• Journal of Veterinary Clinics
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• v.25 no.6
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• pp.506-509
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• 2008

A 2-month-old, intact female white Bull Terrier presented because of suspected deafness. The coat color was predominantly white and the iris color, of both eyes, was brown. The dog did not respond to the owner's voice when the sound stimuli were presented outside of the visual field; however, the dog responded to visual gestures. The other physical, neurological, otoscopic, radiographic, and blood examinations were unremarkable. To assess the apparent deafness, brainstem auditory evoked responses (BAER) were recorded and analyzed in the dog with suspected deafness as well as a normal littermate. The response in the normal littermate consisted of a series of five wave peaks (I-V) with decreased amplitude and prolonged latency as the stimulus intensity decreased. The BAER from the dog suspected of deafness appeared as a flat line and did not reveal identifiable peaks that corresponded to those found in the normal littermate. Thus, congenital, sensorineural and bilateral deafness was confirmed by the BAER.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.115-122
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• 2024

Heat shock protein (HSP) 90 is expressed in most living organisms, and several client proteins of HSP90 are necessary for cancer cell survival and growth. Previously, we found that HSP90 was cleaved by histone deacetylase (HDAC) inhibitors and proteasome inhibitors, and the cleavage of HSP90 contributes to their cytotoxicity in K562 leukemia cells. In this study, we first established mouse xenograft models with K562 cells expressing the wild-type or cleavage-resistant mutant HSP90β and found that the suppression of tumor growth by the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) was interrupted by the mutation inhibiting the HSP90 cleavage in vivo. Next, we investigated the possible function of thioredoxin interacting protein (TXNIP) in the HSP90 cleavage induced by SAHA. TXNIP is a negative regulator for thioredoxin, an antioxidant protein. SAHA transcriptionally induced the expression of TXNIP in K562 cells. HSP90 cleavage was induced by SAHA also in the thymocytes of normal mice and suppressed by an anti-oxidant and pan-caspase inhibitor. When the thymocytes from the TXNIP knockout mice and their wild-type littermate control mice were treated with SAHA, the HSP90 cleavage was detected in the thymocytes of the littermate controls but suppressed in those of the TXNIP knockout mice suggesting the requirement of TXNIP for HSP90 cleavage. We additionally found that HSP90 cleavage was induced by actinomycin D, β-mercaptoethanol, and p38 MAPK inhibitor PD169316 suggesting its prevalence. Taken together, we suggest that HSP90 cleavage occurs also in vivo and contributes to the anti-cancer activity of various drugs in a TXNIP-dependent manner.

• Korean Journal of Veterinary Research
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• v.48 no.2
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• pp.209-213
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• 2008

A four-month-old intact femlae Abyssinian cat was present for routine health evaluation, because her littermate was recently died of ventricular septal defect. Diagnostic imaging studies showed a large caudal paracardiac mass in thoracic radiography and homogenous mass adjacent to heart in the echocardiography. Further echographic study revealed that the mass was liver and the diaphragmatic line was intact. The positive contrast celiogram revealed that no extravasation of the contrast media across the diaphragm and the prolapse of diaphragm into the pleural cavity. Based on our diagnostic imaging studies, the case was diagnosed as diaphragmatic deformity in a cat mimicking a cardiac mass.

• Journal of Life Science
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• v.19 no.9
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• pp.1232-1238
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• 2009

Neurotransmitter release is regulated by various proteins of the active zone in the presynaptic nerve terminals. Dopamine (DA) is an essential neurotransmitter associated with the pathophysiology of diverse behavioral and mental illness such as schizophrenia and drug addiction. We measured synaptosomal DA release of knockout (KO) mice which lacked major genes related to neurotransmitter release. Synaptosomal DA uptake and release were performed and measured using [$^3H$]-DA and superfusion experiments. 3 of the 17 KO mice exhibited altered DA release compared to their littermate controls. In $Rim1{\alpha}$ KO, [$^3H$]-DA release evoked by membrane depolarization significantly decreased. Both basal (physiological buffer-evoked) and membrane depolarization-evoked DA release significantly decreased in dopaminergic conditional KO of $Rim1{\alpha}{\beta}$. Dopaminergic conditional KO of neurexin3 demonstrated a significant increase of membrane depolarization-evoked DA release. These data explain the similarities and distinctions between DA and other classical neurotransmitters such as glutamate and GABA ($\gamma$-aminobutyric acid) release. In conclusion, $Rim1{\alpha}$ and neurexin3 may be important regulators of presynaptic DA release and related to disorders of the nervous system.

• BMB Reports
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• v.41 no.1
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• pp.23-28
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• 2008

The altered amino acid (AA) levels as neurotransmitter closely correlate to neurodegenerative conditions including Alzheimer's disease (AD). Target profiling analysis of nineteen AAs in brain cortex samples from three Tg2576 mice as AD model and three littermate mice as control model was achieved as their N(O,S)-ethoxycarbonyl/tert-butyldimethylsilyl derivatives by gas chromatography. Subsequently, star pattern recognition analysis was performed on the brain AA levels of AD mice after normalization to the corresponding control median values. As compared to control mice, $\gamma$-aminobutyric acid among ten AAs found in brain samples was significantly reduced (P < 0.01) while leucine was significantly elevated (P < 0.02) in AD mice. The normalized AA levels of the three AD mice were transformed into distorted star patterns which was different from the decagonal shape of control median. The present method allowed visual discrimination of the three AD mice from the controls based on the ten normalized AA levels.

• Asian-Australasian Journal of Animal Sciences
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• v.29 no.7
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• pp.1060-1064
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• 2016

With regard to animal welfare concerns, behavioral information of weaned and mixed piglets is great interest in swine production. The aim of this study was to demonstrate the change in behavior of weaned piglets over time in two different groups (littermates and piglets from different litters) after mixing. Two weaned groups of piglets (72 individuals in all) housed either with littermates or with foreign piglets (6 individuals in $1.8m{\times}1.4m$ pens, $28^{\circ}C{\pm}1^{\circ}C$ temperature) were observed with the aid of video technology for 9 consecutive hours on days 1, 2, and 3 after mixing. The behaviors of the weaned piglets in the control and treatment groups were significantly different among the days after mixing. Piglets were, however, more active and aggressive in the groups with foreign piglets. This study reveals a lower level of agonistic behavior in groups of piglets that came from the same litter.

• IMMUNE NETWORK
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• v.2 no.3
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• pp.133-136
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• 2002

Background: The costimulatory molecule 4-1BB, a member of nerve growth factor receptor/tumor necrosis factor (NGFR/TNFR) super family, is involved in cell survival and death. Methods: In this study, female C57BL/6 ($H-2^b$) mice were used as a recipient, and DBA/2 ($H-2^d$) as a donor to assess a mixed lymphocyte reaction (MLR) and CTL response in vitro, and skin graft survival. IL-2, IFN level was measured by ELISA. Results: Mixed lymphocyte reaction (MLR) analysis showed that 4-1BB-deficient responder cells showed enhanced cellular proliferation over littermate controls. In contrast, IL-2 production was diminished only in 4-1BB knockout cultures. The IFN expression, on the other hand, was comparable between the groups. When female C57BL/6 ($H-2^b$) mice were grafted with the trunk skin of DBA/2 ($H-2^d$) mice, the in vivo tissue destruction of 4-1BB-deficient mice was not distinct from the normal littermates. Conclusion: These data suggest that 4-1BB is critical for the induction of alloreactive responses in vitro but 4-1BB alone could not change the course of skin rejection in vivo.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.251-257
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• 2017

Inhibition of $K^+$ outward currents by linopirdine in the outer hair cells (OHCs) of circling mice (homozygous (cir/cir) mice), an animal model for human deafness (DFNB6 type), was investigated using a whole cell patch clamp technique. Littermate heterozygous (+/cir) and ICR mice of the same age (postnatal day (P) 0 -P6) were used as controls. Voltage steps from -100 mV to 40 mV elicited small inward currents (-100 mV~-70 mV) and slow rising $K^+$ outward currents (-60 mV~40 mV) which activated near -50 mV in all OHCs tested. Linopirdine, a known blocker of $K^+$ currents activated at negative potentials ($I_{K,n}$), did cause inhibition at varying degree (severe, moderate, mild) in $K^+$ outward currents of heterozygous (+/cir) or homozygous (cir/cir) mice OHCs in the concentration range between 1 and $100{\mu}m$, while it was apparent only in one ICR mice OHC out of nine OHCs at $100{\mu}m$. Although the half inhibition concentrations in heterozygous (+/cir) or homozygous (cir/cir) mice OHCs were close to those reported in $I_{K,n}$, biophysical and pharmacological properties of $K^+$ outward currents, such as the activation close to -50 mV, small inward currents evoked by hyperpolarizing steps and TEA sensitivity, were not in line with $I_{K,n}$ reported in other tissues. Our results show that the delayed rectifier type $K^+$ outward currents, which are not similar to $I_{K,n}$ with respect to biophysical and pharmacological properties, are inhibited by linopirdine in the developing (P0~P6) homozygous (cir/cir) or heterozygous (+/cir) mice OHCs.

• Journal of Veterinary Clinics
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• v.26 no.5
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• pp.467-471
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• 2009

This report describes Neural Tube Defects (NTDs) with Abdominal Wall Defects (AWDs) on the sibling of Yorkshire terriers. The NTDs and AWDs are rare serious congenital defects. The NTDs are neurulation abnormality that results from to failed transformation of the neurual tube by the incomplete closure of the embryonic neural plate. These dysraphic states range form mild to severe according to developmental malformation that include fusion defects of skull (crania bifida; CB) and fusion defects of vertebrae (spina bifida; SB). The AWDs are genetic defects that results from to failed formation of abdominal wall and cavity. These dysraphic states are omphalocele and gastroschisis. The 12-month dam was delivered by caesarian section and 4 littermate had obvious malformations. One male dead stillbirth fetus (L1) was revealed the extruded abdominal viscera, omphalocele. One female fetus (L2) was died within 1 hour after birth with defects of abdominal muscle upper umbilicus, gastroschisis. 3rd fetus (L3) was died within 36 hours after parturition and revealed a copious dermal and vertebral defects on the midline thorax, upper SB asperta. 4th fetus (L4) is still growing well now at 6 months but at the 2 week age, appears hairy nevus on the frontal cranium and dorsal thoracic portion. The radiograph of L1 and L2 are shown decrease bony density of calvarium and L3 was shown defect of spinose processes of the T9-T13. On our knowledge, this is first report of the SB and CB in Yorkshire terrier. And also sibling of NTDs with AWDs that has not previously been reported in the dog.

• Parasites, Hosts and Diseases
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• v.48 no.3
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• pp.247-251
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• 2010

Feline intestinal tritrichomoniasis by Tritrichomonas foetus was first recognized in USA in 1999 and has so far been reported from UK, Norway, Switzerland, and Australia, but not from the Far East Asian countries. In November 2008, 2 female and male littermate Siamese cats, 6-month old, raised in a household in Korea were referred from a local veterinary clinic with a history of chronic persistent diarrhea. A direct smear examination of fecal specimens revealed numerous trichomonad trophozoites which were isolated by the fecal culture in $InPouch^{TM}$ TF-Feline medium. A PCR testing of the isolate based on the amplification of a conserved portion of the T. foetus internal transcribed spacer (ITS) regions (ITS1 and ITS2) and the 5.8S rRNA gene, and the molecular sequencing of the PCR amplicons confirmed infection with T. foetus. This is the first clinical case of feline intestinal trichomoniasis caused by T. foetus in Korea.