PURPOSE: Periportal low attenuation, defined as a low attenuation rim around the portal vein and its branches which is seen on contrast material-enhanced CT scans, has been described in a variety of conditions. We tried to document that lymphatic obstruction is one of the major cause of periportal low attenuation. METHODS AND MATERIALS: We retrospectively analyzed 57 cases of periportal low attenuation on abdominal CT scans and also reviewed the surgical records in 32 cases. Lymph node enlargement in the hepatoduodenal ligament which is a main lymphatic channel from the liver were analyzed and calculated the ratio of the transeverse diameter between the inferior vena cava and the aorta at the level of right adrenal gland. After complete surgical interruption of the lymphatic drainage from the liver in a dog, follow up CT scans were obtained and correlated with pathologic findings. RESULTS: Fifty patients(88%) had underlying disease which could cause impairment of lymphatic drainage. Periportal low attenuation was identified in several clinical conditions, including surgical lymph node dissection, lymphadenopathy in the hepatoduodenal ligament, blunt trauma. In animal model, CT scan showed prominent periportal low attenuation at 5 days after surgery. Histologic examination revealed numerous dilated lymphatic vessels and a marked lymphedema in the connective tissues surrounding the portal vein and its major branches. CONCLUSION: One of the major.cuase of periportal low attenuation was impaired lymphatic drainage and periportal low attenuation corresponding to the numerous dilated lymphatic vessels and a marked lymphedema in the connective tissues surrounding the portal vein and its major branches.
Adrenal Glands ; Animals ; Aorta ; Connective Tissue ; Dogs ; Drainage ; Follow-Up Studies ; Ligaments ; Liver ; Lymph Node Excision ; Lymph Nodes ; Lymphatic Diseases ; Lymphatic Vessels ; Lymphedema ; Models, Animal ; Portal Vein ; Retrospective Studies ; Tomography, X-Ray Computed ; Vena Cava, Inferior

PURPOSE: Matrix metalloproteinases (MMPs) have been known to participate in various pathologic situations by modulating extracellular matrix. Although MMP-9 upregulation has been reported in some experimental seizure models, the exact role of MMP-9 in hippocampal cell death during epileptogenesis and subsequent mossy fiber sprouting (MFS) is not clear. Here, we investigated the role of MMP-9 on hippocampal cell death and MFS after pilocarpine-induced status epilepticus (SE) in mice, using highly specific hydroxamic MMP-9 inhibitor. METHODS: SE was induced by intraperitoneal pilocarpine administration in adult male C57BL/6 mice. MMP-9 specific inhibitor was administered intracerebroventrically 3 h after pilocarpine-induced SE. Expression and activation of MMP-9 were assessed by zymography and Western blot analysis. TdT-mediated UTP-biotin nick end labeling (TUNEL) and caspase-3 activity assay were also performed. MFS was investigated using Timm staining. RESULTS: Increased expression and activation of MMP-9 after pilocarpine-induced SE were observed in zymography and Western blot analysis. MMP-9 specific inhibitor decreased MMP-9 activity in in situ zymography and hippocampal cell death in cresyl violet staining. DNA fragmentation and caspase-3 activity were also attenuated by MMP-9 specific inhibitor. Four months after pilocarpine-induced SE, MFS was evident in vehicle-treated mice; in contrast, MFS was barely observed in MMP-9 specific inhibitor-treated mice. CONCLUSIONS: This study suggests MMP-9 is associated with hippocampal cell death and MFS after pilocarpine-induced SE. Furthermore, the findings that MMP-9 specific inhibitor ameliorates cell death and MFS offers the possibility of MMP-9 specific hydroxamic inhibitor as novel therapeutic strategy to reduce hippocampal damage and epileptogenesis.
Adult ; Animals ; Apoptosis ; Blotting, Western ; Caspase 3 ; Cell Death* ; DNA Fragmentation ; Extracellular Matrix ; Humans ; Male ; Matrix Metalloproteinase 9 ; Matrix Metalloproteinases ; Mice* ; Mossy Fibers, Hippocampal ; Neurons* ; Pilocarpine ; Seizures ; Status Epilepticus* ; Up-Regulation ; Viola

We observed one patient with large pleural effusion causing severe dyspnea, tachycardia, and severe right atrial collapse, which findings were completely resolved after thoracentesis. Our report shows that massive pleural effusion also can make severe right atrial collapse and symptom like cardiac tamponade, and thoracentesis can improve this condition.
Cardiac Tamponade ; Dyspnea ; Humans ; Pericardial Effusion ; Pleural Effusion* ; Tachycardia*

BACKGROUND AND OBJECTIVES: The prevalence of coronary disease in Korea, with the consequent morbidity and mortality, has rapidly risen during the last two decades. This study aimed to describe the changing pattern in the demographic composition during the 1990s of patients presenting with acute myocardial infarction (AMI) in Korean metropolitan cities. SUBJECTS AND METHODS: Data from the medical record of patients with AMI, admitted to five University Hospitals in Busan and Daegu between January 1990 and December 1999, were sorted according to their age (<30, 3044, 4559, 6074, >75 years) and gender. RESULTS: During the last decade, the number of cases of AMI increased from 283 in 1990, to 988 by 1999 (ratio of AMI/medical patients admitted; 1.68% in 1990 to 2.52% in 1999). The most prevalent age group was 6074 yrs (46.1%), followed by 4559 yrs (34.2%). Generally, the male cases were twice as prevalent as female (68.2% : 31.8%), but the gender ratio was reversed in the highest age group (>75 yrs) (44.6% : 55.4%). During the period in question, the gender ratio and age distribution remained reasonably constant throughout. The proportion of younger AMI patients (<45 yrs) did not increase. CONCLUSION: Admissions due to AMI increased substantially during the 1990s. Almost half the cases were from the 6074 yrs age group, and two third were male. There were little changes in the compositions of age and gender of the AMI cases during this period.
Age Distribution ; Busan ; Coronary Disease ; Daegu ; Female ; Hospitals, University* ; Humans ; Korea ; Male ; Medical Records ; Mortality ; Myocardial Infarction* ; Prevalence

BACKGROUND AND OBJECTIVES: Increased plasma homocysteine(tHcy) has been implicated as an independent risk factor for coronary artery diseas(CAD), but the relationship has not been firmly established. Present study aimed to determine the difference of plasma homocysteine between patients with CAD and normal control, and to identify the relation between plasma homocysteine and genotype variation of its metabolic enzymes, and serological characteristics. METHODS: Plasma homocysteine, fasting and post-methionin loading, folate and vitamin B12 were measured among 149 patients and 80 control subjects. Both group consisted of those younger than 65 years. Frequencies of prevalent mutations of enzymes involved in homocysteine metabolism, cytosine to thymidine transition (C(677)T) of methylentetrahydrofolate reductase (MTHFR) was determined by polymerase chain reaction (PCR) in 85 patients and 47 control. RESULT: There was no significant difference in homocysteine level between patients and control group (fasting tHcy; 10.4 +/- 3.6 vs 11.4 +/- 8.4 ng/ml, post-methionine loading tHcy; 18.8 +/- 4.9 vs 17.2 +/- 9.5 ng/ml, p> 0.05 respectively). Genotype frequency of MTHFR C(677)T was similar between two groups. Plasma homocysteine level did not appear to vary with genotypes of MTHFR both in patients and control subjects. Multiple linear regression analysis identified smoking as the most significant factor affecting plasma homocysteine level, followed by age, MTHFR genotype, obesity, and folate level. CONCLUSION: Homocysteine concentration was not different between controls and patients with CAD. Significant variation of homocysteine level according to genetypic polymorphism of metabolism enzymes was not observed. On multiple linear regression, several factors were identified to be related to homocysteine level, including MTHFR genotype. Further study is warranted to clarify the significance of homocysteine in the development of CAD.
Coronary Artery Disease* ; Coronary Vessels* ; Cystathionine beta-Synthase ; Cytosine ; Fasting ; Folic Acid ; Genotype* ; Homocysteine* ; Humans ; Linear Models ; Metabolism ; Methylenetetrahydrofolate Reductase (NADPH2) ; Obesity ; Oxidoreductases ; Plasma* ; Polymerase Chain Reaction ; Risk Factors* ; Smoke ; Smoking ; Thymidine ; Vitamin B 12

Asthma is a heterogeneous disease whose development is shaped by a variety of environmental and genetic factors. While several recent studies suggest that microbial dysbiosis in the gut may promote asthma, little is known about the relationship between the recently discovered lung microbiome and asthma. Innate lymphoid cells (ILCs) have also been shown recently to participate in asthma. To investigate the relationship between the lung microbiome, ILCs, and asthma, we recruited 23 healthy controls (HC), 42 patients with non-severe asthma, and 32 patients with severe asthma. Flow cytometry analysis showed severe asthma associated with fewer natural cytotoxicity receptor (NCR) + ILC3s in the lung.Similar changes in other ILC subsets, macrophages, and monocytes were not observed. The asthma patients did not differ from the HC in terms of the alpha and beta-diversity of the lung and gut microbiomes. However, lung function correlated positively with both NCR + ILC3 frequencies and microbial diversity in the lung. Sputum NCR + ILC3 frequencies correlated positively with lung microbiome diversity in the HC, but this relationship was inversed in severe asthma. Together, these data suggest that airway NCR + ILC3s may contribute to a healthy commensal diversity and normal lung function.