Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three dogs (two Rottweilers and a Flat-coated retriever) showed various neurological signs, including apathy, depression, circling, a partial decrease in functions associated with cranial nerves, seizures, hyperaesthesia, proprioceptive deficits, and increased spinal reflexes. In all three cases, necropsy revealed a solid, distinct, white mass in the brain and multiple, poorly demarcated, firm nodular proliferations in the lung; in one case the liver was also affected. Histopathological examination showed loosely aggregated, pleomorphic cells, with abundant eosinophilic cytoplasm. The neoplastic cells sometimes contained vacuoles or phagocytized cells. Binucleated and multinucleated giant cells, and mitotic figures, were common. Immunohistochemically, the tumour cells reacted strongly for lysozyme and vimentin, but there was no reaction for S-100 protein, cytokeratin, CD3 or CD79a. The histological and immunohistochemical examinations indicated a histiocytic origin of the tumour cells and malignant histiocytosis was therefore diagnosed.
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PMID:Malignant histiocytosis of the brain in three dogs. 1653 81

Immune status during fracture of lower jaw is a very important factor of pathogenesis. Immune depression is developing shortly after the trauma and it turns out to be a bad prognostic sign, during which the risk of developing the bone wound complications and traumatic osteomyelitis increase, and in case of absence of such complications we are faced with significant extension of a term of healing of bone wounds. We have carried out immune studies in 20 patients with lower jaw fractures. To study SlgA and lysozyme activity we took saliva and studied percentage of T- and B-lymphocytes (and their sub-populations) in blood by the use of micro method. Immunoglobulins were defined by the method of radial immuno diffusion; we determined the interferon system by in vitro stimulation of leucocytes; neutrophilic phagocyte activity was studied by the method of Kost U.A. and Stepko M.I. According to the obtained results, during fractures of lower jaw sharp decrease of interferon system and significant decrease of phagocyte activity was observed. Likewise was decreased lysozyme and SlgA indices, which refer to the depression of immune status of mouth cavity. From the cell immunity indices the decrease of T-activators and T-helpers and reduction of immunoregulation index should be emphasized. Quantity of B-lymphocytes was decreased by 10%. With the practical point of view the obtained results refer, alongside with carrying out the surgical, orthopedic and anti-microbial treatments, to the urgency of application of activators of phagocytosis, interferon and lysozyme immunomodulators. With the view of correction of cell immunity it is necessary to correct factors of T-lymphocytes and to increase activity of SigA and lysozyme, as the factors determining local resistance. The results obtained by us are rather important with the view of both immunology and applied, practical medicine. It enables us to lead the substantiated immune therapy, which will be harmonized with other etiotropic anti microbial therapy and will help us to improve significantly the results of anti-inflammation therapy and to decrease cases of purulent complications.
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PMID:Immune status during fracture of lower jaw. 1657 47

Levamisole, originally synthesized as an anti-helminthic, has been widely used in human and veterinary medicine as an immunomodulator or adjuvant. However, data on its use in fish are scarce, and no information is available for turbot. To study the effects of levamisole treatment on the innate immune system of juvenile turbot, two different doses (D1=500 mg/kg; D2=250 mg/kg dry food) were orally administered for 2 weeks and samplings were performed at -10, 14, 28, 49 and 77 days post treatment (p.t.). Biometrical, haematological, histological and immunological data were obtained. Specific growth rate was higher in the medicated groups than in the control (C), but the difference was statistically significant only for D1 fish at day 49 p.t. The leucocytes/thrombocytes ratio was significantly higher in D1 than in C fish at 14 days p.t., but decreased subsequently. At most samplings, the percentage of the circulating lymphocytes was lower and that of the progranulocytes was higher in the medicated fish than in the C ones. The percentage of fish with high haemotopoietic activity in the kidney was clearly higher in D1 and D2 fish than in C ones at some sampling points. The respiratory burst activity of blood leucocytes was significantly higher in D1 fish than in C ones in all samplings, except at day 77 p.t. when control fish experienced a rebound effect. In all medicated fish, an initial increase of such activity was observed, followed by a further decrease. Their serum peroxidases followed a contrary pattern, with a decrease in the second sampling and a subsequent and non-significant recovery, a situation also observed for serum lysozyme and complement. Therefore, oral levamisole treatment actually affects some turbot immune factors, although stimulation or depression can occur depending on the considered factor and the administered dose. These results point out the interest of further studies on the mechanisms involved in the levamisole action for its adequate use as immunomodulator.
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PMID:Levamisole activates several innate immune factors in Scophthalmus maximus (L.) Teleostei. 1716 95

We previously showed that lysozyme (Lzm-S), derived from leukocytes, caused myocardial depression in canine sepsis by binding to the endocardial endothelium to release nitric oxide (NO). NO then diffuses to adjacent myocytes to activate the cGMP pathway. In a canine right ventricular trabecular (RVT) preparation, Lzm-S also decreased the inotropic response to field stimulation (FSR) during which the sympathetic and parasympathetic nerves were simulated to measure the adrenergic response. In the present study, we determined whether the pathway by which Lzm-S decreased FSR was different from the pathway by which Lzm-S reduced steady-state (SS) contraction. Furthermore, we determined whether the decrease in FSR was due to a decrease in sympathetic stimulation or enhanced parasympathetic signaling. In the RVT preparation, we found that the inhibitory effect of Lzm-S on FSR was prevented by NO synthase (NOS) inhibitors. A cGMP inhibitor also blocked the depressant activity of Lzm-S. However, in contrast to the Lzm-S-induced decline in SS contraction, chemical removal of the endocardial endothelium by Triton X-100 to eliminate endothelial NO release did not prevent the decrease in FSR. An inhibitory G protein was involved in the effect of Lzm-S, since FSR could be restored by treatment with pertussis toxin. Atropine prevented the Lzm-S-induced decline in FSR, whereas beta(1)- and beta(2)-adrenoceptor function was not impaired by Lzm-S. These results indicate that the Lzm-S-induced decrease in FSR results from a nonendothelial release of NO. NO then acts through inhibitory G protein to enhance parasympathetic signaling.
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PMID:Lysozyme, a mediator of sepsis, impairs the cardiac neural adrenergic response by nonendothelial release of NO and inhibitory G protein signaling. 1776 78

Cardiovascular dysfunction in septic shock (SS) is ascribed to the release of inflammatory mediators. Norepinephrine (NE) is often administered to treat low MAP in SS. We recently found that lysozyme c (Lzm-S) released from leukocytes was a mediator of myocardial depression in an Escherichia coil model of SS in dogs. This effect can be blocked in an in vitro preparation by chitobiose, a competitive inhibitor of Lzm-S. In the present study, we examined whether chitobiose treatment can reverse myocardial depression and obviate NE requirements in two respective canine E. coli preparations. In a 6-h study, we administered chitobiose after 3.5 h of E. coli bacteremia and compared stroke work (SW) and MAP at 6 h with a sepsis control group. In a 12-h study, we determined whether chitobiose treatment can reduce the need for NE requirements during 12 h of bacteremia. In the latter study, either chitobiose or NE was given when MAP decreased approximately 20% from the presepsis value in respective groups. In anesthetized, mechanically ventilated dogs, we monitored hemodynamic parameters during continuous E. coli infusion. In the 6-h study, chitobiose improved SW and MAP at the 6-h period as compared with the nontreated sepsis group. In the 12-h study, SW and MAP increased after chitobiose without the necessity of NE administration. These results suggest that inhibitors of Lzm-S such as chitobiose may improve myocardial depression and reduce the need for NE requirements in SS.
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PMID:N,N'-diacetylchitobiose, an inhibitor of lysozyme, reverses myocardial depression and lessens norepinephrine requirements in Escherichia coli sepsis in dogs. 1788 42

In septic shock, systemic vasodilation and myocardial depression contribute to the systemic hypotension observed. Both components can be attributed to the effects of mediators that are released as part of the inflammatory response. We previously found that lysozyme (Lzm-S), released from leukocytes, contributed to the myocardial depression that develops in a canine model of septic shock. Lzm-S binds to the endocardial endothelium, resulting in the production of nitric oxide (NO), which, in turn, activates the myocardial soluble guanylate cyclase (sGC) pathway. In the present study, we determined whether Lzm-S might also play a role in the systemic vasodilation that occurs in septic shock. In a phenylephrine-contracted canine carotid artery ring preparation, we found that both canine and human Lzm-S, at concentrations similar to those found in sepsis, produced vasorelaxation. This decrease in force could not be prevented by inhibitors of NO synthase, prostaglandin synthesis, or potassium channel inhibitors and was not dependent on the presence of the vascular endothelium. However, inhibitors of the sGC pathway prevented the vasodilatory activity of Lzm-S. In addition, Aspergillus niger catalase, which breaks down H(2)O(2), as well as hydroxyl radical scavengers, which included hydroquinone and mannitol, prevented the effect of Lzm-S. Electrochemical sensors corroborated that Lzm-S caused H(2)O(2) release from the carotid artery preparation. In conclusion, these results support the notion that when Lzm-S interacts with the arterial vasculature, this interaction results in the formation of H(2)O(2), which, in turn, activates the sGC pathway to cause relaxation. Lzm-S may contribute to the vasodilation that occurs in septic shock.
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PMID:Lysozyme, a mediator of sepsis that produces vasodilation by hydrogen peroxide signaling in an arterial preparation. 1826 14

A 2-year-old, spayed female domestic shorthair cat was referred with a history of anorexia and depression of 1 week duration. On physical examination, the cat was lethargic and febrile, with splenomegaly, anisocoria and ulcerative stomatitis. A complete blood count (CBC) and a biochemistry profile showed leukocytosis, numerous blast cells in the peripheral blood, thrombocytopenia, hyperglobulinaemia and a positive test for feline leukaemia virus antigen. A diagnosis of acute myelomonocytic leukaemia was made on the basis of the results of bone marrow cytology, histopathology, and immunochemistry (CD3, CD79a, lysozyme, and myeloperoxidase) tests. Following an unexpected 1-month period of clinical and clinicopathological remission without chemotherapy, the cat relapsed and died 1 week later.
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PMID:Acute myelomonocytic leukaemia with short-term spontaneous remission in a cat. 1849 58

Malignant histiocytosis (MH) is a progressive systemic neoplastic proliferation of morphologically atypical histiocytes, well characterised in humans and dogs but only recently identified in the cat. In all species, liver, lung, lymph nodes, spleen and bone marrow are infiltrated by atypical histiocytes, and the disease is rapidly fatal. The purpose of this study was to describe the clinical, histological, immunohistochemical and ultrastructural findings of MH in a cat, together with the diagnostic work-up and a list of differential diagnoses. Clinical evaluation included a complete blood-cell count, serum biochemistry, urinalysis, serology and ultrasound examination. The cat had clinical signs of depression, thinness, dehydration, pale mucous membranes and tachycardia. Abdominal ultrasonography revealed generalised splenomegaly and hepatomegaly. Necroscopy showed whitish nodules, randomly scattered throughout the parenchyma in the spleen and liver. The periportal lymph nodes were greatly enlarged and the cut surface was uniformly greyish-white and translucent. Histological examination revealed pleomorphic proliferation of large round tumour cells, with numerous phagocytic vacuoles containing erytrocytes, leukocytes and haemosiderin. By immunohistochemistry, positivity for lysozyme and alpha1-antitrypsin and a scattered positivity for Mac 387 were observed. Ultrastructural features of tumour cells included cytoplasmic lipid droplets, lysosomes and phagolysosomes. MH in the cat needs to be differentiated from diffuse granulomatous disease, non-Hodgkin's lymphoma and Hodgkin's-like disease. The morphological features of the tumour cells, combined with immunohistochemical and ultrastructural observation, are consistent with a diagnosis of MH in the cat.
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PMID:Morphological characterisation of malignant histiocytosis in a cat. 1908 73

In septic shock, cardiovascular collapse is caused by the release of inflammatory mediators. We previously found that lysozyme (Lzm-S), released from leukocytes, contributed to the myocardial depression and arterial vasodilation that develop in canine models of septic shock. To cause vasodilation, Lzm-S generates hydrogen peroxide (H(2)O(2)) that activates the smooth muscle soluble guanylate cyclase (sGC) pathway, although the mechanism of H(2)O(2) generation is not known. To cause myocardial depression, Lzm-S binds to the endocardial endothelium, resulting in the formation of nitric oxide (NO) and subsequent activation of myocardial sGC, although the initial signaling event is not clear. In this study, we examined whether the myocardial depression produced by Lzm-S was also caused by the generation of H(2)O(2) and whether Lzm-S could intrinsically generate H(2)O(2) as has been described for other protein types. In a canine ventricular trabecular preparation, we found that the peroxidizing agent Aspergillus niger catalase, that would breakdown H(2)O(2), prevented Lzm-S- induced decrease in contraction. We also found that compound I, a species of catalase formed during H(2)O(2) metabolism, could contribute to the NO generation caused by Lzm-S. In tissue-free experiments, we used a fluorometric assay (Ultra Amplex red H(2)O(2) assay) and electrochemical sensor techniques, respectively, to measure H(2)O(2) generation. We found that Lzm-S could generate H(2)O(2) and, furthermore, that this generation could be attenuated by the singlet oxygen quencher sodium azide. This study shows that Lzm-S, a mediator of sepsis, is able to intrinsically generate H(2)O(2). Moreover, this generation may activate H(2)O(2)-dependent pathways leading to cardiovascular collapse in septic shock.
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PMID:Lysozyme, a mediator of sepsis that intrinsically generates hydrogen peroxide to cause cardiovascular dysfunction. 1954 85

Mimivirus was investigated by atomic force microscopy in its native state following serial degradation by lysozyme and bromelain. The 750-nm diameter virus is coated with a forest of glycosylated protein fibers of lengths about 140 nm with diameters 1.4 nm. Fibers are capped with distinctive ellipsoidal protein heads of estimated Mr=25 kDa. The surface fibers are attached to the particle through a layer of protein covering the capsid, which is in turn composed of the major capsid protein (MCP). The latter is organized as an open network of hexagonal rings with central depressions separated by 14 nm. The virion exhibits an elaborate apparatus at a unique vertex, visible as a star shaped depression on native particles, but on defibered virions as five arms of 50 nm width and 250 nm length rising above the capsid by 20 nm. The apparatus is integrated into the capsid and not applied atop the icosahedral lattice. Prior to DNA release, the arms of the star disengage from the virion and it opens by folding back five adjacent triangular faces. A membrane sac containing the DNA emerges from the capsid in preparation for fusion with a membrane of the host cell. Also observed from disrupted virions were masses of distinctive fibers of diameter about 1 nm, and having a 7-nm periodicity. These are probably contained within the capsid along with the DNA bearing sac. The fibers were occasionally observed associated with toroidal protein clusters interpreted as processive enzymes modifying the fibers.
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PMID:Atomic force microscopy investigation of the giant mimivirus. 2055 32


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