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

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

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

Effects of Salt Treatment Time on the Metabolites, Microbial Composition, and Quality Characteristics of the Soy Sauce Moromi Extract

Salt is one of the most important factors for fermented foods, but the effect of salt treatment time on the quality of fermented foods has rarely been studied. In this study, the effect of different salt treatment times (0, 48, and 96 h) after the start of fermentation on the quality of the soy sauce moromi extract (SSME) was investigated. As the salt treatment time was delayed, the population of Aspergillus oryzae, Lactobacillaceae, and Enterococcaecea in SSME increased, whereas the population of Staphylococcaceae and Bacillaceae decreased, leading to changes in the enzymatic activity and metabolite profiles. In particular, the contents of amino acids, peptides, volatile compounds, acidic compounds, sugars, and secondary metabolites were significantly affected by the salt treatment time, resulting in changes in the sensory quality and appearance of SSME. The correlation data showed that metabolites, bacterial population, and sensory parameters had strong positive or negative correlations with each other. Moreover, based on metabolomics analysis, the salt treatment-time-related SSME metabolomic pathway was proposed. Although further studies are needed to elucidate the salt treatment mechanism in fermented foods, our data can be useful to better understand the effect of salt treatment time on the quality of fermented foods