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Abstract Bovine babesiosis is one of the destructive diseases affecting cattle worldwide especially in tropical and subtropical areas. In Egypt, small livestock holder represents the majority of livestock owners affected by the devastating impact of this disease including costs of diagnosis, treatment, control and prevention as well as limitations of production and reproduction of the affected animals. Early and accurate diagnosis of Babesia spp. infection plays an important role in treatment and control. The current study aimed to evaluate the efficacy of Loop-Mediated Isothermal amplification (LAMP) assay as a new molecular technique used for diagnosis of bovine babesiosis in naturally infected cattle. The confirmation of this infection was depended on blood smears, LAMP and Nested-Polymerase chain Reaction (nPCR) assays, which confirmed the infection in 19%, 47.62% and 52.38% of the examined animals, respectively. Tick samples were collected and identified as Rhipicephalus (Boophilus) annulatus, which is the vector of Babesia spp. Evaluation of blood smears and LAMP assay was carried out against nPCR as a reference test. The obtained results revealed that LAMP assay is a sensitive, specific and cost effective test and will be one of the near future applicable tests in epidemiological and diagnostic studies on babesiosis especially in developing countries endemic with this disease.

Mercuric chloride toxicity experimentally induced in mice were associated with chronic neuropathology in brain including ischemic neuronal injury, spongiosis, liqufactive necrosis, perivascular and precellular edema, congestion and hyalinization of chroid plexus of lateral and fourth ventricles of the brain. These changes were observed in cerebral cortex, hypothalamus and cerebellum. The experimental animal showing clinical signs related to neuropathological changes as impared response to noise, loss of perfect movement and sleeping altitude. Co-adminstration of garlic and ginger oil together with mercuric chloride greatly inhept the above mentioned changes and result an improvement and recovery

Mercuric chloride toxicity experimentally induced in mice were associated with chronic neuropathology in brain including ischemic neuronal injury, spongiosis, liqufactive necrosis, perivascular and precellular edema, congestion and hyalinization of chroid plexus of lateral and fourth ventricles of the brain. These changes were observed in cerebral cortex, hypothalamus and cerebellum. The experimental animal showing clinical signs related to neuropathological changes as impared response to noise, loss of perfect movement and sleeping altitude. Co-adminstration of garlic and ginger oil together with mercuric chloride greatly inhept the above mentioned changes and result an improvement and recovery

Mercuric chloride toxicity experimentally induced in mice were associated with chronic neuropathology in brain including ischemic neuronal injury, spongiosis, liqufactive necrosis, perivascular and precellular edema, congestion and hyalinization of chroid plexus of lateral and fourth ventricles of the brain. These changes were observed in cerebral cortex, hypothalamus and cerebellum. The experimental animal showing clinical signs related to neuropathological changes as impared response to noise, loss of perfect movement and sleeping altitude. Co-adminstration of garlic and ginger oil together with mercuric chloride greatly inhept the above mentioned changes and result an improvement and recovery

Objective. The aim of this study was to evaluate an intraarticular injection of different doses of autologous mesenchymal stem cells (MSCs) for improving repair of midterm osteochondral defect. Design. At 4 weeks postoperative marrow stimulation model bilaterally (3 mm diameter; 4 mm depth) in the medial femoral condyle, autologous MSCs were injected into knee joint. Twenty-four Japanese rabbits aged 6 months were divided randomly into 4 groups (n = 6 per group): the control group and and MSC groups including 0.125, 1.25, and 6.25 million MSCs. Repaired tissue was assessed macroscopically and histologically at 4 and 12 weeks after intraarticular injection of MSCs. Results. At 12 weeks, there was no repair tissue in the control group. The gross appearance of the 1.25 and 6.25 million MSC groups revealed complete repair of the defect with white to pink tissue at 12 weeks. An osteochondral repair was histologically significantly better in the 1.25 and 6.25 million MSC groups than in the control and 0.125 million MSC groups at 4 and 12 weeks, due to presence of hyaline-like tissue in the deep layer at 4 weeks, and at 12 weeks hyaline cartilage formation at the periphery and fibrous tissue containing some chondrocytes in the deep layer of the center of the defect. Subchondral bone was restructured in the 1.25 and 6.25 million MSC groups, although it did not resemble the normal bone. Conclusion. An intraarticular injection of 1.25 or 6.25 million MSCs could promote the repair of subchondral bone, even in the case of midterm osteochondral defect.

The aim of this study was to investigate a cell delivery system for repair of severe chronic osteochondral defects using magnetically labeled mesenchymal stem cells (m-MSCs), with the aid of an external magnetic device, through the accumulation of a small number of m-MSCs into a desired area and to detect the suitable number of autologous m-MSCs needed for repair of the defect. Twenty-six male Japanese white rabbits aged 6 months were used. An osteochondral defect was created bilaterally at the weight-bearing surface of the medial femoral condyle of the rabbits’ knees (3 mm diameter; 4 mm depth). At 4 weeks after creation of the defect, autogenic transplantation of the m-MSCs into the defect area was performed, followed by 10-min exposure to an external magnetic device, where animals were divided into four groups: high (1 × 106 m-MSCs), medium (2 × 105 m-MSCs), low (4 × 104 m-MSCs), and control (PBS injection). At 4 and 12 weeks posttransplantation of m-MSCs, repaired tissue was assessed histologically using the Fortier score with toluidine blue staining. Transplantation of a low number of m-MSCs was not enough to improve osteogenesis and chondrogenesis, but the medium and high groups improved repair of the chronic defect with chondrogenic tissues and showed histologically significantly better results than the control and low groups. The use of a magnetic targeting system for delivering m-MSCs has the potential to overcome the clinical hurdles for repair of the severe chronic osteochondral defect. Furthermore, this system is predicted to produce good clinical outcomes for humans, not only to repair osteochondral defects but also to repair a variety of damaged tissues.

Mesenchymal stromal cells (MSCs) have the capacity to differentiate into cells of mesenchymal lineage, such as chondrocytes, and have potential for use in regeneration of equine articular cartilage. MSCs instilled intra-articularly would be exposed to the inflamed environment associated with equine osteoarthritis (OA), which may compromise their function and ability to heal a cartilaginous defect. The aim of this study was to assess the ability of equine adult MSCs to differentiate into chondrocytes when stimulated with pro-inflammatory cytokines. MSCs derived from equine bone marrow (BM) and from synovial fluid (SF) were cultured in chondrogenic induction medium containing transforming growth factor (TGF)-β1. BM-derived MSCs (BMMSCs) and SF-derived MSCs (SFMSCs) were stimulated with 100 ng/mL interferon (IFN)-γ and 10 ng/mL tumor necrosis factor (TNF)-α. Chondrogenic differentiation was measured quantitatively with the glycosaminoglycan (GAG) assay and qualitatively by immunofluorescence (IF) for SOX-9, TGF-β1, aggrecan and collagen II. The viability of equine MSCs was maintained in the presence of IFN-γ and TNF-α, but production of GAGs from both types of MSCs was decreased in stimulated medium. Exposure of BMMSCs to pro-inflammatory cytokines reduced the levels of SOX-9, TGF-β1, aggrecan and collagen II, whereas exposure of SFMSCs to these cytokines reduced the levels of aggrecan only. These data suggest that pro-inflammatory cytokines do not affect proliferation of MSCs, but could inhibit chondrogenesis of MSCs.

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