffuse counterpart of FSCCL does not hold good. These results indicate that DSCCL and ILL/IDL are identical, derived from primary follicular cells or MZB cells of secondary follicles, and should be unified under MZB lymphocyte-derived lymphomas. They are distinguished from FCC-derived lymphomas in morphologic, immunologic, cytogenetic and molecular genetic features. Bcl-1 and bcl-2 genes may be associated with the pathogenesis of FCC-derived lymphoma and MZB lymphocyte-derived lymphoma, respectively.

Antigens, CD↗
PubMed1995

[Gastroduodenal ulcer disease: update on pathogenesis].

Gastroduodenal ulcer disease comprises a heterogeneous group of different diseases resulting uniformly in a mucosal defect reaching beyond the muscularis mucosae. Consequently, a single unifying pathogenesis of ulcer disease does not exist but only a rather general concept that ulcers develop when mucosa-injuring factors outweigh the mucosa-protecting factors. According to this concept, ulcers develop within a broad range of different possibilities in the relation of mucosa-injuring factors to impaired mucosal protection. The main histological and physiological elements for the understanding of peptic ulcer disease are briefly summarized, followed by a short survey of the important known 'traditional' abnormalities of possible pathogenetic importance in duodenal and gastric ulcer patients. Gastroduodenal ulcer disease represents a typical example of a multifactorial disease, where different combinations of both hereditary and environmental factors produce the same morphological lesion. By far the most exciting data of the last ten years originate from the still increasing understanding of the role of Helicobacter pylori in gastroduodenal ulcer disease. The most important evidence and hypotheses are presented of how and where Helicobacter pylori is or could be involved in the complicated pathogenetic network of ulcer disease. The infection of gastric epithelium by Helicobacter pylori has become the second main factor besides acid/pepsin in the pathogenesis of ulcer disease. Beside the improved insights in ulcer pathogenesis, the translation of the new data into clinical medicine has led and will lead to remarkable progress. Most important: a causal therapy of ulcer disease has become available in contrast to the so far practiced sole symptomatic treatment of single ulcer episodes. What has treatment of single ulcer episodes. What has been a domain of ulcer surgery has come into reach of drug therapy.

Anti-Bacterial Agents↗
PubMed1994

Insights into the role of thromboxane A2 and serotonin in the pathogenesis of unstable angina.

New research about platelet and endothelial functions is allowing us to better understand the pathogenesis of myocardial ischemic episodes in patients with unstable angina, creating new perspectives for the rational utilization of therapies. In patients with unstable angina, the episodes of symptomatic and silent ischemia are caused by repeated reductions of coronary blood flow. They are the result of the mechanical effect of the growing thrombus, which causes intermittent episodes of partial obstruction of the arterial lumen, in association with vasoconstriction at the stenotic site and dependent coronary arterial bed, produced by the cyclic release of platelet derived vasoactive products, namely thromboxane A2 and serotonin. Several studies, many of them in animal models of thrombosis, suggest that serotonin and thromboxane A2 are mediators of platelet aggregation, adynamic obstruction and coronary artery thrombosis. Because they cause coronary cyclic flow reductions, they are implicated in the pathogenesis of myocardial ischemic episodes during unstable angina. Drugs that interfere with the arachidonate pathway, and the 5-HT2-receptor antagonists, have been proven to decrease or abolish coronary cyclic flow variations in animal models and man. However, further studies should be done to test the hypothesis that the association of a 5-HT2-receptor antagonist with aspirin may contribute to decrease myocardial ischemia and prevent coronary occlusion in patients with unstable angina. Continuous Holter monitoring during the first week after admission in the hospital should be a good method to evaluate the eventual efficacy of this new class of drugs in abolishing or decreasing the frequency, intensity and duration of myocardial ischemic episodes in patients with unstable angina. The central role of serotonin in the pathogenesis of thrombotic events, and the presumed preventive effect of ketanserin, were the bases of a national multicenter pilot controlled study designed to evaluate the safety and efficacy of ketanserin plus aspirin in the secondary prevention of patients with unstable angina and non-Q wave myocardial infarction (KATUA Trial).

Angina, Unstable↗
PubMedDate not supplied

[Hemostatic-vascular interactions in the pathogenesis and the treatment of adult respiratory distress syndrome].

The complex pathophysiologic alterations occurring in adult respiratory distress syndrome (ARDS) result from the interaction of various humoral and cellular mediators. In this review we examine the events that lead to acute pulmonary injury as discussed in the recent literature as well as the correlations among humoral systems and cell activation involved in the pathogenesis of ARDS. We also consider the mechanisms inducing the appearance of adhesive molecules (ELAM-1 and ICAM-1) on the surface of endothelial cells, the importance of complement and clotting activation, and the role of monocyte-macrophages, platelets and neutrophils. The complexity of alterations among the different mediators involved in the pathogenesis of ARDS is underscored by experimental results demonstrating how the pharmacologic blockade of each system cannot completely prevent the development of lung damage. Understanding of the complex processes involved in the pathogenesis of ARDS provides new prospects for its treatment, such as inhalational nitric oxide and aerosolised prostacyclin. The most promising approach involves the use of monoclonal antibodies which may enable the selective inhibition of different mediators and endotoxins.

Humans↗
PubMed1994

[Brief analytical review of additional possible mechanisms in the pathogenesis of AIDS].

It is generally agreed that HIV itself has the primary role in the initiation and propagation of the pathogenic process of the infection. Nonetheless, a number of important issues concerning the pathogenesis of HIV infection remain unresolved. For example, it remains unclear how CD4+ T cells are lost after HIV infection. The low frequency of infected cells seen even in advanced infection implies that a direct cythopathic effect of HIV on infected CD4+ T cells cannot explain their disappearance. Multiple and diverse mechanisms have been proposed as supplements to the HIV in the destruction of CD4+ cells and the pathogenesis of AIDS. However, it is not yet possible to state confidently which additional mechanism(s) is important. Identification of the nature of this supplemental process has become essential for successful, non-harmful intervention. We propose here a short analytical review of the possible supplemental mechanisms of immunological destruction in AIDS in order to emphasize the complexity of the pathogenesis of the disease.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Insulin resistance, hypersecretion of LH, and a dual-defect hypothesis for the pathogenesis of polycystic ovary syndrome.

OBJECTIVE: To review the literature dealing with the roles of insulin resistance and elevated LH levels in the development of the polycystic ovary syndrome and to outline a new hypothesis of the pathogenesis of this disorder. DATA SOURCES: We reviewed articles on the topics of insulin resistance, elevated LH levels, and polycystic ovary syndrome that were contained in the CD-PLUS MEDLINE system data base for years 1976-1994. METHODS OF STUDY SELECTION: Ninety-one original reports published in English-language, peer-reviewed biomedical journals were selected. DATA EXTRACTION AND SYNTHESIS: The selected studies were reviewed critically and their conclusions were evaluated. The available literature indicates that insulin resistance and increased LH secretion are frequent features of polycystic ovary syndrome and may be important in its pathogenesis. It appears that both the amplitude and the frequency of LH pulses are increased in this disorder. Although the causes of these abnormalities of LH secretion are unknown, they could be either primary (due to increased sensitivity of LH secretion to GnRH) or secondary (due to the effects of sex steroids on LH secretion). The cause of insulin resistance in polycystic ovary syndrome also is unknown. It most likely results from a post-binding defect in the insulin action pathway. There is both in vitro and in vivo evidence that elevated LH and hyperinsulinemia act synergistically to enhance ovarian growth, androgen secretion, and ovarian cyst formation. CONCLUSIONS: Based on the available literature, we propose a "dual-defect" hypothesis of polycystic ovary syndrome. We suggest that in a significant subset of patients, this disorder may be caused by a conjunction of two independent genetic defects: one that produces elevated LH secretion and another that produces insulin resistance. Thus, polycystic ovary syndrome develops as a result of the synergistic action of increased LH levels and hyperinsulinemia on the ovary. This working hypothesis may serve as a useful guide for further studies of the pathogenesis of polycystic ovary syndrome.

Female↗
PubMed1994

[Pathogenesis and treatment of hepatic encephalopathy].

Cirrhotic patients with hepatic encephalopathy show a variety of neuropsychiatric abnormalities. The pathogenesis appears to be ascribable to an increase in gut-derived neurotoxic substances and to functional alteration in inhibitory and excitatory neurotransmission in the brain. On the basis of the potential pathogenesis, therapies are designed by reducing the production and absorption of gut-derived neurotoxins and/or by modifying the balance of central neurotransmission. In this review, the current concept of the pathogenesis and treatment of hepatic encephalopathy is described.

Anti-Bacterial Agents↗
PubMed1994

[A study of pathogenesis and symptoms of Tourette's syndrome--mainly on the importance of "startle reflex" through Latah reaction].

There is no established theory on pathogenesis of Tourette's syndrome, but recently, a theory of the British school of behaviorism; 'transient tics' and the more serious case, Tourette's syndrome which ensues on the fixation of the startle reflex, have received attention. So we determined, whether pathogenesis and symptoms of Tourette's syndrome could be systematically explained by "the startle reflex theory". Authors assumed that the startle reflex was composed of two divided actions, a series of muscular movements which started with eye blinks and terminated in the flexion of lower limbs (the primary startle reflex system), and more purposeful and complicated actions which occasionally arose from these movements (the secondary startle reflex system). On the basis of this supposition, we considered simple tics which are usually called "tics", those are the manifestation of astonishment by the primary startle reflex system, and complex tics; echo phenomena, coprolalia, complex movements, and so on, which are said to be pathognomonic of Tourette's syndrome, are the expression of amazement by the secondary startle reflex system. Furthermore, we formulated a hypothesis that in the latter case, the secondary startle reflex system contains the senses of orientation and defense, and the defense mechanism which is innately imprinted in common throughout human race, and covered through individual development, is released and fixed in the form of complex movements or echo phenomena in an emergency, such as astonishment. To discuss further, we determined Latah reaction minutely (especially in "Imu" of the Ainu race in Japan) in which intricate symptoms had been suggested as one of the senses of defense, were closely related to Tourette's syndrome. For more concrete study, we presented two severe cases of Tourette's syndrome. Considering the circumstances mentioned above, pathogenesis and symptoms of Tourette's syndrome could be explained by the startle reflex theory. Finally, we analyzed several psychiatrical syndromes which were provoked by astonishment, we concluded that it was necessary to emphasize Tourette's syndrome was only a part of those more comprehensive syndromes which could be called "startle syndromes".

Adult↗
PubMed1993

Relevance of tumour necrosis factor-alpha and interleukin-1-alpha in the pathogenesis of hypoxia-related organ failure.

Tumour necrosis factor-alpha (TNF) and Interleukin-1-alpha (IL-1) are both cytokines which are known to be released by stimulated macrophages during septic events. Because of their influence on the function of the vascular endothelium, TNF and IL-1 contribute to the pathogenesis of hypoperfusion and organ dysfunction. The finding of elevated cytokine levels in patients with hypoxic organ failure, suggesting a relation between systemic oxygen supply and humoral mechanisms, led us to perform laboratory investigations on the relevance of TNF and IL-1 for the pathogenesis of hypoxia-related deterioration of the microcirculation. In vivo studies with anaesthetized rats demonstrated a synergism between hypoxaemia and endotoxaemia on the development of lethal organ failure. In vitro studies with human monocytes showed that a hypoxic atmosphere was not able to induce synthesis or release of TNF and IL-1, whereas re-oxygenation after hypoxia initiated a significant increase in TNF and IL-1 synthesis, probably mediated by oxygen radicals. Finally, experiments with human endothelial cells established that hypoxia is able to induce high affinity receptors for TNF in a time- and dose-dependent manner. These studies demonstrate that hypoxia influences humoral mechanisms which are known to contribute to the pathogenesis of vessel dysfunction, probably through a cytokine-dependent pathway of hypoxia-related organ dysfunction.

Animals↗
PubMed1993

Bronchoalveolar lavage and the study of proteinases and antiproteinases in the pathogenesis of chronic obstructive lung disease.

Bronchoalveolar lavage has been used for 15 yrs to investigate the role of proteinases and antiproteinases in the pathogenesis of emphysema, but the results are confused by numerous technical factors, many of which may prove insurmountable. Even if the problems can be overcome, the technique will probably not prove sensitive enough to provide a true insight into the pathogenesis of emphysema in man. Nevertheless, the studies with this technique have provided important information and methodologies that have advanced our scientific, if not pathological, knowledge. Perhaps further applications of the knowledge obtained, to cellular and genetic studies, will eventually establish the true mechanisms involved in determining whether a smoker remains "healthy" or develops disabling disease. Lavage may have played a major role in the study of emphysema, if for no other reasons than to establish the fact that the pathogenesis of the disease is far from clear.

Bronchoalveolar Lavage Fluid↗