http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Juvenile Obesity Aggravates Disease Severity in a Rat Model of Atopic Dermatitis
나흥식,백승근,정근영,이재희,이정진,한태호,이샛별,이현경 대한천식알레르기학회 2015 Allergy, Asthma & Immunology Research Vol.7 No.1
inPurpose: There is increasing epidemiological evidence of an association between childhood obesity and atopic dermatitis, but little is known about the underlying mechanism(s). In the present study, we used a rat model of atopic dermatitis to assess whether juvenile obesity, induced by reduction of litter size, aggravated the signs of atopic dermatitis and, if so, whether this aggravation was associated with changes in plasma concentration of adipokines, such as leptin and adiponectin. Methods: Dermatitis was induced by neonatal capsaicin treatment. Body weight, dermatitis score, serum IgE, skin nerve growth factor (NGF), serum leptin and adiponectin, and cytokine mRNA expression in the skin lesion were compared between small (SL, 5 pups) and large litters (LL, 15 pups). Results: The body weight of juvenile rats up to 6 weeks of age was significantly heavier in the SL group, compared with those in the LL group. The SL group showed more robust development of dermatitis, and higher levels of serum IgE and skin NGF than the LL group. Additionally, the SL group demonstrated higher levels of leptin and pro-inflammatory cytokine mRNA but lower levels of adiponectin than the LL group. Conclusions: These results suggest a causal link between a decrease in immunological tolerance, induced by juvenile obesity, and aggravation of atopic dermatitis.
Attenuated Neuropathic Pain in Ca(V)3.1 Null Mice
나흥식,Soonwook Choi,김준선,Joonoh Park,신희섭 한국분자세포생물학회 2008 Molecules and cells Vol.25 No.2
To assess the role of α1G T-type Ca2+ channels in neuropathic pain after L5 spinal nerve ligation, we examined behavioral pain susceptibility in mice lacking CaV3.1 (α1G −/−), the gene encoding the pore-forming units of these channels. Reduced spontaneous pain responses and an increased threshold for paw withdrawal in response to mechanical stimulation were observed in these mice. The α1G −/− mice also showed attenuated thermal hyperalgesia in response to both low-(IR30) and high-intensity (IR60) infrared stimulation. Our results reveal the importance of α1G T-type Ca2+ channels in the development of neuropathic pain, and suggest that selective modulation of α1G subtype channels may provide a novel approach to the treatment of allodynia and hyperalgesia.
구심성 미주신경과 구심성 하심장 신경에 대한 전기자극이 호흡과 혈압에 미치는 영향
나흥식 고려대학교 의과대학 1987 고려대 의대 잡지 Vol.24 No.1
This experiment was performed to determine the influence on tachypnea evoked by coronary heart diseases with pain in itself or pulmonary congestion secondary to acute congestive heart failure in the anesthetized and vagotomized cats. The results are summarized as follows: 1. The impulse discharges of phrenic efferents resulted from electrical stimulation of the left inferior cardiac nerve were increased by the increment of rate of phrenic efferents during inspiration. These results indicate the hyperpnea that can be produced by excitation of afferent cardiac sympathetic nerve fibers. 2. Cardiac pain evoked by electrical stimulation increases the blood pressure. 3. Not only C fibers but also A delta fibers participated in the change of the respiration and blood pressure. 4. Activation of pulmonary stretch receptor produced apnea. 5. During cold nerve block, activation of J receptor and bronchial receptor caused tachypnea characterized by increased rate of respiration, increased expiratory reserve volume and decreased tidal volume.