PURPOSE: To evaluate the usefulness and diagnostic accuracy of turbo spin-echo(TSE) proton-density andT2-weighted images of meniscal tears of the knee. MATERIALS AND METHODS: We retrospectively evaluated thesensitivity, specificity, and accuracy of TSE proton density and T2-weighted images of meniscal tears confirmedarthroscopically or surgically in 47 patients(98 menisci). The routine TSE parameters used in all patients werethe dual echo sequence with sagittal proton density and T2-weighed images(4000/16, 90/5/2 [TR/effectiveTE/ETL/NEX]), and fat-suppressed coronal proton density and T2-weighted images. The chi-square test was used forstatistical analysis. RESULTS: The sensitivity, specificity, and accuracy of TSE proton density images for thedetection of meniscal tears were 93.9%, 93.8%, and 93.9%, respectively, in the medial meniscus, and 92.9%, 91.4%,and 91.8% in the lateral. On T2-weighted images the corresponding figures were 87.9%, 93.8%, and 89.8%,respectively, in the medial meniscus, and 64.3%, 91.4%, and 83.7 % in the lateral. CONCLUSION: With regard tosensitivity and accuracy, TSE proton density images of meniscal tears were superior to TSE T2-weighted images.
Humans ; Knee* ; Magnetic Resonance Imaging* ; Menisci, Tibial ; Protons ; Retrospective Studies ; Sensitivity and Specificity

Chronic thromboembolic pulmonary hypertension (CTEPH) is considered to be an aberrant outcome of acute pulmonary thromboembolism, due to inadequate thrombus dissolution. However, the mechanism of thrombi dissolution failure remains unclear. With respect to inherited thrombophilia, the co-occurrence of natural anticoagulant deficiencies with CTEPH was found to be rare. Pulmonary thromboendarterectomy (PTE) is a potentially curative surgical procedure for CTEPH, but it is associated with considerable mortality due to postoperative complications, such as reperfusion pulmonary edema and right heart failure. The postoperative course after PTE poses a unique series of ventilatory care and hemodynamic management challenges. We present the case of a 42-year-old woman with unilateral CTEPH combined with thrombophilia (Protein S deficiency). Successful PTE was followed by independent lung ventilation with unilateral nitric oxide (NO) inhalation, which resulted in functional improvement without postoperative complications.
Adult ; Endarterectomy* ; Female ; Heart Failure ; Hemodynamics ; Humans ; Hypertension, Pulmonary* ; Inhalation ; Lung ; Mortality ; Nitric Oxide ; Postoperative Complications ; Protein S Deficiency ; Pulmonary Edema ; Pulmonary Embolism ; Reperfusion ; Thrombophilia ; Thrombosis ; Ventilation

PURPOSE: Hypoxic-ischemic encephalopathy is a significant cause of neonatal morbidity and mortality. Erythropoietin (EPO) is emerging as a therapeutic candidate for neuroprotection. Therefore, this study was designed to determine the neuroprotective role of recombinant human EPO (rHuEPO) and the possible mechanisms by which mitogen-activated protein kinase (MAPK) signaling pathway including extracellular signal-regulated kinase (ERK1/2), JNK, and p38 MAPK is modulated in cultured cortical neuronal cells and astrocytes. METHODS: Primary neuronal cells and astrocytes were prepared from cortices of ICR mouse embryos and divided into the normoxic, hypoxia (H), and hypoxia-pretreated with EPO (H+EPO) groups. The phosphorylation of MAPK pathway was quantified using western blot, and the apoptosis was assessed by caspase-3 measurement and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. RESULTS: All MAPK pathway signals were activated by hypoxia in the neuronal cells and astrocytes (P<0.05). In the neuronal cells, phosphorylation of ERK-1/-2 and apoptosis were significantly decreased in the H+EPO group at 15 hours after hypoxia (P<0.05). In the astrocytes, phosphorylation of ERK-1/-2, p38 MAPK, and apoptosis was reduced in the H+EPO group at 15 hours after hypoxia (P<0.05). CONCLUSION: Pretreatment with rHuEPO exerts neuroprotective effects against hypoxic injury reducing apoptosis by caspase-dependent mechanisms. Pathologic, persistent ERK activation after hypoxic injury may be attenuateed by pretreatment with EPO supporting that EPO may regulate apoptosis by affecting ERK pathways.
Animals ; Anoxia ; Apoptosis* ; Astrocytes ; Blotting, Western ; Caspase 3 ; DNA Nucleotidylexotransferase ; Embryonic Structures ; Erythropoietin* ; Humans ; Hypoxia-Ischemia, Brain ; MAP Kinase Signaling System ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinases ; Mortality ; Neurons ; Neuroprotection ; Neuroprotective Agents* ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Phosphotransferases ; Protein Kinases*

Von Hippel-Lindau (VHL) disease is an autosomal dominant neoplasia syndrome that result from a germline mutation in the VHL gene. Germline mutation in the VHL gene lead to the development of hemangioblastomas of the central nervous system and retina, cysts and clear cell carcinoma of the kidney, cyst adenomas of other organs, and pheochromocytoma. VHL is a tumor suppressor gene on the short arm of chromosome 3. VHL disease has been classified into two main clinical subtypes depending on the presence (type 2) or absence (type 1) of pheochromocytoma. Type 2 has been subdivided into three categories depending on the presence (type 2B) or absence (type 2A) of renal cell carcinoma, with type 2C being a rare subtype in which pheochromocytoma is the sole manifestation of VHL disease. Recently we experienced a family with VHL type 1 who carry C to T (Q73X) transition in codon 217 nonsense germline mutation in exon 1 of VHL gene. The authors report this case with literature review.
Adenoma ; Arm ; Carcinoma, Renal Cell ; Central Nervous System ; Chromosomes, Human, Pair 3 ; Codon ; Exons ; Genes, Tumor Suppressor ; Germ-Line Mutation* ; Hemangioblastoma ; Humans ; Kidney ; Pheochromocytoma ; Retina ; von Hippel-Lindau Disease

The advantages of wielding synthetic polymer are that the pore size, physical strength and chemical composition can be easily controlled. However, the synthetic polymer has hydrophobic character and low affinity to cells and other bio molecules. This study was performed to investigate the effect of plasma glow's discharge on the surface modification of poly(lactic-co-glycolic acid)(PLGA) sponge on the adhesion and bio-activity of chondrocytes in vitro culture. PLGA sponges(lactic acid: glycolic acid = 85 : 15, pore size=200 - 300 mrcro m, dimension=15 x 2 mm) were prepared. The experimental group(n=8) was treated with a radiofrequency plasma glow-discharge(acrylic acid and oxygen: 50 W, 0.2 torr for 30 seconds) but the control group (n=8) was treated with nothing. 1 x 10(6)ml/20 microliter of P3 chondrocytes from rabbit ears were used for seeding. Eight hours after cell seeding, the total DNA amount of chondrocytes attached to the PLGA and the changes of actin were evaluated under a confocal microscope. Type I and II collagen expression were detected by RT-PCR three weeks after seeding for an evaluation of phenotypic maintenance. The total DNA amount of attached chondrocytes was remarkably increased in the experimental group(p < 0.05). After scrutinizing with a confocal microscope, the actin of cells was more spread out and finely arranged in the experimental group than in the control group. Both types of collagen expression were significantly increased in their assigned groups. Plasma treatment of the PLGA sponge could increase the adhesion property of chondrocytes, and provide suitable environment for maintaining the phenotype of chondrocytes.
Actins ; Chondrocytes* ; Collagen ; DNA ; Ear ; Oxygen ; Phenotype ; Plasma* ; Polymers ; Porifera

Recent study showed that peripheral inflammation induced an increased expression of brain-derived neurotrophic factor (BDNF) mRNA which was mediated by nerve growth factor in the dorsal root ganglion (DRG). Therefore, it is conceivable that peripheral inflammation may induce an increase in BDNF synthesis in DRG and consequently enhance the level of BDNF in the spinal cord and that gene expression of trkB mRNA may be altered. In the present study, we evaluated changes in BDNF-immunoreactivity and trkB mRNA in the DRG and spinal cord by means of immunohis-tochemistry and RT-PCR, respectively, following peripheral tissue inflammation produced by intraplantar injection of Freund's adjuvant into rat paws. In addition, coexistence of BDNF and preprotachykinin (PTT) mRNAs, BDNF and CGRP mRNAs or BDNF and trkB mRNAs in the DRG following inflammation was observed by means of in situ hybridization. The results obtained were as follows; 1. Inflammation induced a significant increase of the number of BDNF-immunoreactive (IR) neurons in the ipsilateral DRGs. The increase was observed 1 and 3 days after injection of adjuvant, and the levels had returned to normal by 7 days. In the spinal cord, inflammation also induced an elevation in the expression of BDNF-IR terminals in the medial superficial layers of the ipsilateral dorsal horn and in lamina V 1 and 3 days after injection. 2. There was significant increase of truncated trkB (t-trkB) mRNA in the ipsilateral DRG 3 days following inflammation. Changes in the expression of trkB mRNA in the DRG or trkB and t-trkB mRNAs in the spinal cord were not observed. 3. Many neurons showed increased coexistence of BDNF and PTT mRNAs or BDNF and CGRP mRNAs in the DRG following inflammation. 4. Few neurons showed coexistence of BDNF and trkB mRNAs in the DRG following inflammation. The results suggest a paracrine function for BDNF within the DRG in addition to an important role related with nociception following peripheral inflammation.
Animals ; Brain-Derived Neurotrophic Factor* ; Diagnosis-Related Groups ; Freund's Adjuvant ; Ganglia, Spinal* ; Gene Expression ; Horns ; In Situ Hybridization ; Inflammation* ; Nerve Growth Factor ; Neurons ; Nociception ; Rats* ; RNA, Messenger ; Spinal Cord* ; Spinal Nerve Roots*

The concentration of adenosine in the normal kidney increases markedly during renal hypoxia, ischemia, and inflammation. A recent study reported that an A3 adenosine receptor (A3AR) antagonist attenuated the progression of renal fibrosis. The adriamycin (ADX)-induced nephropathy model induces podocyte injury, which results in severe proteinuria and progressive glomerulosclerosis. In this study, we investigated the preventive effect of a highly selective A3AR antagonist (LJ1888) in ADX-induced nephropathy. Three groups of six-week-old Balb/c mice were treated with ADX (11 mg/kg) for four weeks and LJ1888 (10 mg/kg) for two weeks as following: 1) control; 2) ADX; and 3) ADX + LJ1888. ADX treatment decreased body weight without a change in water and food intake, but this was ameliorated by LJ1888 treatment. Interestingly, LJ1888 lowered plasma creatinine level, proteinuria, and albuminuria, which had increased during ADX treatment. Furthermore, LJ1888 inhibited urinary nephrin excretion as a podocyte injury marker, and urine 8-isoprostane and kidney lipid peroxide concentration, which are markers of oxidative stress, increased after injection of ADX. ADX also induced the activation of proinflammatory and profibrotic molecules such as TGF-β1, MCP-1, PAI-1, type IV collagen, NF-κB, NOX4, TLR4, TNFα, IL-1β, and IFN-γ, but they were remarkably suppressed after LJ1888 treatment. In conclusion, our results suggest that LJ1888 has a renoprotective effect in ADX-induced nephropathy, which might be associated with podocyte injury through oxidative stress. Therefore, LJ1888, a selective A3AR antagonist, could be considered as a potential therapeutic agent in renal glomerular diseases which include podocyte injury and proteinuria.
Adenosine* ; Albuminuria ; Animals ; Anoxia ; Body Weight ; Collagen Type IV ; Creatinine ; Doxorubicin ; Eating ; Fibrosis ; Inflammation ; Ischemia ; Kidney ; Mice* ; Oxidative Stress ; Plasma ; Plasminogen Activator Inhibitor 1 ; Podocytes ; Proteinuria ; Receptors, Purinergic P1* ; Water

Background/Aims: The mucoprotective drug rebamipide is used to treat gastritis and peptic ulcers. We compared the efficacy of Mucosta Ⓡ (rebamipide 100 mg) and its new formulation, AD-203 (rebamipide 150 mg), in treating erosive gastritis. Methods: This double-blind, active control, noninferiority, multicenter, phase 3 clinical trial randomly assigned 475 patients with endoscopically proven erosive gastritis to two groups: AD-203 twice daily or Mucosta Ⓡ thrice daily for 2 weeks. The intention-to-treat (ITT) analysis included 454 patients (AD-203, n=229; Mucosta Ⓡ , n=225), and the per-protocol (PP) analysis included 439 patients (AD-203, n=224; Mucosta Ⓡ , n=215). The posttreatment assessments included the primary (erosion improvement rate) and secondary endpoints (erosion and edema cure rates; improvement rates of redness, hemorrhage, and gastrointestinal symptoms). Drug-related adverse events were evaluated. Results: According to the ITT analysis, the erosion improvement rates (posttreatment) in AD-203-treated and Mucosta Ⓡ -treated patients were 39.7% and 43.8%, respectively. According to the PP analysis, the erosion improvement rates (posttreatment) in AD-203-treated and Mucosta Ⓡ -treated patients were 39.3% and 43.7%, respectively. The one-sided 97.5% lower limit for the improvement rate difference between the study groups was −4.01% (95% confidence interval [CI], –13.09% to 5.06%) in the ITT analysis and −4.44% (95% CI, –13.65% to 4.78%) in the PP analysis. The groups did not significantly differ in the secondary endpoints in either analysis. Twenty-four AD-203-treated and 20 Mucosta Ⓡ -treated patients reported adverse events but no serious adverse drug reactions; both groups presented similar adverse event rates. Conclusions The new formulation of rebamipide 150 mg (AD-203) twice daily was not inferior to rebamipide 100 mg (Mucosta Ⓡ ) thrice daily. Both formulations showed a similar efficacy in treating erosive gastritis.