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Y Song

Publications and source records attributed to Y Song.

At least 361 records · Page 20Linked to original sources

Effects of particulate high-density polyethylene and titanium alloy on tissue ingrowth into bone harvest chamber in rabbits.

The purpose of this study was to determine whether small, phagocytosable particles of titanium alloy (Ti) and high-density polyethylene (HDPE) have an adverse effect on bone ingrowth. The bone harvest chamber (BHC) was implanted bilaterally in the proximal tibial metaphysis of six mature rabbits. The BHC has a transverse 1-mm wide pore providing a continuous canal through the chamber for tissue ingrowth. After an initial 6-week period for osseointegration of the BHC, the contents of the canal were harvested repeatedly at 3 weekly intervals. This could be done with the chamber in place, without disturbing its exterior surface or the surrounding bone. The carrier solution, 1% sodium hyaluronate (Healon) was implanted first. In subsequent implantations, Healon was mixed with particles of HDPE or Ti averaging 4.7 +/- 2.1 and 3.0 +/- 2.6 microns, respectively. The contralateral chamber was left empty and served as a control. The chambers were harvested repeatedly, alternating experimental and control sides. The sections from the control side, and those containing Healon alone demonstrated extensive trabecular bone in a fibrovascular stroma. The sections containing Ti alloy particles were qualitatively and quantitatively similar to the control sections and those containing Healon, except for the presence of small black granules of Ti alloy, dispersed in the fibrovascular stroma or phagocytosed by scattered macrophages. The sections containing HDPE particles were infiltrated and engulfed by mononuclear and multinuclear histiocytic cells in a highly fibrous stroma. The majority of the multinucleated cells present were interpreted as being foreign body giant cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Alloys↗

Intermittent micromotion and polyethylene particles inhibit bone ingrowth into titanium chambers in rabbits.

We performed a histomorphological and morphometric analysis of the effects of short daily periods of micromotion and phagocytosable particles of high density polyethylene (PE) on bone ingrowth into a 1 x 1 x 5 mm canal within a titanium chamber in rabbits. The micromotion chamber (MC) was implanted in the tibia of nine mature New Zealand white rabbits. After osseointegration and first harvest of tissue, 40 micromotions (amplitude = 0.5 mm) were applied daily at a rate of 1 Hz for a 3-week period. The tissue within the chamber was then harvested. For the second treatment, PE particles (10(8)/mL) were placed within the canal. The tissue in the chamber was harvested 3 weeks later. The next treatment was a 3-week rest period, in which neither micromotion nor particles were utilized; a harvest followed. The final treatment combined PE particles and micromotion, followed by a harvest 3 weeks later. Sections from control harvests contained extensive trabecular bone arranged longitudinally throughout the canal in a fibrovascular stroma. Micromotion produced longitudinally oriented fibrous tissue within the chamber. PE particles were associated with macrophages, surrounding and engulfing the birefringent particles. The combination of particles and micromotion produced a fibrous stroma laden with macrophages. PE particles and micromotion, alone or together, produced a similar effect in inhibiting bone ingrowth, compared to nonmoved chambers without particles. In this short-term experiment, no additive or potentiating effect of these two stimuli could be demonstrated.

Animals↗

Surface-associated proteins from Staphylococcus aureus demonstrate potent bone resorbing activity.

Staphylococcus aureus infections are associated with rapid bone destruction in conditions such as osteomyelitis, bacterial arthritis, and infected orthopedic implant failure. How this bacterium induces bone destruction has not been defined. In studies of the role of oral Gram-negative bacteria in periodontal pathology, we have established that cell surface-associated proteins (SAPs) are potent stimulators of bone resorption. The surface-associated components from S. aureus have now been isolated and demonstrated to be extremely potent stimulators of bone resorption in the murine calvarial bone resorption assay. Bone resorption appears to be due to proteins, is not the result of contamination with lipoteichoic acid or muramyl dipeptide, and is potently inhibited by indomethacin and can be completely blocked by high concentrations of interleukin-1 receptor antagonist or TN3-19.12, a neutralizing monoclonal antibody to murine TNF. The SAP fraction can stimulate fibroblasts or monocytes to release osteolytic cytokines, but only at high concentrations. Fractionation of the SAPs by high performance liquid chromatography demonstrated that a number of fractions were osteolytically active. The most active contained a heterodimeric protein of molecular weight 32-36 kD. The presence of this osteolytically active surface-associated fraction may account for the bone resorption associated with local infection with S. aureus.

Animals↗

Relationship between ornithine decarboxylase and cytoskeletal organization in cultured human keratinocytes: cellular responses to phorbol esters, cytochalasins, and alpha-difluoromethylornithine.

Changes in cell shape occur during the cell cycle and influence cell proliferation and differentiation. In order to study how altered cell proliferation and cell shape are interrelated, we have studied ornithine decarboxylase (ODC) regulation in cultured normal human epidermal keratinocytes (NHEK). Cytoskeletal disruptors have been reported to modulate regulation of ODC; the products of ODC, the polyamines, influence actin polymerization rates in vitro, and polyamine auxotrophs have profoundly disrupted cytoskeletons. Therefore, altered ODC levels could be involved in signaling changes in cell shape and an intact cytoskeleton could transduce signals to regulate ODC levels. We had previously observed that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), which profoundly alters cell shape, markedly suppresses ODC biosynthesis in NHEK solely at posttranscriptional/protein synthesis levels. TPA treatment caused NHEK to rapidly assume a rounded morphology that was accompanied by a change in actin organization, as determined by rhodamine-phalloidin labeling. Immunolocalization of ODC showed a perinuclear/nuclear distribution in untreated NHEK and a more diffuse pattern after TPA treatment that was apparent within 15-30 min. Changes in ODC enzyme activity are not significant until 60 min after TPA treatment. NHEK treated with cytochalasin B or D to inhibit actin polymerization exhibited a diffuse ODC localization that could be reversed by removal of the cytochalasin; inhibition of ODC by alpha-difluoromethylornithine caused a diffuse ODC localization. All treatments resulted in cytoskeletal remodeling. These data are the first evidence for a distinct subcellular localization for ODC and suggest that changes in ODC localization may be an initial step in regulation of ODC activity. Furthermore, changes in ODC activity cause an altered cytoskeleton, suggesting one means by which growth regulatory signals can be transduced to the cytoskeleton from various signaling pathways.

Actins↗

beta-Adrenoceptor stimulation activates large-conductance Ca2+-activated K+ channels in smooth muscle cells from basilar artery of guinea pig.

We studied the effect of isoproterenol on the Ca2+-activated K+ (BK) channel in smooth muscle cells isolated from the basilar artery of the guinea pig. Cells were studied in a whole-cell configuration to allow the clamping of intracellular Ca2+ concentration, [Ca2+]i. Macroscopic BK channel currents were recorded during depolarizing test pulses from a holding potential (VH) of 0 mV, which was used to inactivate the outward rectifier. The outward macroscopic current available from a VH of 0 mV was highly sensitive to block by external tetraethylammonium Cl (TEA) and charybdotoxin, and was greatly augmented by increasing [Ca2+]i from 0.01 to 1.0 microM. With [Ca2+]i between 0.1 and 1.0 microM, 0.4 microM isoproterenol increased this current by 58.6 +/- 17.1%, whereas with [Ca2+]i at 0.01 microM a sixfold smaller increase was observed. With [Ca2+]i > or = 0.1 microM, 100 microM dibutyryl -adenosine 3':5: cyclic monophosphate (cAMP) and 1 microM forskolin increased this current by 58.5 +/- 24.1% and 59.7 +/- 10.3%, respectively. The increase with isoproterenol was blocked by 4.0 microM propranolol extracellularly, and by 10 U/ml protein kinase inhibitor intracellularly. Single-channel openings during depolarizing test pulses from a VH of 0 mV recorded in the whole-cell configuration under the same conditions (outside-out-whole-cell recording) indicated a slope conductance of 260 pS. In conventional outside-out patches, this 260-pS channel was highly sensitive to block by external TEA, and in inside-out patches, its probability of opening was greatly augmented by increasing [Ca2+]i from 0.01 to 1.0 microM. Outside-out-whole-cell recordings with [Ca2+]i > or = 0.1 microM indicated that 100 microM dibutyryl-cAMP increased the probability of opening of the 260-pS channel by 152 +/- 115%. In inside-out patches, the catalytic subunit of protein kinase A increased the probability of opening, and this effect also depended on [Ca2+]i , with a 35-fold larger effect observed with 0.1-0.5 microM Ca2+ compared to 0.01 microM Ca2+. We conclude that the BK channel in cerebrovascular smooth muscle cells can be activated by beta-adrenoceptor stimulation, that the effect depends strongly on [Ca2+]i, and that the effect is mediated by cAMP-dependent protein kinase A with no important contribution from a direct G-protein or phosphorylation-independent mechanism. Our data indicate that the BK channel may participate in beta-adrenoceptor-mediated relaxation of cerebral vessels, although the importance of this pathway in obtaining vasorelaxation remains to be determined.

Animals↗

Synthesis and application of hepatitis E virus peptides to diagnosis.

Based on computer analysis of hydrophobicity and prediction of secondary structures for the full-length putative proteins encoded by open reading frame-1 (ORF-1), ORF-2 and ORF-3 of hepatitis E virus (HEV), we selected antigenic regions with hydrophilicity, beta-turn, and beta-sheet, and synthesized 7 peptides of possible epitope-containing regions of the polypeptide encoded by all 3 ORFs of HEV genomic RNA by Merrifield's method of solid-phase synthesis. The synthetic peptides were screened and identified by solid-phase enzyme-linked immunosorbent assay (ELISA). Three of the peptides (EH174 from ORF-1, EH286 from ORF-2 and EH362 from ORF-3) showed antigenic activity and possible application for the development of anti-HEV test kits (the peptide-based ELISA). The laboratory experiments and clinical trials showed that the kits, using a set of 3 synthetic HEV peptides as coating antigens, were of high specificity and exhibited good reproducibility. The small-scale seroepidemiological survey indicated high seroprevalence (14.3%) of anti-HEV in Tibetan populations. Additionally, the results also demonstrated good agreement with clinical findings, suggesting that the test kits will be of major use for immunodiagnosis and seroepidemiological surveys of HEV infection.

Amino Acid Sequence↗

Tumor necrosis factor-alpha and basic fibroblast growth factor decrease glial fibrillary acidic protein and its encoding mRNA in astrocyte cultures and glioblastoma cells.

Tumor necrosis factor-alpha is a pluripotent cytokine that is reportedly mitogenic to astrocytes. We examined expression of the astrocyte intermediate filament component glial fibrillary acidic protein in astrocyte cultures and the U373 glioblastoma cell line after treatment with tumor necrosis factor-alpha. Treatment with tumor necrosis factor-alpha for 72 h resulted in a decrease in content of glial fibrillary acidic protein and its encoding mRNA. At the same time, tumor necrosis factor-alpha treatment increased the expression of the cytokine interleukin-6 by astrocytes. The decrease in glial fibrillary acidic protein expression was greater when cells were subconfluent than when they were confluent. Thymidine uptake studies demonstrated that U373 cells proliferated in response to tumor necrosis factor-alpha, but primary neonatal astrocytes did not. However, in both U373 cells and primary astrocytes tumor necrosis factor-alpha induced an increase in total cellular protein content. Treatment of astrocytes and U373 cells for 72 h with the mitogenic cytokine basic fibroblast growth factor also induced a decrease in glial fibrillary acidic protein content and an increase in total protein level, demonstrating that this effect is not specific for tumor necrosis factor-alpha. The decrease in content of glial fibrillary acidic protein detected after tumor necrosis factor-alpha treatment is most likely due to dilution by other proteins that are synthesized rapidly in response to cytokine stimulation.

Animals↗

Expression of new KDN-gangliosides in rainbow trout testis during spermatogenesis and their structural identification.

The developmental expression of 2-keto-3-deoxy-D-glycero-D-galacto-nononic acid-containing glycosphingolipids (KDN-gangliosides) in rainbow trout testis during spermatogenesis was studied using a monoclonal antibody, mAb.kdn3G, which recognizes the KDN alpha 2-->3Gal beta 1-->epitope. A major KDN-ganglioside found in mature sperm, (KDN)GM3, KDN alpha 2-->3Gal beta 1-->4Glc beta 1-->Cer (where Cer is ceramide), was expressed in testis throughout all stages of its maturation. On the contrary, four new KDN-gangliosides which were reactive with mAb.kdn3G were not detected in mature sperm, although they were identified in immature testis and expressed during spermatogenesis. The structures of these KDN-gangliosides were established by chemical, enzymatic and immunochemical methods as: (i) (KDN)GD1a, KDN alpha 2-->3Gal beta 1-->3GalNAc beta 1-->4(KDN alpha 2-->3)Gal beta 1-->4Glc beta 1-->Cer; (ii) (KDN, Neu5Ac)GD1a, KDN alpha 2-->3Gal beta 1-->3GalNAc beta 1-->4(Neu5Ac alpha 2-->3)Gal beta 1-->4Glc beta 1-->Cer and Neu5Ac alpha 2-->3Gal beta 1-->3GalNAc beta 1-->4(KDN alpha 2-->3)Gal beta 1-->4Glc beta 1-->Cer; (iii) (KDN) GD1 alpha, KDN alpha 2-->3Gal beta 1-->3(KDN alpha 2-->6)GalNAc beta 1-->4Gal beta 1-->4Glc beta 1-->Cer; and (iv) (KDN,Neu5Ac)GD1 alpha, KDN alpha 2-->3Gal beta 1-->3(Neu5Ac alpha 2-->6)GalNAc beta 1-->4Gal beta 1-->4Glc beta 1-->Cer. (KDN)GD1a and (KDN,Neu5Ac)GD1a first appeared at an early stage of spermatogenesis, but (KDN)GD1 alpha and (KDN,Neu5Ac)GD1 alpha were not expressed until 2 months prior to spermiation. While (KDN)GM3 was previously shown to contain only 4-sphingenine (d18:1) acylated with a C16:0 fatty acid, the new KDN-gangliosides discovered in this study were composed of 4-hydroxysphinganine (t18:0) or 4-sphingenine (d18:1), and were acylated with a C24:1 or C16:0 fatty acid. A possible function of these KDN-gangliosides is suggested.

Acylation↗

Ionic basis of the electrophysiological actions of adenosine on cardiomyocytes.

The purpose of this review is to examine the role of the extracellular A1-adenosine (Ado) receptor in modulating membrane potential and currents in cardiac cells. The cellular electrophysiological effects of adenosine are both cell type- and species-dependent. In supraventricular tissues (SA, AV node, and atrium) of all species studied, the "direct" cAMP-independent activation of the inwardly rectifying K+ current IKAdo seems to be the most important action of adenosine. This current is activated by both adenosine and acetylcholine and flows through K+ channels with unitary slope conductance of about 45 pS and an open time constant of 1.4 ms. The density of K(+)-ACh,Ado channels is much less in ventricular than in atrial myocytes, and thus adenosine has little or no effect on the ventricular action potential. In atrial myocytes adenosine has a small inhibitory effect on basal L-type calcium current (ICa,L), but no effect on T-type calcium current (ICa,T). In ventricular myocytes, adenosine does not inhibit ICa,L (except ferret), ICa,T, or the sodium inward current INa. Adenosine has recently been shown to activate IKATP in ventricular membrane patches, but the relevance of this finding remains to be defined. Irrespective of cell type and species, adenosine inhibits membrane currents that are stimulated by beta-adrenergic agonists and other agents known to stimulate the activity of the enzyme adenylyl cyclase. This indirect cAMP-dependent mechanism of action has been shown to be responsible for the inhibition by adenosine of isoproterenol-stimulated ICa,L, delayed rectifier K+ current (IK), chloride current (ICl), the transient inward current ITi, and the pacemaker current IF. The importance of the actions of adenosine on membrane currents in modulation of atrial, ventricular, sinoatrial, and atrioventricular nodal function are discussed. Likewise, the antiarrhythmic and proarrhythmic actions of adenosine are discussed and the clinical implications of these actions are noted.

Adenosine↗

Effect of endogenous insulin on pancreatic exocrine secretion in perfused dog pancreas.

Canine pancreas was perfused with an intraarterial infusion of Krebs-Ringer bicarbonate solution containing 5% dog red blood cells, 0.1% bovine serum albumin, and 3% dextran at 15 ml/min, while portal effluent was continuously collected. Pancreatic juice was obtained in 15-min samples via main pancreatic duct cannulation. After a 1-h basal period, secretin and cholecystokinin-8 (CCK), at doses of 2.5 ng.min-1 each, were simultaneously infused for 10 min, with background infusion of a normal rabbit serum (NRS) or an antiinsulin serum (Anti-I) in 5 ml each via a sidearm of the intraarterial catheter. The infusion of secretin and CCK resulted in a significant increase in pancreatic bicarbonate and protein secretion during the infusion of NRS, whereas the pancreatic secretory response of bicarbonate and protein was profoundly suppressed by the infusion of Anti-I in six pancreata so studied. This suppression by Anti-I coincided with significant increases in somatostatin and pancreatic polypeptide levels in portal venous effluent. In three additional pancreata, simultaneous infusions of Anti-I with antisomatostatin (5 ml) and antipancreatic polypeptide (5 ml) serum failed to inhibit the pancreatic exocrine secretion. These results indicate that secretin- and CCK-stimulated pancreatic secretion of bicarbonate and protein depends heavily on local action of insulin. The suppression by Anti-I of pancreatic secretion is mediated, in part, by local releases of somatostatin and pancreatic polypeptide. Thus, the insuloacinar axis plays an important regulatory role in pancreatic exocrine secretion in the dog, and it involves at least three islet hormones including insulin, somatostatin, and pancreatic polypeptide.

Animals↗

Ontogeny of 2-[125I]iodomelatonin binding sites in the chicken (Gallus domesticus) kidney and spleen.

To understand the possible role of melatonin receptors in the development of renal and immune functions, age-related variations of 2-[125I]iodomelatonin binding sites in the chicken kidney and spleen were investigated by radioreceptor assay. Chickens at embryonic day 20, as well as 2 days, 9 days, 2 weeks, 6 weeks, 12 weeks, and 16 weeks after hatching, were kept under a 12 h light:12 h dark photoperiod and killed at the middle of the light period. Binding sites for 2-[125I]iodomelatonin in membrane preparations of the chicken kidney and spleen were present on embryonic day 20. The maximum binding densities (Bmax) in the kidney increased to a peak between 9 days and 2 weeks of age, then progressively decreased. Bmax values of 2-[125I]iodomelatonin binding sites in the chicken spleen were lower than in the kidney. The peak density in the chicken spleen was recorded at day 2 after hatching and decreased significantly after 6 weeks of age. There were no significant differences in binding affinities (Kd) in kidney and spleen of chicken in the different age groups studied. The unity of Hill coefficients of 2-[125I]iodomelatonin binding sites of the chicken kidney and spleen in all age groups tested suggested that only a single class of binding sites was present in these tissues during development. It is proposed that the developmental changes in 2-[125I]iodomelatonin binding sites in the chicken kidney and spleen may be pertinent to the development of diurnal rhythms of kidney functions and the post-pubertal decline in immune functions of the chicken.

Age Factors↗

2-[125I]iodomelatonin-binding sites in the human kidney and the effect of guanosine 5'-O-(3-thiotriphosphate).

Putative melatonin receptors in normal kidney cortical tissues of patients with transitional cell carcinoma or renal cell carcinoma were characterized using a melatonin agonist, 2-[125I]iodomelatonin, as the radioligand. 2-[125I]Iodomelatonin-binding sites in the human kidney were stable, saturable, reversible, and of high affinity. The binding affinity was 15.2 +/- 2.5 pmol/L, and the binding density was 1.79 +/- 0.19 fmol/mg protein. The unity of the Hill coefficients and linearity of the Scatchard plots suggested that 2-[125I]iodomelatonin was bound to a single class of binding sites. Pharmacological characterization showed that these binding sites were highly specific to 2-iodomelatonin, melatonin, 6-hydroxymelatonin, and 6-chloromelatonin. Guanosine 5'-O-(3-thiotriphosphate) decreased the binding affinity and density of 2-[125I]iodomelatonin-binding sites in the kidney, suggesting that these binding sites are coupled to a G-protein. The characterization of 2-[125I]iodomelatonin-binding sites in normal kidney tissues taken from patients with transitional cell carcinoma or renal cell carcinoma suggests the existence of 2-[125I]iodomelatonin-binding sites in the human kidney cortex, which is in line with the findings of 2-[125I]iodomelatonin-binding sites in kidneys of other mammals and birds. The implication of a direct melatonin action on renal function in the human is proposed.

Adult↗

The patch clamp technique.

The introduction of the patch clamp technique less than two decades ago revolutionized the study of cellular physiology by providing a high-resolution method of observing the function of individual ionic channels in a variety of normal and pathological cell types. By the use of variations of the basic recording methodology, cellular function and regulation can be studied at a molecular level by observing currents through individual ionic channels. At a cellular level, processes such as signaling, secretion, and synaptic transmission can be examined. In addition, by combining the information from high-resolution electrophysiological recordings obtained by the patch clamp method with modern molecular biological techniques, further insight can be gained into the gene expression and protein structure of ionic channels. Given the ubiquity and importance of ionic channels, it is not surprising that their study has led to a new understanding of the mechanisms of certain disease processes and has given insight into treatments for these diseases. This review gives an historical perspective of the development of the patch clamp technique and an overview of the methodologies currently in use. Examples are shown to illustrate typical uses of the patch clamp technique with emphasis on the variety of recording configurations available and the advantages and drawbacks of each method.

Animals↗

Tissue ingrowth and differentiation in the bone-harvest chamber in the presence of cobalt-chromium-alloy and high-density-polyethylene particles.

Particulate wear debris from joint replacements has been implicated in the etiology of periprosthetic bone resorption. However, the effect of high-density-polyethylene or cobalt-chromium-alloy particles on osteoclastic bone resorption in vivo has not been studied previously, to our knowledge. Therefore, we examined the effect of these particles on tissue ingrowth, net bone formation (per cent trabecular bone), and osteoclastic bone resorption (osteoclasts per unit of bone surface) with use of a bone-harvest chamber that had a transverse one-millimeter channel for tissue ingrowth. After an initial six-week period for incorporation of the chamber into the proximal part of the tibia of rabbits, the contents of the channel were harvested repeatedly at three-week intervals. The carrier solution, 1 per cent sodium hyaluronate, was implanted first. In subsequent implantations, the hyaluronate was mixed with high-density-polyethylene or cobalt-chromium particles at concentrations of 10(8) particles per milliliter. The tissue harvested from the chambers that contained no particles was composed of longitudinally oriented trabecular bone in a fibrovascular stroma. Particulate high-density polyethylene evoked a moderate foreign-body reaction and a chronic inflammatory response and decreased net bone formation. When cobalt-chromium particles had been implanted, the tissue exhibited a more florid foreign-body reaction and a chronic inflammatory response, often in a nodular arrangement, in a background of dense connective tissue. Bone was sparse, and areas of cell necrosis and hyaline degeneration were noted. Histomorphometric analyses were carried out to determine the amount of net bone formation and osteoclastic bone resorption in the presence or absence of high-density-polyethylene or cobalt-chromium particles. The amount of bone was greatest in the control specimens, moderately decreased in the presence of high-density-polyethylene particles, and greatly decreased in the presence of cobalt-chromium particles. The number of osteoclasts in Howship lacunae per unit of trabecular bone surface was increased in the presence of high-density polyethylene, indicating that these particles stimulate osteoclastic bone resorption.

Animals↗

The incidence of drug resistant tuberculosis in 1279 Korean patients.

OBJECTIVES: In the past decade, the incidence of tuberculosis has been decreased in Korea and the nationwide survey of tuberculosis from 1965 through 1990 suggested a declining tendency of resistant organisms. But the prevalence rate of multidrug resistance of Mycobacterium tuberculosis is still a serious problem in Korea, and the aim of this study is to check the drug resistance pattern in the patients visiting University Hospital, the 3rd referral center. METHODS: We reviewed 1279 cases (522 female, 757 male, mean age 39.4 +/- 16.7) of bacteriologically proven tuberculosis seen during the period from 1986 to 1992 retrospectively. Of 1093 patients, who were indentified in previous medical history, 454 (41.5%) had a history of prior antituberculous chemotherapy. RESULTS: Resistance rate (resistant to 1 or more drugs) was 33.9%. Eleven percent of patients had resistance to a single drug (INH: 80.6%). Twenty two percent of patients had resistance to 2 or more drugs. Resistance rate is higher (47.4%) in the patients with a history of prior treatment than without a history (25.5%). CONCLUSIONS: These data suggest that the high rate of multidrug resistance in Korea did not show any decreasing tendency. So, mycobacterial culture and sensitivity tests should be recommended at initial treatment of tuberculosis and potent antituberculosis drugs are strongly recommended.

Adult↗

Injury-induced upregulation of bFGF and CNTF mRNAS in the rat retina.

Focal mechanical injury to the retina has been shown to slow or prevent photoreceptor degeneration near the lesion site in two animal models of retinal degeneration, inherited retinal dystrophy in the Royal College of Surgeons (RCS) and light damage in albino rats. Thus, when injured, the rat retina activates a self-protective mechanism to minimize damage. To identify injury responsive factors and cells, we examined the mRNAs for the following factors and some of their receptors: basic and acidic fibroblast growth factors (bFGF, aFGF) and FGF receptor-1 (FGFR1); ciliary neurotrophic factor (CNTF) and CNTF receptor alpha (CNTFR alpha); brain-derived neurotrophic factor (BDNF) and its receptor trkB; and insulin-like growth factor-1 (IGF-1) and IGFR-1 receptor (IGF-1R). After a single mechanical lesion to the subretinal space and retina, there was a substantial increase in bFGF and CNTF expression that persisted for the entire 10 d period of study. The increase in bFGF mRNA after injury was prompt and great in amplitude, while the elevation of CNTF mRNA was relatively slower. In addition, there was a transient increase in FGFR1 mRNA. In situ hybridizations showed that the elevation of bFGF and CNTF was localized to the vicinity of the lesion. The expression of GFAP (glial fibrillary acidic protein) mRNA also increased in response to injury. These findings strongly suggest that increases in endogenous bFGF and/or CNTF play key roles in injury-induced photoreceptor rescue.

Animals↗

[Enzyme-linked immunoadsorbent assays for myelin basic protein and antibodies to myelin basic protein in serum and CSF of patients with diseases of the nervous system].

Simplified enzyme-linked immunoadsorbent assays (ELISA) for myelin basic protein (MBP) and antibodies to myelin basic protein (Anti-MBP) have been used to test 337 patients with diseases of the nervous system including 36 compressive diseases (CMP), 33 multiple sclerosis (MS), 34 cerebrovascular diseases (CVD), 31 inflammatory diseases of central nervous system (ID), 161 epilepsy (EP) and 42 other nervous diseases (OND). Comparison of results among various groups indicates that serum mean MBP values of CMP, MS, CVD, ID and EP groups are significantly higher than those of OND group and normal control (P < 0.01). The serum mean MBP value of 33 acute trauma patients with spine fracture and paraplegia, the majority of CMP group, is the highest compared with MS group (P < 0.05), CVD, ID and EP groups (P < 0.01). CSF mean MBP value of 15 CVD patients is markedly greater than that of OND group (P < 0.05). No statistically significant differences are found in serum MBP values between OND group and normal control, and in serum and CSF Anti-MBP values among six groups by using our method.

Autoantibodies↗

Inhibition of thrombin by antithrombin III and heparin cofactor II in vivo.

The critical role of thrombin in the pathogenesis of venous and arterial thrombosis, and the effectiveness of glycosaminoglycans as antithrombotic drugs are well known. Antithrombin III is a major inhibitor of thrombin and augmentation of its inhibitory actions by heparin is the basis for the clinical uses of heparin. Recent clinical and experimental studies have demonstrated that another glycosaminoglycan, dermatan sulfate, is an effective antithrombotic drug. Dermatan sulfate catalyses the inhibition of thrombin by heparin cofactor II. The concentrations of heparin cofactor II are higher in the plasmas of individuals with congenital antithrombin III deficiency and pregnant women than controls. The role of heparin cofactor II as a physiologic thrombin inhibitor is unknown. Enzyme-linked immunosorbent assays were used to quantify thrombin-heparin cofactor II and thrombin-antithrombin III endogenous to the plasmas of adult antithrombin III-Hamilton deficient subjects, their siblings with normal antithrombin III levels, pregnant women at term and 3 to 5 days after delivery. Both thrombin-antithrombin III and thrombin-heparin cofactor II complexed with vitronectin were detected in all the plasmas. Significantly, the concentrations of thrombin-heparin cofactor II-vitronectin were higher in the plasmas of congenital antithrombin III deficient subjects and in pre- and post-delivery plasmas than those of normal subjects. In addition, the concentrations of thrombin-heparin cofactor II decreased 3 to 5 days after delivery, reflecting the disappearance of the catalytically active dermatan sulfate elaborated by the placenta. Thus, heparin cofactor II normally inactivates thrombin in vivo, with its role increasing in conditions associated with high levels of heparin cofactor II and/or dermatan sulfate.

Adult↗