• The Korean Journal of Physiology
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• v.27 no.1
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• pp.37-49
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• 1993

Ventilatory responses to inhaled $CO_2$ were measured during continuous negative pressure breathing (CNPB) in awake dogs. End expiratory lung volume (EELV) decreased linearly with pressure level during CNPB (correlation coefficient= 0.81, p<0.005) during air breathing. When CNPB was applied during 5% $CO_2$ inhalation, the decrease in EELV was not significantly different (p<0.5) from that during air breathing. As a result of a lowered EELV, tidal volume ($V_T$) significantly decreased by 22% and breathing frequency ($f_B$) increased by 68% in the steady state during air breathing (p<0.0001). These responses were similar during 5% $CO_2$ inhalation, thus the $CO_2$ response curve measured during CNPB shifted upward without a change in sensitivity (p>0.05). These results indicate additive effects of CNPB and $CO_2$ inhalation. The degree of hyperventilation during CNPB at eupnea was estimated to be 63% of that during control ventilation and was significantly greater than zero (p<0.0001), which suggests an alveolar hyperventilation due to CNPB. These results suggest that the mechanical alterations associated with n decrease in lung volume could play an important role in ventilatory control independently of chemical regulation of breathing. Thus, exercise hyperpnea, which is associated with a lowered functional residual capacity (FRC), may in part be explained by this mechanical stimulation of breathing.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.369-374
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• 1995

Aujeszky's disease virus(ADV) was inoculated intranasally into the Korean native goats to investigate pathological findings and pathogenesis of ADV infection by using of histological and immunohistochemical methods and in situ hybridization(ISH). Clinical signs of salvation, pyrexia, pruritus and staggering were followed by death with five days after inoculation, Pathoanatomical findings were edema of the lung and the urinary bladder with hemorrhage and congestion, petechial hemorrhages on the endo-and epicardium, renal congestion, moderate splenomegaly and cystic edema. Main microsocpic lesions observed in all infected goats were confined to the CNS and charcterized by perivascular cuffing with lymphocytes and macrophages, focal gliosis, neuronal degeneration and necrosis, and intranuclear inclusion bodies in the neurons and glial cells. Positive reactions to ADV were detected more frequently in the nuclei than in the cytoplasms of infected nerve cells in the CNS by immunohistochemistry and ISH. Frequenctly localized sites of ADV in the CNS were olfactory bulb, prietal cortex, callosal sulcus and corpus callosum. Positive reactions were also detected in the tonsillar epithelium, and alveolar macrophage and sloughed epithelium of the lung.

• International Journal of Oral Biology
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• v.37 no.3
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• pp.121-129
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• 2012

Previous clinical studies have demonstrated that gabapentin, a drug that binds to the voltage-gated calcium channel ${\alpha}2{\delta}1$ subunit proteins, is effective in the management of neuropathic pain, but there is limited evidence that addresses the participation of glial cells in the antiallodynic effects of this drug. The present study investigated the participation of glial cells in the anti-nociceptive effects of gabapentin in rats with trigeminal neuropathic pain produced by mal-positioned dental implants. Under anesthesia, the left mandibular second molar was extracted and replaced by a miniature dental implant to induce injury to the inferior alveolar nerve. Mal-positioned dental implants significantly decreased the air-puff thresholds both ipsilateral and contralateral to the injury site. Gabapentin was administered intracisternally beginning on postoperative day (POD) 1 or on POD 7 for three days. Early or late treatment with 0.3, 3, or 30 ${\mu}g$ of gabapentin produced significant anti-allodynic effect in the rats with mal-positioned dental implants. On POD 9, in the mal-positioned dental implants group, OX-42, a microglia marker, and GFAP, an astrocyte marker, were found to be up-regulated in the medullary dorsal horn, compared with the naive group. However, the intracisternal administration of gabapentin (30 ${\mu}g$) failed to reduce the number of activated microglia or astrocytes in the medullary dorsal horn. These findings suggest that gabapentin produces significant antinociceptive effects, which are not mediated by the inhibition of glial cell function in the medullary dorsal horn, in a rat model of trigeminal neuropathic pain.

• Tuberculosis and Respiratory Diseases
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• v.69 no.5
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• pp.323-330
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• 2010

A key mechanism in the pathogenesis of chronic obstructive pulmonary disease is thought to be an abnormal inflammatory response in the lungs to the inhalation of toxic particles and gases, derived from tobacco smoke, air pollution, and/or occupational exposures. This review highlights the potential participation of several alternative pathogenetic processes, particularly involving the potential participation of biological and pathobiological processes related to aging, including oxidative stress and enhanced expression of markers of senescence/aging in emphysematous lungs, and the potential for enhanced tissue destruction involving alveolar cell apoptosis.

• Molecules and Cells
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• v.42 no.11
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• pp.763-772
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• 2019

Periodontitis is characterized by the loss of periodontal tissues, especially alveolar bone. Common therapies cannot satisfactorily recover lost alveolar bone. Periodontal ligament stem cells (PDLSCs) possess the capacity of self-renewal and multilineage differentiation and are likely to recover lost alveolar bone. In addition, periodontitis is accompanied by hypoxia, and hypoxia-inducible $factor-1{\alpha}$ ($HIF-1{\alpha}$) is a master transcription factor in the response to hypoxia. Thus, we aimed to ascertain how hypoxia affects runt-related transcription factor 2 (RUNX2), a key osteogenic marker, in the osteogenesis of PDLSCs. In this study, we found that hypoxia enhanced the protein expression of $HIF-1{\alpha}$, vascular endothelial growth factor (VEGF), and RUNX2 ex vivo and in situ. VEGF is a target gene of $HIF-1{\alpha}$, and the increased expression of VEGF and RUNX2 proteins was enhanced by cobalt chloride ($CoCl_2$, $100{\mu}mol/L$), an agonist of $HIF-1{\alpha}$, and suppressed by 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1, $10{\mu}mol/L$), an antagonist of $HIF-1{\alpha}$. In addition, VEGF could regulate the expression of RUNX2, as RUNX2 expression was enhanced by human VEGF ($hVEGF_{165}$) and suppressed by VEGF siRNA. In addition, knocking down VEGF could decrease the expression of osteogenesis-related genes, i.e., RUNX2, alkaline phosphatase (ALP), and type I collagen (COL1), and hypoxia could enhance the expression of ALP, COL1, and osteocalcin (OCN) in the early stage of osteogenesis of PDLSCs. Taken together, our results showed that hypoxia could mediate the expression of RUNX2 in PDLSCs via $HIF-1{\alpha}$-induced VEGF and play a positive role in the early stage of osteogenesis of PDLSCs.

• The Korean Journal of Physiology
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• v.8 no.2
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• pp.49-53
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• 1974

A single dose of pilocarpine was subcutaneously injected into the rabbit in order to clarify the effects of cholinergic activities on the secretion of the pulmonary surfactant. The animal was sacrificed four hours after the injection, and the pressure-volume curve of the excised lung was obtained. The surfactant activities of the lung washings were also measured, and a comparison was made with the normal. The pressure-volume curve of the excised lung by the injection and ejection of air formed a loop (hysteresis) and the mean intra-alveolar pressure at 35 ml of air was 220 $mmH_20$ in the normal. The mean deflation curve of the pilocarpine treated rabbit lungs was shifted to the left compared with the normal. The surfactant activities were slightly increased than the normal. The above results suggest that pilocarpine stimulates the secretion of the pulmonary surfactant from the Type II alveolar epithelial cell.

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.218-225
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• 1995

Background: Airway resistance(Raw) is measured with the body plethysmograph by displaying the relationship between airflow and alveolar pressure($V/P_A$). If the resistance curve on $V/P_A$ tracing is curved or looped, the estimation of Raw is difficult. This study was designed to examine wheather there is any correlation between the shape of resistance curve and the clinical status and the pulmonary function of patients. Methods: The 146 pulmonary disease patients with increased Raw were included in this study. The shapes of resistance curves on $V/P_A$ tracing with body plethysmograph during quiet breathing were analyzed and compared with pulmonary function. Results: The results were as follows ; 1) The shapes of resistance curves were summarized in 5 categories; type 1: linear, type 2: ovoid, type 3: sigmoid, type 4: scoop, type 5: paisley. The type 3 except 1 case, type 4 and type 5 were found to have loop mainly in expiratory phase. 2) Although the shapes of resistance curves were not typical for specific disease, the resistance curves of acute disease tended to belong to type 1 or 2 and those of chronic airflow obstruction tended to belong to type 3, 4 or 5. But resistance curves of bronchial asthma and destructive lung with tuberculosis showed all types in proportion to degree of airflow obstruction or destruction of parenchyme. 3) In the cases of resistance curves going to type 5 rather than type 1 and those with looping, airflow obstuction tended to be severe and airway resistance and residual volume tended to increase. Conclusions: Analysis of resistance curve on $V/P_A$ tracing measuring airway resistance is helpful for judging degree of airflow obstruction and air trapping. Although the shape of resistance curve is not typical for specific disease, there is a close association between looping and airway obstruction.

• Tuberculosis and Respiratory Diseases
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• v.46 no.1
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• pp.75-81
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• 1999

Background : Recently, there are many patients with lipoid pneumonia by ingestion of shark liver oil in Korea, but only a few animal experimentations have been carried out. The purpose of this study is to evaluate sequential change of the lung after aspiration of shark liver oil and to provide the radiologic-pathologic correlation. Methods: A single intratracheal administration of shark liver oil was given to 14 white rabbits. They were then sacrificed sequentially from 1 week to 6 weeks after injection. We investigated the HRCT and pathologic findings Results: One was sudden death immediately after injection. Six of the 13 rabbits showed pneumonic infiltrations on the HRCT. There were air space consolidation with air-bronchogram on the HRCT of the first week. They were associated with the volume loss in the 4th week, and the traction bronchiectasis in the 6th week. The important pathologic findings were peribronchial alveolar inflammation with septal widening and cuboidal metaplasia of the alveolar wall. The number of macrophages in an alveoli was peaked in the second week and then gradually decreased. On the 6th week, we could find the proliferation of fibroblasts. Conclusion: We can prove the development of lipoid pneumonia after aspiration of squalene by animal experimentation, and the understanding of HRCT and pathologic findings may be helpful in proper evaluation of pneumonia due to aspiration of fish-extracted lipid.

• Safety and Health at Work
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• v.10 no.2
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• pp.237-244
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• 2019

Background: Street vendors spend relatively more time near roadways and are vulnerable to air pollution related health disorders. However, there is limited information on the quality of the air they breathe. The objectives of this present study were to calculate the mass concentration of atmospheric particulate matter (PM) in eight size fractions ($PM_{0.4-0.7}$, $PM_{0.7-1.1}$, $PM_{1.1-2.1}$, $PM_{2.1-3.3}$, $PM_{3.3-4.7}$, $PM_{4.7-5.8}$, $PM_{5.8-9.0}$, and $PM_{9.0--0{\mu}m}$) at commercial (CML) and residential site (RSL) in Dehradun city from November 2015 to May 2016. To estimate the corresponding respiratory deposition dose (RDDs) in alveolar (AL), tracheobronchial (TB), and head airway (HD) region on street vendors working at CML and RSL. To find the association of atmospheric PM with RDDs and the incidence of respiratory related disorders among street vendors. Methods: Andersen cascade impactor was employed for calculating the PM mass concentration. Questionnaire based health survey among street vendors were carried out through personal interview. Results: A significant difference (p < 0.05; t-test) between the mean $PM_{0.4-10{\mu}m}$ mass concentration at CML and RSL was observed with ($mean{\pm}SD$) $84.05{\pm}14.5$ and $77.23{\pm}11.7{\mu}g\;m^{-3}$, respectively. RDDs in AL, TB and HD region at CML was observed to be 9.9, 7.8, and 7.3% higher than at RSL, respectively. Health survey revealed 1.62, 0.96, 0.04, and 0.57 times higher incidence of cold, cough, breathlessness, and chest pain, respectively with street vendors at CML compared to RSL. Conclusion: The site characteristics plays a major role in the respiratory health status of street vendors at Dehradun.

• Tuberculosis and Respiratory Diseases
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• v.60 no.5
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• pp.554-563
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• 2006

Background: PM is known to induce various pulmonary diseases, including asthma, cancer, fibrosis and chronic bronchitis. Despite the epidemiological evidence the pathogenesis of PM-related pulmonary diseases is unclear. Methods: This study examined the effects of PM exposure on the secretion of $TNF-{\alpha}$ and $IL-1{\beta}$ in the cultured alveolar macrophages. The cultured primary alveolar macrophages were treated with the medium, PM ($5{\sim}20{\mu}g/cm^2$), LPS (5ng/ml), and PM with LPS for 24h and 48h respectively. ELISA was used to assay the secreted $TNF-{\alpha}$ and $IL-{\beta}$ in the culture medium. Western blotting was used to identify and determine the level of proteins isolated from the culture cells. The cells cultured in the $Lab-Tek^{(R)}$ chamber slides were stained with immunocytochemical stains. Results: PM induced $TNF-{\alpha}$ and $IL-1{\beta}$ secretion in the culturing alveolar macrophages, collected from the SPF and inflammatory rats. However, the effects were only dose-dependent in the inflammatory macrophages. When the cells were co-treated with PM and LPS, there was a significant synergistic effect compared with the LPS in the both cell types. Conclusion: PM might be play an important role in the induction and/or potentiation of various lung diseases by oversecretion of $TNF-{\alpha}$ and $IL-1{\beta}$.