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At least 19 recordsLinked to original sources
PubMed1995

The human glioma pathogenesis-related protein is structurally related to plant pathogenesis-related proteins and its gene is expressed specifically in brain tumors.

We report the cloning of a cDNA encoding GliPR (glioma pathogenesis-related protein), a protein that is structurally similar to plant pathogenesis-related proteins. The GLIPR gene is highly expressed in the human brain tumor, glioblastoma multiforme/astrocytoma, but neither in normal fetal or adult brain tissue, nor in other nervous system tumors. GliPR shares up to 50% amino acid (aa) homology with plant pathogenesis-related proteins, group 1, over a region that comprises almost two thirds of the protein. We speculate that there may be functional similarities between the human and plant proteins as well.

Amino Acid Sequence↗
PubMed1987

Biological function of pathogenesis-related proteins: Four tobacco pathogenesis-related proteins are chitinases.

Four endochitinases (poly[1,4-(N-acetyl-beta-D-glucosaminide)] glycanohydrolase, EC 3.2.1.14) have been purified from leaves of Nicotiana tabacum cv. Samsun NN reacting hypersensitively to tobacco mosaic virus. Two of them are acidic proteins of molecular weights 27,500 and 28,500 and have been identified as 2 of the 10 pathogenesis-related proteins that are known to accumulate in tobacco in response to stress or pathogen attack. These two pathogenesis-related proteins, named "P" and "Q" when their biological function was unknown, account for one-third of tobacco mosaic virus-induced chitinase activity of tobacco leaves. They are serologically closely related to the two other chitinases, which can be considered as new basic pathogenesis-related proteins. These two basic chitinases exhibit higher molecular weights (32,000 and 34,000) and higher specific enzyme activity than the two acidic isoforms.

Journal Article↗
PubMed1992

Pathogenesis, treatment and prognosis of impending myocardial infarction and early post-infarction angina--relation between ST-segment shift during myocardial ischemia and the pathogenesis.

We studied 141 patients to evaluate the pathogenesis and clinical picture of high-risk unstable angina (UA), designated as impending myocardial infarction (IMI) in this study, or severe early post-infarction angina (PIA). IMI and PIA were diagnosed when chest pain appeared at rest and lasted 15 min or more despite extensive pharmacological therapy during hospital stay among consecutive 510 patients with UA. All patients underwent coronary angiography urgently within 72 h after chest pain, and were divided into 2 subgroups according to ST segment shifts during chest pain. In IMI, 42 patients with ST depression had higher incidences of prior myocardial infarction (MI), worsening UA, multivessel disease and complex lesions such as eccentric irregular lesion or ulceration. On the contrary, in 44 with ST elevation, new onset UA, single vessel disease and coronary thrombus (CT) were dominant. In PIA, 32 patients with ST elevation revealed higher incidences in Q wave MI, ST elevation at the MI onset, single vessel disease and CT, compared to 23 with ST depression who showed a high proportion of complex lesions. Thus, it was evident that there was a common link between the pathogenesis of IMI and PIA. The therapeutic options were also different in the groups according to ST segment shift. We conclude that ST segment shifts during chest pain may be useful for determining the pathogenesis and clinical features of high-risk UA.

Angina, Unstable↗
PubMed1998

Structure comparison of human glioma pathogenesis-related protein GliPR and the plant pathogenesis-related protein P14a indicates a functional link between the human immune system and a plant defense system.

The human glioma pathogenesis-related protein (GliPR) is highly expressed in the brain tumor glioblastoma multiforme and exhibits 35% amino acid sequence identity with the tomato pathogenesis-related (PR) protein P14a, which has an important role for the plant defense system. A molecular model of GliPR was computed with the distance geometry program DIANA on the basis of a P14a-GliPR sequence alignment and a set of 1,200 experimental NMR conformational constraints collected with P14a. The GliPR structure is represented by a group of 20 conformers with small residual DIANA target function values, low AMBER-energies after restrained energy-minimization with the program OPAL, and an average rms deviation relative to the mean of 1.6 A for the backbone heavy atoms. Comparison of the GliPR model with the P14a structure lead to the identification of a common partially solvent-exposed spatial cluster of four amino acid residues, His-69, Glu-88, Glu-110, and His-127 in the GliPR numeration. This cluster is conserved in all known plant PR proteins of class 1, indicating a common putative active site for GliPR and PR-1 proteins and thus a functional link between the human immune system and a plant defense system.

Amino Acid Sequence↗
PubMed2006

Rapid pathogenesis induced by a vesicular stomatitis virus matrix protein mutant: viral pathogenesis is linked to induction of tumor necrosis factor alpha.

Vesicular stomatitis virus (VSV) matrix (M) protein blocks host mRNA export from the nucleus and thereby inhibits interferon induction in infected cells. M mutants with mutations of methionine 51 (M51) lack this shutoff function. We examined pathogenesis of a VSV M mutant with a deletion of M51 (VSVDeltaM51) after intranasal infection of BALB/c mice and found an unexpected phenotype. Mice that received VSVDeltaM51 experienced a more rapid but overall less severe weight loss than mice that received the recombinant wild-type VSV (rwtVSV). Rapid weight loss was not explained by faster initial replication because VSVDeltaM51 replication was controlled faster than rwtVSV replication in the lungs and did not spread systemically like rwtVSV. This faster control of VSVDeltaM51 correlated with a more rapid induction of interferon in the lung. Because tumor necrosis factor alpha (TNF-alpha) is associated with weight loss, we examined TNF-alpha induction in mice infected with rwtVSV or VSVDeltaM51. We found more-rapid induction of TNF-alpha by the mutant at early times after infection, while rwtVSV induced more TNF-alpha later in infection. This result suggested that TNF-alpha induction might explain both the rapid weight loss caused by the mutant and the overall greater weight loss caused by the rwtVSV. Using TNF-alpha knockout mice (C57BL/6 background), we showed that weight loss following rwtVSV infection was greatly reduced in the absence of TNF-alpha. Although the rapid weight loss caused by VSVDeltaM51 was less pronounced in C57BL/6 mice, it was eliminated in the absence of TNF-alpha. These results indicate a role for TNF-alpha in the pathogenesis of VSV.

Administration, Intranasal↗
PubMed2002

The immunogenetics and pathogenesis of gastric cancer. Highlights of the First Sino-European Workshop on the Immunogenetics and Pathogenesis of Gastric Cancer.

Clinical scientists from eight European countries and China gathered in the ancient Chinese capital of Xi'an on April 26-28, 2001 to discuss collaboration on a modern approach to gastric cancer prevention. Participants at the First Sino-European Workshop on Immunogenetics and Pathogenesis of Gastric Cancer presented their most up-to-date research results on topics ranging from epidemiology and immune mechanisms to Helicobacter pylori and vaccine development. Researchers then formed groups with their Chinese or European counterparts to plan future research endeavors which will benefit Chinese and European populations alike. After 3 years of organization between the Institute of Digestive Diseases of the Fourth Medical University in Xi'an, China and the Laboratory of Immunogenetics, VU University Medical Center in Amsterdam, the first workshop came into being under the joint sponsorship of the Commission of the European Union, National Natural Science Foundation of China and the Institute of Digestive Diseases, Xi'an, China. As gastric cancer is the most prevalent malignant tumor in China, the workshop was of special significance to the Chinese researchers and to the Chinese population in general. During the workshop, presentations on the epidemiology of gastric cancer showed that this disease is in fact common the world over: it is the second most common cancer next to lung cancer and about 1 million new cases were diagnosed in 2000. Three-quarters of the cases of gastric cancer occur in Asia, and approximately 80% of these cases are in China and Japan. Genetic factors and environmental factors such as diet and H. pylori infection play a role in gastric carcinogenesis. As a recognized cause of gastric cancer, H. pylori was the subject of various presentations ranging from immunological studies, molecular analysis of strains and pathogenesis to vaccine development. Specific areas of discussion included bacterial-epithelial interactions in H. pylori infection, epidemiology in China, global distribution of vacA and cagA genotypes, new evidence for host factors, nonsteroidal antiinflammatory drugs and H. pylori as independent risk factor for gastric cancer, new diagnostic techniques for H. pylori using serum levels of pepsinogen I, and autoimmune processes in corpus atrophy. Vaccine development using a variety of strategies against H. pylori was the subject of an entire session of talks. Oral immunization with urease with Escherichia coli heat labile enterotoxin was shown to be safe and immunogenic in humans as a mucosal adjuvant. Results of a study using attenuated Salmonella typhimurium as a vehicle for DNA-mediated immunization in mice were also presented. A final presentation discussed an ongoing trial comparing strain variability in the vacA and cagA gene sequences and disease expression between H. pylori infection in Europe and China. Researchers also discussed the role of IL1 gene family and TNF gene polymorphisms in gastric pathology and various immune mechanisms involved in gastric cancer, such as down-regulation of NF kappa B, IL-1 and IL-1RA, cyclooxygenase signalling, and identification of MGAg antibodies. An interactive discussion followed each presentation and ideas and suggestions were provided. According to specialty, the presenters were then assigned to groups of four or five to make plans for joint research projects. A number of international and Chinese observers were present, including representatives from the European Commission, the World Health Organization and the Chinese National Center for Biotechnology Development, and offered input on the financial feasibility of such projects.

China↗
PubMed2000

Pathogenesis of atherosclerosis: infectious versus immune pathogenesis. A new concept.

A novel concept for the pathogenesis of atherosclerosis is presented that obviates the need to search for a causative infectious agent. It is shown that LDL stranded in the subendothelium is transformed by enzymatic (non-oxidative) modification to yield an entity with complement- and macrophage-activating properties. This primarily serves to clear the stranded lipoprotein from tissues. However, sustained overactivation of complement and macrophages occurs when LDL-deposition is too extensive. A chronic inflammation then ensuing initiates and promotes the pathology of the atherosclerotic lesion. Atherosclerosis is thus a special form of an immunopathological disease which evolves through overactivation of the most archaic effector components of the immune system by altered self.

Animals↗
PubMed1991

Degradation of tobacco pathogenesis-related proteins : evidence for conserved mechanisms of degradation of pathogenesis-related proteins in plants.

Tobacco (Nicotiana tabacum L.) leaves were found to contain an extracellular proteinase that endoproteolytically cleaves tobacco pathogenesis-related (PR) proteins. This proteinase was partially purified from tobacco leaves and characterized as an aspartyl proteinase with a pH optimum around pH 3 and a molecular mass of 36,000 to 40,000 daltons. In vitro, the enzyme cleaved purified tobacco and tomato PR proteins into discrete fragments. The characteristics of this proteinase were similar to pepsin and identical to those displayed by a previously described tomato 37-kilodalton aspartyl proteinase active against tomato PR proteins (I Rodrigo, P Vera, V Conejero [1989] Eur J Biochem 184: 663-669), suggesting that these extracellular proteases could play a role in a conserved mechanism for PR protein turnover in plants.

Journal Article↗
PubMedDate not supplied

[Experimental study of the pathogenesis of frostbite. Part III. Significance of energy status of muscle tissue in the pathogenesis of frostbite].

The authors have investigated energy status of muscle tissue of the lower legs of Wistar rats subjected to freezing, as well as the dependence of ultrastructure changes in muscle tissue mitochondria on the intensity of freezing. The animals were divided into three experimental groups: two groups were exposed to cryoinjury of different intensity, while the third was the control one. Cryoinjury was applied over an experimental after thawing were taken samples of muscle tissue for the analysis of content of energy phosphates and carbohydrates' metabolites, respectively, as well as for morphometric analysis of mitochondria volume out of frozen right and unfrozen left lower legs. Results obtained from different experimental groups were compared mutually and with control group that was not exposed to cryoinjury, respectively. It was found that the freezing in muscle tissue caused hydrops degeneration of mitochondria, depletion of energy reserves, reduction of energy status and the activation of mechanism of anaerobic metabolism. All these alterations were proportional to the intensity of freezing and considerably influenced contractility function of muscle cells, causing prolonged spasm of arterioles in thawed tissue, i.e., rigor congelationis that was primarily defined as an important factor in the pathogenesis of ischemic impairment of thawed tissues.

Animals↗
PubMed1986

The natural history and pathogenesis of the cranial coronal ring articulations: implications in understanding the pathogenesis of the Crouzon craniostenotic defects.

The craniostenotic birth defects seen in patients with Crouzon syndrome have prompted this developmental study on the system of articulations between the human frontal, sphenoid, and ethmoid bones. The Crouzon facies, including midfacial hypoplasia and exorbitism, have been linked to the premature synostosis of calvarial sutures. However, considerable evidence shows that midfacial positioning is linked to increasing length of the midline cranial base. Thirty-seven typical-for-age (8 to 29 weeks) embryos were histologically prepared, read serially, and three-dimensionally reconstructed to map the so-called coronal ring articulations that continuously join the frontal, sphenoid, and ethmoid bones. A morphologic staging plan was used to show the progressive development of bones and intervening joints. Data show that a coronal ring exists beginning at 8 weeks. Those portions of the ring separating the frontal and sphenoid bones (within the orbit and laterally along the coronal suture) show the typical structure of a five-layered suture. This sutural component of the ring is C-shaped with a cartilaginous bridge between the optic foramina completing the ring. This is the sphenoethmoidal (S-E) synchondrosis of the midline cranial base. It is suggested that this deeply located cartilage joint is the primary site of pathogenesis in the craniostenotic facies and not the coronal sutures which are operated upon. Even though the S-E cartilage would be difficult and potentially morbid to approach surgically, this study would suggest that preoperative computed tomography (CT) of the skull base with special emphasis on the S-E region may provide a better prognosis regarding midface growth effects after surgery. It appears to be the fused S-E synchondrosis and not necessarily the premature closure of the coronal sutures that may tether the midface posteriorly.

Adult↗
PubMed1980

[New viewpoints on the pathogenesis and the treatment of strabismus. First part: pathogenesis of strabismus (author's transl)].

In 1962 the anteroposition of the inferior oblique muscle has been introduced. This surgery enlarges the angle between the muscle and the visual axis favouring the torsional action at the cost of the vertical one. The results of 554 cases with a postoperative follow-up of at least ten years are analysed. The spontaneous recovery of binocular vision and the disappearance of the accommodative component suggest that a sagittalization of the oblique muscles might be an important cause of strabismus. The evolution of the suppression scotoma demonstrates that the position of the eyes depends on the optomotor balance between the nasal and temporal retinal halves. A new concept of the pathogenesis of squint is presented. The sagittalization of the oblique muscles and the hemiretinal suppression are considered to be the keys by means of which the problem of strabismus could be solved.

Adult↗