Copper molybdate synthesized by sonochemistry route at room temperature as an efficient solid catalyst for esterification of oleic acid.

Copper molybdate nanoplates were synthesized by a sonochemical process at room temperature, which we report as a simple and cost-effective route. Structural analysis of the material by the Rietveld method of X-ray diffraction (XRD) data revealed lindgrenite Cu3(MoO4)2(OH)2 in a single-phase structure. All the vibrational modes characteristic of the space group were identified by Raman vibrational and near-infrared (NIR) spectroscopies. The profile obtained for N2 adsorption/desorption was type III hysteresis, characteristic of mesoporous materials, with a surface area of 70.77(1) m2 g-1. The micrographs of the material obtained by scanning electron microscopy showed nanoplates with nanometric sizes and an anisotropic growth aspect. The catalytic activity of lindgrenite was evaluated by esterifying oleic acid with methanol, showing high conversion rate to methyl oleate and good catalyst stability after seven recycling cycles. Above all, the best catalytic performance was reached when we optimized parameters such as oleic acid:methanol molar ratio of 1:5, 5% of catalyst dosage, and reaction time of 5 h, resulting in 98.38% of conversion at 413 K. Therefore, sonochemically synthesized lindgrenite proved to be a high potential material for biofuel production by oleic acid esterification.

Assistive devices: an effective strategy in non-pharmacological treatment for hand osteoarthritis-randomized clinical trial.

This study aims to evaluate the use of assistive devices as a strategy in non-pharmacological treatment for hand osteoarthritis (HOA). This is a randomized, prospective, parallel, assessor-blinded clinical trial, in which patients with a diagnosis of HOA were randomly allocated to an intervention group (IG), where they received assistive devices for daily life activities, or to a control group (CG), where they received a guideline leaflet with information on joint protection and disease features. The primary outcomes considered were occupational performance, measured by the Canadian Occupational Performance Measure (COPM), and hand function was evaluated through the Score for the Assessment and Quantification of Chronic Rheumatoid Affections of the Hands (SACRAH). The secondary outcomes were pain, measured by the visual analog scale (VAS), and quality of life, measured by the World Health Organization Quality of Life Instrument, Short Form (WHOQOL-BREF). We compared both outcomes before and after interventions and outcomes between groups. Participants from the two groups were assessed at the time of inclusion in the study, 30, and 90 days after initial evaluation. Out of the 39 patients included, 19 were allocated to the IG and 20 to the CG. Only two patients from the CG did not complete the follow-up period. The patients' hand function and occupational performance improved after intervention (30 days-SACRAH-p < 0.05; COPM-p < 0.05; VAS-p < 0.05). When comparing results between the groups, there was a statistical difference in COPM (performance-p < 0.001; and satisfaction-p < 0.001), in the first reevaluation carried out. The use of assistive devices has proved to be an effective alternative in non-pharmacological treatment for HOA. CLINICAL TRIAL REGISTRATION: NCT02667145.

Challenges in the rabbit haemorrhagic disease 2 (RHDV2) molecular diagnosis of vaccinated rabbits.

Molecular methods are fundamental tools for the diagnosis of viral infections. While interpretation of results is straightforward for unvaccinated animals, where positivity represents ongoing or past infections, the presence of vaccine virus in the tissues of recently vaccinated animals may mislead diagnosis. In this study, we investigated the interference of RHDV2 vaccination in the results of a RT-qPCR for RHDV2 detection, and possible associations between mean Cq values of five animal groups differing in age, vaccination status and origin (domestic/wild). Viral sequences from vaccinated rabbits that died of RHDV2 infection (n=14) were compared with the sequences from the commercial vaccines used in those animals. Group Cq means were compared through Independent t-test and One-way ANOVA. We proved that RHDV2 vaccine-RNA is not detected by the RT-qPCR as early as 15days post-vaccination, an important fact in assisting results interpretation for diagnosis. Cq values of vaccinated and non-vaccinated infected domestic adults showed a statistically significant difference (p<0.05), demonstrating that vaccination-induced immunity reduces viral loads and delays disease progression. Contrarily, in vaccinated young rabbits higher viral loads were registered compared to non-vaccinated kittens. No significant variation (p=0.3824) was observed between viral loads of non-vaccinated domestic and wild RHDV2-victimised rabbits. Although the reduced number of vaccinated young animals analysed hampered a robust statistical analysis, this occurrence suggests that passively acquired maternal antibodies may inhibit the active immune response to vaccination, delaying protection and favouring disease progression. Our finding emphasises the importance of adapting kitten RHDV2 vaccination schedules to circumvent this interference phenomenon.

Pulmonary and hepatic lesions caused by the dehydropyrrolizidine alkaloid-producing plants Crotalaria juncea and Crotalaria retusa in donkeys.

The effects and susceptibility of donkeys to Crotalaria juncea and Crotalaria retusa poisoning were determined at high and low doses. Seeds of C. juncea containing 0.074% of dehydropyrrolizidine alkaloids (DHPAs) (isohemijunceines 0.05%, trichodesmine 0.016%, and junceine 0.008%) were administered to three donkeys at 0.3, 0.6 and 1 g/kg body weight (g/kg) daily for 365 days. No clinical signs were observed and, on liver and lung biopsies, the only lesion was a mild liver megalocytosis in the donkeys ingesting 0.6 and 1 g/kg/day. Two other donkeys that received daily doses of 3 and 5 g seed/kg showed initial respiratory signs 70 and 40 days after the start of the administration, respectively. The donkeys were euthanized following severe respiratory signs and the main lung lesions were proliferation of Clara cells and interstitial fibrosis. Three donkeys ingested seeds of C. retusa containing 5.99% of monocrotaline at daily doses of 0.025, 0.05 and 0.1 g/kg for 365 days. No clinical signs were observed and, on liver and lung biopsies, the only lesion was moderate liver megalocytosis in each of the three donkeys. One donkey that received a single dose of 5 g/kg of C. retusa seeds and another that received 1 g/kg daily for 7 days both showed severe clinical signs and died with diffuse centrilobular liver necrosis. No lung lesions were observed. Another donkey that received a single dose of 2.5 g/kg of C. retusa seeds showed no clinical signs. The hepatic and pneumotoxic effects observed are consistent with an etiology involving DHPAs. Furthermore, the occurrence of lung or liver lesions correlates with the type of DHPAs contained in the seeds. Similarly as has been reported for horses, the data herein suggest that in donkeys some DHPAs are metabolized in the liver causing liver disease, whereas others are metabolized in the lung by Clara cells causing lung disease.

Periacinar liver fibrosis caused by Tephrosia cinerea in sheep.

Tephrosia cinerea has been associated with ascites and liver fibrosis in sheep in Brazil. The dried plant was fed ad libitum to three sheep for 55-80 days. Three additional sheep were used as controls. All the treated sheep presented with hypoalbuminemia and increased γ-glutamyltransferase and aspartate aminotransferase activities. Anorexia, apathy, rough coat, ascites, and emaciation were observed after 45-60 days of feeding with T. cinerea. At necropsy 55-80 days after feeding of the plant commenced, the treated sheep had ascites, hydrothorax and hydropericardium, and their livers were firm and whitish, with a nodular surface. Histologically, the main hepatic lesions were periacinar fibrosis associated with hemorrhages and necrosis. On electron microscopy, a severe swelling of sinusoidal endothelial cells, frequently obstructing the lumen of the sinusoid was observed. The space of Disse was compressed by the swollen endothelial cells and microvilli usually present on the surface of hepatocytes adjacent to the space of Disse were not apparent. Dense bundles of collagen fibers were present in the spaces of Disse and within the sinusoids between profiles of swollen endothelial cells. It is concluded that T. cinerea causes periacinar fibrosis, similar to poisoning by Galenia africana in sheep and goats and veno-occlusive disease in different species.

Dystrophic epidermolysis bullosa in goats.

Clinical, histopathological and ultrastructural findings of caprine dystrophic epidermolysis bullosa (DEB) with autosomal recessive inheritance are reported. The goats presented with exungulation, erosions, crusts and scars on the skin and ulcers in the oral cavity. Microscopically, the skin showed subepidermal separation with clefts filled occasionally with clear eosinophilic fluid, cellular debris or neutrophils. Ultrastructurally, the site of blister formation was the sublamina densa in the epidermal basement membrane zone. In skin with blister formation and in clinically uninvolved skin, the basal lamina was preserved, but the anchoring fibrils were sparse and rudimentary. A twin brother of an affected kid was mated over 5 years with his mother; three out of the 10 kids born presented with epidermolysis bullosa, indicating that the disease has an autosomal recessive mode of inheritance. It is suggested that the disease is similar to human severe generalized recessive DEB.

Susceptibility to chemical insecticides of two Brazilian populations of the visceral leishmaniasis vector Lutzomyia longipalpis (Diptera: Psychodidae).

OBJECTIVES: To investigate the insecticide susceptibility of two geographically separated Lutzomyia longipalpis populations (Lapinha and Montes Claros) with different histories of insecticide exposure (i.e. no exposure and repeated exposure, respectively). METHODS: (i) Bioassay monitoring of sand fly survival over time when exposed to a range of insecticides; and (ii) analysis of the level of insecticide detoxification enzymes in individual sand flies caught at both study sites. Insecticides tested were the organophosphates malathion and fenitrothion and the pyrethroids lambda-cyhalothrin, permethrin and deltamethrin. RESULTS: Survival analyses showed that whilst there was no overall significant difference in susceptibility of both populations to organophosphates, Lapinha sand flies were significantly more susceptible to pyrethroids than those from Montes Claros. Multiple regression analyses also showed that insecticide susceptibility in both locations varied with sand fly sex. The relative susceptibilities of the two sand fly populations to tested insecticides were also compared. Thus, Montes Claros sand flies were most susceptible to malathion, followed by fenitrothion, deltamethrin and permethrin. Those from Lapinha were most susceptible to lambda-cyhalothrin, followed by malathion, permethrin, deltamethrin and fenitrothion. Biochemical analyses demonstrated that Montes Claros sand flies had significantly lower insecticide detoxification enzyme activity than Lapinha sand flies. CONCLUSIONS: Our results are the first record of significantly reduced susceptibility to the insecticides used in control of wild populations of Lu. longipalpis. They demonstrate the importance of evaluating chemicals against this species by conventional bioassay and microplate assays before and during spraying programmes.

Abortion and neonatal mortality in sheep poisoned with Tetrapterys multiglandulosa.

Tetrapterys spp. have been reported as a cause of cardiac fibrosis, status spongiosus of the nervous system, and abortion. To study the intoxication by Tetrapterys multiglandulosa, 24 sheep were divided into 4 experimental groups of 4 sheep each and 1 control group. Groups 1 to 3, respectively, received 1, 1.5, and 3 g/kg body weight of the dry plant daily, starting on the 90th day of pregnancy. Group 4 received 1.5 g/kg from the 120th day of pregnancy to the end of gestation. All sheep from groups 2 and 3, except 1 that was submitted to cesarean delivery, aborted between 110 and 134 days of pregnancy. Seven fetuses had anasarca. Seven lambs from groups 1 and 4 were weak and died or were euthanatized. The other 2 were born weak with mild nervous signs but recovered. Cardiac fibrosis and status spongiosus of the nervous system were observed in newborn lambs and fetuses.

Spontaneous lysosomal storage disease caused by Sida carpinifolia (Malvaceae) poisoning in cattle.

Clinical and pathologic findings for the spontaneous poisoning by Sida carpinifolia in cattle are described in this study. A survey on field cases of S. carpinifolia in cattle was carried out on farms of Alto Vale do Itajaí, State of Santa Catarina, southern Brazil. Sixteen affected animals were clinically evaluated and 9 were subjected to postmortem examination. The main clinical signs consisted of marching gait, alert gaze, head tremors, and poor growth. Histologic and ultrastructural lesions consisted of vacuolization and distension of neuronal perikarya, mainly from Purkinje cells, and of the cytoplasm of acinar pancreatic and thyroid follicular cells. Clinical signs and lesions varied from mild to severe. Improvement of the clinical signs was observed in cattle after a period of up to 90 days without consuming the plant; however, residual lesions, mainly characterized by axonal spheroids and absence of Purkinje neurons in some areas of the cerebellum, were observed in these cases. It is concluded that the natural chronic consumption of S. carpinifolia was the etiologic cause of storage disease in cattle in this study.

Fatal cytauxzoonosis in captive-reared lions in Brazil.

Fatal cytauxzoonosis is described in a captive reared lioness (Panthera leo) and its 6-month-old cub. Clinical signs in the lioness included loss of weight, depression, anaemia, loss of hair, dark discolored urine, tachypnoea, nystagmus, deaphness and staggering gait. The cub died after a short period of depression. In the lioness, laboratory examination revealed normochromic normocytic anaemia, neutrophilia, lymphopenia, monocytosis, eosinopenia, thrombocytopenia, proteinuria, pyuria, haematuria and increased. At necropsy the lioness showed marked pulmonary edema and slight gelatinous translucent edema in the mediastinum, petechiae and echymosis disseminated in the serosae, and the intestinal content was red and semiliquid. The cub presented hemothorax, endocardial and pulmonary edema, petechiae in the cardiac serosae, hepatic and splenic congestion and segments of the small intestine with blood stained fluid contents and reddish mesenteric lymph nodes. Histopathological examination of liver, spleen, heart, lungs, intestines, pancreas, mesenteric lymph nodes, kidneys, skeletal muscle, brain and skin revealed large number of intravascular macrophages with their cytoplasm filled with various schizogonic stages of a Theileriidae. Electron microscopy confirmed the presence of schizonts in endothelial-associated macrophages. The diagnosis was established by the finding of the pathognomonic schizonts in macrophages within blood vessels in several organs and tissues from both lions. This is the first report of feline cytauxzoonosis in P. leo and of a confirmed infection by Cytauxzoon felis in felidae in South America.

Swainsonine-induced lysosomal storage disease in goats caused by the ingestion of Turbina cordata in Northeastern Brazil.

A disease of the central nervous system in goats was observed in the municipalities of Juazeiro, Casa Nova and Curaça, state of Bahia, and Petrolina, state of Pernambuco, Northeastern Brazil. The disease was produced experimentally in two goats by the administration of dry Turbina cordata mixed with grain. Clinical signs were observed after the ingestion of 62 and 106 g/kg body weight in 28 and 54 days, respectively. The concentration of swainsonine in the plant varied from less than 0.001% to 0.14% (dry weight). Clinical signs of natural and experimental cases included difficulties in standing, ataxia, hypermetria, wide-based stance, intention tremors, spastic paresis mainly in the hind legs, nystagmus, abnormal postural reactions, head tilting, and falling. Diffuse vacuolation of neurons, epithelial cells of pancreas, thyroids, and renal tubules were observed on the histology. From the electron microscopy of Purkinje cells the vacuoles represented dilated lysosomes. These findings demonstrated that T. cordata causes an acquired glycoprotein lysosomal storage disease. The intoxication occurs at least in an area of 27,000 km2 causing severe losses in goats, and some farmers report the disease also in cattle.

Neurohistologic and ultrastructural lesions in cattle experimentally intoxicated with the plant Prosopis juliflora.

Intoxication by pods of Prosopis juliflora (mesquite beans) causes an impairment of cranial nerve function in cattle and goats. In goats, vacuolation of neurons in the trigeminal motor nuclei has been reported. To study the lesions in cattle caused by consumption of P. juliflora pods and dry ground pods, eight 6- to 12-month-old male cattle were divided into 4 groups: group 1 was fed a ration containing 50% of pods; groups 2 and 3 received a ration containing 50 and 75% of dry ground pods, respectively; group 4 was the control. After 200 days, all cattle were killed and sampled for histologic evaluation. Samples of the trigeminal motor nucleus were examined by electron microscopy. All cattle from groups 1, 2, and 3 showed clinical signs resulting from impaired function of cranial nerves V, IX, X, and XII, starting 45-75 days after consumption of the plant. The main histologic lesions were vacuolation and loss of neurons in trigeminal motor nuclei and other motor cranial nerve nuclei with Wallerian-like degeneration in the cranial nerves. Mild denervation atrophy was observed in the masseter and other masticatory muscles. On electron microscopy, neurons of the trigeminal nuclei had markedly swollen mitochondria, with the mitochondrial cristae displaced peripherally, disoriented and disintegrating. Intoxication by P. juliflora seems to have a novel pathogenesis, characterized by a selective, primary, chronic, and progressive injury to mitochondria of neurons of the trigeminal and other cranial nerve nuclei. Cranial nerve degeneration and denervation atrophy of the muscles occurs as a consequence of the neuronal lesion.

Macrophages and giant cell proliferation associated with bone protein synthesis and calcification in the trachea and bronchi of rabbits intoxicated with Solanum glaucophyllum.

A histopathologic, immunohistochemical, and ultrastructural study of the trachea and the bronchi of 6 rabbits experimentally intoxicated with the calcinogenic plant Solanum glaucophyllum was performed. Histologically, infiltration of the mucosa and the submucosa of the trachea and the bronchi by macrophages, multinucleated giant cells, a few lymphocytes and mast cells, and calcium deposits in the basal lamina of the epithelium and in elastic fibers were observed. Expression of osteocalcin, osteonectin, and osteopontin was detected in the mucosa, lamina propria, and epithelium. Electron microscopic study of the corresponding areas showed numerous macrophages in the process of fusion to form multinucleated giant cells, activated mesenchymal cells, and calcium precipitation in the basal lamina of epithelium and in elastic fibers. It is suggested that the high levels of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in the plant induces macrophage proliferation, multinucleated giant-cell formation, mesenchymal cell activation, bone-protein synthesis, and calcification. In addition, the synthesis of 1,25(OH)2D3 by local macrophages may have contributed to the calcification.

Intoxication by Ipomoea sericophylla and Ipomoea riedelii in goats in the state of Paraíba, Northeastern Brazil.

A disease of the nervous system was observed in goats from two farms of the semiarid of the state of Paraíba, northeastern Brazil. Ipomoea sericophylla was found in one farm and I. riedelii in the other. Both plants were administered experimentally to five goats each. Both plants induced clinical signs similar to those observed in spontaneous cases. Two goats died spontaneously and five were euthanatized. Three goats recovered after the withdrawal of the plants. Histological examination showed that all goats that died spontaneously or were euthanized had diffuse vacuolation of neurons, macrophages of lymphatic tissues, and epithelial cells of pancreas, thyroid, renal tubules and liver. On electron microscopy of Purkinje cells, numerous dilated membrane bordered vacuoles were identified as lysosomes. On lectin-histochemical analysis, cerebellar cells gave positive reactions to Concanavalia ensiformis, Triticum vulgaris, and succinylated-T. vulgaris, which indicate the storage of alpha-D-mannose, alpha-D-glucose, beta-D-N-acetyl-glucosamine, and acetyl-neuraminic acid. The chemical analysis of I. sericophylla and I. riedelii showed 0.11 and 0.14% of swainsonine, respectively. The latter also contained calystegines B1, B2 and C1. It is concluded that I. sericophylla and I. riedelli cause a lysosomal storage disease.

Lectin-histochemistry: glycogenosis in cattle.

Ten out of 47 calves that were born in a small Brahman herd from southern Brazil developed progressive muscular weakness and tremors, lethargy and poor body condition. Necropsy was performed on three affected animals. The only gross lesion detected was paleness of the muscles of the trunk and limbs. Multiple cytoplasm vacuoles located in different tissues were the principal microscopic lesions. Vacuoles were particularly evident in skeletal muscles and myocardium. PAS-positive granules were numerous in skeletal muscle fibres and Purkinje fibres of the myocardium, but were also observed in the neurons of the brain and spinal cord, and in the vascular smooth muscle fibres from all the examined tissues. Pretreatment with diastase completely abolished the PAS reactivity. The vacuoles reacted strongly to Griffonia simplicifolia II and Concanavalia ensiformes lectins, whose biding pattern has been reported as useful for demonstration of glycogen. Examination of the electron micrographs revealed that glycogen was free within the cytoplasm or accumulated in membrane-bound granules of several tissues, especially in striated muscle, liver and neurons of the CNS. These findings were consistent with generalized glycogenosis.

Glicogenose hereditária em bovinos Brahman no Brasil / Inherited glycogenosis in Brahman cattle in Brazil

Relata-se uma enfermidade hereditária em bovinos caracterizada por acúmulo lisossomal de glicogênio em diversos órgãos. A doença foi diagnosticada em um rebanho da raça Brahman, no município de Porto Lucena, Rio Grande do Sul, Brasil. Os animais afetados, a partir de 1 mês de idade, apresentavam dificuldade em acompanhar a mãe e crescimento retardado, desenvolviam fraqueza e tremores musculares, letargia e perda de condição corporal progressivos. Todos os bezerros eram descendentes do mesmo touro. Foi realizada necropsia em três bezerros doentes; palidez muscular do tronco e membros foi a única alteração macroscópica encontrada. Vacuolização citoplasmática de diversos órgãos foi a principal alteração histológica observada. Os vacúolos citoplasmáticos eram mais evidentes na musculatura esquelética, miocárdio, especialmente nas fibras de Purkinje e em neurônios do Sistema Nervoso Central (SNC). Nos tecidos mais afetados foi observada grande quantidade de grânulos ácido periódico de Schiff (PAS), positivos e negativos quando o tecido era tratado previamente com diastase. Uma mutação no gene da glicosidase alfa ácida, causadora da glicogenose generalizada em bovinos Brahman, a 1057?TA, foi detectada pela técnica de reação em cadeia de polimerase (PCR) em tecidos dos animais necropsiados. Também foi detectada a presença dessa mutação em amostras de sangue de animais parentes dos bezerros doentes. Os achados clínicos, patológicos e moleculares são semelhante ás descrições de glicogenose tipo II em bovinos da raça Brahman descritos na Austrália. Não foram encontrados relatos anteriores em revistas indexadas sobre glicogenose hereditária em bovinos Brahman no Brasil.

Tremorgenic syndrome in goats caused by Ipomoea asarifolia in Northeastern Brazil.

Green leaves of Ipomoea asarifolia were dosed to 10 goats. Nine goats ingesting 5-37 g/kg bw daily had clinical signs in 4-38 days. One goat ingesting 2.5 g/kg bw daily during 125 days and two control goats had no clinical signs. Clinical signs were characteristic for a tremorgenic syndrome. Five goats recovered in 4-9 days after the withdrawal of the plant. Two goats died spontaneously and three were euthanased for histologic and ultrastructural studies. No significant lesions were observed at necropsies or on the histologic and ultrastructural studies. Samples of the plant analyzed for enzymatic inhibitors were negative for calystegines and contained an almost undetectable amount of swainsonine (less than 0.001%). It is concluded that I. asarifolia causes a tremorgenic syndrome due to an unknown tremorgenic phytotoxins or mycotoxins.

Symmetric focal degeneration in the cerebellar and vestibular nuclei in swine caused by ingestion of Aeschynomene indica seeds.

A vestibulocerebellar disorder was observed in 2- to 4-month-old swine after consumption of broken rice contaminated with 13% Aeschynomene indica seeds. Affected animals recovered in 2-14 days after removal of the contaminated food. To reproduce the syndrome, 10 pigs were fed 13% A. indica seeds in commercial pig ration or rice. They showed clinical signs similar to those observed in the spontaneous cases, 1 hour to 6 days after ingestion. Three pigs recovered after the withdrawal of the contaminated food. The others were killed. Two pigs that were fed for 25 days with food containing 3% and 6% seeds and two control pigs did not show clinical signs. Histologic lesions were characterized by symmetric focal degeneration in the cerebellar and vestibular nuclei. The initial lesion, observed 24 hours after the first ingestion, was characterized by vacuolation of the neuropil. Subsequently, there was progressive loss of parenchyma, vascular reaction, a few small spheroids, astrocytosis, and accumulation of gitter cells. The brains from four pigs were perfused with a buffered solution of glutaraldehyde-paraformaldehyde 12-48 hours after they started to ingest the seeds. No ultrastructural lesions were observed in the cerebellar nuclei after 12 hours of seed consumption. At 24 hours, endothelial cells and pericytes were separated by empty spaces from astrocyte foot processes, suggesting perivascular edema. The astrocytes were enlarged, consistent with intracellular fluid accumulation. These results suggest that A. indica seeds are toxic, causing functional derangement of the vestibulocerebellar system, followed by alterations in the microvasculature in the cerebellar and vestibular nuclei.

Cell differentiation and bone protein synthesis in the lungs of sheep with spontaneous calcinosis.

The lungs of three sheep with spontaneous enzootic calcinosis induced by the calcinogenic plant Nierembergia veitchii (Nv) were examined electron microscopically and immunohistochemically. The main ultrastructural changes were activation of fibroblasts and modified smooth muscle cells (SMCs) in the pulmonary interstitium, with an increase in extracellular matrix and precipitation of calcium, either in a laminated pattern or as amorphous aggregates. Macrophages and multinucleated giant cells, some with calcium crystals in the cytoplasm, were found in areas of increased extracellular matrix. Thickening and replication of the basal lamina of capillaries were prominent. The bone proteins osteocalcin, osteopontin and osteonectin were detected immunohistochemically in the cytoplasm of activated fibroblasts, in modified SMCs and in the extracellular matrix. It is suggested that 1,25-dihydroxyvitamin D(3)in Nv induces cellular differentiation and the synthesis of a calcifiable matrix.

Lysosomal storage disease caused by Sida carpinifolia poisoning in goats.

A neurologic disease characterized by ataxia, hypermetria, hyperesthesia, and muscle tremors of the head and neck was observed for 2 years in a flock of 28 Anglo-Nubian and Saanen goats on a farm with 5 ha of pasture. Six newborns died during the first week of life, and five abortions were recorded. The predominant plant in the pasture was Sida carpinifolia. The disease was reproduced experimentally in two goats by administration of this plant. Three goats with spontaneous disease and the two experimental animals were euthanatized and necropsied. No significant gross lesions were observed. Fragments of several organs, including the central nervous system, were processed for histopathology. Small fragments of the cerebellar cortex, liver, and pancreas of two spontaneously poisoned goats and two experimentally poisoned goats were processed for electron microscopy. Multiple cytoplasm vacuoles in hepatocytes, acinar pancreatic cells, and neurons, especially Purkinje cells, were the most striking microscopic lesions in the five animals. Ultrastructural changes included membrane-bound vacuoles in hepatocytes, Kupffer cells, acinar pancreatic cells, Purkinje cells, and the small neurons of the granular cell layer of the cerebellum. Paraffin-embedded sections of the cerebellum and pancreas were submitted for lectin histochemical analysis. The vacuoles in different cerebellar and acinar pancreatic cells reacted strongly to the following lectins: Concanavalia ensiformis, Triticum vulgaris, and succinylated Triticum vulgaris. The pattern of staining, analyzed in Purkinje cells and acinar pancreatic cells coincides with results reported for both swainsonine toxicosis and inherited mannosidosis.