Isolated lymph node amyloidosis.
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Biomedical subjects
Publications and source records attributed to A Jover.
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Crystal structures of p-xylene-crystallized deoxycholic acid (3alpha,12alpha-dihydroxy-5beta-cholan-24-oic acid) and its three epimers (3beta,12alpha-; 3alpha,12beta-; and 3beta,12beta-) have been solved. Deoxycholic acid forms a crystalline (P21) complex with the solvent with a 2:1 stoichiometry whereas crystals of the three epimers do not form inclusion compounds. Crystals of the 3beta,12beta-epimer are hexagonal, whereas the 3alpha,12beta-and 3beta,12alpha-epimers crystallize in the P2(1)2(1)2(1) orthorhombic space group. The three hydrogen bond sites (two hydroxy groups, i. e. O3-H, and O12-H, and the carboxylic acid group of the side chain, O24bO24a-H) simultaneously act as hydrogen bond donors and acceptors. The hydrogen bond network in the crystals was analyzed and the following sequences have been observed: two chains (abcabc... or acbacb... ) and two rings (abc or acb), which constitute a complete set of all the possible sequences which can be drawn for an intermolecular hydrogen bond network formed by three hydrogen bond donor/acceptor sites forming crossing hydrogen bonds. The orientation of O3-H (alpha or beta) determines the sequence of the acceptor and the donor groups involved in the pattern: O24a --> O12 --> O3 --> O24b when it is alpha and O24a --> O3 --> O12--> O24B when it is beta. These observations were used to predict the hydrogen bond network of p-xylene-crystallized 3-oxo,12alpha-hydroxy-5beta-cholan-24-oic acid. This compound has two hydrogen bond donor and three potential hydrogen bond acceptor sites. According to the previous sequence set, this compound should crystallize in the monoclinic P21 system, should form a complex with the solvent, O24b should not participate in the hydrogen bond network, and the chain sequence O24a --> O12 --> O3 would be followed. All predictions were confirmed experimentally.
To date, two isoforms of estrogen receptors (ER) have been identified, cloned, and characterized from several species, estrogen receptor-alpha (ERalpha) and estrogen receptor-beta (ERbeta). Although the presence of ERalpha has been demonstrated in normal and tumoral canine mammary tissues, the issue of ERbeta expression has not been addressed in the dog. In this study, we have analyzed the expression of ERbeta in formalin-fixed, paraffin-embedded tissue samples of nonaltered mammary gland, 30 malignant (six complex carcinoma, 12 simple carcinoma, three carcinosarcoma, and nine carcinoma or sarcoma in benign tumor), and five benign (one fibroadenoma, one complex papilloma, one complex adenoma, and two benign mixed tumors) mammary tumors of the dog by using a polyclonal ERbeta antibody and the avidin-biotin-peroxidase complex immunohistochemical technique. Our results show that high numbers of normal ductal and acinar epithelium and approximately one third of canine mammary tumors express ERbeta. This expression was higher in benign than in malignant tumors. Furthermore, expression was higher in complex and mixed histologic subtypes of malignant tumors when compared with simple subtypes.
This paper report on the lesions occurred in the thymus in experimental acute African swine fever (ASF). Twenty-one pigs were inoculated with the highly virulent ASF virus (ASFV) isolate Spain-70. Animals were slaughtered from 1 to 7 days post infection (dpi). Three animals with similar features were used as controls. Thymus samples were fixed in 10% buffered formalin solution for histological and immunohistochemical study and in 2.5% glutaraldehyde for ultrastructural examination. For immunohistochemical study, the avidin-biotin-peroxidase complex (ABC) technique was used to demonstrate viral protein 73 and porcine myeloid-histiocyte antigen SWC3 using specific monoclonal antibodies. Cell apoptosis was evaluated by the TUNEL assay. Blood samples were taken daily from all pigs and were used for leukocyte counts. The results of this study show a severe thymocyte apoptosis not related to the direct action of ASFV on these cells, but probably to a quantitative increase in macrophages in the thymus and their activation. A decrease in the percentage of blood lymphocytes was observed at the same time No significant vascular changes were observed in the study. With these results we suggest that ASFV infection of the thymus does not seem to play a critical role in the acute disease. Although severe apoptosis was observed, animals died because of the severe lesions found in the other organs.
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Porcine enzootic pneumonia (PEN), caused by Mycoplasma hyopneumoniae (Mh), has been described in pigs in all geographic areas. The disease is characterized by high morbidity and low mortality rates in intensive swine production systems. A morphologic and immunohistochemical study was done to determine the cellular populations present in lung parenchyma of infected pigs, with special attention to the bronchus-associated lymphoid tissue (BALT). Polyclonal and monoclonal antibodies were used for the detection of antigens of Mh, T lymphocytes (CD3+, CD4+, and CD8+), IgG+ or IgA+ lymphocytes, and cells containing lysozyme, S-100 protein, major histocompatibility complex class II antigen or myeloid-histiocyte antigen. Findings in lung tissues associated with Mh infection were catarrhal bronchointerstitial pneumonia, with infiltration of inflammatory cells in the lamina propria of bronchi and bronchioles and alveolar septa. Hyperplasia of mononuclear cells in the BALT areas was the most significant histologic change. The BALT showed a high morphologic and cellular organization. Macrophages and B lymphocytes were the main cellular components of germinal centers. T lymphocytes were primarily located in perifollicular areas of the BALT, lamina propria and within the airway epithelium, and plasma cells containing IgG or IgA at the periphery of the BALT, in the lamina propria of bronchi and bronchioles, in alveolar septa, and around bronchial submucosal glands. The hyperplastic BALT in PEN cases consisted of macrophages, dendritic cells, T and B lymphocytes, and IgG+ and IgA+ plasma cells. CD4+ cells predominated over CD8+ cells. Local humoral immunity appears to play an important role in the infection.
Histopathological, immunohistochemical and ultrastructural cutaneous changes are described in acute and subacute forms of experimental African Swine Fever (ASF). Fourteen 3-month-old Large White cross pigs were infected intramuscularly with the Dominican Republic 78 (DR78) ASF virus isolate and euthanized in pairs on alternatives days (3 to 17) post-inoculation (dpi). Three pigs were found dead at 8, 10 and 13 dpi, respectively. Antibodies against viral antigen Vp73, human fibrinogen, glycoprotein IIIa and Factor VIII-ra were used to evaluate viral antigen distribution, fibrin microthrombi and platelets in dermal vessels, respectively. Cutaneous lesions were characterised by vascular changes ranging from hyperaemia, mild oedema, scarce fibrin microthrombi and microhaemorrhages in euthanized animals, to generalized fibrin microthrombosis and microhaemorrhages in dead pigs. Secondary pustules and superficial folliculitis were observed in two animals dead at 10 and 13 dpi. Diffuse cytoplasmic Vp73 labelling was found in numerous intravascular monocytes and dermal macrophages. Ultrastructural studies showed mature viral particles in the lumen of dermal vessels but viral replication was not observed; nonetheless, microtubuloreticular structures were observed in the cytoplasm of some endothelial cells and macrophages which showed cytopathic effects, signs of cell activation or degeneration. Morphological and immunohistochemical evidences of platelet activation, degranulation and consumption were observed from 5 dpi onward.
This paper describes major pathogenetic mechanisms of African and Classical Swine Fever virus infections. The interactions between both viruses and the monocyte-macrophage-system result in the release of mediator molecules, which are important for the further progression of the diseases. The causes of the thrombocytopenia and the mechanisms of the haemorrhages, which are characteristic in both infections, are described. Apoptotic cell death is regarded as the predominant cause of lymphopenia in both virus infections.
Atrophy of the thymic cortex and loss of thymocytes were studied in 32 pigs inoculated with the virulent strain "Alfort" of classical swine fever (CSF) virus and killed at intervals from 2 to 15 days after infection. Immunohistochemical, ultrastructural, ELISA and TUNEL methods were used. The results suggested that direct action of CSF virus on thymocytes played no more than a minor role. The massive lymphoid depletion observed in the thymus, may, however, have been associated with the numerical increase in monocytes-macrophages in this organ, and their secretory activation, leading to synthesis and release of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1alpha and C1q complement component as main chemical mediators, and IL-1beta and IL-6 as minor mediators. These cytokines (TNF-alpha and IL-1alpha) may have played a role in the apoptosis of thymocytes, demonstrated by TUNEL and ultrastructural methods. The pathogenetic mechanism outlined may contribute to the lymphoid depletion observed in others organs in CSF and may explain the lymphopenia characteristic of the disease.
We describe the cytological features of a soft-tissue high-grade spindle and pleomorphic sarcoma. The smears showed hypercellularity composed of pleomorphic round and elongated cells, and a striking population of multinucleated osteoclast-type giant cells. Microscopically the tumor showed multiple patterns such as highly cellular pleomorphic, less cellular, and hyalinized areas with neoplastic cartilage and osteoid, and areas with hemorrhage and multicystic appearance with numerous osteoclastic giant cells, resembling aneurysmal bone cysts. Immunohistochemical studies showed positivity for vimentin, while chondroid tissue was positive for S-100, and osteoclastic giant cells stained positively for CD68. Due to the varied microscopic patterns, the differential diagnosis included many tumors containing osteoclastic giant cells and osteochondroid tissue.
To gain further insight into the pathogenesis of classical swine fever (CSF), the changes induced by hog cholera (HC) virus in pulmonary intravascular macrophages (PIMs) were examined. Twelve pigs were inoculated by the intramuscular route with a virulent strain of HC virus (Quillota strain) and killed in groups of three at 4, 7, 10 and 14 days post-inoculation. Immunohistochemical and ultrastructural examination revealed HC virus infection in endothelial cells, PIMs, and interstitial and alveolar macrophages. In addition to viral replication, a predominant feature was the secretory activation of PIMs, characterized by expanded rough endoplasmic reticulum and hyperplastic Golgi complexes. The results obtained suggest that macrophage activation and the subsequent release of pro-inflammatory mediators play an important role in the pathogenesis of CSF.
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Twelve miniature pigs were infected experimentally with the moderately-virulent Spanish isolate of African swine fever virus E75. The disease was reproduced acutely and subacutely, and six days after infection the animals showed severe clinical and pathological signs characterised by diffuse haemorrhages in lymphoid and non-lymphoid organs. An immunohistopathological study, using two different methods, and a monoclonal antibody (mAb) (18BG3) were used to analyse the distribution of the virus protein 73 (VP73) and IgM and IgG. VP73 was observed primarily in cells of the mononuclear phagocyte system, and in many megakaryocytes, some tubular epithelial cells of the kidneys, tonsillar epithelium, some hepatocytes, and in a few endothelial cells and neutrophils in the later stages of the infection. The histological findings and the distribution of VP73 and IgM and IgG indicated that the virus caused haemorrhagic lesions through its effect on various haemostatic mechanisms.
An ultrastructural study of Kupffer cells and pulmonary intravascular macrophages (PIMs) of healthy and African Swine Fever (ASF)-infected pigs was carried out. A vascular perfusion method was performed in order to obtain an optimal intravascular morphology and tissue fixation. The infection developed acute ASF lesions in both organs. Both Kupffer cells and PIMs were studied at different stages of infection. The differences observed in both macrophagic cells from uninfected and infected tissues are shown and discussed.