Mice were infected by feeding the embryonated eggs of Toxocara canis and Ascaris lumbricoides. Each mouse was killed daily for a week and then at several days interval after infection and the distribution of larvae in the various tissues of mice was investigated after the macerating the tissues and digesting with artificial gastric juice. It was confirmed that the migratory behaviour of larvae of T. canis and A. lumbricoides is referred to as the somatic and tracheal type of migration in the mice respectively. Toxocara larvae were found in the carcass on the third day after infection and in the brain after the sixth day of infection. From the thirty-fifth day to the seventy-sixth day after infection, Toxocara larvae were not found in the tissues of mice except in the carcass and brain and they did not develop further than the second-stage larvae. The size of Ascaris larvae, from the embryonated eggs was 0.228-0.271 mm length by 0.010-0.013 mm width and in the third day of infection the size of larvae was 0.271-0.343 mm length by 0.017-0.020 mm width. Between the fifth and tenth day after infection, lavrae molted twice in the lungs and grew to the fouth-stage larvae; 1.357-2.0 mm by 0.034-0.071 mm. These larvae migrated to the intestinal canal after the tenth day of infection and disappeared from the mouse after the twenty-fifth day of infection. No larvae were found in the carcass and brain. The inflammatory reactions in the tissues of infected mice were also observed.
: parasitology-helminth-nematode-Toxocara cani ; Ascaris lumbricoides ; mouse ; migration ; animal

Adult worms of Parvatrema spp. (Digenea: Gymnophallidae) were found in the intestines of 2 species of migratory birds, i.e., a great knot, Calidris tenuirostris, and 2 Mongolian plovers, Charadrius mongolus, in the coastal area of Gunsan-si, Jeollabuk-do in October 2009. The recovered Parvatrema worms were 79 in total number and composed of 2 species. The worms from a great knot were 289 micrometer in length with the oral and ventral sucker ratio of 2 : 1. They had a single vitellarium, and their intrauterine eggs were 25.0 x 17.5 micrometer in size. These findings were compatible with P. duboisi (Dollfus, 1923) Bartoli, 1974 (syn. P. timondavidi Bartoli, 1963). The worms recovered from the Mongolian plovers were smaller in length than P. duboisi and had 2 vitellaria. The oral and ventral sucker ratio was 2.5 : 1, and the eggs were 17.5 x 8.8 micrometer in size. These worms were assigned to be P. homoeotecnum James, 1964. This is the first report on the natural final hosts of Parvatrema spp. in Korea.
*Animal Migration ; Animals ; Bird Diseases/*parasitology ; Charadriiformes/*parasitology/physiology ; Trematoda/anatomy & histology/*isolation & purification ; Trematode Infections/parasitology/*veterinary

Macrophage migration inhibitory factor (MIF) is originally identified in the culture medium of activated T lymphocytes as a soluble factor that inhibits the random migration of macrophages. MIF is now recognized as a multipotent cytokine involved in the regulation of immune and inf lammatory responses. In rheumatoid arthritis (RA), MIF promotes inf lammatory responses by inducing proinflammatory cytokines and tissue-degrading molecules, promoting the proliferation and survival of synovial fibroblasts, stimulating neutrophil chemotaxis, and regulating angiogenesis and osteoclast differentiation. Expression of MIF in synovial tissue and synovial fluid levels of MIF are elevated in RA patients. Specifically, MIF levels correlate with RA disease activity and high levels are associated with bone erosion. In animal models of RA, the genetic and therapeutic inhibition of MIF has been shown to control inflammation and bone destruction. Based on the role of MIF in RA pathogenesis, small molecular inhibitors targeting it or its receptor pathways could provide a new therapeutic option for RA patients.
Arthritis, Rheumatoid* ; Chemotaxis ; Cytokines ; Fibroblasts ; Humans ; Inflammation ; Macrophage Migration-Inhibitory Factors ; Macrophages* ; Models, Animal ; Neutrophils ; Osteoclasts ; Synovial Fluid ; T-Lymphocytes

Cortical malformation-associated epileptic seizures are resistant to conventional anticonvulsant drugs. Relatively little research has been conducted on the effects of antiepileptic drugs (AEDs) on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate (MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of ethosuximide (ETX) in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed and age-matched vehicle-injected control animals. Field potential recordings were used to monitor the amplitude and number of population spikes, and paired pulse inhibition in response to stimulation of the commissural pathway. Pharmaco-resistance was tested by measuring seizure latencies after pilocarpine administration (320 mg/kg, i.p.) with and without pre-treatment with ETX. Pre-treatment with 300 mg of ETX significantly prolonged the latency to the status epilepticus (SE) in both control and MAM-treated groups. Pre-treatment with ETX 100mg and ETX 200 mg had little effect in MAM-exposed rats. However, ETX 200 mg prolonged the latency to the SE in control groups. Spontaneous field potential and secondary after-discharges were higher for MAM-treated rat in comparison with control rats injects with ETX. The main findings of this study are that acute seizures initiated in MAM-exposed rats are relatively resistant to standard ETX assessed in vivo. These data suggest that ETX do not prolong seizure latencies in MAM-rats exposed to pilocarpine.
Animals ; Anticonvulsants ; Brain ; Epilepsy ; Ethosuximide* ; Methylazoxymethanol Acetate ; Models, Animal* ; Neuronal Migration Disorders* ; Neurons* ; Pilocarpine* ; Rats* ; Seizures* ; Status Epilepticus

OBJECTIVETo analyze the spatial distribution of highly pathogenic avian influenza (HPAI) and to explore environmental factors associated with HPAI using geographic information system (GIS) techniques in Mainland China.

METHODSDatabases were set up using the information of HPAI during epidemics in 2004, and linked to digital maps at provincial and county administrative layers in the country through the ArcGIS 8.3 software. Spatial cluster analyses, spatial statistics analyses and tracking analyses on epidemic situation of HPAI were implemented. Environmental factors associated with HPAI were also analyzed on data related to weather, vegetation and migratory birds etc.

RESULTSFindings from spatial cluster analyses showed that high incidence area was centralized in 113.261 degrees ordm; east longitude and 23. 119 degrees ordm; north latitude with a radius of 1090.52 kilometers (relative risk= 2.646, P value= 0.001). Spatial statistical analyses showed that HPAI took place mainly in capital cities of provinces and surrounding areas as well as in the circumference areas of arterial rivers, lakes and seacoasts. Results also showed that HPAI occurrences were associated with low air temperature, high relative humidity and high air pressure as well as with east & central migration routes of migratory birds. The average normalized difference vegetation index was 0.36 +/- 0.11 in epidemic areas of HPAI.

CONCLUSIONHPAI was unrandomly distributed and geographically clustered in China.

Animal Migration ; Animals ; Atmospheric Pressure ; Birds ; virology ; China ; epidemiology ; Cluster Analysis ; Environment ; Geographic Information Systems ; Humidity ; Influenza A Virus, H5N1 Subtype ; pathogenicity ; Influenza in Birds ; epidemiology ; Temperature

OBJECTIVE: To detect the expression of macrophage migration inhibitory factor(MIF) in the brain and spinal cord of chronic non-remitting model of experimental autoimmune encephalomyelitis(EAE) mouse, and to discuss their effect on EAE/MS. METHODS: Seventy-two female SPF C57BL/6J mice, aged 6k8 weeks, were randomly divided into an EAE group, a blank group, and an adjuvant group. The mice were immuned by mMOG35-55 and CFA. Immunohistochemic technique was used to detect the expression of MIF in the brain and spinal cord. RESULTS: In the EAE group, we observed up-regulation of MIF of central nervous system(CNS) at onset, peak and chronic phase. During each phase, the difference of MIF between the EAE group and each of the other 2 groups was significant (P<0.05). In the EAE group, the expression of MIF was the highest at the peak, which was different from other periods (P<0.05). CONCLUSION MIF significanty expressed during the procedure of EAE disease, and may be related with the onset and exacerbation of EAE.
Animals ; Brain ; metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental ; chemically induced ; metabolism ; Female ; Macrophage Migration-Inhibitory Factors ; biosynthesis ; Mice ; Mice, Inbred C57BL ; Random Allocation ; Up-Regulation

PURPOSE: A majority of patients with neuronal migration disorders(NMDs) in cortical structures suffer from medically intractable epilepsy. The role of NMDs on seizure susceptibility or epileptogenecity has not been well documented. In the present study, we established an experimental model of NMDs in Sprague-Dawley rats by exposing fetal rats to external irradiation in order to demonstrate epileptogenic effect of NMDs lesions. METHODS: Pregnant rats were exposed to 240cGy of external X-irradiation delivered by a linear accelerator source on gestational day 16 and 17 to produce NMDs lesions in rat brain. RESULTS: Microcephaly was evident on gross examination of the affected brains. Seizure susceptibility was tested by a small dose of kainate(0.1mg/kg) injected intraperitoneally, and the irradiated animals showed increased susceptibility to kainate. Histopathologic examination revealed cortical dysplasia consisting of dyslamination of cerebral cortex and appearance of cytomegalic neurons, neuronal heterotopia in periventricular white matter, dispersion of pyramidal layer and hippocampal dentate gyrus, and agenesis of corpus callosum. Histopathologic change of the cerebral cortex and hippocampus was closely correlated with seizure activity. Quantitative autoradiography of [H]muscimol binding to GABAA receptors was significantly reduced in NMDs lesions(P=0.02). CONCLUSION: In utero irradiation of fetal rats resulted in histopathologic abnormalities that mi- miced several characteristic features of human neuronal migration disorders, and hyperexcitability appears to be associated with reduction in density of GABAp receptors in the brain, particularly in hippocampus and neocortex.
Agenesis of Corpus Callosum ; Animals* ; Autoradiography ; Brain ; Cerebral Cortex ; Dentate Gyrus ; Epilepsy ; Hippocampus ; Humans ; Kainic Acid ; Kinetics* ; Malformations of Cortical Development ; Mice ; Microcephaly ; Models, Animal* ; Models, Theoretical ; Neocortex ; Neuronal Migration Disorders* ; Neurons* ; Particle Accelerators ; Rats ; Rats, Sprague-Dawley ; Seizures

Climate change induced by recent global warming may have a significant impact on vector-borne and zoonotic diseases. For example, the distribution of Japanese encephalitis virus (JEV) has expanded into new regions. We surveyed the levels of hemagglutination-inhibition (HI) antibodies against JEV (Family Flaviviridae, genus Flavivirus) in wild birds captured in Korea. Blood samples were collected from 1,316 wild birds including the following migratory birds: Oceanodroma castro (n = 4), Anas formosa (n = 7), Anas penelope (n = 20), Fulica atra (n = 30), Anas acuta (n = 89), Anas crecca (n = 154), Anas platyrhynchos (n = 214), Aix galericulata (n = 310), and Anas poecilorhyncha (n = 488). All were captured in 16 locations in several Korea provinces between April 2007 and December 2009. Out of the 1,316 serum samples tested, 1,141 (86.7%) were positive for JEV. Wild birds captured in 2009 had a higher seroprevalence of ant-JEV antibodies than those captured in 2007. Wild birds with an HI antibody titer of 1 : 1,280 or higher accounted for 21.2% (280/1,316) of the animals tested. These findings indicated that wild birds from the region examined in our study have been exposed to JEV and may pose a high risk for introducing a new JEV genotype into Korea.
Animal Migration ; Animals ; Animals, Wild ; Bird Diseases/*epidemiology/virology ; Birds ; Encephalitis Virus, Japanese/genetics/*isolation & purification ; Encephalitis, Japanese/blood/epidemiology/*veterinary/virology ; Genotype ; Hemagglutination Inhibition Tests ; Population Surveillance ; Republic of Korea/epidemiology ; Seroepidemiologic Studies

PURPOSE: To investigate the effect of macrophage migration inhibitory factor (MIF) on corneal sensitivity after laser in situ keratomileusis (LASIK) surgery. METHODS: New Zealand white rabbits were used in this study. A hinged corneal flap (160-microm thick) was created with a microkeratome, and -3.0 diopter excimer laser ablation was performed. Expressions of MIF mRNA in the corneal epithelial cells and surrounding inflammatory cells were analyzed using reverse transcription polymerase chain reaction at 48 hours after LASIK. After LASIK surgery, the rabbits were topically given either 1) a balanced salt solution (BSS), 2) MIF (100 ng/mL) alone, or 3) a combination of nerve growth factor (NGF, 100 ug/mL), neurotrophine-3 (NT-3, 100 ng/mL), interleukin-6 (IL-6, 5 ng/mL), and leukemia inhibitory factor (LIF, 5 ng/mL) four times a day for three days. Preoperative and postoperative corneal sensitivity at two weeks and at 10 weeks were assessed using the Cochet-Bonnet esthesiometer. RESULTS: Expression of MIF mRNA was 2.5-fold upregulated in the corneal epithelium and 1.5-fold upregulated in the surrounding inflammatory cells as compared with the control eyes. Preoperative baseline corneal sensitivity was 40.56 +/- 2.36 mm. At two weeks after LASIK, corneal sensitivity was 9.17 +/- 5.57 mm in the BSS treated group, 21.92 +/- 2.44 mm in the MIF treated group, and 22.42 +/- 1.59 mm in the neuronal growth factors-treated group (MIF vs. BSS, p < 0.0001; neuronal growth factors vs. BSS, p < 0.0001; MIF vs. neuronal growth factors, p = 0.815). At 10 weeks after LASIK, corneal sensitivity was 15.00 +/- 9.65, 35.00 +/- 5.48, and 29.58 +/- 4.31 mm respectively (MIF vs. BSS, p = 0.0001; neuronal growth factors vs. BSS, p = 0.002; MIF vs. neuronal growth factors, p = 0.192). Treatment with MIF alone could achieve as much of an effect on recovery of corneal sensation as treatment with combination of NGF, NT-3, IL-6, and LIF. CONCLUSIONS: Topically administered MIF plays a significant role in the early recovery of corneal sensitivity after LASIK in the experimental animal model.
Animals ; Epithelium, Corneal/*drug effects/innervation/physiology ; Female ; Humans ; Interleukin-6/pharmacology ; Keratomileusis, Laser In Situ/*methods ; Leukemia Inhibitory Factor/pharmacology ; Macrophage Migration-Inhibitory Factors/genetics/*pharmacology ; Models, Animal ; Nerve Growth Factor/pharmacology ; Nerve Regeneration/*drug effects/physiology ; Neurotrophin 3/pharmacology ; RNA, Messenger/metabolism ; Rabbits ; Recovery of Function/*drug effects/physiology ; Sensation/*drug effects/physiology

The aim of this study was to, from the point of neurogenic inflammation, explore the pathogenesis of colitis and to provide direct evidence for the neurogenic colitis hypothesis. Male Sprague-Dawley rats (180-220 g) anesthetized with chloral hydrate were intrathecally (ith) implanted with polyethylene-10 (PE-10) catheter to reach the spinal cord T₁₂-L₅ level. Substance P (SP) was ith injected once a day for 14 d. The disease active index (DAI) score was calculated by rat body weight and stool. The macroscopic and HE staining-microscopic pathologies of colon/spinal tissue were evaluated. By immunofluorescence staining, the protein expression of a pro-inflammatory cytokine, migration inhibitory factor (MIF), in colon tissue was detected and was semi-quantitatively analyzed. The results showed that in the colon tissue, inflammation was dose-dependently aggravated by ith SP 10 μ and 20 μ, whereas in the spinal tissue, only slight edema and congestion were seen in SP 20 μ group. The MIF protein of colon tissue was increased in ith SP 10 μ and 20 μ groups (P<0.05, P<0.01 as compared to normal saline group respectively), but in the spinal tissue, there was no obvious MIF protein expression either in SP groups or in normal saline group. Pretreatment with neurokinin-1 (NK₁) receptor antagonist ([D-Pro2, D-Trp7, 9] -SP, 22.4 μ, ith, 10 min before ith SP) prolonged the latency of DAI rising and reduced the DAI amplitude, as well as prevented the high MIF expression induced by ith SP. These results suggest that rat colitis can be induced by direct SP stimulation in lumbar spine via activating central NK₁ receptor; and that colonic MIF is possibly one of the inflammatory factors involved in this pathogenesis. These data provide a reasonable support to the hypothesis of colitis being a neurogenic inflammation. In addition, a potential clinical significance for the finding that higher concentration of spinal SP can induce colitis via NK₁ receptor is discussed.
Animals ; Colitis ; chemically induced ; Colon ; pathology ; Disease Models, Animal ; Inflammation ; pathology ; Injections, Spinal ; Intramolecular Oxidoreductases ; metabolism ; Macrophage Migration-Inhibitory Factors ; metabolism ; Male ; Neurokinin-1 Receptor Antagonists ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1 ; metabolism ; Spinal Cord ; pathology ; Substance P ; adverse effects