• Tuberculosis and Respiratory Diseases
• /
• 제73권4호
• /
• pp.231-233
• /
• 2012

Tadalafil is a phosphodiesterase-5 inhibitor (PDE5I), which is widely used to treat erectile dysfunction. Although PDE5Is have excellent safety profiles, and most of the side effects are mild, rare serious adverse events have been reported in association with PDE5Is. Thrombosis is one of those events, and a few previous reports have suggested the association of PDE5Is with thrombosis. We report the case of a 61-year-old male who developed pulmonary embolism combined with pulmonary infarction directly after taking tadalafil. Both the patient and the physician suspected tadalafil as the culprit drug, as the patient was in an otherwise healthy condition. However, after extensive evaluation, we noticed that factor VIII levels were elevated. Prior reports suggesting the association between thrombosis and PDEIs either lack complete information on coagulation factors, or show inconsistencies in their results. Physicians should operate caution prior to accepting the diagnosis of adverse drug reaction.

• Tuberculosis and Respiratory Diseases
• /
• 제57권6호
• /
• pp.573-578
• /
• 2004

저자들은 폐색전증과 파종성혈관내응고를 동반한 특발성 과호산구 증후군 1례를 경험하였다. 환자는 스테로이드 투여로 빠른 호전이 없어 시클로스포린을 추가하여 호전되었다.

• BMB Reports
• /
• 제44권5호
• /
• pp.298-305
• /
• 2011

Most intracellular reactive oxygen species (ROS), especially superoxide anion ($O_2^{{\bullet}_-}$) that is converted from oxygen, are overproduced by excessive electron leakage from the mitochondrial respiratory chain. Intracellular oxidative stress that damages cellular components can contribute to lifestyle-related diseases such as diabetes and arteriosclerosis, and age-related diseases such as cancer and neuronal degenerative diseases. We have previously demonstrated that the excessive mitochondrial $O_2^{{\bullet}_-}$ production caused by SDHC mutations (G71E in C. elegans, I71E in Drosophila and V69E in mouse) results in premature death in C. elegans and Drosophila, cancer in mouse embryonic fibroblast cells and infertility in transgenic mice. SDHC is a subunit of mitochondrial complex II. In humans, it has been reported that mutations in SDHB, SDHC or SDHD often result in inherited head and neck paragangliomas (PGLs). Recently, we established Tet-mev-1 conditional transgenic mice using our uniquely developed Tet-On/Off system, which equilibrates transgene expression to endogenous levels. These mice experienced mitochondrial respiratory chain dysfunction that resulted in $O_2^{{\bullet}_-}$ overproduction. The mitochondrial oxidative stress caused excessive apoptosis leading to low birth weight and growth retardation in the neonatal developmental phase in Tet-mev-1 mice. Here, we briefly describe the relationships between mitochondrial $O_2^{{\bullet}_-}$ and aging phenomena in mev-1 animal models

• Clinical and Experimental Pediatrics
• /
• 제53권12호
• /
• pp.994-999
• /
• 2010

Purpose: Mitochondrial dysfunction can present with various symptoms depending on the organ it has affected. This research tried to analyze the ophthalmologic symptoms and ophthalmologic examination (OE) results in patients with mitochondrial disease (MD). Methods: Seventy-four patients diagnosed with mitochondrial respiratory chain complex defect with biochemical enzyme assay were included in the study. They were divided into 2 groups based on the OE results by funduscopy and were analyzed on the basis of their clinical features, biochemical test results, morphological analysis, and neuroimaging findings. Results: Thirty-seven (50%) of the 74 MD patients developed ophthalmologic symptoms. Abnormal findings were observed in 36 (48.6%) patients during an OE, and 16 (21.6%) of them had no ocular symptoms. Significantly higher rates of prematurity, clinical history of epilepsy or frequent apnea events, abnormal light microscopic findings in muscle pathology, diffuse cerebral atrophy in magnetic resonance imaging, and brainstem hyperintensity and lactate peaks in magnetic resonance spectroscopy were noted in the group with abnormal OE results. Conclusion: Although the ophthalmologic symptoms are not very remarkable in MD patients, an OE is required. When the risk factors mentioned above are observed, a more active approach should be taken in the OE because a higher frequency of ocular involvement can be expected.

• Tuberculosis and Respiratory Diseases
• /
• 제40권4호
• /
• pp.416-423
• /
• 1993

경북대학교 의과대학 호흡기내과에서 운동시 호흡곤란을 호소하며 입원하여 개흉폐생검, 경기관지 폐생검 및 기관폐포세척을 하여 광학현미경 및 전자현미경소견상 특징적인 lamellar body가 보이는 폐포단백증으로 진단된 3예를 경험하였기에 문헌고찰과 함께 보고하였다.

• Tuberculosis and Respiratory Diseases
• /
• 제38권1호
• /
• pp.25-33
• /
• 1991

The immune staus is known to be decreased in malignant disease and radiation therapy (RT), used as a therapeutic tool, further decrease this-attenuated immune status. We measured the number of peripheral lymphocytes, its subsets and lymphoblast transformation for PPD, PHA, monoclonal antibodies including anti-CD3 and anti-CD2 before and after RT in 19 patients with squamous cell lung cancer to search the fine mechanism behind the RT-induced attenuation of lymphoblast transformtion for mitogens and antigen. The results were as follows; 1) The number of lymphocytes and its subsets decreased significantly after RT, but the percentages of lymhocyte subsets did not change aftr RT except interleukin-2 receptor positive T lymphocytes. 2) The function of lymphoctes, measured by lymphoblast tranformation for PHA and PPD, decrased after RT and the compositions of PBMC used for lymphoblast transformtion were not different before and after RT. 3) The mitosis of lymphocytes to anti-CD2 or anti-CD3 decreased significantly after RT. And IL-2 plus anti-CD3 increased the mitosis than that of anti-CD3 only after RT, but before RT there was no difference. In conclusion, we suggested the fine mechanism behind the RT-induced attenuation of immune response might be the dysfunction of lymphocytes in terms of impaired synthesis of IL-2 rather than the decrease of circulating lymphocyte numbers.

• Genes and Genomics
• /
• 제40권12호
• /
• pp.1269-1277
• /
• 2018

Bcl2-associated athanogene 3 (BAG3) mutations have been reported to cause the myofibrillar myopathy (MFM) which shows progressive limb muscle weakness, respiratory failure, and cardiomyopathy. Myopathy patients with BAG3 mutation are very rare. We described a patient showing atypical phenotypes. We aimed to find the genetic cause of Korean patients with sensory motor polyneuropathy, myopathy and rigid spine. We performed whole exome sequencing (WES) with 423 patients with sensory motor polyneuropathy. We found BAG3 mutation in one patient with neuropathy, myopathy and rigid spine syndrome, and performed electrophysiological study, whole body MRI and muscle biopsy on the patient. A de novo heterozygous p.Pro209Leu (c.626C>T) mutation in BAG3 was identified in a female myopathy. She first noticed a gait disturbance and spinal rigidity at the age of 11, and serum creatine kinase levels were elevated ninefolds than normal. She showed an axonal sensory-motor polyneuropathy like Charcot-Marie-Tooth disease (CMT), myopathy, rigid spine and respiratory dysfunction; however, she did not show any cardiomyopathy, which is a common symptom in BAG3 mutation. Lower limb MRI and whole spine MRI showed bilateral symmetric fatty atrophy of muscles at the lower limb and paraspinal muscles. When we track traceable MRI 1 year later, the muscle damage progressed slowly. As far as our knowledge, this is the first Korean patient with BAG3 mutation. We described a BAG3 mutation patient with atypical phenotype of CMT and myopathy, and those are expected to broaden the clinical spectrum of the disease and help to diagnose it.

• 대한소아치과학회지
• /
• 제46권1호
• /
• pp.119-126
• /
• 2019

수면호흡장애는 구강악안면 근육 기능부전을 유발하여 안모의 형태이상 및 부정교합을 유발할 수 있다. 소아치과 영역에서 수면호흡장애의 조기 진단과 치료는 이러한 합병증을 차단하여 정상적인 안모 성장을 유지할 수 있다는 점에서 중요하다. 수면호흡장애의 치료법 중에 하나로 근기능요법이 있으며 기성 근기능 장치가 보조적으로 사용될 수 있다. 본 증례들에서는 수면호흡장애가 있는 부정교합 환자들에게 기성 근기능 장치를 사용하여 수면호흡장애를 해소하는 결과를 얻었기에 보고하는 바이다. 하지만 총생의 개선 효과는 그 정도에 따라 차이가 발생할 수 있으므로 이에 대한 한계점은 고려할 필요가 있다.

• IMMUNE NETWORK
• /
• 제22권2호
• /
• pp.18.1-18.15
• /
• 2022

Dysfunction of mitochondrial metabolism is implicated in cellular injury and cell death. While mitochondrial dysfunction is associated with lung injury by lung inflammation, the mechanism by which the impairment of mitochondrial ATP synthesis regulates necroptosis during acute lung injury (ALI) by lung inflammation is unclear. Here, we showed that the impairment of mitochondrial ATP synthesis induces receptor interacting serine/threonine kinase 3 (RIPK3)-dependent necroptosis during lung injury by lung inflammation. We found that the impairment of mitochondrial ATP synthesis by oligomycin, an inhibitor of ATP synthase, resulted in increased lung injury and RIPK3 levels in lung tissues during lung inflammation by LPS in mice. The elevated RIPK3 and RIPK3 phosphorylation levels by oligomycin resulted in high mixed lineage kinase domain-like (MLKL) phosphorylation, the terminal molecule in necroptotic cell death pathway, in lung epithelial cells during lung inflammation. Moreover, the levels of protein in bronchoalveolar lavage fluid (BALF) were increased by the activation of necroptosis via oligomycin during lung inflammation. Furthermore, the levels of ATP5A, a catalytic subunit of the mitochondrial ATP synthase complex for ATP synthesis, were reduced in lung epithelial cells of lung tissues from patients with acute respiratory distress syndrome (ARDS), the most severe form of ALI. The levels of RIPK3, RIPK3 phosphorylation and MLKL phosphorylation were elevated in lung epithelial cells in patients with ARDS. Our results suggest that the impairment of mitochondrial ATP synthesis induces RIPK3-dependent necroptosis in lung epithelial cells during lung injury by lung inflammation.

• Journal of Chest Surgery
• /
• 제3권1호
• /
• pp.3-12
• /
• 1970

During the last 10 years of period, one hundred patients with various pulmonary diseases were pneumonectomized upon at the Department of Chest Surgery of Pusan University Hospital. This paper is concerned with the clnical results of these patients along with the serious postoperative complications such as postoperative intrapleural infection and hemorrhage. The results were obtained as follows. 1.Left pneumonectomy was done in sixty-six of 100 patients [66 %] and the right one was done in the rest thirty-four[34 %]. The ratio between left and right was nearly 2:1. 2.Of all oostoperative complications, the intrapleural infection was most common, and these were 53 % in empyema thoracis and 12.7 % in pulmonary tuberculosis respectively. 3.More postoperative complications could be seen after right pneumonectomy than the left one. 4.It was thought that the postoperative intrapleural infection was closely correlated with the methods of pleural dissection at pneumonectomy,postoperatlve tube drainage, time of operation, massive hemorrhage during operation, prolongation of bleeding time, and dysfunction of the liver. 5.The repeated thoracenteses with infusion of neomycin into the infected thoracic cavity and intravenous administrations of the high units of penicillin were effective in treatment of the postoperative intrapleural infection, however, the refractory cases have to be cured by thoracoplasty with open window. 6.Immediate secondary open thoracotomy appears to be the method of choice in life saving who developed massive intrathoracic hemorrhage after pneumonectomy. 7.The mortality rate was 10 % in our cases and the main causes of death were postoperative respiratory insufficiency, pulmonary edema, hemorrhage and sudden cardiac arrest.