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Biomedical subjects

S Kim

Publications and source records attributed to S Kim.

At least 577 records · Page 32Linked to original sources
PubMed1999

Pediatric atlantoaxial instability: management with screw fixation.

Sixteen pediatric patients (age range 3-15 years; mean 9.4 years) with atlantoaxial instability underwent screw fixation at Columbus Children's Hospital between 1992 and 1998. Three patients with type II odontoid fractures underwent odontoid screw fixation. The remaining group of 13 patients had posterior C1-2 transarticular screw fixation and Sonntag C1-2 fusion. The group included 3 patients with rotatory C1-2 fixation, 4 patients with os odontoideum, 4 patients with congenital atlantoaxial instability and 2 patients with traumatic C1-2 instability. Postoperatively, all patients were placed in a Miami-J collar only. At 3 months follow-up, all patients achieved fusion. Bony fusion across the fracture line was clearly evident in patients with odontoid screws. The only complications in this series were a transient swallowing difficulty that resolved spontaneously in 2 weeks, and another patient's C1-2 fusion had extended to C2-3 at 9 months follow-up. This study demonstrates that children at 3 years of age and older, who sustain a type II odontoid fracture with an intact transverse ligament, can be safely managed with odontoid screws if the fracture is less than 4 weeks old. Posterior C1-2 transarticular screw fixation can be done safely and results in a high fusion rate in children older than 4 years of age. The technical difficulties of screw fixation in children are discussed.

Adolescent↗
PubMed1999

Correlation between flow-mediated vasodilatation of the brachial artery and intima-media thickness in the carotid artery in men.

Endothelial dysfunction has been reported to be the initial step in atherosclerosis. A noninvasive technique that uses ultrasound to measure the intima-media thickness of the carotid artery has been applied to evaluate localized atherosclerosis. This study was undertaken to elucidate whether endothelial dysfunction in the brachial artery is related to the intima-media thickness of the carotid artery. Thirty-four men with atherosclerosis (mean+/-SE age 61+/-2 years) and 33 age-matched men without clinical atherosclerosis were examined. The intima-media thickness and plaque formation of the common carotid artery were assessed by B-mode ultrasonography. We also noninvasively measured brachial artery diameter by the same ultrasound machine when the subjects were at rest, during reactive hyperemia, which causes endothelium-dependent vasodilatation, and after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. The atherosclerosis group had a significantly greater intima-media thickness of the common carotid artery than did the control group (1. 02+/-0.04 versus 0.91+/-0.03 mm, P<0.05). The flow-mediated diameter (FMD) increase (percent FMD=DeltaD/D x 100) in the atherosclerosis group was significantly smaller than that in the control group (2. 8+/-0.4% versus 5.1+/-0.6%, P<0.01). A significant negative correlation between the intima-media thickness of the carotid artery and percent FMD was found in all of the subjects. On multiple regression analysis, percent FMD showed a significant negative correlation with the intima-media thickness of the common carotid artery. These findings support the concept that endothelial dysfunction is significantly related to atherogenesis.

Arteriosclerosis↗
PubMed1999

Effects of candesartan and cilazapril on rats with myocardial infarction assessed by echocardiography.

The purpose of this study was to compare the angiotensin II type 1 receptor antagonist candesartan cilexitil (candesartan) and the angiotensin-converting enzyme inhibitor cilazapril on cardiac function, assessed by Doppler echocardiography and cardiac gene expression associated with cardiac remodeling, in rats with myocardial infarction. Candesartan or cilazapril was administered after myocardial infarction. At 1 and 4 weeks after myocardial infarction, cardiac function and mRNA expression in noninfarcted myocardium were analyzed. Candesartan and cilazapril equally prevented increases in hypertrophy in noninfarcted myocardium, left ventricular dilatation, and ejection fraction at 4 weeks. The E-wave/A-wave velocity ratio and the rate of E-wave deceleration, measures of diastolic function, increased to 9.2+/-0.6 and 26.3+/-2. 6 m/s2 at 1 week after myocardial infarction. Candesartan and cilazapril, administered at a dose of 1 mg/kg per day, prevented increases in E-wave/A-wave velocity ratio and E-wave deceleration at 1 and 4 weeks. Candesartan and cilazapril significantly suppressed increased mRNA expression of beta-myosin heavy chain, alpha-skeletal actin, and atrial natriuretic peptide in noninfarcted ventricle at 1 and 4 weeks and expression of collagen I and III at 4 weeks to a similar extent. When given at a dose of 10 mg/kg per day, both candesartan and cilazapril prevented cardiac dysfunction and gene expression to the same extent as when given at 1 mg/kg per day. In conclusion, Doppler echocardiography showed that candesartan and cilazapril equally improved systolic and diastolic function and that ventricular remodeling accompanied modulation of cardiac gene expression.

Angiotensin Receptor Antagonists↗
PubMed1999

Contribution of extracellular signal-regulated kinase to angiotensin II-induced transforming growth factor-beta1 expression in vascular smooth muscle cells.

We have previously demonstrated that angiotensin II (Ang II) contributes to the increase in aortic transforming growth factor-beta(1) (TGF-beta(1)) mRNA levels in hypertensive rats. However, the molecular mechanism whereby Ang II promotes TGF-beta(1) expression in vascular smooth muscle cells (VSMCs) is poorly understood. In this study, we examined the role of extracellular signal-regulated kinase (ERK) in Ang II-mediated TGF-beta(1) expression in VSMCs and the role of Ang II in aortic ERK activity of stroke-prone spontaneously hypertensive rats. Treatment of quiescent VSMCs with 100 nmol/L Ang II induced rapid phosphorylation and activation of ERK1 and ERK2 with a peak at 5 minutes followed by an increase in activator protein-1 (AP-1) DNA binding activity, as shown by gel mobility shift assay. An increase in TGF-beta(1) mRNA was shown by Northern blot analysis. Treatment of VSMCs with PD98059, a specific inhibitor of the ERK pathway, attenuated both the activation of AP-1 and the increase in TGF-beta(1) mRNA induced by Ang II. Inhibition of Ang II-induced AP-1 activation with c-fos antisense oligodeoxynucleotide led to a significant reduction of TGF-beta(1) mRNA in VSMCs. Furthermore, in vivo treatment of stroke-prone spontaneously hypertensive rats with losartan, an Ang II type 1 receptor antagonist, decreased aortic ERK activity. Thus, we show that ERK, through AP-1 activation, is involved in Ang II-induced TGF-beta(1) mRNA expression in VSMCs and suggest that ERK may participate in vascular remodeling of hypertension. However, it remains to be determined whether the increase in TGF-beta(1) mRNA leads to the increase in its active protein.

Angiotensin II↗
PubMed1999

Enhanced in vivo human immunodeficiency virus-1 replication in the lungs of human immunodeficiency virus-infected persons with Pneumocystis carinii pneumonia.

The relationship of serum human immunodeficiency virus-1 (HIV-1) RNA levels to HIV-1 RNA levels in other compartments, such as the lungs, is not well characterized. The purpose of this study was to determine the viral burden of HIV-1 in the lungs by comparing HIV-1 RNA in cell-free bronchoalveolar lavage fluid (BALF) with that in serum. Specimens were examined from 77 HIV-seropositive adults (CD4(+) cell counts: 0 to 700 cells/mm(3); 48% receiving prescribed antiretroviral agents), comprising 43 asymptomatic individuals who were compared with 34 persons with active lung disease caused by Pneumocystis carinii (n = 26), bacteria (n = 3), Mycobacterium avium complex (n = 2), Nocardia sp. (n = 1), Aspergillus sp. (n = 1), or pulmonary Kaposi's sarcoma (n = 1). For serum HIV-1 RNA, the proportion of subjects with detectable levels and the mean values were similar for asymptomatic individuals and persons with active lung disease (85% versus 86%, respectively) (6.64 x 10(4) versus 1. 81 x 10(5) HIV-1 RNA copies/ml; p = 0.13). In contrast, HIV-1 RNA in BALF was more often detected (16% versus 62%; p = 0.001), and mean values were higher (1.04 x 10(5) versus 3.31 x 10(6) HIV-1 RNA copies/ml; p = 0.032), in subjects with active lung disease than in asymptomatic subjects, independent of early or advanced clinical stages of HIV-related disease. For both study groups, HIV-1 RNA levels in BALF exceeded those in serum in 56% of cases by up to 66-fold, and did not correlate with local levels of tumor necrosis factor-alpha, granulocyte-macrophage colony-stimulating factor, or interleukin-16. HIV-1 proviral DNA in cells from BALF was detected in up to 86% of subjects, more frequently in persons with advanced HIV disease (p = 0.0496), and often involved > 10% of BALF cells, but did not correlate with HIV-1 RNA detected in BALF. These data provide evidence for active HIV-1 replication in the lungs. HIV-1 replication is compartmentalized relative to serum, may be restricted, is independent of HIV-1 proviral DNA and clinical stage of HIV, and may be influenced by pulmonary disease such as P. carinii pneumonia or by other local or lung-specific factors. The lungs represent a large reservoir for HIV-1, and may present a source of persistent HIV-1 replication even during periods of apparent clinical latency of HIV-1 infection.

AIDS-Related Opportunistic Infections↗
PubMed1999

SDQR migrations in Caenorhabditis elegans are controlled by multiple guidance cues and changing responses to netrin UNC-6.

The netrin guidance cue, UNC-6, and the netrin receptors, UNC-5 and UNC-40, guide SDQR cell and axon migrations in C. elegans. In wild-type larvae, SDQR migrations are away from ventral UNC-6-expressing cells, suggesting that UNC-6 repels SDQR. In unc-6 null larvae, SDQR migrations are towards the ventral midline, indicating a response to other guidance cues that directs the migrations ventrally. Although ectopic UNC-6 expression dorsal to the SDQR cell body would be predicted to cause ventral SDQR migrations in unc-6 null larvae, in fact, more migrations are directed dorsally, suggesting that SDQR is not always repelled from the dorsal source of UNC-6. UNC-5 is required for dorsal SDQR migrations, but not for the ventral migrations in unc-6 null larvae. UNC-40 appears to moderate both the response to UNC-6 and to the other cues. Our results show that SDQR responds to multiple guidance cues and they suggest that, besides UNC-6, other factors influence whether an UNC-6 responsive cell migrates toward or away from an UNC-6 source in vivo. We propose that multiple signals elicited by the guidance cues are integrated and interpreted by SDQR and that the response to UNC-6 can change depending on the combination of cues encountered during migration. These responses determine the final dorsoventral position of the SDQR cell and axon.

Animals↗
PubMed1999

Total synthesis and chemical biology of the sarcodictyins.

The sarcodictyins A-F and eleutherobin comprise a family of marine-derived diterpenoids with potent cytotoxicities against various tumor cell lines. Investigations have revealed that several of these compounds exert their cytotoxic effects through tubulin binding in a mechanism analogous to that of the clinical anticancer drug Taxol. The biological importance, challenging molecular architecture, and relative scarcity of these natural products have prompted several groups to undertake their total chemical synthesis. In this review, we summarize the current synthetic efforts and examine the preliminary structure-activity relationships which have emerged from early combinatorial libraries.

Animals↗
PubMed1999

Hemodynamic characteristics during treadmill and bicycle exercise in chronic heart failure: mechanism for different responses of peak oxygen uptake.

The exercise capacity of patients with chronic heart failure (CHF) is greater when assessed by the treadmill rather than the bicycle ergometer, but the mechanism of this difference has not been clarified. The present study aimed to determine the difference between the hemodynamics of these exercise modes and the mechanism underlying the different peak oxygen uptake (VO2). Patients (n = 18) underwent a bicycle test and treadmill test using individual ramp protocols. Respiratory gas analysis and hemodynamic measurements with an opti-catheter were performed during both exercise tests. The peak VO2 was significantly larger in the treadmill test than the bicycle test (1410+/-292 vs. 1630+/-331 ml/min, p<0.001). Both the peak cardiac output (Q; 10.2+/-2.2 vs. 10.9+/-2.1 L/min, p<0.001) and the peak arteriovenous oxygen difference (a-v 02 diff; 13.9+/-1.5 vs. 15.0+/-1.2 vol%, p<0.001) were also significantly higher in the treadmill test. The relative contribution of Q and a-v O2 diff to the increased peak VO2 was equivalent, which suggests that both Q and a-v O2 diff. Contribute equally to the different peak VO2 responses in CHF.

Bicycling↗
PubMed1999

Effects of activation of renal adenosine A2 receptor on renal function and renin release in dogs.

Direct effects of adenosine A2 receptor activation on renal function were examined in dogs. When renal perfusion pressure was maintained constant at 100 mmHg, renal administration of a selective A2 receptor agonist, CGS 21680C (sodium salt of CGS 21680, 2-[p-(2-carboxyethyl) phenethylamino]-5'-N-ethylcarboxamido adenosine) (1 microg x kg(-) x min (-1)), although it decreased blood pressure by 20 mmHg, increased renal blood flow and renin release, whereas glomerular filtration rate and urine flow were unaffected. These results suggest that stimulation of renal A2 receptor led to both afferent and efferent arteriolar dilatation, whereas renal A2 receptor plays a minor role in urine formation. CGS 21680C induced renin release and tachycardia that were blocked by propranolol, indicating these effects of A2 receptor stimulation appeared to be indirect.

Adenosine↗
PubMed1999

No participation of adenosine A1 receptor in acute nephrotoxicity by 4-pentenoic acid administration in dogs.

Intrarenal infusion of 4-pentenoic acid is known to lower renal cortical ATP content and cause a reduction in glomerular filtration rate (GFR). The alteration in nucleotide metabolism might augment the production of adenosine, thereby eliciting the fall in GFR. This study was conducted to examine whether 4-pentenoic acid stimulates renal production of adenosine, and if so, to examine the role of adenosine A1 receptor in the reduction of GFR by 4-pentenoic acid. With infusion of 4-pentenoic acid (1 micromol x kg(-1) x min(-1)) into the renal artery of anesthetized dogs, GFR gradually decreased and reached minimum at 60 min with values ranging from 33.9+/-2.2 to 20.2+/-2.8 ml/min. Neither renal blood flow nor mean arterial pressure was affected, but tubular reabsorption of water and sodium was significantly attenuated. Renal venous plasma concentration and urinary excretion of adenosine rose markedly (20-fold) without any change in arterial concentration, suggesting that renal adenosine production was augmented by 4-pentenoic acid. However, KW-3902 (8-(noradamantan-3-yl)-1,3-dipropylxanthine), a selective antagonist of the adenosine A1 receptor, did not affect the action of 4-pentenoic acid on GFR or renal handling of water and sodium. It is concluded that 4-pentenoic acid markedly increases renal adenosine production, but adenosine A1 receptor is not involved in the 4-pentenoic acid-induced nephrotoxicity.

Acute Kidney Injury↗
PubMed1999

Activation of mitogen-activated protein kinases in cardiovascular hypertrophy and remodeling.

Extracellular signal-regulated kinases (ERKs) and c-jun NH2-terminal kinases (JNKs), which belong to the family of mitogen-activated protein kinases (MAPKs), play a key role in the regulation of cell growth or apoptosis or various gene expressions. In spite of the critical importance of MAPKs for cell function in vitro, the role of MAPKs in the pathophysiology of the cardiovascular system in vivo is poorly understood. Recently, we have examined the activities of MAPKs in various cardiovascular disease models. JNKs activity is chronically enhanced in cardiac hypertrophy of hypertensive rats or angiotensin II-infused rats, which is followed by the increase in activator protein-1 (AP-1) activity composed of c-Fos and c-Jun proteins. In chronic hypertensive rats, vascular ERKs and JNKs activities are continuously increased compared with normotensive rats, with the development of vascular thickening. Furthermore, balloon injury rapidly and transiently activates vascular ERKs and JNKs, followed by the activation of AP-1. This activation of ERKs and JNKs in injured artery is in part mediated by angiotensin AT1 receptor. Thus, the enhanced activation of JNKs or ERKs occurs in various cardiovascular disease models, supporting the notion that MAPKs may be a useful target for treatment of cardiovascular hypertrophy and remodeling.

Animals↗
PubMed1999

Assessment of pancreatic invasion in patients with advanced gastric carcinoma: usefulness of the sliding sign on sonograms.

OBJECTIVE: The purpose of our study was to determine the value of the sliding sign on sonograms in evaluating direct pancreatic invasion of advanced gastric carcinoma. SUBJECTS AND METHODS: Sonography was performed prospectively on 70 patients with pathologically proven advanced gastric carcinoma. Sonography was directed at the detection of motion between the gastric mass and the pancreas. When the gastric mass showed complete sliding motion against the pancreas or partial sliding motion with a preserved echogenic fat plane between the two organs on respiration or on extrinsic compression with a transducer (positive sliding sign), patients were considered to have no pancreatic invasion. When the gastric mass had no sliding motion against the pancreas or partial sliding motion with a disrupted echogenic fat plane between the two organs (negative sliding sign), patients were considered to have pancreatic invasion. After sonography, all patients underwent surgery and the results of sonography were compared with the findings at surgery and pathology. RESULTS: Of the 70 patients, 17 had pancreatic invasion and 53 had no evidence of pancreatic invasion at surgery and pathology. The sliding sign on sonography yielded an 80% sensitivity, 96% specificity, and 90% accuracy for the diagnosis of pancreatic invasion. CONCLUSION: Application of the sliding sign on sonography was simple and highly accurate in the diagnosis of pancreatic invasion by advanced gastric carcinoma. The sliding sign may prove useful in the preoperative detection of pancreatic invasion by gastric carcinoma when CT has been inconclusive.

Carcinoma↗
PubMed1999

Fas is expressed in murine pancreatic islet cells and an insulinoma cell line but does not mediate their apoptosis in vitro.

CD4+ lymphocytes are the most important effector cells in autoimmune diabetes of NOD mice, although some role of CD8+ T cells has been demonstrated. However, it is unknown how CD4+ lymphocytes are able to destroy pancreatic beta-cells that do not express MHC (major histocompatibility complex) class II molecules. Apoptotic cell death mediated by an interaction of Fas with Fas ligand (FasL) could be a mechanism by which MHC class II-negative pancreatic beta-cells are destroyed by CD4+ T lymphocytes. We have examined the expression of Fas molecules in pancreatic islet cells, as well as in a NOD-derived mouse insulinoma cell line (MIN6N8). In addition, the role of Fas-mediated apoptosis in pancreatic islet cell death was explored in vitro. Although Fas expression was not detected by flow cytometric analysis, Fas transcripts were demonstrated in MIN6N8 cells and pancreatic islet cells by the sequencing analysis of the cloned reverse transcription polymerase chain reaction products using Fas-specific primers. IFN (interferon)-gamma, tumor necrosis factor-alpha, interleukin-1 and their combinations failed to enhance Fas expression. Unsorted activated splenocytes from diabetic NOD mice had cytotoxic T lymphocyte activity of a small degree against IFN-gamma-treated MIN6N8 cells with FasL upregulation. However, agonistic anti-Fas antibody with or without cycloheximide did not exert cytotoxicity against MIN6N8 cells or pancreatic islets. FasL transfectant cells also did not kill MIN6N8 cells. Our data indicate that pancreatic beta-islet cells express a small amount of Fas molecules but Fas molecules do not mediate apoptosis of islet cells at least in vitro.

Animals↗
PubMed1999

Role of netrin UNC-6 in patterning the longitudinal nerves of Caenorhabditis elegans.

The nervous system of Caenorhabditis elegans comprises circumferential and longitudinal axon tracts. Netrin UNC-6 is required for the guidance of circumferential axon migrations and is expressed by ventral neuroglia and neurons in temporally and spatially regulated patterns. Migrating axons mediate the UNC-6 signal through the UNC-5 and UNC-40 receptors. It is thought that UNC-6 is secreted and becomes associated with basement membranes and cell surfaces to form gradients that direct circumferentially migrating axons toward or away from the ventral UNC-6 sources. Little is known about the effects of UNC-6 on longitudinally migrating axons. In unc-6, unc-5, and unc-40 null mutants, some longitudinal nerves are dorsally or ventrally misdirected. Furthermore, the organization of axons are disrupted within nerves. We show that cells ectopically expressing UNC-6 can redirect the migrations of some neighboring longitudinal axons, suggesting that the gradients postulated to direct circumferential migration also help specify the dorsoventral positions of these longitudinal nerves. We also manipulated the temporal and spatial expression pattern of UNC-6 by two different means. First, we removed the PVT midline neuron which expresses UNC-6 for a short time during axon outgrowths. Second, we expressed UNC-6 uniformly in the nervous system throughout development. The results suggest that changing UNC-6 expression patterns modify the distribution of the cue by providing new localized sources. This new guidance information is critical for organizing the axons of longitudinal nerves.

Animals↗
PubMed1999

Health problems of Asian and Latino immigrants.

Many different circumstances influence Asian and Latino immigration to the United States, including poverty, war, educational opportunities, and protection of financial assets. Such varying circumstances point clearly to a different set of expected health problems. Immigrants often lack resources necessary to acquire quality health care. These resources involve language skills, knowledge of US health care and social services, and insurance. Risk factors to which immigrants may have been exposed include poor nutrition, lack of immunizations and vaccinations, inadequate or inappropriate treatment, and inadequate or inaccurate beliefs about illness and treatment. Frequent health problems among Latino and Asian immigrants are tuberculosis, hepatitis B, sexually transmitted diseases, cancer, diabetes, and substance abuse. The nursing care of immigrants involves not only attention to reducing risk and treating illness, but also attention to the provision of resources. Nurses face several ethical dilemmas in the health care of immigrants including a public anti-immigrant sentiment, and political attempts to limit health care and education to immigrants.

Asian↗
PubMed1999

A two-year study of microscopic urinalysis competency using the urinalysis-review computer program.

BACKGROUND: The microscopic examination of urine sediment is one of the most commonly performed microscope-based laboratory tests, but despite its widespread use, there has been no detailed study of the competency of medical technologists in performing this test. One reason for this is the lack of an effective competency assessment tool that can be applied uniformly across an institution. METHODS: This study describes the development and implementation of a computer program, Urinalysis-ReviewTM, which periodically tests competency in microscopic urinalysis and then summarizes individual and group test results. In this study, eight Urinalysis-Review exams were administered over 2 years to medical technologists (mean, 58 technologists per exam; range, 44-77) at our academic medical center. The eight exams contained 80 test questions, consisting of 72 structure identification questions and 8 quantification questions. The 72 structure questions required the identification of 134 urine sediment structures consisting of 63 examples of cells, 25 of casts, 18 of normal crystals, 8 of abnormal crystals, and 20 of organisms or artifacts. RESULTS: Overall, the medical technologists correctly identified 84% of cells, 72% of casts, 79% of normal crystals, 65% of abnormal crystals, and 81% of organisms and artifacts, and correctly answered 89% of the quantification questions. The results are probably a slight underestimate of competency because the images were analyzed without the knowledge of urine chemistry results. CONCLUSIONS: The study shows the feasibility of using a computer program for competency assessment in the clinical laboratory. In addition, the study establishes baseline measurements of competency that other laboratories can use for comparison, and which we will use in future studies that measure the effect of continuing education efforts in microscopic urinalysis.

Educational Measurement↗