Efficacy of liver free and Chitosan against Eimeria tenella in chickens.

Eimeria spp. are the pathogen that causes coccidiosis, a significant disease that affects intensively reared livestock, especially poultry. Anticoccidial feed additives, chemicals, and ionophores have routinely been employed to reduce Eimeria infections in broiler production. Therefore, the shift to antibiotic-free and organic farming necessitates novel coccidiosis preventive strategies. The present study evaluated the effects of potential feed additives, liver free and chitosan, against Eimeria tenella infection in White Leghorn broiler female chickens. One hundred sixty-five 1-day-old White Leghorn broiler female chicks were divided into 11 groups (15 female chicks per group), including the positive control group (G1), the negative control group (G2), a chitosan-treated group (G3), a chitosan-treated-infected group (G4), the liver free-treated group (G5), the liver free-treated-infected group (G6), the liver free-and-chitosan-treated group (G7), the liver free-and-chitosan-infected group (G8), the therapeutic liver free-and-chitosan-treated-infected group (G9), the sulfaquinoxaline-treated group (G10), and the sulfaquinoxaline-treated-infected group (G11). Chitosan was fed to the chicks in G3 and G4 as a preventative measure at a dose of 250 mg/kg. The G5 and G6 groups received 1.5 mg/kg of Liverfree. The G7 and G8 groups received chitosan and Liverfree. The G10 and G11 groups were administered 2 g/L of sulfaquinoxaline. From the moment the chicks arrived at Foshan University (one-day-old chicks) until the completion of the experiment, all medications were given to them as a preventative measure. G8 did; however, receive chitosan and liver free as therapeutic supplements at 7 dpi. The current study showed that the combination of liver free and chitosan can achieve better prophylactic and therapeutic effects than either alone. In E. tenella challenged chickens, G8 and G9 chickens showed reduced oocyst shedding and lesion score, improved growth performance (body weight, body weight gain, feed intake, feed conversion ratio, and mortality rate), and cecal histology. The current study demonstrates that combining liver free and chitosan has superior preventive and therapeutic benefits than either alone, and they could also be used as alternative anticoccidial agents.

Assessment of oxidative stress and tissue damage in Echinococcus granulosus naturally infected bovine liver.

Echinococcus granulosus is a zoonotic parasite infects many livestock species, especially cattle, sheep, goat and buffalo, causing cystic echinococcosis. The aim of this study was to demonstrate the presence of the parasite and parasitic tissue damage histopathologically and to determine the role of oxidative stress in the tissue damage through the immunohistochemical detection of the oxidative damage-marker malondialdehyde (MDA) and the antioxidant response-marker superoxide dismutase (SOD). The material of the study consisted of 20 liver samples with Echinococcus cysts and 10 E.granulosus- negative healthy liver samples obtained from different cattle at various times from slaughterhouses in Kirikkale province, Turkey. Histopathologically, Echinococcus cysts of various sizes were observed along with the surrounding fibrous connective tissue. Giant cells, mononuclear cells, and eosinophilic leukocytes were found between the fibrous connective tissue and the cyst. In the parenchymal tissue distant from the cyst, inflammatory changes were observed, including vacuolation and necrosis in hepatocytes, congestion and dilation sinusoidal capillaries. Immunohistochemically, MDA immunopositivity was observed in both hepatocytes surrounding the cyst and areas distant from the cyst, while SOD immunopositivity was mainly detected in fibrous connective tissue and hepatocytes surrounding the Echinococcus cysts. A significant increase in MDA immunoreactivity was observed in E.granulosus s.l.-infected livers. Although no statistically significant change was observed in SOD immunopositivity in the liver tissues with cystic echinococcosis, regional variations were noted. Germinal layer (GL) of Echinococcus cyst showed immunopositive staining for MDA, while laminated layer (LL) exhibited immunonegative staining. To the authors' best understanding, this study represents a pioneering effort in showcasing and evaluating the immunoreactivities of MDA and SOD within the liver tissue afflicted with Echinococcus cysts. Simultaneously, the examination extends to encompass tissue damage and the infiltration of inflammatory cells. This study highlights the role of oxidative stress in the pathogenesis of Cystic Echinococcosis (CE) and the need for further investigation of antioxidant defense mechanisms and their regional variations.

ADAMTS-13 and HMGB1-induced oxidative stress in Taenia multiceps-infected animals.

This study investigated the cytotoxic effects of oxidative stress (OS), high mobility group box 1 (HMGB1), ADAMTS (A disintegrin and metalloproteinase with thrombospondin motifs), and neuropathology associated with coenurus cerebralis (Taenia multiceps). ADAMTS-13, HMGB1, glutathione reductase (GR), copper/zinc superoxide dismutase (Cu/Zn SOD), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) expression levels were studied. The study found that ADAMTS-13 (P < 0.005), HMGB1 (P < 0.005), GR (P < 0.005), Cu/Zn SOD (P < 0.005), and 8-OHdG (P < 0.005) levels were significantly higher in T. multiceps (c. cerebralis)-infected animals compared to healthy control animals. This study's most important finding was that HMGB1 up-regulation in neurons, endothelial cells, and glial cells can directly cause brain parenchymal destruction and that HMGB1-mediated oxidative stress plays a crucial role in the neuropathogenesis of coenurosis. The results also showed that increased levels of ADAMTS-13 may play a pivotal role in regulating and protecting the blood-brain barrier integrity and neuroprotection. These findings also suggest that ADAMTS-13 and HMGB1 compete in the prevention or formation of microthrombi, which was regarded as a remarkable finding. ADAMTS-13 and HMGB1 are valuable biomarkers for disease risk assessment, estimating host neuropathy following T. multiceps (c. cerebralis) exposure, and providing a new therapeutic target. This is the first study to show that HMGB1 and ADAMTS-13 are expressed in reactive cells and are associated with neuroimmunopathology in coenurosis.

Effect of Local and Systemic Dimethylsulfoxide on Peripheral Nerve Repair: A Controlled Randomized Experimental Study.

INTRODUCTION: We investigated the possible beneficial effect of dimethylsulfoxide (DMSO) on peripheral nerve repair in rats. Methods: Seventy rats were divided into four groups: control, sham, DMSO-L, and DMSO-IP. Except in the control group, nerve repair was done at the right sciatic nerve. DMSO was administered locally and intraperitoneally for 12 weeks to the DMSO-L and DMSO-IP groups, respectively. No therapeutic agent was administered to the other groups. Nerve regeneration was assessed by behavioral, electrophysiological, histopathological, and immunohistochemical tests. Results: With the exception of S-100 protein expression, all results indicate that DMSO has a beneficial effect on peripheral nerve regeneration. Functional nerve recovery was notably more evident in the DMSO-L than in the DMSO-IP group. Under macroscopic examination, nerve scores of the regeneration area in the DMSO-L group was also better than in the others. Discussion: We believe that DMSO can improve peripheral nerve regeneration in rats.

Research on the Effects of Levetiracetam in Spinal Cord Injury Model in Rats: An Experimental Study.

Purpose: Despite advances in spinal biomechanic research, surgical techniques, and rehabilitation processes, no significant improvement has been identified in the treatment of spinal cord injury (SCI) and neurological recovery. Aim of the Study: This study was designed to investigate the potential therapeutic effects of methylprednisolone and levetiracetam on SCI. Materials and Methods: In this study, 42 male Wistar Albino rats, each weighing 300-350 g, were separated into three main groups: control group, acute and subacute stage groups. With the exception of the control group, a T7-8 dorsal laminectomy was performed on the spinal column of the rats. A temporary vascular aneurysm clip was then applied to the spinal cord for 1 min to create SCI and methylprednisolone or levetiracetam was administered intraperitoneally to all except the control and SHAM control groups. The damaged spinal cord was removed for histopathological and biochemical examinations. Results: Both pharmacological agents were determined to have improved the histopathological architecture in damaged neural tissues during the acute period of SCI, but could not sustain this activity in the subacute period. Neither pharmacological agent affected the biochemical data in the acute nor subacute stages. Conclusions: Both pharmacological agents showed histopathological healing effects in injured tissues during the acute phase of SCI in this rat model but these effects could not be sustained in the subacute period. No effect on biochemical data was seen in either the acute or subacute period. There is a need for further advanced studies to determine the effects of levetiracetam on the healing processes in SCI.

First description of enhanced expression of transforming growth factor-alpha (TGF-α) and glia maturation factor-beta (GMF-ß) correlate with severity of neuropathology in border disease virus-infected small ruminants.

Border disease (BD) is caused by Pestivirus and characterized by severe neuropathology, and histopathologically observed severe hypomyelination. We have previously shown that small ruminants infected with border disease virus (BDV) play an important role for neuropathology and pathogenesis of severe oxidative damage in brain tissue, neuronal mtDNA; in the production of high pathologic levels of nitric oxide; in glial cell activation and stimulation of intrinsic apoptosis pathway. This study aimed to investigate the relationship between glia maturation factor beta (GMF-ß) and transforming growth factor alpha (TGF-α) expressions and the causes of BDV-induced neuropathology and to investigate their role in neuropathogenesis in a way that was not presented before. Expression levels of GMF-ß and TGF-α were investigated. Results of the study revealed that the levels of GMF-ß (P < 0.005) and TGF-α (P < 0.005) expression in the brain tissue markedly increased in the BDV-infected animals compared to the non-infected healthy control group. While TGF-α expressions were predominantly observed in neurons, GMF-ß expressions were found in astrocytes, glial cells and neurons. These results were reasonable to suggest that BDV-mediated increased GMF-ß might play a pivotal role neuropathogenesis and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of BD. The results also indicated that increased levels of GMF up-regulation in glial cells and neurons causes neuronal destruction, suggesting pathological pathway involving GMF-mediated brain cell cytotoxicity. It is clearly indicated that the cause of astrogliosis is due to severe TGF-a expression. This is the first study to demonstrate the expression of GMF-ß and TGF-α in neurons and reactive glial cells and its association with neuropathology in BD.

Effectiveness of the Biophysical Barriers to the Peridural Fibrosis in Rat Laminectomy Model.

Purpose: Peridural fibrosis which could occur after the spinal surgery could adhere neural tissue closely and may cause to neural entrapment symptoms and require surgical reintervention. Aim of the study: Present study was designed to reduce occurrence of peridural fibrosis in rat laminectomy model by using biophysical barriers called hyaluronic acid (HAS) dural barrier, activated polyethylene glycol and polyethylene imine (PEG) dural barrier, and platelet-rich plasma (PRP). Materials and methods: In this study, 2 of 26 male Wistar albino rats (325-350 g body weight), which were not included into study groups were sacrificed by removing their total blood and their blood was used for preparation of PRP, and remaining rats were randomly delivered into four groups called SHAM, HAS, PEG, and PRP groups. Then L3-4-5 laminectomy was performed to all animals and experimental agents were administered to the selected groups mentioned above. Spinal colons of all animals were removed gross total after 6-week period and investigated histopathologically. Additionally, real-time-polymerase chain reaction was used to obtain collagen type I and type III, transforming growth factor-1ß, and tumor necrosis factor-α gene expressions. Results: All results demonstrated that polyethylene glycol and polyethylene imine dural barrier and PRP could decrease peridural fibrosis formation efficiently in rat. Conclusion: Present study results suggested that to reduce or block formation of peridural fibrosis, either polyethylene glycol and polyethylene imine dural barrier or PRP could be used effectively in human subjects after they will be closely investigated in future studies.

The Investigation of the Cox-2 Selective Inhibitor Parecoxib Effects in Spinal Cord Injury in Rat.

Aim: Today, spinal cord injury (SCI) can be rehabilitated but cannot be treated adequately. This experimental study was conducted to investigate possible beneficial effects of methylprednisolone and parecoxib in treatment of SCI. Materials and methods: Forty-eight male Wistar albino rats were assigned into CONTROL, acute (MP-A, PX-A, and PXMP-A), and subacute (MP-S, PX-S, and PXMP-S) stage groups. Then, to induce SCI, a temporary aneurysm clip was applied to the spinal cord following T7-8 laminectomy, except in the CONTROL group. Four hours later parecoxib, methylprednisolone, or their combination was administered to rats intraperitoneally except CONTROL, SHAM-A, and SHAM-S groups. Rats in the acute stage group were sacrificed 72 h later, and whereas rats in the subacute stage were sacrificed 7 days later for histopathological and biochemical investigation and for gene-expression analyses. Results: Parecoxib and methylprednisolone and their combination could not improve histopathological grades in any stage. They also could not decrease malondialdehyde or caspase-3, myeloperoxidase levels in any stage. Parecoxib and methylprednisolone could decrease the TNF-α gene expression in subacute stage. Methylprednisolone could increase TGF-1ß gene-expression level in acute stage. Conclusion: Neither of the experimental drugs, either alone or in combination, did not show any beneficial effects in SCI model in rats.

Tracking acute phase protein response during acute and chronic Toxoplasma gondii infection.

Toxoplasmosis is a disease caused by the protozoan Toxoplasma gondii, which occurs worldwide in mammals and birds. Brain is the primary target organ because Toxoplasma gondii is a ubiquitous intracellular parasite that causes most frequently life-threatening encephalitis in immunocompromised patients. Relation of tissue cysts number, histopathology score and acute phase proteins were investigated. In this study, 36 mice are infected with Me49 strain of Toxoplasma gondii. The control group has 6 healthy mice. After inoculation of Toxoplasma gondii, at 10., 15., 20., 30., 45., 60. days, 6 each mice euthanized after collection of blood samples. Hemopexin, haptoglobulin, macroglobulin, serum amyloid A and clusterin levels are determined by ELISA. Then, brain tissues were investigated histopathologically and lesions were scored. The average cyst numbers were determined by counting three samples (25 µl each) of each brain homogenate under light microscopy. Inflammatory reaction was observed on day 10 days after inoculation (d.a.i.) The lesions were characterized by perivascular mononuclear cell infiltration, focal mononuclear cell infiltration in the meninges, and glial proliferation. Tissue cysts were observed in all Toxoplasma gondii-infected groups. The highest lesion score was observed at 60 d.a.i. And the most tissue cyst number were on day 30. d.a.i. Serum levels of hemopexin, haptoglobulin, macroglobulin, serum amyloid A and clusterin were significantly higher than the control group on day 10-20., 10., 10-30., 10.,10-45 d.a.i., respectively. High level of acute phase proteins in mice on certain days infected with Toxoplasma gondii was exhibited a relationship between brain lesions and tissue cysts.

Cerebral ischaemia/reperfusion injury could be managed by using tramadol.

OBJECTIVES: No valid treatment modality that will repair stroke damage and provide neurological recovery has yet been identified in literature. Studies demonstrated that adequate quality of life could be provided if post-stroke pain could be treated sufficiently and timely. Besides its pain relief effects, tramadol has oedema-reducing and anti-inflammatory properties. With these in mind, this study investigated the influence of tramadol in acute and/or chronic ischaemia/reperfusion (I/R) injury. METHODS: Putting aside the Control group, 23 Wistar albino rats were distributed to four groups to investigate the acute (Sham-A, TR-A) and chronic (Sham-C, TR-C) periods of I/R injury, and temporary aneurysm clips were applied to their internal carotid arteries for 30 min. Four hours after clippage, tramadol was administered to animals of TR-A and TR-C groups intraperitoneally. After sacrificing all animals, pyknotic and necrotic neuronal cells in hippocampal cornu ammonis (CA)1, CA2, CA3 and parietal cortical regions were counted, and perivascular oedema, intercellular organization disorder (IOD) and inflammatory cell infiltration were scaled histopathologically. Additionally, tissue interleukin (IL)-1ß, IL-10, malondialdehyde, nitric oxide, tumour necrosis factor-α, caspase-3, beclin-1, Atg12, LC3II/LC3I levels were measured biochemically. RESULTS: Tramadol could minimize perivascular oedema, IOD, parietal and hippocampal neuronal necrosis, inflammatory cell infiltration in both periods of I/R injury histopathologically. Apart from inhibiting apoptosis and enhancing autophagy, tramadol had no influence on any other biochemical result. DISCUSSION: Tramadol can ameliorate the histopathological structure of ischaemic tissue in both periods of I/R injury in rat. We suggest further research investigating various dosages with different administration methods of tramadol in stroke should be conducted by adopting different explorative techniques.

Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat.

BACKGROUND: Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today. AIMS OF THE STUDY: Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat. METHODS: Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically. RESULTS: Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1ß, IL-6, MPO, NO, and TNFα levels. It could increase IL-1ß levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels. CONCLUSION: Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.

First description of enhanced expression of glia maturation factor-beta in experimental toxoplasmic encephalitis.

Objective We previously showed that Toxoplasma gondii infection induces severe neuropathology in the form of oxidative stress, high nitric oxide production, glial activation, and apoptosis. This study examined the association between glia maturation factor-beta (GMF-ß) expression, activated astrocytes/microglia, and neuropathology in toxoplasmic encephalitis (TE). Methods Mouse brain GMF expression was examined by immunohistochemistry on days 10 and 30 post- T. gondii infection. Results Neuropathology of infected mice was associated with increased GMF expression in reactive glial cells and neurons compared with healthy controls. Specific up-regulation of GMF-ß expression in glial cells was associated with increased gliosis in TE. Conclusions GMF up-regulation in glial cells causes neuronal destruction, suggesting a TE pathological pathway involving GMF-mediated brain cell cytotoxicity. GMF-ß may therefore be a good biomarker for disease risk assessment and to estimate host neuropathy after exposure to T. gondii, as well as providing a new therapeutic target. This is the first study to demonstrate the expression of GMF-ß in reactive glial cells and its association with neuropathology in TE.

Effects of DMSO on a rabbit ear hypertrophic scar model: A controlled randomized experimental study.

Dimethyl sulfoxide (DMSO) is an anti-inflammatory, antibacterial, analgesic drug widely used to treat several diseases as reported in the literature. It has a detractive effect on collagen deposition in the abnormal tissue. This study aimed to investigate the possible therapeutic effects of DMSO on hypertrophic scar formation in rabbits. Twenty-four New Zealand male albino rabbits were randomly divided into four groups: control, sham, DMSO, and TRA (triamcinolone acetonide). Except the control group, punch biopsy defects were created on each animal's right ear. Following the hypertrophic scar formation on day 28, intralesional DMSO and triamcinolone acetonide were administered once a week for 4 weeks into these scars of the DMSO and TRA groups, respectively. No therapeutic agent was administered to the control and sham groups. One week after the last injection, ear samples were collected for histopathological, immunohistochemical, and real-time polymerase chain reaction gene expression analyses. Histopathological examination revealed that the epithelium in the DMSO group was thicker than that in the control and TRA groups, but thinner than that in the sham group. Connective tissue thickness and vascularity level of the sham group were higher than those of the control, DMSO, and TRA groups. The collagen type I immunoreactivity level of the sham and TRA groups was higher than those of the control and DMSO groups. The collagen type III immunoreactivity level was higher in the sham group than in all other groups. Collagen type I/type III immunoreactivity ratios were lower in the DMSO group. The alignment of collagen fibers was normal in the DMSO group, but was irregular in the sham and TRA groups. The collagen type I gene expression levels of the DMSO and TRA groups were lower than that of the sham group. Collagen type III and IFN-γ mRNA expression levels were almost similar among the groups. TGF-1ß mRNA expression levels were higher in the DMSO and TRA groups than in the control and sham groups. On the basis of the results, it can be concluded that intralesional administration of DMSO decreases hypertrophic scar formation easily and safely.

Role of oxidative stress in the pathophysiology of Toxoplasma gondii infection.

Oxidative stress (OS) plays an essential role in the pathogenesis of common neurodegenerative diseases. We have previously shown that Toxoplasma gondii (T. gondii) induces high nitric oxide (NO) production, glial activation, and apoptosis that altogether cause severe neuropathology in toxoplasma encephalitis (TE). The objective of this study was to investigate the cytotoxic effect of OS and to identify a correlation between the causes of T. gondii induced neuropathology. Expression levels of glutathione reductase (GR), Cu/Zn superoxide dismutase (SOD1), neuron specific enolase (NSE), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were investigated. Results of the study revealed that the levels of GR (P <0.005) and NSE (P <0.001) expression in the brain tissue markedly increased while SOD1 activity decreased (P <0.001) in the infected group compared to the non-infected group. In addition, intense staining for 8-OHdG (P <0.05) was observed both in the nucleus and the cytoplasm of neurons and glial cells that underwent OS. These results were reasonable to suggest that T. gondii-mediated OS might play a pivotal role and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of TE. The results also clearly indicated that increased levels of NO and apoptosis might contribute to OS-related pathogenesis of TE. As a result, OS and expression of NSE might give an idea of the disease progress and may have a critical diagnostic significance for patients with T. gondii infection.

Increased expressions of ADAMTS-13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice.

Toxoplasma gondii (T. gondii) is a protozoan parasite with the potential of causing severe encephalitis among immunocompromised humans and animals. Our previous study showed that T. gondii induces high nitric oxide (NO) production, high glial activation (GFAP) and neurofilament expressions, leading to severe neurodegeneration in toxoplasma encephalitis (TE) in the central nervous system (CNS). The aim of this experimental study was to investigate ADAMTS-13 expression and apoptosis in CNS and to identify whether they have any correlation with toxoplasmosis neuropathology and neurodegeneration. Mice were infected with ME49 strain T. gondii and the levels of ADAMTS-13, caspase 3, caspase 8, caspase 9, TNFR1 and Bcl-xL expressions were examined in brain tissues by immunohistochemistry, during the development and establishment of chronic infections at 10, 30 and 60 days post-infection. Results of the study revealed that the levels of ADAMTS-13 (P < 0.005), caspase 3 (P < 0.05), caspase 8 (P < 0.05), caspase 9 (P < 0.005) and TNFR1 (P < 0.05) expressions in the brain markedly increased while Bcl-xL expression decreased (P < 0.005). The most prominent finding from our study was that 10, 30 and 60 days post-infection ADAMTS-13 increased significantly and this may play an important role in the regulation and protection of the blood-brain barrier integrity and CNS microenvironment in TE. These results also suggest that T. gondii-mediated apoptosis might play a pivotal role and a different type of role in the mechanism of neurodegeneration and neuropathology in the process of TE. Furthermore, expression of ADAMTS-13 might give an idea of the progress and is critical for diagnosis of this disease. To the best of the authors' knowledge, this is the first report on ADAMTS-13 expression in the CNS of T. gondii-infected mice.

Nitric oxide production increases during Toxoplasma gondii encephalitis in mice.

Toxoplasma gondii is an intracellular parasite with the potential of causing severe encephalitis among immunocompromised human and animals. The aim of this experimental study was to investigate the immunomodulatory and immunopathological role of nitric oxide (NO) in central nervous systems and to identify any correlation between toxoplasmosis neuropathology and investigate the consequences of the cellular responses protect against T. gondii. Mice were infected with ME49 strain T. gondii and levels of endothelial, neuronal and inducible nitric oxide synthase (eNOS, nNOS, iNOS), glial fibrillary acidic protein (GFAP) and neurofilament (NF) were examined in brain tissues by immunohistochemistry, during the development and establishment of a chronic infection at 10 30 and 60 days post infection. Results of the study revealed that the levels of eNOS (p < 0.05), nNOS (p < 0.05), iNOS (p < 0.005), GFAP (p < 0.005) and NF (p < 0.005) were remarkably higher in T. gondii-infected mice than in uninfected control. The most prominent finding from our study was 10 and 30 days after inoculation data indicating that increased levels of NO not only a potential neuroprotective role for immunoregulatory and immunopathological but also might be a molecular trigger of bradyzoite development. Furthermore, this findings were shown that high expressed NO origin was not only inducible nitric oxide synthase but also endothelial and neuronal. We demonstrated that activation of astrocytes and microglia/macrophages is a significant event in toxoplasma encephalitis (TE). The results also clearly indicated that increased levels of NO might contribute to neuropathology related with TE. Furthermore, expression of NF might gives an idea of the progress and critical for diagnostic significance of this disease.

eNOS and iNOS trigger apoptosis in the brains of sheep and goats naturally infected with the border disease virus.

In this study, apoptotic and anti-apoptotic mechanisms and if present, which pathway to trigger the apoptosis in the brains of Border Disease Virus (BDV) infected lambs (n=10) and goat kids (n=5) were investigated. Briefly, apoptotic (caspase 3, caspase 9) and anti-apoptotic markers (Bcl-2), cytokine response (TNF-α, INF-γ), reactive gliosis and myelin loss were examined. eNOS, iNOS, caspase 9, caspase 3 and GFAP expressions were higher in BDV infected tissues compared to control animals (6 kids and 6 lambs) (p<0.05). Double immunoperoxidase test revealed that TUNEL positive apoptotic cells showed significant association with increased eNOS-iNOS and iNOS-BDV expressions. However, no significant differences were found for TNFR1, TNF-α and INF-γ expressions in BD (p>0.05). There was a positive correlation between the intensity of myelin loss, GFAP activity and severity of infection. Inconclusion, as a novel finding, it is established that eNOS and iNOS overexpressions are co-associated with apoptosis in BDV infected neurons and neuroglia. The results also strongly suggested that BDV infected apoptotic cells mainly prefer the intrinsic pathway that might be most likely related to increased nitric oxide levels.

Increased expressions of ADAMTS-13, neuronal nitric oxide synthase, and neurofilament correlate with severity of neuropathology in Border disease virus-infected small ruminants.

Border Disease (BD), caused by Pestivirus from the family Flaviviridae, leads to serious reproductive losses and brain anomalies such as hydranencephaly and cerebellar hypoplasia in aborted fetuses and neonatal lambs. In this report it is aimed to investigate the expression of neuronal nitric oxide synthase (nNOS), A Disintegrin And Metalloprotease with Thrombospondin type I repeats-13 (ADAMTS-13), and neurofilament (NF) in the brain tissue in small ruminants infected with Border Disease Virus (BDV) and to identify any correlation between hypomyelinogenesis and BD neuropathology. Results of the study revealed that the levels of ADAMTS-13 (p<0.05), nNOS (p<0.05), and NF (p<0.05) were remarkably higher in BDV-infected brain tissue than in the uninfected control. It was suggested that L-arginine-NO synthase pathway is activated after infection by BDV and that the expression of NF and nNOS is associated with the severity of BD. A few studies have focused on ADAMTS-13 expression in the central nervous system, and its function continues to remain unclear. The most prominent finding from our study was that ADAMTS-13, which contain two CUB domains, has two CUB domains and its high expression levels are probably associated with the development of the central nervous system (CNS). The results also clearly indicate that the interaction of ADAMTS-13 and NO may play an important role in the regulation and protection of the CNS microenvironment in neurodegenerative diseases. In addition, NF expression might indicate the progress of the disease. To the best of the authors'knowledge, this is the first report on ADAMTS-13 expression in the CNS of BDV-infected small ruminants.

A rare case of feline congenital Toxoplasma gondii infection: fatal outcome of systemic toxoplasmosis for the mother and its kitten.

This report describes a case of fatal systemic toxoplasmosis in a 2.5-year-old mixed breed pregnant cat and its kittens. The pregnant cat was presented to the gynecology clinic with symptoms of dystocia. The ultrasound examination revealed the presence of five fetuses in the uterus, three of which were not alive, and consequently a cesarean section was performed. However, the mother cat and the remaining two live kittens died two and ten days after cesarean section, respectively. Pathologically, severe alveolar edema, tachyzoite-like structures in the alveolar macrophages and multifocal necroses in the lungs of mother cat were observed. An intense Toxoplasma gondii immunopositive reaction was observed in the cytoplasms of alveolar macrophages, bronchial and bronchiolar epithelia, necrotic foci in the lungs, and Kupffer cells of the liver. PCR analyses amplified T. gondii DNA in tissue samples of the mother cat and kittens. The present study provides strong evidence for a transplacental transmission of T. gondii infection with deadly outcome for the mother cat, fetuses and kittens. As to the authors' knowledge, this report is the first case of fatal congenital toxoplasmosis in domestic cats in Turkey.

Characterization of chondrocytes cultured on catechin-loaded alginate-chitosan scaffolds.

Bovine chondrocytes were seeded into scaffolds of a high molecular weight chitosan and alginate with a pore size of 50-350 µm with or without catechin. In polymerase chain reaction (PCR), unlike type II, collagen type I was no longer expressed at day 14. The DNA content increased until day 8 and began declining, indicating cell detachment. The GAG content increased during the first 12 days. The percentage of round and collagen type II immunoreactive cells increased over the time. Catechin has some protective properties on chondrocytes seeded on the alginate-chitosan scaffolds during the first 12 days by means of DNA and chondrocyte morphology (p < 0.05).