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Supplementary Figures S1-S13 and Table S1. Confirmation of KIAA1324 mRNA expression in primary tissues from gastric cancer (GC) patients and GC cell lines (S1). Analysis of correlation between copy number variation (CNV) and KIAA1324 mRNA expression in gastric cancer cell lines (S2). KIAA1324 enhanced cisplatin- and etoposide-induced apoptosis of gastric cancer cells (S3). KIAA1324 knockdown reduced staurosporine-induced apoptosis (S4). KIAA1324 did not have a considerable effect on cell cycle (S5). KIAA1324 did not affect autophagy of gastric cancer cells (S6). KIAA1324 â–³C caused growth inhibition and apoptosis in gastric cancer cells (S7). KIAA1324 â–³N did not induce apoptosis of gastric cancer cells (S8). 1-303 a.a. of KIAA1324 was required for KIAA1324-mediated apoptosis (S9). Subcellular localization of KIAA1324 (S10). 1-303 a.a. of KIAA1324 bound to GRP78. (A) A schematic model of KIAA1324 fragments (S11). GRP78 knockdown induced apoptosis of MKN28 cells (S12). A schematic model of the anti-tumorigenic ability of KIAA1324 through regulation of GRP78 activity (S13). Semi-quantitative and quantitative RT-PCR primers (Table S1).

Recent advances in genome and transcriptome analysis have contributed to the identification of many potential cancer-related genes. Furthermore, biological and clinical investigations of the candidate genes provide us with a better understanding of carcinogenesis and development of cancer treatment. Here, we report a novel role of KIAA1324 as a tumor suppressor in gastric cancer. We observed that KIAA1324 was downregulated in most gastric cancers from transcriptome sequencing data and found that histone deacetylase was involved in the suppression of KIAA1324. Low KIAA1324 levels were associated with poor prognosis in gastric cancer patients. In the xenograft model, KIAA1324 significantly reduced tumor formation of gastric cancer cells and decreased development of preformed tumors. KIAA1324 also suppressed proliferation, invasion, and drug resistance and induced apoptosis in gastric cancer cells. Through protein interaction analysis, we identified GRP78 (glucose-regulated protein 78 kDa) as a KIAA1324-binding partner. KIAA1324 blocked oncogenic activities of GRP78 by inhibiting GRP78–caspase-7 interaction and suppressing GRP78-mediated AKT activation, thereby inducing apoptosis. In conclusion, our study reveals a tumor suppressive role of KIAA1324 via inhibition of GRP78 oncoprotein activities and provides new insight into the diagnosis and treatment of gastric cancer. Cancer Res; 75(15); 3087–97. ©2015 AACR.

Supplementary Materials and Methods

The 2019 coronavirus disease (COVID-19) pandemic has had a profound impact on the mental health of people worldwide. This study examined dysfunctional coronavirus anxiety in nonpsychotic psychiatric outpatients during the pandemic using the coronavirus anxiety scale (CAS) and examined the relationship between coronavirus anxiety and clinical symptoms using network analysis.In this cross-sectional study, 192 patients who first visited the psychiatric outpatient clinic of Severance Hospital during the COVID-19 pandemic with chief complaints of depressed mood, anxiety, somatic symptoms, or insomnia were included. We compared the clinical characteristics of patients with and without dysfunctional coronavirus anxiety. Network analysis was conducted to estimate the network of coronavirus anxiety and depressive, anxious, and hypochondriacal psychopathology.The results showed that 7.8% of patients exhibited dysfunctional coronavirus anxiety (CAS ≥ 5). Patients with dysfunctional coronavirus anxiety showed higher levels of health worry, somatic preoccupation, and subjective anxiety compared to patients without dysfunctional coronavirus anxiety. In the network analysis, the health worry node (Item 6 of the WI) showed the greatest number of connections with coronavirus anxiety nodes.These findings suggest that health worry may be an important bridge symptom that connects coronavirus anxiety and other clinical psychopathology. Patients with elevated health worries should be carefully monitored during the COVID-19 pandemic for exacerbation of previous symptoms and COVID-19-related psychopathology. Understanding the psychological factors in the face of the pandemic and their relationships with clinical psychiatric symptoms would help people prevent and overcome mental health problems during the pandemic.

Suicidality in obsessive-compulsive disorder (OCD) is underestimated and it is important for clinicians to understand the factors that contribute to suicidal ideation. The present study aimed to estimate a network of the core clinical symptoms of OCD including obsessions, compulsions, and obsessive-compulsive (OC) symptom dimensions, depressive symptoms, and psychological traits, and to examine which symptoms contribute to suicidal ideation in patients with a primary diagnosis of obsessive-compulsive disorder.A total of 444 patients with OCD were assessed with the Yale-Brown Obsessive-Compulsive Scale, the Montgomery-Asberg Depression Rating Scale, and various other measures. Network analysis was conducted to estimate the network of obsessive-compulsive and depressive symptoms, psychological traits including alexithymia and impulsivity, and demographic covariates. Symptoms directly related to suicidal ideation in the network were examined for their relative contribution to suicidal ideation.Suicidal ideation was directly related to degree of control over compulsive behaviors, distress associated with compulsive behaviors, time spent performing compulsive behaviors, and unacceptable thoughts, along with depressive symptoms and alexithymia. In the network of OC and depressive symptoms the most central symptoms among the former were interference due to compulsive behaviors and interference due to obsessive thoughts, and among the latter were pessimistic thoughts and reported sadness.The findings suggest that along with depressive symptoms and alexithymia, compulsions and unacceptable thoughts dimension may contribute to suicidality, and thus, should be carefully monitored in patients with OCD.

Background: The present study examined whether mitochondrial DNA copy number (mtDNAcn) and telomere length — key markers of cellular aging — were altered in male and female participants with obsessive–compulsive disorder (OCD) compared to healthy controls. We also tested for associations between these alterations and OCD-related clinical features and inflammatory index. Methods: A total of 235 patients with OCD (38.7% female) and 234 healthy controls (41.5% female) were included. We quantified whole-blood mtDNAcn and leukocyte telomere length using quantitative polymerase chain reaction. We also calculated the neutrophil-to-lymphocyte ratio from complete blood cell counts. Results: Multivariate analysis of covariance showed that OCD status had a significant overall effect on cellular aging markers in men (Wilks λ = 0.889, F2,275 = 17.13, p < 0.001) and women (Wilks λ = 0.742, F2,182 = 31.61, p < 0.001) after controlling for age, body mass index and childhood trauma. In post-hoc comparisons, men with OCD had lower mtDNAcn than controls (p < 0.001), but we found no between-group difference for telomere length (p = 0.55). Women with OCD had a significantly lower mtDNAcn (p < 0.001) and shortened telomere length (p = 0.023) compared to controls. Moreover, the lower mtDNAcn shown in the OCD group was significantly correlated with an increase in systemic inflammation for both sexes, as measured by neutrophil-to-lymphocyte ratio. Limitations: The present cross-sectional design did not allow us to infer a causal relationship between OCD disease status and cellular aging markers. Conclusion: The present study is, to our knowledge, the first to demonstrate alterations in mtDNAcn and telomere shortening in OCD. These results suggest that aging-associated molecular mechanisms may be important in the pathophysiology of OCD.

Early life stress (ELS) leads to increased susceptibility to serious psychiatric problems such as alcohol dependence, but the mechanisms through which ELS affects alcohol dependence are unclear. We investigated the mediating role of multi-dimensional impulsivity in the associations between ELS and alcohol dependence. 330 male patients with alcohol dependence (mean age = 48.39) completed self-rating scales of ELS and several self-report measures of impulsivity as well as balloon analogue risk task (BART). After classifying different dimensions of impulsivity using factor analysis, structural equation modeling was conducted to test the mediation effects of impulsivity between ELS and alcohol dependence severity and social onset of hazardous drinking. Among the participants, 64.8%, 42.1% and 47.9% reported at least one episode of childhood maltreatment, sexual abuse and parental conflict, respectively. Response impulsivity-sensation seeking, reflection impulsivity and aggression partially mediated the association between ELS and severity of alcohol dependence (CFI = 0.902 and RMSEA = 0.079). Reflection impulsivity dimension partially mediated the association between ELS and social onset of hazardous drinking (CFI = 0.939, RMSEA = 0.091). These finding imply that stabilizing vulnerabilities such as reflection impulsivity via intervention programs that target young individuals with ELS may be helpful in delaying the onset of hazardous drinking and prevent alcohol dependence.

Recent advances in genome and transcriptome analysis have contributed to the identification of many potential cancer-related genes. Furthermore, biological and clinical investigations of the candidate genes provide us with a better understanding of carcinogenesis and development of cancer treatment. Here, we report a novel role of KIAA1324 as a tumor suppressor in gastric cancer. We observed that KIAA1324 was downregulated in most gastric cancers from transcriptome sequencing data and found that histone deacetylase was involved in the suppression of KIAA1324. Low KIAA1324 levels were associated with poor prognosis in gastric cancer patients. In the xenograft model, KIAA1324 significantly reduced tumor formation of gastric cancer cells and decreased development of preformed tumors. KIAA1324 also suppressed proliferation, invasion, and drug resistance and induced apoptosis in gastric cancer cells. Through protein interaction analysis, we identified GRP78 (glucose-regulated protein 78 kDa) as a KIAA1324-binding partner. KIAA1324 blocked oncogenic activities of GRP78 by inhibiting GRP78–caspase-7 interaction and suppressing GRP78-mediated AKT activation, thereby inducing apoptosis. In conclusion, our study reveals a tumor suppressive role of KIAA1324 via inhibition of GRP78 oncoprotein activities and provides new insight into the diagnosis and treatment of gastric cancer. Cancer Res; 75(15); 3087–97. ©2015 AACR.

Rett syndrome (RTT), associated with mutations in methyl-CpG-binding protein 2 (Mecp2), is linked to diverse neurological symptoms such as seizures, motor disabilities, and cognitive impairments. An altered GABAergic system has been proposed as one of many underlying pathologies of progressive neurodegeneration in several RTT studies. This study for the first time investigated the temporal- and location-specific alterations in the expression of γ-amino butyric acid (GABA) transporter 1 (GAT-1), vesicular GABA transporter (vGAT), and glutamic acid decarboxylase 67kD (GAD67) in wild type (WT) and knockout (KO) mice in the Mecp2m1.1Bird/ymouse model of RTT. Immunohistochemistry (IHC) co-labeling of GAT-1 with vGAT identified GABAergic synapses that were quantitated for mid-sagittal sections in the frontal cortex (FC), hippocampal dentate gyrus (DG), and striatum (Str). An age-dependent increase in the expression of synaptic GABA transporters, GAT-1, and vGAT, was observed in the FC and DG in WT brains. Mecp2 KO mice showed a significant alteration in this temporal profile that was location-specific, only in the FC. GAD67-positive cell densities also showed an age-dependent increase in the FC, but a decrease in the DG in WT mice. However, these densities were not significantly altered in the KO mice in the regions examined in this study. Therefore, the significant location-specific downregulation of synaptic GABA transporters in Mecp2 KO brains with unaltered densities of GAD67-positive interneurons may highlight the location-specific synaptic pathophysiology in this model of RTT.

BACKGROUND/AIMS Loss of transforming growth factor beta1 (TGF-beta1) exhibits a similar pathology to that seen in a subset of individuals infected with Helicobacter pylori, including propagated gastric inflammation, oxidative stress, and autoimmune features. We thus hypothesized that gastric mucosal TGF-beta1 levels could be used to determine the outcome after H. pylori infection. METHODS Northern blot for the TGF-beta1 transcript, staining of TGF-beta1 expression, luciferase reporter assay, and enzyme-linked immunosorbent assay for TGF-beta1 levels were performed at different times after H. pylori infection. RESULTS The TGF-beta1 level was markedly lower in patients with H. pylori-induced gastritis than in patients with a similar degree of gastritis induced by nonsteroidal anti-inflammatory drugs. There was a significant negative correlation between the severity of inflammation and gastric mucosal TGF-beta1 levels. SNU-16 cells showing intact TGF-beta signaling exhibited a marked decrease in TGF-beta1 expression, whereas SNU-638 cells defective in TGF-beta signaling exhibited no such decrease after H. pylori infection. The decreased expressions of TGF-beta1 in SNU-16 cells recovered to normal after 24 hr of H. pylori infection, but lasted very spatial times, suggesting that attenuated expression of TGF-beta1 is a host defense mechanism to avoid attachment of H. pylori. CONCLUSIONS H. pylori infection was associated with depressed gastric mucosal TGF-beta1 for up to 24 hr, but this apparent strategy for rescuing cells from H. pylori attachment exacerbated the gastric inflammation.

The item-level visibility which can be secured by RFID technology can help the inventory records of a supply chain correspond closer to the actual inventories. More accurate and timely tracking of chain-wide inventories provides a great potential for optimised on-line control of supply chains. In this paper, we develop an on-line neural network controller that optimises a three-stage supply chain. With the inventory data feedback from an RFID system, the neural network controller minimises the total cost of the supply chain rapidly while satisfying a target order fulfilment ratio. As a test bed of the neural network controller, we develop the beer game model of the supply chain. We demonstrate through simulation-based experiments that the neural network controller shows the highest performance when the inventory data is secured from item-level RFID data.

Dysregulation of transforming growth factor-beta (TGF-beta) signaling has been implicated in the pathogenesis of a variety of diseases including cancer; therefore, pharmacological inhibitors that target the TGF-beta signaling pathway might be promising drugs for disease therapy. In this study, we investigated the mechanism of inhibition of TGF-beta signaling by the Hsp90 inhibitor geldanamycin (GA). Treatment with GA suppressed TGF-beta signaling, as evidenced by inhibition of TGF-beta-induced phosphorylation and transcriptional activity of Smad3 and decreased induction of target genes. Western blot analysis revealed that GA induced degradation of TGF-beta type I and type II receptors through a proteasome-dependent pathway. Notably, induction of Hsp70 by GA correlated with inhibition of TGF-beta signaling. Suppression of Hsp70 expression by Hsp70 siRNA or KNK437, an inhibitor of Hsp70 synthesis, blocked the inhibition of TGF-beta signaling by GA. Furthermore, Hsp70 interacted directly with TGF-beta receptors following GA treatment. Our results suggest that GA-mediated induction of Hsp70 and its subsequent interaction with TGF-beta receptors plays a crucial role in inhibition of TGF-beta signaling.

Transforming growth factor-beta1 (TGF-beta1) performs diverse cellular functions, including anti-inflammatory activity. The inhibitory Smad (I-Smad) Smad6 was previously shown to play an important role in TGF-beta1-induced negative regulation of Interleukin-1/Toll-like receptor (IL-1R/TLR) signaling through binding to Pellino-1, an adaptor protein of interleukin-1 receptor associated kinase 1(IRAK1). However, it is unknown whether Smad7, the other inhibitory Smad, also has a role in regulating IL-1R/TLR signaling. Here, we demonstrate that endogeneous Smad7 and Smad6 simultaneously bind to discrete regions of Pellino-1 upon TGF-beta1 treatment, via distinct regions of the Smad MH2 domains. In addition, the Smad7-Pellino-1 interaction abrogated NF-kappaB activity by blocking formation of the IRAK1-mediated IL-1R/TLR signaling complex, subsequently causing reduced expression of pro-inflammatory genes. Double knock-down of endogenous Smad6 and Smad7 genes by RNA interference further reduced the anti-inflammatory activity of TGF-beta1 than when compared with single knock-down of Smad7. These results provide evidence that the I-Smads, Smad6 and Smad7, act as critical mediators for effective TGF-beta1-mediated suppression of IL-1R/TLR signaling, by simultaneous binding to discrete regions of Pellino-1.

The expression of 14-3-3 proteins is dysregulated in various types of cancer. This study was undertaken to investigate the effects of 14-3-3 zeta and 14-3-3 sigma on cell growth inhibition mediated by transforming growth factor-beta 1 (TGF-beta1). Mouse mammary epithelial cells (Eph4) that are transformed with oncogenic c-H-Ras (EpRas) and no longer sensitive to TGF-beta1-mediated growth inhibition displayed increased expression of 14-3-3 zeta and decreased expression of 14-3-3 sigma compared with parental Eph4 cells. Using small interfering RNA-mediated knockdown and overexpression of 14-3-3 sigma or 14-3-3 zeta, we showed that 14-3-3 sigma is required for TGF-beta1-mediated growth inhibition whereas 14-3-3 zeta negatively modulates this growth inhibitory response. Notably, overexpression of 14-3-3 zeta increased the level of Smad3 protein that is phosphorylated at linker regions and cannot mediate the TGF-beta1 growth inhibitory response. Consistent with this finding, mutation of the 14-3-3 zeta phosphorylation sites in Smad3 markedly reduced the 14-3-3 zeta-mediated inhibition of TGF-beta1-induced p15 promoter-reporter activity and cell cycle arrest, suggesting that these residues are critical targets of 14-3-3 zeta in the suppression of TGF-beta1-mediated growth. Taken together, our findings indicate that dysregulation of 14-3-3 sigma or 14-3-3 zeta contributes to TGF-beta1 resistance in cancer cells.

Growing evidence suggests that overexpression of TrkC, a member of the Trk family of neurotrophin receptors, could drive tumorigenesis, invasion and metastatic capability in cancer cells. However, relatively little is known about the mechanism of TrkC-mediated oncogenesis. The TrkC gene is a partner of the Tel-TrkC (ETV6-NTRK3) chimeric tyrosine kinase, a potent oncoprotein expressed in tumors derived from multiple cell lineages. Recently, we have shown that ETV6-NTRK3 suppresses transforming growth factor-beta (TGF-beta) signaling by directly binding to the type II TGF-beta receptor (TbetaRII). Here, we report that expression of TrkC also suppresses TGF-beta-induced Smad2/3 phosphorylation and transcriptional activation. Silencing TrkC expression by small interfering RNA in the highly metastatic 4T1 mammary tumor cell line expressing endogenous TrkC significantly enhanced TGF-beta-induced Smad2/3 phosphorylation and restored TGF-beta growth inhibitory activity. In contrast, expression of TrkC in 67NR cells, in which TrkC is not expressed, suppressed TGF-beta transcriptional activation. Moreover, we show that TrkC directly binds to the TbetaRII, thereby preventing it from interacting with the type I TGF-beta receptor (TbetaRI). These results indicate that TrkC is an inhibitor of TGF-beta tumor suppressor activity.

Ischemia in the immature brain is an important cause of neonatal seizures. Temporal evolution of acquired neonatal seizures and their response to anticonvulsants are of great interest, given the unreliability of the clinical correlates and poor efficacy of first-line anti-seizure drugs. The expression and function of the electroneutral chloride co-transporters KCC2 and NKCC1 influence the anti-seizure efficacy of GABAA-agonists. To investigate ischemia-induced seizure susceptibility and efficacy of the GABAA-agonist phenobarbital (PB), with NKCC1 antagonist bumetanide (BTN) as an adjunct treatment, we utilized permanent unilateral carotid-ligation to produce acute ischemic-seizures in post-natal day 7, 10, and 12 CD1 mice. Immediate post-ligation video-electroencephalograms (EEGs) quantitatively evaluated baseline and post-treatment seizure burdens. Brains were examined for stroke-injury and western blot analyses to evaluate the expression of KCC2 and NKCC1. Severity of acute ischemic seizures post-ligation was highest at P7. PB was an efficacious anti-seizure agent at P10 and P12, but not at P7. BTN failed as an adjunct, at all ages tested and significantly blunted PB-efficacy at P10. Significant acute post-ischemic downregulation of KCC2 was detected at all ages. At P7, males displayed higher age-dependent seizure susceptibility, associated with a significant developmental lag in their KCC2 expression. This study established a novel neonatal mouse model of PB-resistant seizures that demonstrates age/sex-dependent susceptibility. The age-dependent profile of KCC2 expression and its post-insult downregulation may underlie the PB-resistance reported in this model. Blocking NKCC1 with low-dose BTN following PB treatment failed to improve PB-efficacy.

Ischemia in the immature brain is an important cause of neonatal seizures. The exact timing of neonatal stroke onset is usually unclear and the diagnosis delayed until presentation with seizures a few to several hours later. Optimal seizure treatment in neonates remains uncharacterized and the widely used drug phenobarbital has limited clinical efficacy. Developmental profiles of chloride co-transporter expression and function in immature brains have been proposed to dictate the age dependent anti-seizure efficacy of GABA-agonists and this switch is known to occur in P8-9 mouse pups. To investigate the anti-seizure efficacy of the first line anticonvulsant and GABA A -agonist phenobarbital (PB) and NKCC1 antagonist bumetanide (BTN) as adjunct treatment on neonatal ischemic-seizures, we utilized synchronous video-EEG and unilateral carotid-ligation to produce acute ischemic-seizures in postnatal day 7 and 10 CD1 mice. Quantitative analyses of pre- and post-treatment EEGs were done using Pinnacle (Pinnacle technology Inc., KS) seizure scoring and Insight software (Persyst development corp., AZ) for evaluation of seizure grades (clinical vs. subclinical or electrographic) and treatment efficacy. Severity of acute ischemic seizures and incidence of subclinical seizures was higher at P7 and a gender-specific susceptibility was detected in males that correlated with a lag in KCC2 expression levels in naïve males compared to age-matched females, not detected at P10. However, the P7 brains were comparatively more resistant to infarcts unlike at P10 when they occurred frequently. PB showed a better efficacy at P10. BTN treatment 1h following PB however failed to act as an efficacious adjunct therapy and aggravated subclinical seizures in P10 females. At P7, both PB and add-on BTN treatment failed to stop seizures. EEG power (0.5-32 Hz) was lowered after PB treatment at both ages. Post-ischemic down-regulation of KCC2 expression was detected at both ages tested compared to age-matched naïve brains. This study showed that 1. Quantification of subclinical ictal events better evaluate anti-seizure efficacy of treatments and 2. The down-regulation of KCC2 in ischemia may further decrease the efficacy of drug actions that are dependent on a hyperpolarizing chloride gradient for their anticonvulsant action. This decrease in efficacy failed to be rescued by blocking the immature chloride co-transporter NKCC1.

Lung cancer is the leading cause of cancer related death in the world. Although recent advances in development of new chemotherapeutics offer a great promise to clinical outcome, drug resistance is still major concern of clinician. Cisplatin is platinum based drug that variously, combined with many other chemotherapeutics, have been widely used in the treatment of cancer. However, tumors usually become resistant to cisplatin during treatment. We performed RNA sequencing with 7 lung cancer cell lines and selected candidate genes to identify novel drug-resistance genes. RNA sequence analysis showed that one of these genes contained CT45A6. CT45A6 is a member of CT45 family. CT45 is a cancer/testis antigen family 45 that is located in Xq26.3 and expressed normally in testis and various cancers including lung cancer. However, little is known about its biological function, especially about drug resistance. Here, we show that CT45A6 confers cisplatin resistance into lung cancer cell lines. CT45A6 gene is significantly over-expressed in A549PR (cisplatin-resistant A549 lung cancer cell line) compared with wild type A549 lung cancer cell line. Interestingly, overexpression of CT45A6 in CT45A6-low NCI-H2009 and NCI-H358 lung cancer cell lines showed increased resistance to cisplatin and G2 phase population. Inversely, knockdown of CT45A6 in A549PR cells significantly decreased cisplatin-resistance. Thus, our findings indicate that CT45A6 may be a potential target to overcome drug resistance. Citation Format: Shin-Tae Kim, Seong-Jin Kim. CT45A6, cancer/testis antigen 45 family member, confer drug resistance to lung cancer cell lines. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 955. doi:10.1158/1538-7445.AM2013-955

Sang-Ha Kim, M.D. 1 , Joo Young Park, M.D. 2 , Hyun Sook Park, 2 , Hee Seok Seo, 2 , Shin Tae Kim, M.D. 1 , Chong Whan Kim, M.D. 1 , Bu Ghil Lee, M.D. 1 , Seok Jeong Lee, M.D. 1 , Shun Nyung Lee, M.D. 1 , Jin Kyu Noh, M.D. 1 , Min Su Lee, M.D., Won Yeon Lee, M.D., Suk Joong Yong, M.D., Kye Chul Shin, M.D. Department of Internal Medicine, Microbiology, Yonsei University Wonju College of Medicine, Wonju, Korea

M. pneumoniae는 지역사회폐렴의 중요한 원인균으로 대개 경증의 임상상을 보이지만 급성호흡곤란증후군을 일으킬 정도로 중증의 폐렴을 보이는 경우가 드물게 보고 되고 있다. 저자들은 일반적인 임상적인 경과와 달리 심한 폐침윤과 호흡곤란을 호소한 M. pneumoniae 폐렴 2예를 보고한다. 이들은 M. pneumoniae 폐렴의 전형적인 임상양상을 보이지 않았으나 중증지역사회폐렴의 양상을 보여 처음부터 새로운 퀴놀론이나 마크로라이드가 포함된 경험적 항생제 투여를 시작하였다. 또한 처음부터 M. pneumoniae IgG또는 IgM의 의미있는 상승과 추적검사에서 더욱 상승된 항체가를 보이고 혈청 검사에서 다른 감염증의 가능성을 배제하여 M. pneumoniae 폐렴으로 진단하였으며 합병증을 남기지 않고 치료가 되었다. 두 증례를 통하여 저자들은 M. pneumoniae 감염이 중증의 지역사회폐렴의 원인의 하나로 고려되어야 하며, 중증 폐렴소견을 보이는 경우에도 마크로라이드나 퀴놀론을 포함한 경험적 항생제 치료가 필요할 수 있음을 경험하여 보고한다.

Primary lung cancer can metastasize by a direct local extension, hematogenous dessemination, and lymphatic spread. However, it less commonly metastasizes via a transbronchial invasion. Approximately half of all patients with lung cancer have metastases at the initial presentation. Autopsy data showed that there are an average of 4.8 metastatic sites. The most common sites for metastases include the lymph nodes, liver, adrenal gland, bone, and brain. However clinically significant metastases isolated in the small bowel seldom occur. Here we report a case of lung cancer with a small bowel metastasis.

Background : ADA is an enzyme found in most cells, and is involved in purine metabolism, but its chief role concerns the proliferation and differentiation of lymphocytes, especially T-lymphocytes. For that reason ADA has been looked on as a marker of cell-mediate immunity, which is the key mechanism of the tuberculous pleural effusion. Thus, the pleural fluid ADA activity is increased in the tuberculous pleural effusion. Age associated immune decline is characterized by decreases in both B and T-lymphocyte function and the former may be largely a result of the latter. Therefore, the pleural fluid ADA activity would be lower in old rather than in young, patients with tuberculous pleural effusion. We studied the relationship between age, and pleural fluid ADA activity, in patients with tuberculous pleural effusion. Materials and Methods : In the 46 patients with tuberculous pleural effusion enroll in this study, the pleural fluid ADA activities were measured by means of an automated kinetic method. Results : The mean age of the patients was years, with a male to female ratio of 30:16. The patients were divided into two groups, young patients, regarded as years with 28 and 18 patients, respectively. The pleural fluid ADA activity in both groups show significant differences : IU/L(young patients) Vs. IU/L(old patients)(p

Lymphangiomas in the mediastinum are rare benign tumors, characterized proliferating lymphatic vessels. They are usually found in children and young adults, but rarely in order adults. Most are located in the neck, with less than 1 percent found in the mediastinum, with mediastinal lymphangiomas comprising 0.7-4.5 percent of all tumors in this location. They are often classified pathologically according to the size of the cystic spaces within them, as simple or capillary, cavernous and cystic, or just cystic, hygromas, Of the 3 types above, the cavernous type of mediastinal lymphangioma is very rare. We report a case of a mediastinal lymphangioma of the cavernous type that was confirmed from pathological findings, a CT and MRI scan.