No abstract available.
Aneurysm

BACKGROUND: Puromycin aminonucleoside (PAN) is a known podocytotoxin. PAN-induced nephrosis is a widely used animal model for studying human idiopathic nephrotic syndrome. Abnormal protein accumulation associated with podocyte-specific endoplasmic reticulum (ER) stress damages cells structurally and functionally, which in turn induces apoptosis and severe proteinuria. In the present study, we investigated the effect of PAN on ER stress and apoptosis in podocytes in vitro. METHODS: Mouse podocytes were cultured and treated with various concentrations of PAN. ER stress markers were then evaluated by western blotting, and apoptosis was evaluated by fluorescence-activated cell sorting (FACS) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. RESULTS: PAN treatment increased ER stress markers such as activating transcription factor (ATF) 6α and caspase-12 in a dose-dependent manner at 12 and 24 hours, respectively. These markers were reduced by chemical chaperones, such as sodium 4-phenylbutyric acid and tauroursodeoxycholic acid. PAN treatment also increased 78 kD glucose-regulated protein (GRP78)/binding immunoglobulin protein (BiP) at the earlier stage of 12 hours. PAN significantly induced podocyte apoptosis in concentration- and time-dependent manners, as seen using FACS and TUNEL assays. This result was improved by Nox4 siRNA, ATF6 siRNA, and chemical chaperones. LY294002, a PI3-kinase inhibitor, significantly boosted ER stress and apoptosis. PAN-induced ER stress increased oxidative stress and subsequently induced apoptosis, and could be mitigated by inhibition of PI3-kinase signaling. CONCLUSION: Our findings suggest that PAN induces ER stress in podocytes mainly through the GRP78/BiP, ATF6α, and caspase-12 pathways, which trigger apoptosis via induction of oxidative stress. This stress is mitigated by inhibiting PI3-kinase signaling.
Animals ; Apoptosis* ; Blotting, Western ; Caspase 12 ; DNA Nucleotidylexotransferase ; Endoplasmic Reticulum Stress* ; Endoplasmic Reticulum* ; Flow Cytometry ; Humans ; Immunoglobulins ; In Situ Nick-End Labeling ; In Vitro Techniques ; Mice ; Models, Animal ; Nephrosis ; Nephrotic Syndrome ; Oxidative Stress ; Phosphatidylinositol 3-Kinases ; Podocytes* ; Proteinuria ; Puromycin Aminonucleoside* ; Puromycin* ; RNA, Small Interfering ; Sodium ; Transcription Factors

The authors would like to publish this corrigendum to correct the spells of an author's name in the above article.

Invasive aspergillosis (IA) is most commonly seen in patients with risk factors, such as cytotoxic chemotherapy, prolonged neutropenia, corticosteroids, transplantation and acquired immune deficiency syndrome. IA commonly occurs in the respiratory tract. Extrapulmonary aspergillosis is usually a part of a disseminated infection, and primary invasive intestinal aspergillosis is very rare. Herein, we report a case of an immunocompetent 53-year-old male who suffered recurrent septic shock in the intensive care unit (ICU) and was finally diagnosed as invasive intestinal aspergillosis without dissemination. IA is rarely considered for patients who do not have an immune disorder. Thus, when such cases do occur, the diagnosis is delayed and the clinical outcome is often poor. However, there is a growing literature reporting IA cases in patients without an immune disorder, mostly among ICU patients. Primary intestinal aspergillosis should be considered for critically ill patients, especially with severe disrupted gastrointestinal mucosal barrier.
Acquired Immunodeficiency Syndrome ; Adrenal Cortex Hormones ; Aspergillosis* ; Critical Illness ; Diagnosis ; Drug Therapy ; Gastrointestinal Diseases ; Humans ; Immune System Diseases ; Immunocompromised Host* ; Intensive Care Units ; Male ; Middle Aged ; Neutropenia ; Respiratory System ; Risk Factors ; Shock, Septic

PURPOSE: The purpose of this study was to determine the role of CT and MR imagings in the diagnosis aortic dissection and differentiation between the true and false lumen. MATERIALS AND METHODS: We retrospectively studied forty patients with aortic dissection(AD) diagnosed imagings or surgery. Of the forty patients, 19 were examined with only CT, 14 with CT and MR, and 7 with MI~: Our points of view were(1) the classification of AD according to configuration of intimal flap by cross-sectional imaging, (2) differentiation between the true and false lumens, (3) the course of the false lumen, and (4)! detectability of the origin of major branch vessels of the abdominal aorta. RESULTS: The classification by corss-sectional imaging were crescentic(65%), circumferential(15%), flat(12%), and irregular(8%) type, in which false negative diagnosis was made in 1 case of crescentic and circumferential type, respectively. In 2 case of flat type and 1 case of irregular type, the differentiation between the true and false lumen was impossible with CT. The course of the false lumen in descending thoracic aorta revealed countrclock wise rotation(66%), clockwise rotation(5%) or fixed(29%) apperance. MR imaging was superior to CT in the detection of the origin of major branch vessels of the abdominal aorta. The determination of the origin of major branches of abdominal aorta arising from the true and false lumen were impossible in 2 cases in which only CT was done. CONCLUSION: Diagnosis of crescentic and circumferential types of AD with narrow and thrombosed false lumen was problematic in both CT and MR with no difference of diagnostic accuracy between the two modalities. The differentiation between the true and false lumen was difficult in flat and irregular types with only CT. Therefore, when surgical treatment is considered as in type B aortic dissection, MR imaging is recommended in order to determine the origin of major branch vessels.
Aorta, Abdominal ; Aorta, Thoracic ; Classification ; Diagnosis* ; Humans ; Magnetic Resonance Imaging ; Retrospective Studies

No abstract available.
Colon* ; Colonic Neoplasms* ; Humans ; Sparganosis* ; Ultrasonography*

No abstract available.
Nevus*

We found an error in this article. The Fig. 1A.

No abstract available.
Antibodies, Monoclonal* ; Herpesvirus 4, Human* ; Humans* ; Tetanus Toxoid* ; Tetanus*

No abstract available.
Adaptive Immunity ; Animals ; Cell Line* ; Rats*