Biomedical subjects

L Y Chen

Publications and source records attributed to L Y Chen.

At least 73 records · Page 4Linked to original sources

PubMed1998

Developmental profile of a caltrin-like protease inhibitor, P12, in mouse seminal vesicle and characterization of its binding sites on sperm surface.

We examined the developmental profile of a kazal-type trypsin inhibitor (P12) of Mr 6126 in mouse seminal vesicle, characterized its binding sites on the surface of sperm, and assessed its effect on Ca2+ uptake by spermatozoa. Among the genital tracts of adult mice, P12 was found only in the male accessory glands including seminal vesicle, coagulating gland, and prostate. It was immunolocalized on the luminal epithelium of the primary and secondary folds in both the seminal vesicle and coagulating gland, and on the folds projecting into the lumen of the glandular alveolus in the prostate. The protein and its RNA message in seminal vesicle did not appear in the prepubertal period, but expression coincided with maturation. Castration of adult mice resulted in cessation of P12 expression. Treatment of the castrated mice with testosterone propionate in corn oil restored the protein expression in the seminal vesicle. Spermatozoa collected from caudal epididymis were devoid of P12. Cytochemical study illustrated a P12-binding region on the anterior acrosomes of cells preincubated with P12. Analysis of equilibrium data from the binding assay using 125I-P12 with a Scatchard plot showed a single type of P12-binding sites on sperm, with an apparent dissociation constant of 70.15 +/- 5.25 nM and the capacity of 1.49 +/- 0.06 x 10(6) binding sites/cell. The protein could serve as a calcium transport inhibitor to suppress a great extent of Ca2+ uptake by spermatozoa. The immunohistochemical staining patterns of testis revealed that the P12-binding sites appeared on postmeiotic cells such as spermatids and spermatozoa, but were absent in Leydig cells, Sertoli cells, spermatogonia, and spermatocytes in seminiferous tubules.

Animals↗

PubMed1998

Evidence for the presence of L-arginine-nitric oxide pathway in human red blood cells: relevance in the effects of red blood cells on platelet function.

There is a renewed interest in the role of red blood cells (RBCs) in the regulation of vascular tone and platelet homeostasis. To examine whether human RBCs synthesize NO from L-arginine, which may mediate the antiplatelet effects of these cells, purified RBCs (10(7)-10(8)/ml) were incubated with [3H]L-arginine, and its conversion into [3H]L-citrulline determined. RBCs consistently converted [3H]L-arginine to [3H]L-citrulline in a Ca2+-dependent fashion, and this conversion was inhibited by two different specific NO synthase inhibitors. Suspension of RBCs (10(7)-10(8)/ml) reduced platelet aggregation, and the RBC-mediated inhibition of platelet aggregation was blocked by pretreatment of RBCs with NO synthase inhibitor and potentiated by pretreatment with superoxide dismutase. Release of serotonin by aggregating platelets also was inhibited in the presence of RBCs. Western analysis with a specific mouse monoclonal antibody provided direct evidence for the presence of human endothelium-type constitutive NO synthase with a molecular mass approximately 140 kDa in the RBC cytosol. These observations suggest that RBCs possess endothelium-type NO synthase and may regulate platelet function at least in part by in situ release of NO.

Animals↗

PubMed1998

[Pupillary responses evoked by spatial patterns].

Human pupillary responses evoked by visual spatial patterns were investigated. Experimental data revealed that: (1) pupillary constriction can be induced not only by increment of luminance but also by change of gratings or checkerboards without change of space-averaged luminance; (2) constriction amplitude increases with increasing difference of spatial frequency; (3) pupillary response can be evoked by changing from uniform brightness to checkerboard patterns or from checkerboard to darkness, without any increment of the local luminance. These results indicate that the human pupillary response system is not merely controlled by luminous flux but also receives and processes visual pattern information.

Evoked Potentials, Visual↗

PubMed1998

Cleidocranial dysplasia: a rare case associated with congenital hypothyroidism and severe neonatal hyperbilirubinemia.

Cleidocranial dysplasia is an autosomal dominant disorder affecting skeletal ossification and tooth development. This disorder can be rarely associated with blood, intestinal and vascular anomalies. There has been no case reported in previous literature that discusses this disorder in association with congenital hypothyroidism and severe neonatal hyperbilirubinemia. Herein, we report on a 4-year-old boy who in an outpatient clinic was diagnosed as having cleidocranial dysplasia, with defective ossification over bilateral hypoplastic clavicles, narrowed thoracic cage on chest x-ray and prominent wormian bones over the lambdoid sutures on skull x-ray. Physical examination revealed a 4-fb wide open anterial fontanel, frontal bossing and malalignment of teeth. He was a primpara with birth weight of 2350 gm and gestation age of 33 weeks. He had received blood exchange transfusion on the 4th postnatal day at Ping-Tong Christian Hospital because of severe neonatal hyperbilirubinemia. Congenital hypothyroidism was diagnosed on the 10th day. He was then treated with thyroxine and transferred to our hospital. Thyroid scan revealed diffusely decreased radioactivity in bilateral lobes of the thyroid gland. According to out clinic findings at his regular follow ups, with continued use of thyroxine supplement, he now has a normal thyroid function and has a body length of about 50 percentile.

Child, Preschool↗

PubMed1997

A role for Ras signaling in coreceptor regulation during differentiation of a double-positive thymocyte cell line.

Evidence suggests that the Ras/mitogen-activated protein kinase signaling pathway is required for positive selection of thymocytes. We have asked whether Ras activation is also sufficient to mediate changes in gene expression that are associated with positive selection. To accomplish this, we expressed a constitutively active form of Ras in the immature CD4+ 8+ DPK thymocyte cell line. DPK cells that express active Ras have reduced levels of CD8alpha and CD8beta at the level of cell surface protein and mRNA. These data provide evidence of a direct link between Ras signaling pathways and coreceptor regulation during positive selection. They also suggest that a sustained or potent Ras signal may play a critical role in directing thymocytes into the CD4 lineage. DPK cells that express active Ras, however, were not fully differentiated, indicating that Ras signaling provides only a partial signal for double-positive thymocyte differentiation.

Animals↗

PubMed1997

Lead exposure causes generation of reactive oxygen species and functional impairment in rat sperm.

The relationships between blood lead, sperm lead, sperm reactive oxygen species (ROS) level, and sperm fertile capability were investigated to understand the effects of lead exposure on sperm function and the mechanism of these effects. Male Sprague-Dawley rats, 7 weeks old, were randomly divided into control group and lead-treated group. The controls and lead-treated animals received intraperitoneal injection of 10 mg sodium acetate and 10 mg lead acetate/kg body weight, respectively, weekly for 6 or 9 weeks. The blood lead and epididymal sperm lead were analyzed by graphite furnace atomic absorption spectrophotometer. Chemiluminescence was measured to evaluate the generation of sperm ROS. Sperm-oocyte penetration rate (SOPR) was measured to evaluate sperm function. After 6 weeks of lead exposure, the rats had average blood lead levels of 32 microg/dl, sperm lead levels of 0.67 +/- 0.11 microg/10(9) sperm, unchanged epididymal sperm counts, percent of motile sperms, and motile epididymal sperm counts compared with control animals. However, after 9 weeks of lead exposure, the rats had average blood lead levels of 48.0 +/- 4.3 microg/dl, sperm lead levels of 0.88 +/- 0.16 microg/10(9) sperm, statistically lower epididymal sperm counts, and lower motile epididymal sperm counts. There was a good correlation between the blood lead and sperm lead(r2 = 0.946, P < 0.001). The sperms of lead-exposed rats produced significantly higher counts ofchemiluminescence than did those from the control rats (P < 0.001). The chemiluminescence counts were positively associated with sperm lead level (r2 = 0.613, P < 0.001). Epididymal sperm counts, motility and motile epididymal sperm counts were negatively associated with sperm chemiluminescence (r2 = 0.255, 0.152, and 0.299; P < 0.01, 0.05, and 0.01, respectively). The SOPR were positively associated with epididymal sperm counts, motility and motile epididymal sperm counts (r2 = 0.136, 0.285, and 0.264; P < 0.05, 0.01, and 0.001, respectively). The sperm chemiluminescence was negatively associated with SOPR (r2 = 0.519, P < 0.001). It is concluded that lead exposure probably affected the sperm function by activating one of the pathways of ROS generation.

Animals↗

PubMed1997

Induction of the early growth response (Egr) family of transcription factors during thymic selection.

There is little known about the regulation of gene expression during TCR-mediated differentiation of immature CD4+8+ (double positive) thymocytes into mature T cells. Using the DPK CD4+8+ thymocyte precursor cell line, we demonstrate that the early growth response-1 gene (Erg-1), encoding a zinc finger transcription factor, is rapidly upregulated after TCR stimulation. We also report that Egr-1 is expressed by a subset of normal double positive thymocytes in the thymic cortex, as well by a majority of medullary single positive thymocytes. Expression of Egr-1 is dramatically reduced in the thymus of major histocompatibility complex knockout mice, but can be induced by anti-CD3 antibody stimulation of isolated thymocytes from these animals. These and other data suggest that high level expression of Egr-1 in the thymus is a consequence of selection. A similar pattern of expression is found for family members Egr-2 and Egr-3. Using the DPK cell line, we also demonstrate that expression of Egr-1, 2, and 3 is dependent upon ras activation, as is the initiation of differentiation to a single positive cell. In contrast, the calcineurin inhibitor cyclosporin A, which inhibits DPK cell differentiation as well as positive selection, inhibits expression of Egr-2 and Egr-3, but not Egr-1. The identification of the Egr family in this context represents the first report of a link between the two known signaling pathways involved in positive selection and downstream transcriptional regulators.

Animals↗

PubMed1997

Reperfusion injury in the endotoxin-treated rat heart: reevaluation of the role of nitric oxide.

1. The role of nitric oxide (NO) in ischaemia-reperfusion injury to the heart continues to be debated. 2. The role of NO released during endotoxemia on myocardial reperfusion injury was examined in rats given saline or lipopolysaccharide (LPS, 10 mg. kg-1). 3. Aortic rings from LPS-treated rats showed a markedly decreased contractile response to both noradrenaline (NA) and U46619, and a diminished relaxation response to acetylcholine, thrombin and aggregating platelets. Treatment of rat aortic rings from LPS-treated rats with the NO synthesis inhibitor N omega-nitro-L-arginine (L-NOARG) reversed the diminished contractile response to NE and U46619. 4. Before ischaemia-reperfusion, baseline force of cardiac contraction (FCC) and coronary perfusion pressure (CPP) were lower and coronary flow was higher in hearts from LPS-treated rats (all P < 0.05 vs. saline-treated group). Treatment of hearts from LPS-treated rats with L-NOARG increased baseline FCC and CPP. 5. After ischaemia-reperfusion, hearts from saline-treated rats showed a 36 +/- 5% fall in FCC, a 38 +/- 6% rise in CPP and a 38 +/- 5% fall in coronary flow, whereas hearts from LPS-treated rats revealed only a 16 +/- 9% fall in FCC, a 10 +/- 3% rise in CPP and a 20 +/- 4% fall in coronary flow (all P < 0.05 vs. changes in saline-treated group). Fewer hearts from LPS-treated rats developed reperfusion arrhythmias (6% vs. 60% hearts from saline-treated rats, P < 0.02). Myocardial superoxide dismutase activity was higher in the LPS-treated group (P < 0.05). 6. NO synthesis, measured as formation of nitrite, was higher (P < 0.05) in cardiac and aortic tissues from LPS-treated rats. Prostacyclin (PGI2) release in coronary effluent was greater in LPS-treated rat hearts (P < 0.05 vs. saline-treated rats). 7. Thus LPS-treated hearts demonstrate a basal decrease in FCC and coronary vascular resistance. These hearts demonstrate a modest protection from reperfusion injury. Induction of NO synthesis, and possibly PGI2 release, may underlie cardioprotection from ischaemia-reperfusion.

Animals↗

PubMed1997

A crossover comparison of intermittent oral and intravenous administration of calcitriol on the parathyroid hormone concentration in hemodialysis patients.

Active vitamin D3 is used commonly in hemodialysis patients with severe secondary hyperparathyroidism. Intermittent pulse therapy with active vitamin D3, either orally or intravenously, has been proven to be effective with less hypercalcemic complication than daily oral vitamin D3. We therefore designed a three-phase crossover study to compare the effect of oral and intravenous calcitriol given by intermittent pulse therapy. Thirteen regular hemodialysis patients were enrolled. In phase 1, 1 microgram calcitriol was given orally at bedtime twice a week for 4 months, and then was stopped for 1 month to washout. In phase 2, 1 microgram calcitriol was given intravenously immediately after hemodialysis twice a week for 2 months, and then was stopped for 1 month to washout. Phase 3 repeated phase 1 but lasted for only 2 months. Calcium carbonate was given as the sole phosphate-binding agent if there was no severe hypercalcemia or hyperphosphatemia. Serum parathyroid hormone (PTH) levels decreased dramatically in all three phase therapies. As a result, mid-molecule PTH decreased from 5.71 +/- 2.65 to 3.97 +/- 2.92 ng/ml in phase 1 (p = 0.010), from 4.34 +/- 3.39 to 1.98 +/- 1.76 ng/ml in phase 2 (p = 0.007), and from 2.72 +/- 0.97 to 1.67 +/- 0.71 ng/ml in phase 3 (p = < 0.001). However, there was no difference in the calculation of the PTH declination among the three phases (32, 50 and 42%, respectively). The incidence of hypercalcemia was higher in using calcitriol than without it (23 vs. 6%, p < 0.05), but there was no difference between intravenous and oral calcitriol (35 vs. 19%). The above results suggested that both oral and intravenous calcitriol, with lower doses and intermittent pulse therapy, were equally effective in controlling secondary hyperparathyroidism. The incidences of hypercalcemia were similar in both oral and intravenous calcitriol using 3.5 mEq/1 dialysate calcium concentration and calcium carbonate as the chief phosphate binder.

Administration, Oral↗

PubMed1997

Downregulation of nitric oxide synthase activity in human platelets by nitroglycerin and authentic nitric oxide.

BACKGROUND: Besides endothelial cells, platelets possess active nitric oxide synthase (NOS) enzyme, which converts L-arginine to NO and L-citrulline. Nitroglycerin (NTG) inhibits platelet aggregation by increasing intracellular cGMP levels, an effect similar to that of NO. In this study we examined the regulation of platelet NOS activity by NTG and authentic NO. METHODS AND RESULTS: Nitric oxide synthase activity was measured as formation of L-citrulline from L-arginine. As expected, incubation of platelet-rich plasma with NTG resulted in a concentration-dependent (40-400 mumol/L) increase in nitrite levels and an increase in cGMP accumulation. Concurrently, NTG was found to exert an inhibitory effect on platelet NOS activity. Exposure of washed platelets to authentic NO also resulted in approximately 50% decrease in NOS activity. Western analysis showed that NTG and authentic NO had no effect on NOS protein expression in human platelets. CONCLUSIONS: This study indicates that NO, either authentic or derived from NTG, decreases NOS activity without affecting NOS protein expression in human platelets. The downregulation of NOS activity may have a bearing on the phenomenon of nitrate tolerance.

Blood Platelets↗

PubMed1997

Measurement of the radiation doses absorbed by jaw bones during irradiation of nasopharyngeal cancers.

BACKGROUND: Nasopharyngeal carcinoma (NPC) occurs more frequently for Chinese than for other ethnic groups. The most common treatment for NPC is radiotherapy, but there is no report of the doses of radiation absorbed by the mandibular and maxillary bones, although exposure to radiation is one of the most important references for those patients who need to have oral surgical treatments. METHODS: Thermoluminescent dosimeter (TLD) was used to measure radiation absorbed by a rando phantom and cancer patients. RESULTS: The results showed that the doses absorbed by the mandible and maxilla depend on the dose applied, field size, and field shape. In the rando phantom, the range of absorption in the mandible was, for the central incisor 1.89-3.36 Gy, canine 1.96-3.78 Gy, bicuspid 2.24-14.14 Gy, second molar 4.34-31.92 Gy, internal pterygoid muscle region 70 Gy. In the maxilla the range was, for the central incisor 2.17-2.94 Gy, canine 2.24-3.36 Gy, bicuspid 3.15-4.41 Gy, second molar 7.00-7.42 Gy. In nasopharyngeal carcinoma patients, the mean radiation absorbed by the bicuspid vestibular region of the mandible was 3.09 Gy, by the bicuspid vestibule of the maxilla 3.35 Gy and by the midline vestibule 2.31 Gy. The radiation doses absorbed by maxilla and mandible from the incisor to the second premolars were less than 20% of the dose to the primary tumor. CONCLUSIONS: The doses absorbed by the mandible and maxilla are relatively low in NPC patients receiving radiation therapy.

Adult↗

PubMed1996

Identification of a fungal protein of Syncephalastrum racemosum as aspartic proteinase.

During purification of fungal deoxyribonuclease (DNase) from Syncephalastrum racemosum, a protein which was functionally unknown and persistently existed in the DNase-containing fractions through chromatography over DEAE-cellulose, hydroxylapatite, and phenyl-Sepharose was identified. The protein was finally separated from DNase after affinity chromatography on a cibacron blue-Sepharose column and purified to apparent homogeneity after gel chromatography on a Superdex 200 HR column. Ten tryptic peptides of this protein were isolated and sequenced. Searching in the sequence data bank with the aid of the computer program PC/Gene, we found that this protein was highly homologous to aspartic proteinases, such as pepsin and rhizopuspepsin. Because of its fungal origin and because the protein indeed showed catalytic cleavage on peptide bonds of bovine serum albumin, RNase, and carbonic anhydrase, we termed this protein syncephapepsin. The molecular weight of syncephapepsin is 38,000 daltons, based on gel filtration and sodium dodecyl sulfate-polyacrylamide electrophoresis.

Amino Acid Sequence↗

PubMed1996

Oxidized LDL decreases L-arginine uptake and nitric oxide synthase protein expression in human platelets: relevance of the effect of oxidized LDL on platelet function.

BACKGROUND: Oxidized LDL (ox-LDL) promotes vasoconstriction and platelet activation. The present study was undertaken to determine the involvement of the L-arginine-nitric oxide (NO) pathway in ox-LDL-mediated platelet activation. METHODS AND RESULTS: Washed human platelets were incubated with native LDL or ox-LDL for 1 hour at 37 degrees C followed by measurement of platelet function and indexes of the L-arginine-NO pathway. Ox-LDL but not native LDL caused a concentration-dependent increase in thrombin-induced platelet aggregation and 14C-serotonin release. These effects of ox-LDL were inhibited by pretreatment of platelets with L-arginine, the precursor of NO. Ox-LDL also caused a concentration-dependent reduction in the uptake of 3H-L-arginine by platelets. In addition, NO synthase activity, measured as conversion of 3H-L-arginine to 3H-L-citrulline, decreased on incubation of platelet cytosol with ox-LDL. Nitrite production was also reduced by treatment of platelets with ox-LDL. These effects of ox-LDL on NO synthase activity and nitrite production were reversed by pretreatment of platelets with L-arginine. Concurrent with the decrease in NO production, cytosolic cGMP was inhibited in ox-LDL-treated platelets. The inhibitory effects of ox-LDL were dependent in part on the increase of cholesterol in the platelets. Western blot analysis demonstrated approximately 50% reduction in the expression of NO synthase protein in platelets treated with ox-LDL. CONCLUSIONS: These observations indicate that the L-arginine-NO pathway is involved in the effects of ox-LDL on platelet function and that ox-LDL stimulates platelet function primarily by diminishing NO synthase expression as well as decreasing the uptake of L-arginine.

Arginine↗

PubMed1996

XpsD, an outer membrane protein required for protein secretion by Xanthomonas campestris pv. campestris, forms a multimer.

XpsD is an outer membrane lipoprotein, required for the secretion of extracellular enzymes by Xanthomonas campestris pv. campestris. Our previous studies indicated that when the xpsD gene was interrupted by transposon Tn5, extracellular enzymes were accumulated in the periplasm (Hu, N.-T., Hung, M.-N., Chiou, S.-J., Tang, F., Chiang, D.-C. Huang, H.-Y. and Wu, C.-Y. (1992) J. Bacteriol. 174, 2679-2687). In this study, we constructed a series of substitutions and deletion mutant xpsD genes to investigate the roles of NH2- and COOH-terminal halves of XpsD in protein secretory function. Among these secretion defective xpsD mutations, one group (encoded by pCD105, pYLA, pKdA6, and pKD2) caused secretion interference when co-expressed with wild type xpsD, but the other (encoded by pMH7, pKdPs, and pKDT) did not. Cross-linking studies and gel filtration chromatography analysis indicated that the wild type XpsD protein forms a multimer in its native state. Similar gel filtration analysis of xpsD mutants revealed positive correlations between multimer formation and secretion interfering properties exerted by the mutant XpsD proteins in the parental strain XC1701. Those mutant XpsD proteins (encoded by pCD105, pYL4, pKdA6, and pKD2) that caused secretion interference formed multimers that are similar to the wild type XpsD multimers and those (encoded by pMH7, pKdPs, and pKDT) that did not formed smaller ones. Furthermore, gel filtration and anion exchange chromatography analyses indicated that the wild type XpsD protein co-fractionated with XpsD (delta 29-428) or XpsD (delta 448-650) protein but not with XpsD (delta 74-303) or XpsD (delta 553-759) protein. We propose that the mutant XpsD (delta 29-428) protein caused secretion interference primarily by forming mixed nonfunctional multimers with the wild type XpsD protein in XC1701 (pCD105), whereas the mutant XpsD (delta 74-303) did so by competing for unknown factor(s) in XC1701(pYL4).

Bacterial Outer Membrane Proteins↗

PubMed1996

Reversal by high-density lipoprotein of the effect of oxidized low-density lipoprotein on nitric oxide synthase protein expression in human platelets.

Oxidized low-density lipoproteins (ox-LDLs) induce vasoconstriction and platelet activation, and high-density lipoproteins (HDLs) reverse these effects of ox-LDL. To determine the involvement of the L-arginine-nitric oxide (NO) pathway in the effects of lipoproteins on platelets, washed human platelets were incubated with native-LDL, ox-LDL, or HDL plus ox-LDL, but not native LDL, potentiated thrombin-induced platelet aggregation and carbon 14-labeled serotonin release, and these effects of ox-LDL were blocked by pretreatment of platelets with HDL. Incubation of ox-LDL with platelets resulted in reduction in the uptake of tritiated L-arginine by intact platelets and in NO synthase activity in platelet lysate. These effects of ox-LDL on platelet NO synthase activity were also reversed by pretreatment of platelets with HDL. Western blot analysis demonstrated about a 50% reduction in the expression of NO synthase protein in platelets treated with ox-LDL. Whereas HDL alone had no effect on NO synthase protein expression, it blocked the decrease in NO synthase expression caused by ox-LDL. Thus ox-LDL stimulates platelet function primarily by diminishing NO synthase expression, and this effect of ox-LDL can be blocked by pretreatment of platelets with HDL.

Arginine↗

PubMed1996

Further evidence of the presence of constitutive and inducible nitric oxide synthase isoforms in human platelets.

Previous studies have suggested the presence of nitric oxide synthase (NOS) enzyme in human platelets. We herein provide definitive evidence for the presence of both endothelial constitutive NOS (ecNOS) and inducible NOS (iNOS) isoforms and their mRNA in human platelets. Total RNA was isolated from human platelets, and reverse-transcription polymerase chain reaction (RT-PCR) demonstrated the expression of the ecNOS and iNOS isoforms in platelets. High-stringency Southern analysis confirmed the molecular authenticity of the RT-PCR products for each NOS isoform. Western analysis with mouse monoclonal antibody against human ecNOS consistently demonstrated a band with a molecular weight of 140-150 kDa. Western analysis with mouse monoclonal antibody against rat macrophage iNOS showed a single 200-kDa band in both resting and lipopolysaccharide (LPS)-plus interferon-gamma (IFN-gamma)-stimulated platelets. Immunoprecipitation further confirmed the presence of the 200-kDa iNOS band. Expression of iNOS protein, measured with densitometry, was increased in LPS- and IFN-gamma-stimulated platelets (p < 0.01 vs. resting platelets). Thus, human platelets possess both ecNOS and iNOS isoforms and their mRNA, and iNOS exhibits molecular weight and kinetic characteristics distinct from those of ecNOS.

Adult↗

PubMed1996

Recombinant lys-plasminogen given before, but not after, recombinant tissue-type plasminogen activator markedly improves coronary thrombolysis in dogs: relationship of thrombolytic efficacy with parameters of fibrinolysis.

Recombinant tissue-type plasminogen activator (rt-PA) administration rapidly restores blood flow in thrombosed coronary arteries, but coronary arteries often reocclude after initial thrombolysis. This occurs because of the short half-life of rt-PA and rapid increase in plasminogen activator inhibitor (PAI-1) and alpha2-antiplasmin levels in plasma. We hypothesized that administration of lys-plasminogen, which binds to fibrin with 10 times greater affinity and results in a loose fibrin structure (as compared with native glu-plasminogen), before rt-PA would enhance the thrombolytic efficacy of rt-PA and modulate parameters of fibrinolysis. To examine this hypothesis, dogs with electrically induced stable thrombus in the left anterior descending coronary artery (LAD) were treated with saline (group A, n = 9) or lys-plasminogen (group B, 2 mg/kg, n = 5), followed 10 min later by rt-PA (1 mg/kg in 20 min). Four other dogs with occlusive LAD thrombus were first given rt-PA, followed by lys-plasminogen (2 mg/kg) 50 min later (group C). Lys-plasminogen given before rt-PA restored flow in all dogs in 14 +/- 4 min (vs. 22 +/- 9 min in group A, p < 0.05), continuing > 2 h (vs. 41 +/- 15 min in group A, p < 0.02). Lys-plasminogen given after rt-PA did not potentiate the effect of rt-PA. Plasma t-PA antigen concentrations were highest in group B dogs at 2 h after rt-PA infusion. PAI-1 and alpha2-antiplasmin plasma levels were suppressed in all dogs receiving lys-plasminogen whether it was given before or after rt-PA. Therefore, lys-plasminogen given before rt-PA markedly potentiates the effect of rt-PA and alters the parameters of fibrinolysis. In contrast, lys-plasminogen given after rt-PA does not influence the thrombolytic effect of rt-PA, whereas it suppresses PAI-1 and alpha2-antiplasmin levels in plasma. This study also suggests that binding of plasminogen to the clot is more important than the plasma levels of PAI-1 and alpha2-antiplasmin.

Animals↗

PubMed1996

Imaging approach to the diagnosis of pulmonary sequestration.

PURPOSE: To describe the characteristic features of pulmonary sequestration (PS), to evaluate the usefulness of various imaging modalities, and to find a rational approach to accurate diagnosis. MATERIAL AND METHODS: Twenty-four patients with PS proved by operation and pathology were reviewed retrospectively. Plain chest films were done in all patients, bronchography in 3, sonography in 14, CT in 6 (including CT angiography in 1 case), MR in 8 (including MR angiography in 1 case) and aortography in 12 (including DSA in 1 case). RESULTS: Plain chest films demonstrated a solid mass in 14 patients and a cystic mass in 10. Bronchograms showed displacement of adjacent bronchi with no filling of contrast medium within the lesion in 2 cases, while another case had a blind intermediate portion of the right bronchus (hypoplasia of middle and lower lobes associated with extralobar sequestration). Sonography demonstrated a solid lung mass in 12 cases and a solid mass with cystic areas in 2, and detected vessel-like structures within the mass or in its surroundings in 12. Doppler analysis showed arterial spectral wave confirming a feeding artery. CT revealed a solid mass in all patients, a mass with low density area in 4, and emphysema surrounding the mass in 3. MR imaging depicted anomalous arteries in all patients and venous drainage in 4 cases. Aortography demonstrated anomalous systemic arterial supply to the PS in all patients. In this series, 21 cases (87.5%) were correctly diagnosed preoperatively by the imaging modalities. CONCLUSION: Plain chest films can provide a diagnostic clue to PS. Sonography, CT and MR are helpful for showing arterial blood supply and for making a definite diagnosis. We recommend a rational imaging approach for the diagnosis of PS.

Adolescent↗