A case in which contrast-enhanced transoral carotid ultrasonography was useful for pre- and post-procedural evaluation in carotid artery stenting

Contrast-enhanced transoral carotid ultrasonography (CETOCU) is a novel examination modality that is superior to other modalities in the cases of pseudo-occlusion with severe arteriosclerotic stenosis of the distal internal carotid artery (ICA), and is also useful for noninvasively evaluating changes over time in the vessel distal to the stent following carotid artery stenting (CAS). We report a case of a patient who we evaluated with CETOCU for a pseudo-occlusive ICA before and after CAS.     

Ultrasound-Guided Resuscitative Endovascular Balloon Occlusion of the Aorta in the Resuscitation Area

Background

In trauma resuscitation with resuscitative endovascular balloon occlusion of the aorta (REBOA), urgent and accurate placement of the catheter in the resuscitation area without fluoroscopy can shorten the time from admission to REBOA, allowing rapid, temporary control of bleeding.

Protective effects of coenzyme q(10) on decreased oxidative stress resistance induced by simvastatin

The effects of simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase (HMG-CoA reductase), on oxidative stress resistance and the protective effects of coenzyme Q (CoQ) were investigated. When simvastatin was administered orally to mice, the levels of oxidized and reduced CoQ(9) and CoQ(10) in serum, liver, and heart, decreased significantly when compared to those of control. The levels of thiobarbituric acid reactive substances induced by Fe(2+)-ascorbate in liver and heart mitochondria also increased significantly with simvastatin. Furthermore, cultured cardiac myocytes treated with simvastatin exhibited less resistance to oxidative stress, decreased time to the cessation of spontaneous beating in response to H(2)O(2) addition, and decreased responsiveness to electrical field stimulation. These results suggested that oral administration of simvastatin suppresses the biosynthesis of CoQ, which shares the same biosynthesis pathway as cholesterol up to farnesyl pyrophosphate, thus compromising the physiological function of reduced CoQ, which possesses antioxidant activity. However, these undesirable effects induced by simvastatin were alleviated by coadministering CoQ(10) with simvastatin to mice. Simvastatin also reduced the activity of NADPH-CoQ reductase, a biological enzyme that converts oxidized CoQ to the corresponding reduced CoQ, while CoQ(10) administration improved it. These findings may also support the efficacy of coadministering CoQ(10) with statins.     

A case of nephrotic syndrome due to lupus nephritis which was controlled with low-density lipoprotein apheresis.

Our report discusses a 29 year old female patient with nephrotic syndrome due to lupus nephritis, biopsy-proven World Health Organization classification Types IVb and V that was controlled with low-density lipoprotein (LDL) apheresis. She was initially treated with steroid therapy, including methylprednisolone pulse therapy, and the serological activity of her systemic lupus erythematosus was suppressed. However, her nephrotic state, accompanied by severe hyperlipidemia, persisted despite the steroid therapy. Since we could not obtain her consent to administer immunosuppressants such as cyclophosphamide, we tried to treat her using LDL apheresis (LDL-A). We found that her urine protein excretion, hyperlipidemia, hypoalbuminemia, and renal function improved following the initiation of LDL-A. This suggests that LDL-A may be an effective therapy for nephrotic syndrome due to lupus nephritis through short-term amelioration of hyperlipidemia.     

Carotid artery ultrasound and intravascular ultrasound

Lipid lowering therapy is associated with a significant reduction in cardiocerebral events. But, additional studies are necessary to identify patients in whom atheroma may results in developing coronary events. Intravascular ultrasound(IVUS) and carotid artery echocardiography have significantly contributed to the understanding of nature of atherosclerosis and have validated the concepts of vascular remodeling and vulnerable plaque. Actually, intimal-medial thickness(IMT) in carotid echo is good predictors of cardiovascular events. Positive remodeled plaque with soft characteristics is more likely to rupture and cause acute coronary syndrome. Thus, studies using IVUS and carotid echo may lead to important insights into how risk factor reduction stabilizes plaque and reduces the risk of acute coronary events.     

High-affinity autoantibodies specifically eliminate granulocyte-macrophage colony-stimulating factor activity in the lungs of patients with idiopathic pulmonary alveolar proteinosis

Deficiency of granulocyte-macrophage colony-stimulating factor (GM-CSF) in mice results in pulmonary alveolar proteinosis (PAP) from impaired surfactant catabolism by alveolar macrophages (AMs). Recently, we have shown that neutralizing anti-GM-CSF autoantibodies develop specifically in patients with idiopathic pulmonary alveolar proteinosis (iPAP). Analogous to murine PAP models, it is plausible that the autoantibodies reduce GM-CSF activity, resulting in AM dysfunction and surfactant accumulation. To examine this hypothesis, we estimated the neutralizing activity of the autoantibodies in the lungs of patients and characterized their biologic properties. GM-CSF bioactivity was completely abrogated in the bronchoalveolar lavage fluid (BALF) of patients with iPAP but not in healthy subjects. Autoantibodies were present in the alveoli in high concentrations and colocalized with GM-CSF. They recognized human GM-CSF with high avidity (K(AV) = 20.0 +/- 7.5 pM) and high specificity, reacting with its superstructure and neutralizing GM-CSF activity to a level 4000 to 58 000 times the levels of GM-CSF normally present in the lung. Although target epitopes varied among patients, GM-CSF amino acids 78 to 94 were consistently recognized. Thus, autoantibodies bind GM-CSF with high specificity and high affinity, exist abundantly in the lung, and effectively block GM-CSF binding to its receptor, inhibiting AM differentiation and function. Our data strengthen the evidence associating anti-GM-CSF autoantibodies with the pathogenesis of this disease.     

Lipid analyses for the management of vascular diseases

Despite a long history of studies on lipid abnormalities, numerous problems in laboratory technologies and techniques remain unresolved. One of the most commonly tested molecules is low-density lipoprotein (LDL) cholesterol, and a homogenous assay technique for measurement of this molecule has recently been introduced. Although the method represents remarkable technological breakthroughs with great potential for improving lipoprotein analysis, some discrepancies exist among assay protocols. Even for direct measurement of high-density lipoprotein (HDL) cholesterol, which has widely been accepted, there are still large discrepancies among data obtained by different protocols. Oxidatively modified LDL is an independent factor that is considered to directly contribute to the pathogenesis of early atherosclerosis. Lipid peroxidation products, surface charge, and spectrophotometric patterns are all applicable to the evaluation of in vitro oxidation. Only enzyme-linked immunosorbent assays using monoclonal antibodies have a potential for clinical use, but such methods are not yet standardized. There is also increasing evidence for the presence of anti-oxidized LDL autoantibodies in human sera, but the diagnostic utility remains controversial. In addition, small dense LDL has recently attracted much attention as an independent risk factor. Although this is a potential target of oxidization, a robust and simple analytical method does not yet exist. This review presents the current state of laboratory technologies for testing lipid abnormalities.     

Establishment and characterization of an opisthorchiasis-associated cholangiocarcinoma cell line （KKU-100）

AM: To establish and characterize a new cholangiocarcinoma cell line from a patient living in the Opisthorchis viverrini (O. viverrini) endemic area of Northeast Thailand. METHODS: Fresh liver biopsy and bile specimens were obtained from a 65-year-old Thai woman with cholangiocarcinoma of the ports hepatis. After digestion, the cells were cultured in Ham's F12 media. The established cell line was then characterized for growth kinetics, cell morphology, imm-unocytochemistry and cytogenetics. Tumorigenicity of the cell line was determined by heterotransplanting in nude mice. RESULTS: The primary tumor was a poorly differentiated tubular adenocarcinoma. Examination of the bile revealed malignant cells with O. viverrin eggs. The cholangiocarcinoma cell line KKU-100 was established 4 mo after the primary culture-population doubling time was 72 h. KKU-100 possesses compact and polygonal-shaped epithelial cells. Immunocytochemically, this cell line exhibited cytokeratin, EMA, CEA, and CA125, but not a-fetoprotein (AFP), CA19-9, desmin, c-met, or p53. Such protein expressions parallel those of the primary tumor. Cytogenetic analysis identified aneuploidy karyotypes with a modal chromosome number of 78 and marked chromosomal structural changes. Inoculation of KKU-100 cells into nude mice produced a transplantable, poorly differentiated aden-ocarcinoma, similar to the original tumor. CONCLUSION: KKU-100 is the first egg-proven, Opisthorchis- associated cholangiocarcinoma cell line, which should prove useful for further investigations of the tumor biology of this cancer.     

A case of pulmonary infection caused by Mycobacterium szulgai

We report a case of pulmonary non-tuberculous mycobacteriosis caused by Mycobacterium szulgai. A thirty-nine-year-old man with no relevant significant past history underwent an annual medical check. His chest X-ray and CT scan showed an infiltrative shadow with a cavity in the right upper lobe. As it was suggestive of pulmonary tuberculosis, he was referred to our hospital. Smear tests of his sputum, gastric fluid, and transbronchial fluid showed no mycobacterial organisms, but culture of the samples revealed growth of mycobacteria. The organism was identified as M. szulgai using a DNA-DNA hybridization method, and the case was diagnosed as pulmonary non-tuberculous mycobacteriosis caused by M. szulgai. By anti-mycobacterial drug treatment with isoniazid, rifampicin, and ethambutol, the infiltrative shadow on chest roentogenogram and CT showed improvement. Culture of his sputum and gastric fluid showed no growth of mycobacteria after starting treatment.