Enhanced cardiac expression of two isoforms of matrix metalloproteinase-2 in experimental diabetes mellitus.

BackgroundDiabetic cardiomyopathy (DM CMP) is defined as cardiomyocyte damage and ventricular dysfunction directly associated with diabetes independent of concomitant coronary artery disease or hypertension. Matrix metalloproteinases (MMPs), especially MMP-2, have been reported to underlie the pathogenesis of DM CMP by increasing extracellular collagen content.PurposeWe hypothesized that two discrete MMP-2 isoforms (full length MMP-2, FL-MMP-2; N-terminal truncated MMP-2, NTT-MMP-2) are induced by high glucose stimulation in vitro and in an experimental diabetic heart model.MethodsRat cardiomyoblasts (H9C2 cells) were examined to determine whether high glucose can induce the expression of the two isoforms of MMP-2. For the in vivo study, we used the streptozotocin-induced DM mouse heart model and age-matched controls. The changes of each MMP-2 isoform expression in the diabetic mice hearts were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical stains were conducted to identify the location and patterns of MMP-2 isoform expression. Echocardiography was performed to compare and analyze the changes in cardiac function induced by diabetes.ResultsQuantitative RT-PCR and immunofluorescence staining showed that the two MMP-2 isoforms were strongly induced by high glucose stimulation in H9C2 cells. Although no definite histologic features of diabetic cardiomyopathy were observed in diabetic mice hearts, left ventricular systolic dysfunction was determined by echocardiography. Quantitative RT-PCR and IHC staining showed this abnormal cardiac function was accompanied with the increases in the mRNA levels of the two isoforms of MMP-2 and related to intracellular localization.ConclusionTwo isoforms of MMP-2 were induced by high glucose stimulation in vitro and in a Type 1 DM mouse heart model. Further study is required to examine the role of these isoforms in DM CMP

Clinical Role of Interstitial Pneumonia in Patients with Scrub Typhus: A Possible Marker of Disease Severity

Interstitial pneumonia (IP) frequently occurs in patients with scrub typhus, but its clinical significance is not well known. This study was designed to evaluate interstitial pneumonia as a marker of severity of the disease for patients with scrub typhus. We investigated clinical parameters representing the severity of the disease, and the chest radiographic findings for 101 patients with scrub typhus. We then compared these clinical factors between patients with and without IP. We also studied the relationship between IP and other chest radiographic findings. The chest radiography showed IP (51.4%), pleural effusion (42.6%), cardiomegaly (14.9%), pulmonary alveolar edema (20.8%), hilar lymphadenopathy (13.8%) and focal atelectasis (11.8%), respectively. The patients with IP (n=52) had higher incidences in episode of hypoxia (p=0.030), hypotension (p=0.024), severe thrombocytopenia (p=0.036) and hypoalbuminemia (p=0.013) than the patients without IP (n=49). The patients with IP also had higher incidences of pleural effusion (p<0.001), focal atelectasis (p=0.019), cardiomegaly (p<0.001), pulmonary alveolar edema (p=0.011) and hilar lymphadenopathy (p<0.001) than the patients without IP. Our data suggest that IP frequently occurs for patients with scrub typhus and its presence is closely associated with the disease severity of scrub typhus

A Family Harboring CMT1A Duplication and HNPP Deletion

Charcot-Marie-Tooth disease type 1A (CMT1A) is associated with duplication of chromosome 17p11.2-p12, whereas hereditary neuropathy with liability to pressure palsies (HNPP), which is an autosomal dominant neuropathy showing characteristics of recurrent pressure palsies, is associated with 17p11.2-p12 deletion. An altered gene dosage of PMP22 is believed to the main cause underlying the CMT1A and HNPP phenotypes. Although CMT1A and HNPP are associated with the same locus, there has been no report of these two mutations within a single family. We report a rare family harboring CMT1A duplication and HNPP deletion

Tristetraprolin down-regulates IL-23 expression in colon cancer cells.

mRNA 3&apos;UTR demonstrated that the ARE cluster between the third and fifth AREs was responsible for TTP-mediated destabilization of IL-23 mRNA. A RNA electrophoretic mobility shift assay confirmed that TTP binds to this ARE cluster. Taken together, these results demonstrate that TTP acts as a negative regulator of IL-23 gene expression in mouse colon cancer cells and suggest its potential application as a novel therapeutic target to control IL-23-mediated tumor promotion

Balloon Dilatation for Corrosive Esophageal Strictures in Children: Radiologic and Clinical Outcomes

Objective: We retrospectively evaluated the effectiveness of the esophageal balloon dilatation (EBD) in children with a corrosive esophageal stricture. Materials and Methods: The study subjects included 14 patients (M:F = 8:6, age range: 17-85 months) who underwent an EBD due to a corrosive esophageal stricture. The causative agents for the condition were glacial acetic acid (n = 9) and lye (n = 5). Results: A total of 52 EBD sessions were performed in 14 patients (range 1-8 sessions). During the mean 15-month follow-up period (range 1-79 months), 12 patients (86%) underwent additional EBD due to recurrent esophageal stricture. Dysphagia improved after each EBD session and oral feeding was possible between EBD sessions. Long-term success (defined as dysphagia relief for at least 12 months after the last EBD) was achieved in two patients (14%). Temporary success of EBD (defined as dysphagia relief for at least one month after the EBD session) was achieved in 17 out of 52 sessions (33%). A submucosal tear of the esophagus was observed in two (4%) sessions of EBD. Conclusion: Only a limited number of children with corrosive esophageal strictures were considered cured by EBD. However, the outcome of repeated EBD was sufficient to allow the children to eat per os prior to surgical management.Doo EY, 2009, CLIN RADIOL, V64, P265, DOI 10.1016/j.crad.2008.10.001PARK JY, 2009, KOREAN J PEDIAT, V52, P446Hyoung J, 2008, J VASC INTERV RADIOL, V19, P736, DOI 10.1016/j.jvir.2008.01.015Ko HK, 2006, J VASC INTERV RADIOL, V17, P1327, DOI 10.1097/01.RVI.0000232686.29864.0AWeintraub JL, 2006, J VASC INTERV RADIOL, V17, P831, DOI 10.1097/01.RVI.0000217964.55623.19Wilkinson AG, 2004, PEDIATR RADIOL, V34, P414, DOI 10.1007/s00247-004-1164-1Huang YC, 2004, PEDIATR SURG INT, V20, P207, DOI 10.1007/s00383-004-1153-3Lan LCL, 2003, J PEDIATR SURG, V38, P1712, DOI 10.1016/S0022-3468(03)00638-9Fasulakis S, 2003, PEDIATR RADIOL, V33, P682, DOI 10.1007/s00247-003-1011-9Hamza AF, 2003, J PEDIATR SURG, V38, P828Kukkady A, 2002, PEDIATR SURG INT, V18, P486, DOI 10.1007/s00383-002-0798-zYEMING W, 2002, J PEDIATR SURG, V37, P398Jayakrishnan VK, 2001, PEDIATR RADIOL, V31, P98Lisy J, 1998, ACAD RADIOL, V5, P832Yararbai O, 1998, HEPATO-GASTROENTEROL, V45, P59KIM IO, 1993, RADIOLOGY, V189, P741HAN HY, 1993, J KOREAN RADIOL SOC, V29, P1181SONG HY, 1992, RADIOLOGY, V184, P373GUNDOGDU HZ, 1992, J PEDIATR SURG, V27, P767LOVEJOY FH, 1990, NEW ENGL J MED, V323, P668MAYNAR M, 1988, RADIOLOGY, V167, P703DELANGE EE, 1988, RADIOLOGY, V167, P45SATO Y, 1988, AM J ROENTGENOL, V150, P639MCLEAN GK, 1987, RADIOLOGY, V165, P35GOLDTHORN JF, 1984, RADIOLOGY, V153, P655LONDON RL, 1981, GASTROENTEROLOGY, V80, P173MUHLETALER CA, 1980, AM J ROENTGENOL, V134, P1137RAGHEB MI, 1976, SURGERY, V79, P494