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A study of the pathogenesis of bovine ephemeral fever confirmed that the major clinical signs were fever lasting no more than 2 days, with increased respiratory rate, dyspnoea and some degree of lameness. Haematological observations revealed a neutrophilia with a left shift and a lymphopaenia at the time of peak clinical reaction. The net result was a slight leucopaenia on the day after this reaction. The most prominent pathological changes involved the lungs and synovial joints. Pulmonary emphysema and alveolar collapse with bronchiolitis, degenerative changes in synovial membranes and increased synovial fluid were observed. Specific fluorescence indicating the presence of BEF viral antigen could be detected at the time of peak clinical response in individual cells in the lungs, spleen and lymph nodes as well as neutrophils. Before and after the peak fever some fluorescence was seen in cells which appeared to be reticular cells in the lymph nodes. Viral isolation in mice could be made from blood, lungs, spleen and lymph nodes over a period of no more than 3 days. It is postulated that viral growth takes place mainly in the reticuloendothelial cells in the lungs, spleen and lymph nodes and not in vascular endothelium or lymphoid cells.
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PMID:Studies on the pathogenesis of bovine ephemeral fever. 33 60

In 26 dogs, a single subcutaneous injection of N-nitroso-N-methylurethane produced acute lung injury characterized by tachypnea cyanosis, increased static lung recoil, and decreased lung compliance. During the first few days, light microscopic examination revealed widespread interstitial and perivascular edema and alveolar collapse. At the same time, electron microscopy showed the major alteration to be widespread necrosis of both types of alveolar epithelial cells without significant injury to the vascular endothelium. During recovery, new epithelial cells appeared which probably were derived from granular pneumocytes. These cells developed into mature granular pneumocytes through a phase in which they resembled fetal granular pneumocytes. The late stage was characterized by a picture resembling diffuse interstitial fibrosis but which was due to irreversible closure of clusters of small airspaces with no apparent increase in collagen. Elastic recoil of the lungs, as reflected by peak inspiratory airway pressure, increased during the acute phase and showed a return toward normal that was coincident with the appearance of mature granular pneumocytes in the regenerating epithelium. Lung compliance decreased during the acute phase and in most animals returned toward normal during the recovery phase. These observations strongly suggest that the alteration in lung mechanics is related to epithelial necrosis and that recovery is related to epithelial regeneration.
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PMID:Experimental acute alveolar injury in the dog. Morphologic--mechanical correlations. 125 90

Cyclosporine A (CyA) given to prevent xenograft rejection induces renal function impairment. In the last few years many studies have been devoted to understanding the mechanism(s) of CyA-induced renal insufficiency. In humans, several specific findings--interstitial fibrosis, toxic tubulopathy, peritubular capillary congestion, arteriolopathy--have been associated with CyA administration. It is now recognized that CyA renal toxicity mainly manifests under three different syndromes: (1) acute reversible decrease in glomerular filtration rate (GFR), (2) acute microvascular disease with the pattern of thrombotic microangiopathy, and (3) chronic irreversible renal damage. This review analyzes the available evidence that the clinical syndromes of CyA nephrotoxicity are related to changes induced by CyA on renal vessels. Experimental studies have failed to document that the activation of renin-angiotensin axis or sympathetic nervous system plays a relevant role in the development of CyA-associated renal vasoconstriction, which is the main causal factor of acute reversible decrease in GFR, whereas it is possible that changes in arachidonic acid metabolites with vasoactive properties contribute to this CyA-induced phenomenon. In this context, findings of increased urinary TxB2 and protective effect of TxA2 receptor blocking are of particular interest. Since the introduction of CyA in clinical practice, a syndrome of thrombotic microangiopathy resembling hemolytic uremic syndrome/thrombotic thrombocytopenic purpura has been recognized in humans and reproduced in experimental animals. This is a rare form of vascular toxicity attributed to CyA which may have a poor prognosis and possibly results from a direct toxic effect of CyA on vascular endothelium. The syndrome of chronic progressive deterioration of renal function associated with CyA was first recognized in humans. Until recently the possibility of reproducing this syndrome in animals in order to better understand its nature was not addressed. As in humans, when animals are given CyA for greater than 2 months they may develop chronic renal insufficiency with tubular arteriopathy and interstitial fibrosis. A peculiar form of tubulointerstitial damage has been recognized in association with CyA, and called striped interstitial fibrosis, that is probably due to tubular collapse induced by afferent vasoconstriction. This lesion may be improved by withdrawal of CyA, but renal function usually does not normalize.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal vascular and thrombotic effects of cyclosporine. 265 May 37

Although a variety of renal lesions may occur in acquired immune deficiency syndrome (AIDS), a rare but aggressive form of focal and segmental glomerulosclerosis with capillary collapse has been considered a possible component of this disorder. It is manifested by heavy proteinuria and progression to renal failure in a short time. We studied renal biopsies from nine patients with HIV infection and the above clinical features and compared the renal tissues to biopsies from HIV-positive individuals with immune complex glomerulonephritis and to biopsies from patients with heroin abuse nephropathy. The HIV-associated nephropathy was characterized by a combination of lesions: focal and segmental glomerulosclerosis, often in an early stage of evolution and with prominent degenerative changes of visceral epithelium; tubular necrosis without identifiable nephrotoxic or hemodynamic etiology; interstitial edema; large plasma protein-containing tubular casts in all segments of the nephron associated with marked tubular dilatation; and widespread tubuloreticular structures in vascular endothelium. In contrast, neither the sclerosing glomerular changes nor the tubulointerstitial abnormalities were present in HIV-infected patients with immune complex glomerulonephritis. Similarly, the tubular and interstitial changes and widespread tubuloreticular structures were absent in heroin-abuse nephropathy. The lesions of HIV-associated nephropathy occurred in patients with AIDS, AIDS-related complex, and in individuals clinically asymptomatic for HIV infection. Their morphological features in asymptomatic patients are sufficiently specific to allow for accurate diagnosis of HIV infection.
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PMID:HIV-associated nephropathy. A unique combined glomerular, tubular, and interstitial lesion. 307 May 50

The histopathological effect of photodynamic therapy (PDT) was investigated in an intraocular retinoblastoma-like tumour in vivo. Eighty-two tumours were studied by light microscopy and 8 by electron microscopy. Damage of the vascular endothelium with dilation of the organelles was evident 1 h after treatment, followed by leakage of the blood vessels, tissue hemorrhages, and vascular collapse. Histopathological examination showed an overall pattern of shrinkage of the cytoplasm and pycnosis of the nuclei in most of the tumour cells 3-5 days after treatment. The tumour recurrence often developed from the periphery of the tumours and in a few cases from small islets of viable tissue. Use of high doses of Photofrin II or light energy was associated with damage in the light irradiated area both to the conjunctiva or cornea in the form of leucocyte infiltration or ulcers, and to the retina, which often developed edema and appeared severely disorganized, with damage of the photoreceptors.
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PMID:Histopathological changes in an intraocular retinoblastoma-like tumour following photodynamic therapy. 336 72

We describe experiments on the cryopreservation of the rabbit common carotid artery aimed at improving upon previous results. We describe the design of a double clamp which holds the artery during transportation and storage, preventing twisting, shortening, and collapse of the vessel. The device allowed perfusion with solutions as desired and markedly reduced the extent of endothelial loss during procurement and processing. We also studied the effects of three vehicle solutions; a modified Hanks' solution, a solution originally developed for the cryopreservation of smooth muscle (K-Pipes), and a solution designed for corneal endothelium (CP-Tes). The criteria used to make the assessments were smooth muscle contractility and the structure and function of the vascular endothelium. A new staining method for vascular endothelium (combining propidium iodide with silver nitrate) is described. We found that there was significantly more endothelial cell damage in rabbit carotid arteries frozen in Hanks' solution than in the other solutions, and the recovery of smooth muscle contractility was lowest in the Hanks' group. Arteries cryopreserved using CP-Tes as the vehicle solution showed less endothelial cell damage than arteries preserved with either K-Pipes or Hanks' solution, and these arteries also exhibited the greatest relaxation response to acetylcholine. We conclude that careful handling of the vessels is important; of the solutions studied, CP-Tes is preferred for the cryopreservation of rabbit carotid artery with Me2SO.
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PMID:Cryopreservation of the common carotid artery of the rabbit. 752 24

A case of thrombotic microangiopathy presenting as a hemolytic uremic syndrome complicated by untreatable hypertension and ultimately requiring bilateral nephrectomy is discussed. Severe hypertension and renal failure may complicate the course of vascular diseases of the kidney, including thrombotic microangiopathy, chronic hypertension, and scleroderma. Toxins, pressure stress, and immune material may trigger the initial injury to vascular endothelium. The malignant course of these renal vascular diseases seems linked to the severity of vascular injury. Endothelial injury manifests with swelling and detachment of endothelial cells from the basement membrane, expansion of the subendothelial space, and newly formed basement membrane-like material. In arterioles, endothelial injury precedes myointimal swelling and proliferation, leading to vascular lumina narrowing or obliteration and secondary glomerular ischemia, with glomerular tuft collapse and garland-like wrinkling and thickening of the capillary wall. Endothelial cell injury is very likely the common determinant of a cascade of events that lead to irreversible renal failure. When the initial insult (toxins, mechanical stress, antibodies) is promptly removed, lesions are self-limiting and the patient usually recovers. However, a severe insult persisting for some time can lead to chronic and irreversible vascular lesions that, through renal ischemia, trigger maximal activation of the renin angiotensin system with a brisk elevation in arterial blood pressure that may combine to further vascular injury and renal ischemia. Moreover, enhanced shear stress in the severely narrowed microcirculation, through abnormal von Willebrand factor processing, can also favor endothelial injury and platelet aggregation, which may further worsen the vascular lesions and sustain the microangiopathic process. Plasma manipulation, arteriolar vasodilators, and angiotensin-converting enzyme inhibitors normally control the vicious circle, but in few severe cases bilateral nephrectomy remains the last chance to save the patient's life.
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PMID:Malignant vascular disease of the kidney: nature of the lesions, mediators of disease progression, and the case for bilateral nephrectomy. 867 55

Re-expansion pulmonary oedema is a recognised but rare complication following the rapid drainage of a large pleural effusion or pneumothorax [1,2], usually occurring on the side of re-inflation. The pathogenesis of the pulmonary oedema is poorly understood but is thought to be due to micro-vascular shearing resulting in neutrophil activation and adhesion to the vascular endothelium resulting in increased micro-vascular permeability [3-7]. Few reports appear in the literature of invasive haemodynamic monitoring following this catastrophe. We describe a patient who sustained fatal pulmonary oedema arising in the contralateral lung, with pulmonary flow catheter data documenting the initial circulatory collapse following the aspiration of a massive pulmonary effusion.
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PMID:Catastrophic circulatory collapse following re-expansion pulmonary oedema. 878 12

CBA/CaH-kdkd mice develop a spontaneous and chronic tubulointerstitial renal disease which is characterised by mononuclear cell infiltration, tubular collapse and cystic dilatation of tubules. The pathogenic mechanisms of renal injury have not been fully elucidated in this model. We have analysed the nature of infiltrating cells and the expression of MHC class II antigens, cytokines and adhesion molecules in CBA/CaH-kdkd kidneys at various disease stages. Using immunohistochemical techniques we found that kdkd kidneys are characterised by abundant macrophage and dendritic cell infiltration with fewer T cells with CD4+ and CD8+ phenotypes. Interestingly, MHC class II antigens were not induced on renal tubules. The proinflammatory cytokine, TNF-alpha, was markedly enhanced in kdkd kidney (up to fourfold), whereas the T cell-specific cytokine, IFN-gamma, increased less (less than twofold). ICAM-1 and VCAM-1 were markedly overexpressed by injured proximal tubules. ICAM-2 and PECAM-1 were constitutively expressed on glomerular capillaries and vascular endothelium in normal kidneys and did not change in CBA/CaH-kdkd mice. In conclusion, tubulointerstitial nephritis in CBA/CaH-kdkd mice is characterised by prominent macrophage infiltration and abundant expression of ICAM-1 and VCAM-1 on injured renal tubules. The lack of MHC class II antigens on injured tubules suggests that the kd gene defect could generate a secondary renal inflammatory response which is characterised by prominent macrophage infiltration and a relative scarcity of T cells.
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PMID:Characterisation of cellular infiltration and adhesion molecule expression in CBA/CaH-kdkd mice with tubulointerstitial renal disease. 934 17

Genes of an influenza A (H5N1) virus from a human in Hong Kong isolated in May 1997 were sequenced and found to be all avian-like (K. Subbarao et al., Science 279:393-395, 1998). Gene sequences of this human isolate were compared to those of a highly pathogenic chicken H5N1 influenza virus isolated from Hong Kong in April 1997. Sequence comparisons of all eight RNA segments from the two viruses show greater than 99% sequence identity between them. However, neither isolate's gene sequence was closely (>95% sequence identity) related to any other gene sequences found in the GenBank database. Phylogenetic analysis demonstrated that the nucleotide sequences of at least four of the eight RNA segments clustered with Eurasian origin avian influenza viruses. The hemagglutinin gene phylogenetic analysis also included the sequences from an additional three human and two chicken H5N1 virus isolates from Hong Kong, and the isolates separated into two closely related groups. However, no single amino acid change separated the chicken origin and human origin isolates, but they all contained multiple basic amino acids at the hemagglutinin cleavage site, which is associated with a highly pathogenic phenotype in poultry. In experimental intravenous inoculation studies with chickens, all seven viruses were highly pathogenic, killing most birds within 24 h. All infected chickens had virtually identical pathologic lesions, including moderate to severe diffuse edema and interstitial pneumonitis. Viral nucleoprotein was most frequently demonstrated in vascular endothelium, macrophages, heterophils, and cardiac myocytes. Asphyxiation from pulmonary edema and generalized cardiovascular collapse were the most likely pathogenic mechanisms responsible for illness and death. In summary, a small number of changes in hemagglutinin gene sequences defined two closely related subgroups, with both subgroups having human and chicken members, among the seven viruses examined from Hong Kong, and all seven viruses were highly pathogenic in chickens and caused similar lesions in experimental inoculations.
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PMID:Comparisons of highly virulent H5N1 influenza A viruses isolated from humans and chickens from Hong Kong. 965 15


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