Biomedical subjects

S Y Kim

Publications and source records attributed to S Y Kim.

At least 145 records · Page 8Linked to original sources

PubMed2000

Mapping of a new target region of allelic loss at 21q22 in primary gastric cancers.

To determine the minimal region of deletion on 21q22 in gastric cancer, we performed a high-density loss of heterozygosity (LOH) study with eight polymorphic microsatellite markers. Among the 43 tumors examined, 20 (50%) of 40 informative carcinomas showed LOH at one or more loci. The peak LOH frequency was identified at D21S1820 (34.2%) in 21q22.3. This data suggests that this locus might harbor a new tumor suppressor gene in an area <0.332 Mb in physical map distance defined by D21S1820 and D21S49. Thus, we speculate that trefoil factor family 1 (TFF1), located in this narrow region, might be the most probable candidate gene involved in gastric cancer carcinogenesis.

Adenocarcinoma↗

PubMed2000

In vivo determination of substrate specificity of hepatitis C virus NS3 protease: genetic assay for site-specific proteolysis.

Hepatitis C virus (HCV) NS3 protease is responsible for the processing of the viral polyprotein and is considered as a primary target for the development of anti-HCV therapy. We have developed a genetic method in yeast to screen for good substrate sequences of the NS3 protease. A library of fusion proteins was constructed with a transcription factor, GAL4, linked to the intracellular domain of an integral membrane protein, STE2, by a randomized protease substrate sequence. In yeast cells expressing NS3 protease, the substrate sequences in the fusion proteins were specifically recognized and cleaved. This cleavage resulted in the release of GAL4 from the cytoplasmic membrane and the subsequent activation of reporter genes by GAL4, which was detected by the growth of yeast cells on selective media. Based on the analysis of 69 isolated substrate sequences, a consensus sequence was deduced: (Glu/Asp)-X-Val-Val-(Leu/Pro)-Cys / (Ser/Ala), with the scissile bond being located between Cys and Ser or Ala and X not being determined. This is largely consistent with the previous results obtained by biochemical methods. An oligopeptide containing the deduced sequence was highly efficiently cleaved in vitro by the purified NS3 protease. These data demonstrated that the present genetic method could be used as an efficient tool for the in vivo determination of substrate specificity of proteases.

Amino Acids↗

PubMed2000

Factors involved in hepatic glutathione depletion induced by acute ethanol administration.

Factors implicated in changes of the hepatic glutathione concentration following acute ethanol administration were examined in rats. Adult female rats were treated with either ethanol (4 g/kg, p.o.) or an isocaloric glucose solution. The hepatic reduced glutathione (GSH) concentration decreased rapidly after ethanol intake with a maximum diminution, approximately 50% of the control value, being observed at t = 6 h. The hepatic GSH concentration gradually increased, and finally rebounded at 24 h after ethanol ingestion. The dose of ethanol induced a transient increase in the oxidized glutathione (GSSG)/GSH ratio, which was associated with a significant reduction in GSH rather than elevation in GSSG [corrected]. The activity of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme for glutathione synthesis, and the cysteine concentration in liver were also measured. The GCS activity was depressed to approximately 80% of the control value at t = 2.5 h followed by rapid recovery, but no difference in the hepatic cysteine concentration between control and ethanol treated rats was observed for 24 h, suggesting that the reduction in glutathione synthesis may not play a major role in the significant depletion of this tripeptide in liver. The total glutathione concentration was measured both in prehepatic and posthepatic inferior vena cava blood. The glutathione concentration in posthepatic blood was approximately twice as high as that of prehepatic blood in control rats. Acute ethanol administration doubled the elevation of glutathione in posthepatic blood measured at t = 2.5 h. The sinusoidal efflux of glutathione estimated from the increase in blood glutathione concentration was greater than the total amount of its depletion in the liver of rats treated with ethanol. The results suggest that in the liver of rats treated acutely with ethanol, glutathione efflux plays the most important role in the reduction of this tripeptide, which would be aggravated by a transient decrease in glutathione synthesis and by increased consumption in association with its metabolism.

Alcoholic Intoxication↗

PubMed2000

Effect of Jindangwon on streptozotocin-induced diabetes.

The inhibitory effects of the traditional herbal medicine Jindangwon (JDW) on streptozotocin (ST)-induced diabetic mellitus were studied using the ST-treated diabetic model. Glucokinase activity of pancreatic islets was severely impaired by ST treatment. However, when ST-treated islets were treated with 1 mg/ml of JDW, the enzyme activities of glucokinase and hexokinase were protected, glucose-6-phosphatase was not. When the effects of JDW on ST-induced ATP/ADP ratio of islets were assayed, JDW was effective in restoring of ATP/ADP ratio. In addition, ST decreased the enzyme activities of PDH, while JDW had a protective effect on the enzyme. ST-induced cGMP accumulation was significantly inhibited by JDW treatment. Furthermore, ST-induced nitrite formation was significantly inhibited by JDW treatment. JDW also showed the suppressed nitrite production in ST-treated pancreatic islet cells. When the islets (200/condition) were treated with ST (5 mM for 30 min), and then JDW was added to the ST-treated cells, 1.0 mg/ml of JDW showed the activated and recovered aconitase activity in pancreatic islet cells. When the effect of ST on the gene expression of pancreatic GLUT2 and glucokinase were examined, the level of GLUT2 and glucokinase mRNA in pancreatic islets was significantly decreased. However, JDW protected and improved the expression of protein and genes, indicating that JDW is effective on ST-induced inhibition of gene expression of GLUT2, glucokinase and proinsulin in islets. These results suggested that JDW is effective in this model to treat ST-induced diabetes.

Adenosine Diphosphate↗

PubMed2000

Role of lipid peroxidation and poly(ADP-ribose) polymerase activation in oxidant-induced membrane transport dysfunction in opossum kidney cells.

This study was undertaken to examine the role of lipid peroxidation and poly(ADP-ribose) polymerase (PARP) activation in H(2)O(2)-induced inhibition of Na(+)-dependent phosphate (Na(+)-Pi) uptake in opossum kidney (OK) cells. H(2)O(2) inhibited Na(+)-Pi uptake in a dose-dependent manner. H(2)O(2)-induced inhibition of Na(+)-Pi uptake was prevented by dithiothreitol and glutathione. A potent antioxidant, DPPD, had no effect on H(2)O(2) inhibition of Na(+)-Pi uptake, despite completely inhibiting lipid peroxidation induced by H(2)O(2). However, in primary cultured rabbit proximal tubular cells, the effect of H(2)O(2) on Na(+)-Pi uptake was significantly prevented by DPPD, suggesting a species difference in the role of lipid peroxidation in the inhibition of Na(+)-Pi uptake occurring with H(2)O(2). t-Butylhydroperoxide (tBHP) caused the inhibition of Na(+)-Pi uptake that was prevented by DPPD in OK cells and rabbit proximal tubular cells. The PARP inhibitor 3-aminobenzamide completely protected the inhibition of Na(+)-Pi uptake induced by H(2)O(2) but not by tBHP. H(2)O(2)-induced ATP depletion was prevented by 3-aminobenzamide but not by DPPD. tBHP-induced ATP depletion was prevented by DPPD, whereas it was not altered by 3-aminobenzamide. Effects of H(2)O(2) and tBHP on Na(+)-Pi uptake and ATP depletion were prevented by an iron chelator, deferoxamine, suggesting that the oxidants inhibit Na(+)-Pi uptake through an iron-dependent mechanism. The extent of DNA damage by tBHP was similar to that by H(2)O(2). These results indicate that the effect of H(2)O(2) on membrane transport function in OK cells is associated with PARP activation but not lipid peroxidation, whereas the effect of tBHP is associated with lipid peroxidation.

Animals↗

PubMed2000

Overexpression of phospholipase Cbeta-1 protects NIH3T3 cells from oxidative stress-induced cell death.

Oxidative stress has been implicated in a wide range of cellular damage which includes DNA oxidation, membrane lipid peroxidation, and apoptosis. In our study, we found that overexpression of PLC-beta1 in NIH3T3 fibroblasts protected them from cell death occuring in response to oxidative stress. Cell death caused by treatment with prooxidant tert-butylhydroperoxide (TBH), H2O2, or CdCl2 was considerably suppressed in PLC-beta1 overexpressed NIH/beta1-14 cells in comparison to control NIH/neo cells. However, overexpression of PLC-beta1 failed to protect the cells from toxicity by diamide or KCN. In addition, while accumulation of c-fos mRNA was observed within 30 min of TBH treatment in vector transfected NIH/neo cells, TBH-induced c-fos mRNA generation was completely suppressed in NIH/beta1-14 cells, while that of c-jun and GAPDH was not affected. These findings suggest that PLC-beta1 may play a role in process that can protect cells from oxidative stress-induced cell death.

3T3 Cells↗

PubMed2000

Poly(ethylene oxide)-poly(propylene oxide)-poly(ethylene oxide)/poly(epsilon-caprolactone) (PCL) amphiphilic block copolymeric nanospheres. II. Thermo-responsive drug release behaviors.

Amphiphilic block copolymers composed of relatively hydrophilic PEO-PPO-PEO block copolymer (Pluronic) and poly (epsilon-caprolactone) with hydrophobic character were synthesized by ring-opening polymerization of epsilon-caprolactone in the presence of PEO-PPO-PEO block copolymer using stannous octoate as a catalyst. Pluronic/PCL block copolymeric nanospheres with core-shell structure were prepared by dialysis method. They showed the average diameter of 116-196 nm depending on the type of copolymer. All the nanosphere samples exhibited a narrow size distribution. The critical micelle concentrations of Pluronic/PCL amphiphilic block copolymers determined by fluorescence spectroscopy were lower than that of the common low molecular weight surfactant. Their core-shell structure was confirmed by 1H NMR spectroscopy. Pluronic/PCL block copolymeric nanospheres exhibited the reversible change of size depending on the temperature. Release behaviors of indomethacin from Pluronic/PCL block copolymeric nanospheres also showed temperature dependence and a sustained release pattern. In addition, cytotoxicity test using an MTT assay method revealed that these indomethacin-loaded Pluronic/PCL nanospheres could remarkably reduce the cell damage compared with the unloaded free indomethacin.

Algorithms↗

PubMed2000

Sporadic inclusion body myositis correlates with increased expression and cross-linking by transglutaminases 1 and 2.

Sporadic inclusion body myositis (SIBM) is characterized by vacuolar degeneration of muscle fibers and intrafiber clusters of paired helical filaments with abnormal amyloid deposition. Because of their potential involvement in other degenerative disorders, we have examined the expression of transglutaminases (TGases) in normal and SIBM tissues. We report that at least two different enzymes, the ubiquitous TGase 2 as well as the TGase 1 enzyme, are present in muscle tissues. However, in comparison with normal tissue, the expression of TGases 1 and 2 was increased 2.5- and 4-fold in SIBM, accompanied by about a 20-fold higher total TGase activity. By immunohistochemical staining, in normal muscle, TGase 2 expression was restricted to some endomysial connective tissue elements, whereas TGase 1 and beta-amyloid proteins were not detectable. In SIBM muscle, both TGases 1 and 2 as well as amyloid proteins were brightly expressed and co-localized in the vacuolated muscle fibers, but none of these proteins colocalized with inflammatory cell markers. Next, we isolated high molecular weight insoluble proteins from SIBM muscle tissue and showed that they were cross-linked by about 6 residues/1000 residues of the isopeptide bond. Furthermore, by amino acid sequencing of solubilized tryptic peptides, they contain amyloid and skeletal muscle proteins. Together, these findings suggest that elevated expression of TGases 1 and 2 participate in the formation of insoluble amyloid deposits in SIBM tissue and in this way may contribute to progressive and debilitating muscle disease.

Amyloid beta-Protein Precursor↗

PubMed2000

ABFs, a family of ABA-responsive element binding factors.

Abscisic acid (ABA) plays an important role in environmental stress responses of higher plants during vegetative growth. One of the ABA-mediated responses is the induced expression of a large number of genes, which is mediated by cis-regulatory elements known as abscisic acid-responsive elements (ABREs). Although a number of ABRE binding transcription factors have been known, they are not specifically from vegetative tissues under induced conditions. Considering the tissue specificity of ABA signaling pathways, factors mediating ABA-dependent stress responses during vegetative growth phase may thus have been unidentified so far. Here, we report a family of ABRE binding factors isolated from young Arabidopsis plants under stress conditions. The factors, isolated by a yeast one-hybrid system using a prototypical ABRE and named as ABFs (ABRE binding factors) belong to a distinct subfamily of bZIP proteins. Binding site selection assay performed with one ABF showed that its preferred binding site is the strong ABRE, CACGTGGC. ABFs can transactivate an ABRE-containing reporter gene in yeast. Expression of ABFs is induced by ABA and various stress treatments, whereas their induction patterns are different from one another. Thus, a new family of ABRE binding factors indeed exists that have the potential to activate a large number of ABA/stress-responsive genes in Arabidopsis.

Abscisic Acid↗

PubMed2000

A distinct tumor suppressor gene locus on chromosome 15q21.1 in sporadic form of colorectal cancer.

The SM1311 family is an Ashkenazi family with dominantly inherited predisposition to colorectal adenomas and carcinomas and has a high-penetrance locus in chromosome 15q, with a multipoint logarithm of the odds score of 3.06 at marker D15S118. In the present study, we performed a high-density loss of heterozygosity study with 13 polymorphic microsatellite markers, including D15S118, spanning 15q15.3-q22.1, on 70 cases of the sporadic form of colorectal tumors. Our deletion mapping data showed a locus at D15S968 in chromosomal sub-band 15q21.1 may harbor a tumor suppressor gene in an area <0.521 Mb in physical map distance defined by markers D15S514 and D15S222. THBS1, 0.185 Mb proximal to D15S968, is the nearest known gene to this specific narrow loss of heterozygosity region. Thus, we speculate that THBS1 might be the most probable candidate gene involved in colorectal cancer carcinogenesis.

Adenocarcinoma↗

PubMed2000

Upregulation of phospholipase D in astrocytes in response to transient forebrain ischemia.

Previous in vitro studies using cell cultures or brain slices have demonstrated that phospholipase D (PLD) in the nervous system is involved in the signaling mechanism in response to a variety of agonists. However, little is known about the pathophysiological role of PLD-mediated signaling in the adult brain. We examined the changes in the expression of a PLD isozyme, PLD1, in the adult rat hippocampus, using immunological approaches and an assay for PLD activity after transient forebrain ischemia (four-vessel occlusion model) that results in the selective delayed death of CA1 pyramidal cells and induces reactive astrocytes in the CA1 subfield. In the control hippocampus, PLD1 the level of immunoreactivity was very low. After ischemia, in parallel with the results of Western blot analysis and the PLD activity assay, immunohistochemical analysis of PLD1 demonstrated that the immunoreactive proteins peaked at 7-14 days and were most prominent in the CA1 and the dentate hilar region. The temporal and spatial patterns of immunoreactivity of both PLD1 and glial fibrillary acidic protein (GFAP) were very similar, indicating that reactive astrocytes express PLD1, confirmed by double staining for PLD1 and GFAP. These results demonstrate that reactive astrocytes upregulate PLD in vivo after injury in the adult rat hippocampus.

Animals↗

PubMed2000

LCC, a cerebroside from Lycium chinense, protects primary cultured rat hepatocytes exposed to galactosamine.

Primary cultures of rat hepatocytes exposed to galactosamine (GalN) were used as a screening system to assess whether a new cerebroside, LCC, isolated from the fruits of Lycium chinense, exhibits hepatoprotective activity. Cultured rat hepatocytes injured with GalN routinely release glutamic pyruvic transaminase (GPT) and sorbitol dehydrogenase (SDH) into the culture medium. Treatment of these GalN-injured primary cultures with LCC markedly blocked the release of both GPT and SDH in a dose-dependent manner over concentrations of LCC ranging from 1 microM to 10 microM. To investigate the mechanism of action for the hepatoprotective activity of LCC, the extent of [(3)H]-uridine incorporation into RNA was measured in GalN-injured cultures of rat hepatocytes. [(3)H]-Uridine incorporation was significantly decreased in injured hepatocytes. LCC, however significantly restored the incorporation of [(3)H]-uridine into RNA in a dose-dependent manner over concentrations ranging from 1 microM to 10 microM. LCC also blocked the suppression of RNA synthesis caused by actinomycin D in a dose-dependent manner. These data suggest that LCC may have prominent hepatoprotective activity and that its therapeutic value should be investigated further.

Animals↗

PubMed2000

Effects of physostigmine on the pharmacokinetics of intravenous parathion in rats.

It was reported that the area under the plasma concentration-time curve from time zero to time infinity (AUC) of parathion was significantly smaller, and the time-averaged total body clearance (Cl) of parathion was significantly faster after intravenous administration of parathion to rats pretreated with dexamethasone than those in control rats. This was supported by significantly faster intrinsic clearance of parathion to form paraoxon in hepatic microsomal fraction of rats pretreated with dexamethasone. The above data suggested that parathion was metabolized to paraoxon by dexamethasone-inducible hepatic cytochrome P450 (CYP) 3A in rats. The purpose of this study is to explain the protective effects of physostigmine against paraoxon toxicity by suppressing CYP3A, and hence, decreasing formation of a toxic metabolite, paraoxon. The pharmacokinetic changes of parathion and paraoxon were investigated after intravenous administration of parathion, 3 mg/kg, to control Sprague-Dawley rats, and the rats pretreated with physostigmine (100 microg/kg, intraperitoneal injection 30 min before parathion administration). After a 1-min intravenous infusion of parathion to rats pretreated with physostigmine, the AUC of parathion (60.4 compared with 73.7 microg min/mL) was significantly greater, Cl of parathion (49.7 compared with 40.7 mL/min/kg) was significantly slower, and amount of paraoxon recovered from liver, mesentery and large intestine at 5 min was smaller than those in control rats. Based on in vitro rat hepatic microsomal studies, physostigmine inhibited significantly the erythromycin N-demethylase activity (1.03 compared with 0.924 nmol/mg protein/min), mainly mediated by hepatic cytochrome P450 3A in rats. The above data suggested that the formation of paraoxon was inhibited in rats pretreated with physostigmine by inhibiting CYP3A.

Animals↗

PubMed2000

Synthesis and biological activity of conformationally controlled 2-PAM derivatives.

A series of conformationally controlled 2-PAM derivatives were prepared from 2-acetylpyridine and 2,3-pyrido[b]cycloalkenones in two steps and their reactivities towards parathion poisoned AChE were evaluated. The most planar 2,3-pyrido[b]cyclohexanone oxime methiodide showed an activity comparable to 2-PAM implying E-syn is that the most active conformation of 2-PAM in the biological system.

Acetylcholinesterase↗

PubMed2000

Antitumor activity of Bifidobacterium spp. isolated from a healthy Korean.

The antitumor activity of Bifidobacterium breve K-110, and K-111, and B. infantis K-525 was investigated. These Bifidobacterial cells and their cell wall preparations (WPG) significantly increased the survival rate of mice who had been intraperitoneally implanted with sarcoma 180 cells. Solid tumor growth was inhibited even when the sarcoma 180 cells were implanted into the groins of the mice. However, the Bifidobacterial cells did not show in vitro cytotoxicity against tumor cell lines. Cell kinetic studies revealed that these WPGs induced neutrophils, which were followed by macrophages, at the site of peritoneal injection. The WPGs directly activated these cells to inhibit the growth of tumor cells in in vitro assays. Our results suggest that Bifidobacterial WPGs induce and activate nonspecific phagocytes in situ to reject growing tumor cells in the mouse peritoneal cavity.

Animals↗

PubMed2000

High glucose-induced intercellular adhesion molecule-1 (ICAM-1) expression through an osmotic effect in rat mesangial cells is PKC-NF-kappa B-dependent.

AIMS/HYPOTHESIS: Infiltration of mononuclear cells and glomerular enlargement accompanied by glomerular cell proliferation are very early characteristics of the pathophysiology of diabetes. To clarify the mechanism of early diabetic nephropathy, we measured [3H]-thymidine incorporation and cell numbers to show the influence of a high ambient glucose concentration and the osmotic effect on rat mesangial cell proliferation. We also measured the effect of high glucose on the expression of intercellular adhesion molecule-1 and vascular adhesion molecule-1 by flow cytometry and semiquantitative RT-PCR in mesangial cells and the adhesion of leukocytes to mesangial cells. METHODS/RESULTS: Cells exposed to high D-glucose (30 mmol/l) caused an increase in [3H]-thymidine incorporation and cell numbers at 24 and 48 h and normalized at 72 h (p < 0.05), whereas these changes were not found in high mannitol (30 mmol/l), IL-1 beta, or TNF alpha-stimulated mesangial cells. Cells exposed to high-glucose (15, 30, or 60 mmol/l) or osmotic agents (L-glucose, raffinose and mannitol) showed that intercellular adhesion molecule-1 expression began to increase after 24 h, reached its maximum at 24 and 48 h and gradually decreased afterwards. The stimulatory effects of high glucose and high mannitol on mRNA expression were observed as early as 6 h and reached its maximum at 12 h. Up-regulation of ICAM-1 protein and mRNA was also found in IL-1-beta and TNF-alpha-stimulated mesangial cells. Neither vascular adhesion molecule-1 protein nor mRNA expression was, however, affected by high glucose and high mannitol. Notably, the protein kinase C inhibitors calphostin C and staurosporine reduced high glucose- or high mannitol-induced intercellular adhesion molecule-1 mRNA expression and high glucose-induced proliferation. Furthermore, the NF-kappa B inhibitor N-tosyl-L-phenylalanine chloromethyl ketone reduced high glucose- or high mannitol-induced intercellular adhesion molecule-1 mRNA expression and high glucose-induced proliferation. Results showed that high glucose (15, 30 mmol/l) or high concentrations of osmotic agents remarkably increased the number of adherent leukocytes to mesangial cells (p < 0.01) compared with control cells (5 mmol/l D-glucose). Functional blocking of intercellular adhesion molecule-1 on mesangial cells with rat intercellular adhesion molecule-1 monoclonal antibody, calphostin C, staurosporine, or N-tosyl-L-phenylalanine chloromethyl ketone significantly inhibited high glucose- or high mannitol-induced increase in leukocyte adhesion (p << 0.05). CONCLUSION/INTERPRETATION: These results suggest that high glucose can upregulate intercellular adhesion molecule-1 protein and mRNA expression but not vascular adhesion molecule-1 expression in mesangial cells and promote leukocyte adhesion through up-regulation of intercellular adhesion molecule-1 through osmotic effect, possibly depending on the protein kinase C nuclear factor-kappa B (PKC-NF-kappa B) pathway. High glucose itself can also promote mesangial cell proliferation through the PKC-NF-kappa B pathways. We conclude that hyperglycaemia in itself seems to be an important factor in the development of early diabetic nephropathy.

Animals↗

PubMed2000

Effect of exercise on the mitochondrial DNA content of peripheral blood in healthy women.

Exercise decreases insulin resistance and increases maximal exercise capacity as estimated from maximal oxygen uptake (VO2max). Recent reports have demonstrated that the mitochondrial DNA (mtDNA) content of blood is correlated with VO2max in healthy subjects (mean age 31 years) and is inversely correlated with insulin resistance parameters. The aim of this study was to determine the effect of regular exercise on the mtDNA content in the peripheral blood of 16 healthy young women of mean age 24.8 (SD 6.2) years and 14 healthy older women of mean age 66.7 (SD 5.8) years. The exercise programme lasted for 10 weeks and consisted of three sessions a week, each of 1 h and aiming to attain 60%-80% of VO2max. The mtDNA content of peripheral blood was measured by competitive polymerase chain reaction. The VO2max had significantly increased following the exercise programme [from 33.1 (SD 3.4) to 35.2 (SD 3.4) ml x kg(-1) min(-1) in the young and from 24.3 (SD 5.3) to 30.3 (SD 7.3) ml x kg(-1) x min(-1) in the older women, both P < 0.05]. Exercise decreased systolic blood pressure, and concentrations of triglyceride, low density lipoprotein-cholesterol (LDL-C), glucose and insulin in the blood of the young and of total cholesterol, LDL-C and glucose in that of the older women. High density lipoprotein-cholesterol (HDL-C) in the young women was increased by exercise. The mtDNA content significantly increased following the exercise programme in both groups [from 27.1 (SD 17.9) to 52.7 (SD 44.6) amol x 5 ng(-1) genomic DNA in the young and from 15.3 (SD 10.2) to 32.1 (SD 30.0) amol x 5 ng(-1) genomic DNA in the older women, both P < 0.05]. There was a significant positive correlation between the change in mtDNA content and the change in VO2max (r = 0.74 in the young and r = 0.71 in the older women, both P < 0.01). In conclusion, 10 weeks of moderate intensity, regular exercise increased the mtDNA content in peripheral blood and decreased insulin resistance parameters. This data suggests that increase in the mtDNA content may be associated with increased insulin sensitivity.

Adolescent↗

PubMed2000

Wegener's granulomatosis presenting as mediastinal soft tissue mass invading the tracheal wall.

Wegener's granulomatosis (WG) is a clinicopathologic entity of unknown cause characterised by a necrotising granulomatous vasculitis affecting multiple organs, especially the upper and lower respiratory tracts, lung and kidney. The lung is the most frequently, and sometimes the only involved organ. Single or multiple nodules, with or without cavitation, are the most common pulmonary manifestations in WG, but mediastinal involvement is atypical. The sole tracheal involvement is rare and hilar and mediastinal involvement has been thought not to be part of the clinical feature. We experienced a rare case of WG presenting as paratracheal mediastinal lesions with tracheal wall invasion, which responded dramatically to corticosteroid treatment. We present this case with a review of the literature.

Adult↗