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Biomedical subjects

N Kim

Publications and source records attributed to N Kim.

At least 37 records · Page 2Linked to original sources
PubMed2001

No protective role of Helicobacter pylori in the pathogenesis of reflux esophagitis in patients with duodenal or benign gastric ulcer in Korea.

Little is known about the relationship between H. pylori infection and reflux esophagitis. To evaluate whether or not H. pylori plays a protective role in the pathogenesis of reflux esophagitis, the prevalence rates of reflux esophagitis depending on H. pylori status in consecutively diagnosed duodenal ulcer or benign gastric ulcer patients were evaluated. In addition, the incidence rates of reflux esophagitis depending on H. pylori status were evaluated for those patients who received follow-up endoscopy at least 6 months after eradication treatment. The prevalence rates of reflux esophagitis were 8.0% (2 patients) in the 25 H. pylori-negative duodenal ulcer group patients and 6.5% (36 patients) in the 555 H. pylori-positive duodenal ulcer group patients, and there was no statistical difference. Similarly, that of gastric ulcer patients was 9.4% (32 patients) in the 340 H. pylori-positive group patients, slightly higher than that in the 41 H. pylori-negative group patients 4.9% (2 patients), but without statistical significance. After eradication treatment the reflux esophagitis incidence rates were 2.5% (2 patients) in the 81 H. pylori-eradicated duodenal ulcer group patients and 7.7% (3 patients) in the 39 noneradicated duodenal ulcer group patients, and there was no statistical difference. Similarly, those of gastric ulcer patients were 6.8% (3 patients) in the 44 H. pylori-eradicated and 8.7% (2 patients) in the 23 noneradicated group patients again without statistical difference. These results suggest that H. pylori does not play a protective role in the pathogenesis of reflux esophagitis in patients with duodenal or gastric ulcer in Korea.

Adult↗
PubMed2001

The effect of vaccination with DNA encoding murine T-cell epitopes on the Der p 1 and 2 induced immunoglobulin E synthesis.

BACKGROUND: Immunization with naked plasmid DNA leads to strong and persistent cell-mediated and humoral immune response to plasmid encoded antigen. Vaccination of DNA encoded whole allergen has been tried, but little information is currently available on the efficacy of DNA encoding T-cell epitopes in allergic disease. The purpose of this study was to determine whether the vaccination of naked plasmid DNA encoding only T-cell epitopes suppresses the allergic reaction as effectively as naked DNA encoding whole segments of allergen. METHODS: We immunized mice with a mixed naked plasmid DNA encoding the five classes of murine T-cell epitopes on Der p 1 and Der p 2 three times at weekly intervals via an intramuscular injection of BALB/c mice. Control mice were injected with the pcDNA 3.1 blank vector. After 3 weeks, the mice were actively sensitized twice and allowed to inhale the Der p extracts intranasally six times at weekly intervals. RESULTS: The vaccinated mice showed a significant attenuated induction of Der p-specific immunoglobulin E synthesis compared to controls. In terms of the Der p-specific IgG2a antibody response, the vaccinated mice showed more prominent responses than the control mice group. In addition, analysis of the cytokine profile after Der p stimulation of the lymph-node cells revealed that the level of the mRNA expression of the interferon-gamma gene was higher in the vaccinated mice than in the controls. Histologic studies showed a much reduced infiltration of inflammatory cells in lung tissue of the gene-vaccinated mice in comparison with the controls. CONCLUSIONS: These results suggest that vaccination with DNA encoding T-cell epitopes effectively inhibits allergen-induced IgE synthesis and reduces cell infiltration in lung tissue. Thus, gene therapy using T-cell epitope-encoding DNA presents an ideal way of combating allergic disease in the future.

Animals↗
PubMed2001

Experimental models for the investigation of female sexual function and dysfunction.

There have been limited anatomic and physiological investigations of the female sexual arousal response. A broader understanding of the physiologic mechanisms of female sexual arousal function is required to improve the management of women with sexual dysfunction. Three experimental test systems have been developed to understand better the biochemical and physiological mechanisms of female sexual arousal response. An in vivo animal model was developed to record physiological and hemodynamic changes in the clitoris and vagina following pelvic nerve stimulation and administration of vasoactive agents and physiological modulators. In vitro organ baths of clitoral and vaginal tissue were utilized to investigate mechanisms involved in the regulation of smooth muscle contractility. In addition, primary cell cultures of human and animal clitoral and vaginal smooth muscle cells were developed to investigate signal transduction pathways modulating smooth muscle tone. In vivo studies revealed hemodynamic changes in vagina and clitoris in response to pelvic nerve stimulation, vasodilators and physiological modulators. Organ bath studies have demonstrated that clitoral and vaginal smooth muscle tone is affected by non-adrenergic and non-cholinergic neurotransmitters, and the presence of functional alpha 1 and alpha 2 adrenergic receptors in these tissues has been established through biochemical studies. These changes are regulated by the tone of vascular and non-vascular smooth muscle in the vagina and clitoris. Primary cell culture studies have suggested that several physiological modulators such as vasoactive intestinal polypeptide (VIP), nitric oxide (NO), and prostaglandin E (PGE) regulate vaginal smooth muscle contractility. Data from experimental models have provided a preliminary understanding of the mechanisms of the female sexual arousal response.

Animals↗
PubMed2001

Computed tomography assessment of abdominal aortic aneurysm morphology after endograft exclusion.

OBJECTIVES: Assessment of the long-term function of endografts to exclude abdominal aortic aneurysm (AAA) includes determination of aneurysm dimensions and morphologic changes that occur after implantation. This study reports the dimensional analysis of patients treated with AneuRx bifurcated endoprostheses with postintervention, 1-year (n = 51), 2-year (n = 28), and 3-year (n = 10) postimplantation contrast computed tomography data. METHODS: Maximal diameter (D) and cross-sectional area (CSA) of the AAA were measured from axial computed tomography images. Total volume, AAA thrombus volume (AAA volume minus the volume of the device and luminal blood flow), diameter of the aorta at the level of the renal arteries and within the device, distance from the renal arteries to the device, length of the device limbs, and the angle of the proximal neck were also determined at the same follow-up intervals after deployment with computed tomography angiograms reconstructed in an interactive environment. RESULTS: Fifty-one of 98 consecutively treated patients with the AneuRx bifurcated prosthesis (29 "stiff" and 22 "flexible" body devices) had complete data from the postprocedure and follow-up computed tomography studies available for analysis. Max D, CSA, total volume of the AAA, and AAA thrombus volume decreased sequentially from year to year compared with the postimplantation values. D and CSA decreased or were unchanged in all except four patients, two who had unrestricted enlargement of the aneurysm with eventual rupture and one who had surgical conversion for continued expansion despite four diagnostic angiograms and attempted embolizations. Total volume of the AAA increased in 11 of 51 patients at 1 year, eight of whom had endoleaks at some interval during the follow-up. Thrombus volume increased more than 5% in four of these patients, including the two with eventual rupture and the one conversion. Patients with endoleaks who had spontaneous thrombosis or were successfully treated either remained at the same volume or had decreased volume on subsequent examinations. D at the renal arteries increased an average of 0.9 mm during the first year, with a concomitant increase of 2.8 mm within the proximal end of the device related to the self-expanding nature of the Nitinol suprastructure. Subsequent enlargement of the proximal neck continued at a slow rate in some cases but never exceeded the diameter of the endoluminal device. The distance from the renal arteries to the device increased by an average of 3 mm over the first year, with the greatest increases occurring in patients with a "stiff" body device and those with rapid regression (>10% total volume) in 1 year. As regression of the AAA occurred, the angle of the proximal neck varied from -5 degrees to +25 degrees from the original alignment. Limb length varied from -8 mm to +10 mm, with no consistent pattern for the change, that is, ipsilateral or contralateral limb. CONCLUSION: Significant variation in the quantitation of aneurysm size occurs depending on the technique of computed tomography assessment used. In most patients diameter assessment is adequate, although volumetric analysis appears to be very helpful in certain patients who do not show aneurysm regression, or in whom the diameter increases or where endoleaks persist. Three-dimensional reconstruction and volumetric analysis are also useful to assess the mechanism by which the endovascular device accommodates to morphology changes and to determine criteria for reintervention.

Angiography↗
PubMed2001

Endovascular exclusion of descending thoracic aortic aneurysms and chronic dissections: Initial clinical results with the AneuRx device.

OBJECTIVE: The objective of this study was to analyze a single-center experience in which descending thoracic aortic aneurysms (TAAs) were treated with a new self-expanding endovascular prosthesis (Medtronic AVE). METHODS: Twenty-six patients (13 men, 13 women) with American Society of Anesthesiology grades II to IV and ages ranging from 53 to 92 years (average, 74 years) consented as part of a Phase I Food and Drug Administration-approved trial. Treated lesions included TAAs that were 5 to 10 cm in diameter, 12 diffuse dilations or fusiform aneurysms, and four saccular aneurysms. There were also nine chronic dissections (2 aneurysmal dilations and 7 symptomatic acute recurrent dissections). Three patients (2 with diffuse/fusiform and 1 with dissection) presented with hemothorax, contrast extravasation, or both. RESULTS: Twenty-five of the 26 patients who consented (96% technical success) were treated successfully with no surgical conversions. Eighteen patients have been followed up from 1 to 22 months (average, 9 months). One patient is lost to follow-up, and six patients have died (24%). One procedure-related death (4%) occurred within the 30-day postoperative period and was caused by diffuse embolization. There were no device-related deaths. Five additional patients (20%) have died during the study of comorbid conditions. Complications included one massive myocardial infarction 24 hours after the procedure requiring balloon counterpulsation and long-term dialysis, one cardiac tamponade resulting from central line placement before the procedure, one progression of aneurysm dilation proximal to the device at 1 year, and one bilateral lower extremity paralysis occurring 12 hours after successful deployment. Seven patients (5 women) had femoral artery reconstructions or iliac artery grafts to repair injuries during deployment catheter passage. Other significant parameters included average procedure time (2 hours 40 minutes; range, 1 hour 30 minutes to 5 hours 30 minutes), 450 cc average blood loss (n = 25; 100-3000 cc) being replaced by means of autotransfusion with only two patients receiving banked blood products, and an average 2 days to resumption of normal diet, 1 day in the intensive care unit, and 5 days' hospitalization postprocedure in uncomplicated cases (n = 22). One patient had an endoleak immediately after the procedure that sealed without treatment. Follow-up of all patients ranging from 1 to 22 months (average, 9 months; n = 18) demonstrates continued exclusion of the aneurysm with no endoleaks and either stable or decreasing aneurysm volume, except in one patient with volume increase and no obvious etiology who continues to be investigated. CONCLUSIONS: The study suggests that endovascular prosthesis exclusion of TAAs with an AneuRx self-expanding tubular device may be effective in many patients who are at significant risk for open surgical repair and substantiates further clinical investigation to confirm these findings.

Aged↗
PubMed2001

TDAG51 is not essential for Fas/CD95 regulation and apoptosis in vivo.

Fas/CD95 is a key regulator of apoptotic signaling, which is crucial for the maintenance of homeostasis in peripheral lymphoid organs. TDAG51 has been shown to play critical roles in the up-regulation of Fas gene expression and T-cell apoptosis in vitro. In order to identify the role of TDAG51 in vivo, we generated TDAG51-deficient (TDAG51-/-) mice. Northern blotting revealed no expression of TDAG51 in TDAG51-/- mice, indicating that the TDAG51 gene was successfully targeted. TDAG51-/- mice were healthy and showed no gross developmental abnormalities. While Fas-deficient mice display marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51-/- mice had no apparent defects in secondary lymphoid organs. Although TDAG51 is required for up-regulation of Fas expression in T-cell hybridomas, TDAG51-/- mice expressed normal levels of Fas and had normal T-cell apoptosis. Therefore, we conclude that TDAG51 is not essential for Fas up-regulation and T-cell apoptosis in vivo. There are several known homologs of TDAG51, and these homologs may substitute for TDAG51 in TDAG51-/- mice.

Animals↗
PubMed2001

Ca2+-induced contraction of cat esophageal circular smooth muscle cells.

ACh-induced contraction of esophageal circular muscle (ESO) depends on Ca2+ influx and activation of protein kinase Cepsilon (PKCepsilon). PKCepsilon, however, is known to be Ca2+ independent. To determine where Ca2+ is needed in this PKCepsilon-mediated contractile pathway, we examined successive steps in Ca2+-induced contraction of ESO muscle cells permeabilized by saponin. Ca2+ (0.2-1.0 microM) produced a concentration-dependent contraction that was antagonized by antibodies against PKCepsilon (but not by PKCbetaII or PKCgamma antibodies), by a calmodulin inhibitor, by MLCK inhibitors, or by GDPbetas. Addition of 1 microM Ca2+ to permeable cells caused myosin light chain (MLC) phosphorylation, which was inhibited by the PKC inhibitor chelerythrine, by D609 [phosphatidylcholine-specific phospholipase C inhibitor], and by propranolol (phosphatidic acid phosphohydrolase inhibitor). Ca2+-induced contraction and diacylglycerol (DAG) production were reduced by D609 and by propranolol, alone or in combination. In addition, contraction was reduced by AACOCF(3) (cytosolic phospholipase A(2) inhibitor). These data suggest that Ca2+ may directly activate phospholipases, producing DAG and arachidonic acid (AA), and PKCepsilon, which may indirectly cause phosphorylation of MLC. In addition, direct G protein activation by GTPgammaS augmented Ca2+-induced contraction and caused dose-dependent production of DAG, which was antagonized by D609 and propranolol. We conclude that agonist (ACh)-induced contraction may be mediated by activation of phospholipase through two distinct mechanisms (increased intracellular Ca2+ and G protein activation), producing DAG and AA, and activating PKCepsilon-dependent mechanisms to cause contraction.

Adrenergic beta-Antagonists↗
PubMed2001

Oral administration of collagen conjugated with cholera toxin induces tolerance to type II collagen and suppresses chondritis in an animal model of autoimmune ear disease.

B10.RIII (H-2r) mice were orally administered cyanogen bromide peptide 11 (CB11) or cholera toxin B (CTB)-conjugated CB11 to induce tolerance in collagen-induced autoimmune ear disease. Oral administration of a high dosage of CB11 provided partial protection from chondritis. However, administration of a tiny amount of CTB-CB11 conjugate effectively suppressed chondritis. Oral administration of CTB-CB11 conjugate did not alter the stimulation of T cells in vitro or the fine specificities of B cells. The oral administration of CTB-CB11 caused a higher level of type II collagen-specific IgG and its subclass. Interestingly, increases of TH1 cytokine (interferon-gamma) in Peyer's patches and of TH1/TH2 cytokines (interleukin-2 and interleukin-4) in lymph nodes were detected in mice that had been fed CTB-CB11. An increase of CD8+ T cells in the Peyer's patches with a decrease of CD8+ T cells in lymph nodes was seen in mice that had been fed CTB-CB11. These results suggest that protection from chondritis by oral administration of minute amounts of CTB-CB11 conjugate can be achieved by a mechanism distinct from that of conventional oral tolerance induction.

Administration, Oral↗
PubMed2001

Purification of saponin compounds in Bupleurum falcatum by solvent partitioning and preparative LC.

Saponin compounds (saikosaponin c, a, and d) in Bupleurum falcatum were partially purified by solvent partitioning of the herbal extract using diethyl ether, distilled water, n-butanol, and acetone. After separation of the saponins by preparative LC, the purity of each saikosaponin was more than 94%. The identities of purified individual saikosaponins were confirmed by TLC, analytical LC, and fast-atom bombardment mass spectrometry.

Bupleurum↗
PubMed2001

Clinical features of vivax malaria.

Plasmodium vivax malaria reemerged in the Republic of Korea in 1993 near the Demilitarized Zone (DMZ). We reviewed clinical features of 101 symptomatic patients with vivax malaria. Of the patients, 77 patients (76.3%) were veterans who had served near the DMZ; their median age was 23 years. The duration of the minimum latent period was > 6 months in 66.2% (51 of 77) of the patients (median, 278 days). Tertian fever developed in 69 patients (68.3%). Severe thrombocytopenia with platelet counts < 60,000/microL was common (29.6% of patients). The parasite densities ranged 32-52,127 parasites per microliter of blood (geometric mean, 1,287). The only complication was a splenic rupture in one patient. All patients responded promptly to chloroquine therapy. Our data suggest that the clinical features of reemerging vivax malaria may be similar to those of Korean vivax malaria reported in the past.

Adolescent↗
PubMed2001

Evidence that the rat osteopetrotic mutation toothless (tl) is not in the TNFSF11 (TRANCE, RANKL, ODF, OPGL) gene.

The toothless (tl) osteopetrotic mutation in the rat affects an osteoblast-derived factor that is required for normal osteoclast differentiation. Although the genetic locus remains unknown, the phenotypic impact of the tl mutation on multiple systems has been well characterized. Some of its actions are similar to tumornecrosis factor superfamily member 11(TNFSF11; also called TRANCE, RANKL, ODF and OPGL) null mice. TNFSF11 is a recently described member of the tumor necrosis factor superfamily which, when expressed by activated T cells, enhances the survival of antigen-presenting dendritic cells, and when expressed by osteoblasts, promotes the differentiation and activation of osteoclasts. The skeletal similarities between tl rats and TNFSF11(-/-) mice include 1) profound osteoclastopenia (TNFSF11-null mice, 0% and tl rats 0-1% of normal); 2) persistent, non-resolving osteopetrosis that results from 3) a defect not in the osteoclast lineage itself, but in an osteoblast-derived, osteoclastogenic signal; and 4) a severe chondrodysplasia of the growth plates of long bones not seen in other osteopetrotic mutations. The latter includes thickening of the growth plate with age, disorganization of chondrocyte columns, and disturbances of chondrocyte maturation. These striking similarities prompted us to undertake studies to rule in or out a TNFSF11 mutation in the tl rat. We looked for expression of TNFSF11 mRNA in tl long bones and found it to be over-expressed and of the correct size. We also tested TNFSF11 protein function in the tl rat. This was shown to be normal by flow cytometry experiments in which activated, spleen-derived T-cells from tl rats exhibited normal receptor binding competence, as measured by a recombinant receptor assay. We also found that tl rats develop histologically normal mesenteric and peripheral lymph nodes, which are absent from TNFSF11-null mice. Next, we found that injections of recombinant TNFSF11, which restores bone resorption in null mice, had no therapeutic effect in tl rats. Finally, gene mapping studies using co-segregation of polymorphic markers excluded the chromosomal region containing the TNFSF11 gene as harboring the mutation responsible for the tl phenotype. We conclude that, despite substantial phenotypic similarities to TNFSF11(-/-) mice, the tl rat mutation is not in the TNFSF11 locus, and that its identification must await the results of further studies.

Animals↗
PubMed2000

Regulation of peripheral lymph node genesis by the tumor necrosis factor family member TRANCE.

Proper lymph node (LN) development requires tumor necrosis factor-related activation-induced cytokine (TRANCE) expression. Here we demonstrate that the defective LN development in TRANCE(-/)- mice correlates with a significant reduction in lymphotoxin (LT)alphabeta(+)alpha(4)beta(7)(+)CD45(+)CD4(+)CD3(-) cells and their failure to form clusters in rudimentary mesenteric LNs. Transgenic TRANCE overexpression in TRANCE(-/)- mice results in selective restoration of this cell population into clusters, and results in full LN development. Transgenic TRANCE-mediated restoration of LN development requires LTalphabeta expression on CD45(+) CD4(+)CD3(-) cells, as LNs could not be induced in LTalpha(-/)- mice. LTalpha(-/)- mice also showed defects in the fate of CD45(+)CD4(+)CD3(-) cells similar to TRANCE(-/)- mice. Thus, we propose that both TRANCE and LTalphabeta regulate the colonization and cluster formation by CD45(+) CD4(+)CD3(-) cells in developing LNs, the degree of which appears to correlate with the state of LN organogenesis.

Animals↗
PubMed2000

Effect of initial carbon sources on the performance of microbial fuel cells containing Proteus vulgaris.

Mediator-coupled microbial fuel cells containing Proteus vulgaris were constructed and the cell performance was tested. Fuel cell efficiency depended on the carbon source in the initial medium of the microorganism. Maltose and trehalose were not utilized substantially by P. vulgaris; however, their presence in the initial medium resulted in enhanced cell performance. In particular, galactose showed 63% coulombic efficiency in a biofuel cell after P. vulgaris was cultured in a trehalose-containing medium. This work demonstrates that optimum utilization of carbon sources by microorganisms, which leads to the maximization of fuel cell performance, is possible simply by adjusting initial carbon sources.

Bioelectric Energy Sources↗
PubMed2000

RAS transformation causes sustained activation of epidermal growth factor receptor and elevation of mitogen-activated protein kinase in human mammary epithelial cells.

Activation of the ras oncogene is an important step in carcinogenesis. Human MCF-10A mammary epithelial cells were transformed with a point-mutated form of the Ha-ras oncogene. Epidermal growth factor receptor (EGFR) phosphorylation levels were chronically elevated after EGF induction and the EGFR ligand-driven internalization rate was slower in Ha-ras transformed MCF-10A cells. Additionally, basal levels of p42/44 mitogen-activated protein kinase (MAPK) expression and enzyme activity were significantly higher in Ha-ras transformed cells, localized predominantly in the nucleus. The anti-EGFR monoclonal antibody (MAb) 225 and the EGFR tyrosine kinase inhibitor PD153035 blocked anchorage-independent growth of Ha-ras transformed cells in soft agar and were more effective when used in combination. The MEK inhibitor PD98059 and anti-erbB-2 MAb L26 also suppressed colony formation of Ha-ras transformed cells in soft agar. Therefore, Ha-ras transformation leads to an augmentation in signaling through the EGFR as a result of an increase in ligand-dependent phosphorylation, a decrease in its internalization and an up-regulation in basal p44/42 MAPK levels. These effects may contribute to uncontrolled growth of Ha-ras-transformed human mammary epithelial cells.

Antibodies, Monoclonal↗
PubMed2000

Diverse roles of the tumor necrosis factor family member TRANCE in skeletal physiology revealed by TRANCE deficiency and partial rescue by a lymphocyte-expressed TRANCE transgene.

Tumor necrosis factor-related, activation-induced cytokine (TRANCE), a tumor necrosis factor family member, mediates survival of dendritic cells in the immune system and is required for osteoclast differentiation and activation in the skeleton. We report the skeletal phenotype of TRANCE-deficient mice and its rescue by the TRANCE transgene specifically expressed in lymphocytes. TRANCE-deficient mice showed severe osteopetrosis, with no osteoclasts, marrow spaces, or tooth eruption, and exhibited profound growth retardation at several skeletal sites, including the limbs, skull, and vertebrae. These mice had marked chondrodysplasia, with thick, irregular growth plates and a relative increase in hypertrophic chondrocytes. Transgenic overexpression of TRANCE in lymphocytes of TRANCE-deficient mice rescued osteoclast development in two locations in growing long bones: excavation of marrow cavities permitting hematopoiesis in the marrow spaces, and remodeling of osteopetrotic woven bone in the shafts of long bones into histologically normal lamellar bone. However, osteoclasts in these mice failed to appear at the chondroosseous junction and the metaphyseal periosteum of long bones, nor were they present in tooth eruption pathways. These defects resulted in sclerotic metaphyses with persistence of club-shaped long bones and unerupted teeth, and the growth plate defects were largely unimproved by the TRANCE transgene. Thus, TRANCE-mediated regulation of the skeleton is complex, and impacts chondrocyte differentiation and osteoclast formation in a manner that likely requires local delivery of TRANCE.

Animals↗
PubMed2000

Micellar electrokinetic chromatography for the analysis of D-amygdalin and its epimer in apricot kernel.

We have developed a simple, rapid and reproducible method for the determination of D-amygdalin and its epimer by using micellar electrokinetic chromatography (MEKC). Separation of D-amygdalin was performed in a 20 mM sodium borate buffer (pH 8.5) containing 300 mM sodium dodecyl sulfate using a bare fused-silica capillary. The eluates were monitored by the absorbance at 210 nm. The applied electric field was 278 V/cm, and the time needed for the separation of D-amygdalin did not exceed 6 min. The calibration curve for D-amygdalin showed excellent linearity in the concentration range of 5-500 microg/ml. The migration time and the corrected peak area show relative standard deviations (n=6) of 0.86% and 1.48%, respectively. The limit of detection (S/N=3) for D-amygdalin was 2 microg/ml. Under acidic and neutral conditions, amygdalin exists only as the D-form; however, under basic conditions, it shows both the D- and L-forms with a concentration ratio of 1:1.3 (D-amygdalin/L-amygdalin). Results of HPLC, UV-Vis spectrophotometry, and mass spectrometry reconfirmed the identification of D-amygdalin and its epimer. The number of theoretical plates of D-amygdalin is about 100,000 in MEKC, which is significantly higher than approximately 8,000 of HPLC. This method has been successfully applied to the determination of amygdalin epimers in various apricot kernel extracts and pharmaceutical products.

Amygdalin↗
PubMed2000

Operational characteristics of an antibody-immobilized QCM system detecting Salmonella spp.

A quartz crystal microbalance (QCM) system detecting Salmonella spp. was developed by an anti-Salmonella antibody immobilization onto one gold surface of a piezoelectric quartz crystal surface with sulfosuccinimidyl 6-[3-(2-pyridyldithio)propionamido]hexanoate (sulfo-LC-SPDP) thiolation. The optimum temperature and pH for the antibody-immobilized sensor were 35 degrees C and 7.2, respectively. The frequency shifts obtained were correlated with the Salmonella concentrations in the range 3.2 x 10(6)-4.8 x 10(8) CFU per ml. The system was quite specific to Salmonella spp. and applicable for repetitive use after a regeneration step employing 1.2 M NaOH. A model sample measurement was done for a market milk spiked with Salmonella typhimurium.

Animals↗