An inflammatory process was induced by intratendinous injection of bacterial collagenase into the superficial digital flexor tendon (SDFT) of the left thoracic limb of 10 horses. One week later, the tendons in five of the horses (group 1) were treated with glycosaminoglycan polysulphate (GAGPS), and the tendons of the other five (group 2) were treated with saline solution. The horses were euthanased 150 days after the collagenase injections, and samples of the SDFTs were frozen at -14 degrees C, sectioned at 5 to 7 mum longitudinally and transversely, and stained by the picrosirius red method. Morphometric analysis was used to quantify the organised and disorganised bundles of collagen in the samples from groups 1 and 2. Significantly more organised bundles of collagen were observed in the tendons treated with GAGPS.
Golden Retriever (GR) muscular dystrophy is an inherited degenerative muscle disease that provides an excellent model for Duchenne muscular dystrophy in humans. This study defined the histopathologic lesions, including the distribution of type I and II muscle fibers (FTI and FTII), in 12 dystrophic and 3 nondystrophic dogs between 7 and 15 months of age. The authors were interested in studying the influence on disease phenotype from crossing the base GR breed with Yellow Labrador Retrievers. The dystrophic dogs were divided according to breed: GRs and Golden Labrador Retrievers (GLRs). On hematoxylin and eosin staining, histopathologic lesions were more severe in GRs than GLRs. Six of eight GR muscles (75%) had a severe lesion grade (grade 3). In contrast, seven GLR muscles (87.5%) had mild lesions (grade 2), and only one had severe lesions (grade 3). Changes in fiber-type distribution were more pronounced in GRs versus GLRs. FTI:FTII ratio inversion was observed in three dystrophic GRs but only one GLR. The mean diameter of FTI and FTII was smaller in GRs and GLRs than in nondystrophic dogs (P < .01). The FTI of five GR muscles (62.5%) were larger than those of GLRs, whereas only one GLR muscle was larger (P < .05). The differential was less pronounced for FTII, with four GR muscles being larger and three GLR being larger. Observations indicate that crossing the base GR breed with Labrador Retrievers lessened the severity of the GR muscular dystrophy phenotype.
Epilepsy is a common and devastating neurological disease affecting more than 50 million people worldwide. Accumulating experimental and clinical evidence suggests that inflammatory pathways contribute to the development of seizures in various forms of epilepsy. In this context, while the activation of the PGE EP2 receptor causes early neuroprotective and late neurotoxic effects, the role of EP2 receptor in seizures remains unclear. We investigated whether the systemic administration of the highly selective EP2 agonist ONO-AE1-259-01 prevented acute pentylenetetrazole (PTZ)- and pilocarpine-induced seizures. The effect of ONO-AE1-259-01 on cell death in the hippocampal formation of adult male mice seven days after pilocarpine-induced status epilepticus (SE) was also evaluated. ONO-AE1-259-01 (10μg/kg, s.c.) attenuated PTZ- and pilocarpine-induced seizures, evidenced by the increased latency to seizures, decreased number and duration of seizures episodes and decreased mean amplitude of electrographic seizures. ONO-AE1-259-01 and pilocarpine alone significantly increased the number of pyknotic cells per se in all hippocampal subfields. The EP2 agonist also additively increased pilocarpine-induced pyknosis in the pyramidal cell layer of CA1 but reduced pilocarpine-induced pyknosis in the granule cell layer of the dentate gyrus (DG). Although the systemic administration of ONO-AE1-259-01 caused a significant anticonvulsant effect in our assays, this EP2 agonist caused extensive cell death. These findings limit the likelihood of EP2 receptor agonists being considered as novel potential anticonvulsant drugs.
Visceral leishmaniasis (VL) is a zoonosis that affects both animals and man. Dogs are the etiological agent's main reservoir. The aim of this study was to evaluate the clinical laboratory aspects and renal histopathology of VL dogs. Thirtyfour symptomatic (case) and 17 asymptomatic (control) VL seropositive dogs of different breeds, sexes, and ages from Teresina, Piauí State, Brazil, were used. Diagnosis was confirmed by enzyme-linked immunosorbent assay and indirect immunofluorescence test. Clinical and laboratory tests included blood cell count and renal function analysis (urea and creatinine). Animals were subjected to euthanasia and necropsy. Renal fragments were prepared by the usual histological techniques and stained with hematoxylin-eosin and periodic acid-Schiff. Physical examination showed that lymph node hypertrophy (85.29%) and skin lesions (35.29%) were frequent in the case group. Anemia was found in 55.88% of the case and in 11.76% of the control group. There was a significant difference between groups by Fisher's exact test. Two case-group dogs showed azotemia. Renal histopathological evaluation showed that 61.76% case and 17.65% control-group dogs had membranoproliferative glomerulonephritis. Mesangial proliferative glomerulonephritis was seen in 32.35% case and 64.70% control-group animals. There was a significant difference for both types of glomerulonephritis between groups. Amastigote forms of Leishmania were found in the renal parenchyma, in the inflammatory infiltrate of one case-group dog. We concluded that, in canine VL, regardless of the clinical signs at physical examination, the kidneys are frequently compromised.
Polycystic ovary syndrome (PCOS) affects women during their entire lifespan. Evidence from the literature suggests an association of PCOS with decreased bone formation markers (osteocalcin and P1NP), although no conclusive data about the incidence of fractures exist. In the present study, we investigated the consequences of androgenization in rats on bone markers and femur microCT and the changes in these parameters after ovariectomy. This study was approved by the local Animal Ethics Committee. Briefly, Wistar rats (n= 38) were divided in 4 groups: 1) “Control OVX” (single dose of corn oil s.c. at day 5 of life and ovariectomy at day 100, n=9); 2) “Control SHAM” (n=9); 3) “Androgenized OVX”(single dose of testosterone propionate 1.25 mg s.c. at day 5 of life and ovariectomy at day 100, n=10); and 4) “Androgenized SHAM” (n=10). Full characterization of estrous cycles and weight was performed during growth, and all animals were euthanized at day 180 during metestrus/diestrous. Evaluation of glucose levels, lipids, estradiol, P1NP levels (a marker of bone formation), and analysis of the femur micro CT Skyscan 1174 (Aartselaar, Belgium) was performed in at least eight animals of each group. Ovariectomy increased the weight of Androgenized OVX rats on day 180: these animals were heavier than Control OVX, Control SHAM, or Androgenized SHAM (ANOVA p<0.001). However, metabolic changes were observed in ovary-intact Androgenized SHAM rats who exhibited higher total cholesterol (ANOVA p<0.001), increased LDL (ANOVA p=0.03), and elevated TyG index, a marker of insulin resistance (ANOVA p<0.001) against all other three groups. This group (Androgenized SHAM rats)also exhibited an increase in MicroCt bone density (g/cm-3) (mean + SEM) of 1.117 + 0.06 against the other - Control SHAM 0.8433 + 0.03, Control OVX 0.5527 + 0.001, and Androgenized OVX 0.6284 + 0.02 (ANOVA p< 0.001). Although the values of bone density between Control OVX and Androgenized OVX groups were similar, gonadal removal produced a different pattern of bone density reduction between Control OVX and Androgenized OVX (Two-Way ANOVA p=0.001). Moreover, we found P1NP levels significantly decreased in the Androgenized OVX group (mean + SEM) of 58.57 + 4.41 ng/ml against 88.02 + 8.49 ng/ml in Control OVX versus (ANOVA p<0.0001) indicating lower bone formation. Our results suggest that bone and metabolic features of Androgenized rats are affected by ovariectomy with a negative impact on bone formation.
Evidence from the literature is contentious about the impact of polycystic ovary syndrome (PCOS) on the skeleton, suggesting a possible negative role of this condition on non-obese women. We investigated this hypothesis employing a well-characterized testosterone propionate (TP) rodent model of PCOS to address the consequences of androgenization on bone microarchitecture, histology, and mechanical strength. For this study, Wistar rats (n= 38) were divided in 4 groups: 1) “Control OVX” (single dose of corn oil s.c. at day 5 of life and ovariectomy at day 100, n=9); 2) “Control SHAM” (n=9); 3) “Androgenized OVX”(single dose of TP 1.25 mg s.c. at day 5 of life and ovariectomy at day 100, n=10); and 4) “Androgenized SHAM” (n=10). Full characterization of estrous cycles and weight was performed during growth, and all animals were euthanized at day 180. Successful ovariectomy was confirmed by neglected levels of serum estradiol. Endpoints evaluated include bone micro CT (femur and spinal column), bone histology (number of osteoclasts and osteoblasts in the femur), and mechanical tests. The study was approved by the local Ethics Committee. At the end of the study (day 180), Androgenized OVX rats were heavier than the other three groups. MicroCT Analysis: Androgenized SHAM rats exhibited a significantly higher trabecular mass in the spine (BV/BT) (mean + SEM) 49.21 + 2.42 % versus Control SHAM 36.42 + 1.39 % (Student T-test p=0.001). Following ovariectomy, BV/BT in Androgenized OVX was 40.4 + 2.83 % against 20.34 + 1.85 % in Control OVX (Student T-test p=0.0003). Lumbar trabecular thickness(μm) was also higher in Androgenized OVX (p=0.0065) as well the Trabecular number (n/mm)(p=0.0003). A similar increase in trabecular mass was observed in the femur. Androgenized SHAM rats had a significant higher BV/BT (%), trabecular thickness(μm), and decreased trabecular separation (p < 0.001). However, a significant reduction in cortical bone (thickness) was noted (Student T-test p=0.001). A histological study of the distal femur of Androgenized SHAM rats also show a significantly increased number of osteoclasts and decreased number of osteoblasts than Control SHAM (0< 001). When submitted to the mechanical test, Androgenized Sham rats presented a decreased strength (p<0.01) in relation to its controls. After ovariectomy, there was a reduction in bone in all oophorectomized groups. However, differently than the vertebral bones, no differences regarding bone mechanical strength or stiffness as well microCT values, or bone histology parameters were noted in the femur of Control OVX or Androgenized OVX. Our results suggest that androgenization in a rodent model of PCOS leads, at the same time, to a generalized increase in trabecular (cancellous) bone mass (especially in the spine), associated with a reduced cortical bone mass and decreased strength of the femur.
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