Serological, sequence, and in vitro host range analyses of feline parvovirus (FPV) isolates in Vietnam and Taiwan revealed that more than 80% of the isolates were of the canine parvovirus (CPV) type, rather than feline panleukopenia virus (FPLV). Although parvovirus isolates from three Vietnamese leopard cats were genetically related to CPV type 2a or 2b, they had a natural mutation of VP2 residue 300 Gly to an Asp, resulting in remarkable changes in their antigenic properties. These results indicated the possibility that CPV-2a/2b-type viruses can spread in cats more efficiently than conventional FPLV under natural conditions and that CPV-2a/2b viruses are further evolving in cats.

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Serum samples from two leopard cats (Felis bengalensis) and four Formosan gem-faced civets (Paguma larvata taivana) in Taiwan, September 1995, and nine leopard cats in Vietnam, August and December 1997, were examined for the prevalence of antibodies against feline parvovirus, feline herpesvirus type 1, feline calicivirus and feline immunodeficiency virus. All civets and nine of 11 leopard cats were shown to have antibodies against feline parvovirus (FPV), and FPV's were isolated from mononuclear cells in the peripheral blood of the six leopard cats.

Feline parvovirus (FPV) was isolated rather frequently from the peripheral blood mononuclear cells (PBMCs) of cats in northern Vietnam by coculturing with MYA-1 cells (an interleukin -2 -dependent feline T lymphoblastoid cell line) or Crandell feline kidney (CRFK) cells (a feline renal cell line). Efficiency of virus isolation was higher in MYA-1 cells than in CRFK cells. Interestingly, among the 17 cats from which FPV was isolated, 9 cats were positive for virus neutralizing (VN) antibody against FPV, indicating that FPV infected PBMCs and was not eliminated from PBMCs even in the presence of VN antibodies in the cats.

The root of Polygala tenuifolia WILLD (PT) (Japanese name: Onji) is a well-known traditional Chinese medicine used as an expectorant, a tonic, a tranquillizer and an anti-dementia drug. However, basic researches of the anti-dementia effects are very few in spite of PT being generally recognized as a good herbal drug for amnesia. It was reported that 80% ethanol extract of PT and the methanol extract of PT reverse scopolamine-induced cognitive impairments in rats. 1,2) Acetylcholinestrase (AChE) activity is inhibited in vitro by 80% ethanol extract of PT.1,3) Onjisaponin F, a constituent in PT, increases cholineacetyltransferase (ChAT) mRNA level in rat basal forebrain cell, and. Taken together, transient enhancement of cholinergic systems by PT may be involved in the memory improvement seen in like the scopolamine model. However, practical dementia is caused by irreversible neuronal damage involving neuronal death, neuritic atrophy and synaptic loss. Especially in case of Alzheimer's disease, neuritic atrophy and synapse loss are earlier events than neuronal death are, and are critical for memory disorder. [4][5][6][7][8] Previous our studies suggested that compounds which showed synaptic regeneration activity in cultured neurons were also active for memory impairment in vivo using Alzheimer's disease model mice.9-11) Although protective effects of PT on neuronal death were shown in amyloid b (Ab), glutamate or NMDA-induced neuronal damage, effects of PT on atrophy of neuritis and synaptic loss never have been investigated yet.1,12) Therefore, we aimed in this study to characterize activities of PT under Ab-induced neuritic damage. MATERIALS AND METHODS MaterialsThirty gram of roots of Polygala tenuifolia WILLD (PT) was extracted with 600 ml of water at 100°C for 40 min. This crude drug was purchased from Tochimoto Tenkaido (Osaka, Japan). The decoction was evaporated under reduced pressure and freeze-dried of extract powder (yield: 8.02 g). The extract was then dissolved in sterilized distilled water at 1000 times concentrations of final concentrations. Ab (25-35) (Sigma, Saint Louis, MO, U.S.A.) was dissolved in sterile distilled water at a concentration of 5 mM, and was incubated at 37°C for 3 d to allow fibril formation. [Gly 14 ]-Humanin was purchased from Phoenix Pharmaceuticals (Belmont, CA, U.S.A.) as a positive control for neuronal protection. A monoclonal antibody to phosphorylated neurofilament-H (NF-H) was purchased from Sternberger Monoclonals (Lutherville, MD, U.S.A.). A monoclonal antibody to microtubule-associated protein 2 (MAP2), an antiserum to MAP2, polyclonal antibody to MAP2 and a monoclonal antibody to synaptophysin were purchased from Chemicon (Temecula, CA, U.S.A.). Alexa Fluor 488-conjugated goat anti-mouse IgG and Alexa Fluor 546-conjugated goat antirabbit IgG were purchased from Molecular Probes (Eugene, OR, U.S.A.). Aqua Poly Mont was purchased from Polyscience (Warrington, PA, U.S.A.).Primary Culture Embryos were removed from pregnant Sprague Dawley rats (Japan SLC, Shizuoka, J...

Nasogastric tube syndrome named by Sofferman et al in 1981 is a laryngeal complication presenting with lifethreatening vocal cord abductor paralysis derived from peroforation of the NG tube-induced esophageal ulcer. As compared with the previously reported cases of this syndrome, our 4 autopsied patients were so peculiar in the following two points that vocal cord abductor paralysis developed repeatedly and no esophageal ulcer was present in spite of the presence of the laryngeal abductor muscle injury. We hypothesized that the etiology of such a variant form was circulatory injury of the laryngeal abductor muscle which was caused by the compression of the postcricoid blood vessels perfusing this muscle. Nasogastric tube syndrome, which is treatable by decannulation, cannot be ruled out even if no esophageal ulcer is detected by fiberoptic laryngoscopy.

ABSTRACT. Previously, we reported that a feline T lymphoid cell line, FL74 cells, was very sensitive to feline parvovirus (FPV) infection. In the present study, we developed new quantitative methods for detection of FPV and virus neutralizing antibody against FPV using FL74 cells. The methods presented here were very simple and applicable to both canine parvovirus and feline panleukopenia virus. -KEY WORDS: CPV, FPLV, neutralization test.J. Vet. Med. Sci. 60(8): 973-974, 1998 dose (TCID50) was calculated by the method of BehrensKärber. For detection of FPLV or CPV antigen in CRFK cells, the indirect immunofluorescence (IF) assay was performed as reported previously using an anti-VP2 monoclonal antibody 2D9, which can react with both FPLV and CPV [5,9]. Firstly, to compare the sensitivity of CRFK, FL74 and CL-1 cells against FPLV and CPV, we titrated TU1 or Cp49 strain in the three cell lines. The assay was carried out in a 96-well flat bottom microplate. Ten-fold serially diluted viruses (1:5 to 1:5 × 10 7 ) were distributed at 100 µl/well into 12 wells of a 96-well microplate. Then 100 µl of CRFK, FL74 or CL-1 cells (2 × 10 4 cells/ml) were added to the wells in quadruplicates. Consequently, the total volume was 200 µl/well and each well contained the diluted viruses ranged from 1:10 to 1:10 8 . The inoculated CRFK cells were harvested by trypsinization 7 days post inoculation (p.i.) and FPLV or CPV infection was examined by the indirect IF assay. On the other hand, in FL74 and CL-1 cells, the virus infection was determined by appearance of their CPE.The titers of TU1 and Cp49 strains in CRFK cells reached 10 4.25 and 10 4.5 TCID 50 /100 µl, respectively. In FL74 cells, the ten-fold diluted FPLV or CPV showed the typical CPE as early as 1 day p.i. and the end point dilution of FPLV or CPV showed the CPE 3 or 4 days p.i., respectively. The titers of TU1 and Cp49 strains in FL74 cells reached 10 4.5 and 10 5.25 TCID 50 /100 µl, respectively. In CL-1 cells, the ten-fold diluted CPV showed the typical CPE as early as 2 days p.i. and the end point dilution of CPV showed the CPE 9 days p.i. The titer of Cp49 strain in CL-1 cells reached 10 2.0 TCID 50 /100 µl. In addition, although TU1 strain did not show any CPE in the CL-1 cells in the present study, it was repeatedly confirmed that TU1 strain could grow and cause CPE in CL-1 cells when the cells were infected with the virus at much higher multiplicity of infection. From these results, it was clearly demonstrated that the system using FL74 cells was most sensitive to FPLV and CPV infections among the three cell lines. By using FL74 cells, we could determine the titer of FPLV or CPV within 4 days. Mochizuki et al. [8] previously indicated the possibility that transmission of parvovirus occurred between Feline panleukopenia virus (FPLV) and canine parvovirus (CPV) are classified as host range variants of the feline parvovirus (FPV). FPLV causes acute depression, gastroenteric symptoms such as diarrhea and vomiting, and lymphopenia, with a high mortality among non...

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