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Biomedical subjects

M Pan

Publications and source records attributed to M Pan.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Addison's disease in pregnancy: a report of six cases].

OBJECTIVE: To review six cases of pregnancy with Addison's disease at Obstetrics and Gynecology Hospital, Shanghai Medical University from 1949 to 1994. METHOD: This is a clinical retrospective analysis. Five of the 6 patients were treated with hormone replacement therapy, and the remaining one received no hormone treatment due to lack of symptoms during pregnancy and neglect of previous adrenal surgery by obstetricians. RESULTS: The patient received no treatment occurred Addisonian crisis and died soon after delivery. The other five patients had smooth course of delivery and postpartum period. CONCLUSIONS: Hormone replacement therapy is important for patients with Addison's disease in pregnancy especially for acute decompensation of adrenal function. Pregnant women with history of adrenal surgery should be monitored carefully even without any symptoms and hormone treatment is necessary. Vaginal delivery is encouraged unless there is obstetric indication.

Addison Disease↗
PubMed1995

Protein kinase C-dependent regulation of L-arginine transport activity in Caco-2 intestinal cells.

The regulation of plasma membrane L-arginine transport activity was investigated in differentiated and undifferentiated states of the human intestinal cell line, Caco-2. The sodium-independent, leucine-insensitive uptake of L-arginine measured in this study has been assigned by us previously to system y+ in Caco-2 cells. Treatment of cells with serum-free media containing epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), or the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA), stimulated system y+ arginine transport activity in Caco-2 cells. Transport upregulation by these growth factors or by TPA was blocked by cycloheximide or the PKC inhibitor chelerythrine. Arginine uptake was diminished during the course of differentiation, attributable to a reduction in the transport system y+ capacity (Vmax) with no change in apparent affinity (Km). TPA stimulated arginine uptake required at least 3 h of continual exposure, and increased the membrane's transport capacity (Vmax) in both undifferentiated and differentiated cells. TPA elevated the diminished transport Vmax of differentiated cells TPA to the elevated Vmax value associated with undifferentiated cells. We conclude that upregulation of arginine transport is part of a pleiotropic response to EGF/TGF alpha, and that this involves PKC and de novo synthesis of polypeptides associated with system y+ transport activity.

Alkaloids↗
PubMed1995

Differentiation- and protein kinase C-dependent regulation of alanine transport via system B.

The regulation of sodium-dependent L-alanine transport is described for the first time in intestinal cells. Substrate analogue inhibition patterns and Dixon analyses indicated that uptake occurred via transport system B, an epithelial cell variant of systems B0,+ and ASC. System B served > 95% of the Na(+)-dependent alanine uptake in both undifferentiated (2 days postpassaging) and differentiated (> 9 days postpassaging) states of the human Caco-2 cultured intestinal cell line. (Methylamino)isobutyric acid-inhibitable system A transport accounted for < 5% of total alanine uptake. System B activity was greater in undifferentiated cells compared with the differentiated state, and activity at any differentiation state was stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA). The maximal stimulation, determined by TPA dose-response/exposure time data, was attributable to a change in cell transport capacity (Vmax), with Km unaffected. The Vmax of system B was greater in 2-day-old cells (2.79 +/- 0.21 nmol min-1 mg of protein-1; Km = 164 +/- 26 microM alanine), decreasing to Vmax = 0.51 +/- 0.03 nmol min-1 mg of protein-1 (Km = 159 +/- 14 microM) in 9-day-old cells. Regardless of differentiation status, the sodium-activation Hill coefficient was 1.06 +/- 0.10, and the alanine passive diffusion permeability coefficient was 0.53 +/- 0.08 microliter min-1 mg of protein-1. Phorbol ester up-regulated the Vmax of system B in 2-day-old cells to Vmax = 6.32 +/- 0.37 nmol min-1 mg of protein-1 (Km = 169 +/- 18 microM), and in 9-day-old cells to Vmax = 1.42 +/- 0.05 nmole min-1 mg of protein-1 (Km = 180 +/- 10 microM). Phorbol ester stimulation of transport occurred after at least 6 h of continual exposure, and was blocked by the protein kinase C inhibitors chelerythrine or photoactivated calphostin C. Protein synthesis inhibitors cycloheximide and actinomycin D each blocked the phorbol ester up-regulation of system B activity. It is concluded that Caco-2 cells regulate carrier-mediated sodium-dependent transport of L-alanine by changing the membrane capacity to transport alanine via system B and that this regulation involves de novo protein synthesis under the control of protein kinase C.

Alanine↗
PubMed1995

Protein kinase C activation inhibits glutamate transport by endothelial cells.

The role of protein kinase C (PKC) in regulating endothelial cell glutamate transport was investigated. Glutamate transport studies were performed in confluent human umbilical vein endothelial cells which were treated with the phorbol ester 12-myristate 13-acetate (TPA, 0-1000 nM), a compound which directly activates PKC. TPA inhibited Na(+)-independent System xAG- glutamate transport by 70% but only slightly reduced Na(+)-dependent activity. The TPA-mediated reduction in transport activity was dose-dependent, beginning at 5 min and lasting for at least 24 hr. TPA inhibition of glutamate transport had two distinctive phases: an acute phase (< 1 hr, not affected by either cycloheximide or actinomycin D) in which TPA decreased System xAG- glutamate transporter affinity (TPA Km = 522 +/- 25 microM vs control Km = 329 +/- 85 microM, P < 0.01) but did not alter transporter capacity (TPA Vmax = 4426 +/- 230 pmole/mg/min vs control Vmax = 4535 +/- 750 pmole/mg/min, P = NS) and a chronic phase (4-24 hr) in which TPA inhibition of glutamate transport was due to a reduced transporter capacity (Vmax = 2895 +/- 570 pmole/mg/min) without altering transporter affinity (Km = 370 +/- 60 microM glutamate) and was abrogated by cycloheximide or actinomycin D. The protein kinase C inhibitor chelerythrine chloride abrogated TPA's inhibition effect in both the acute and chronic phases. These data indicate that protein kinase C activation decreases glutamate transport in human umbilical vein endothelial cells via protein synthesis dependent and independent mechanisms.

Biological Transport↗
PubMed1995

Tumor necrosis factor stimulates system XAG- transport activity in human endothelium.

System xAG- is responsible for the carrier-mediated Na(+)-independent transport of anionic amino acids such as glutamate and aspartate across the plasma membrane of cells. In order to examine a possible role for cytokines in regulating System xAG- activity, the effect of TNF on [3H]glutamate transport in cultured human umbilical vein endothelial cells (HUVECs) was studied. Carrier-mediated glutamate uptake was accomplished by two high-affinity carriers, predominantly by a Na(+)-independent carrier (System xAG-, 75% of total glutamate uptake) and, to a lesser extent by a Na(+)-dependent carrier (System XAG-, 24% of total uptake). TNF treatment (10 ng/ml for 10 hr) resulted in an 80% increase in Na(+)-independent glutamate transport activity with no change in System XAG- activity. The TNF stimulatory effect was blocked by actinomycin D and cycloheximide. TNF treatment increased System xAG- glutamate transporter Vmax by 51% (control Vmax = 2359 +/- 345 pmole/mg protein/min vs TNF Vmax = 3569 +/- 436 pmole/mg protein/min, P < 0.01) without altering transporter affinity (control Km, 229 +/- 40 microM glutamate vs TNF Km = 224 +/- 60 microM glutamate, P = NS). The protein kinase C (PKC) inhibitor chelerythrine chloride had no effect on the TNF-stimulated glutamate transport, indicating that the augmented glutamate transport was not mediated by PKC activation. These data indicate that the TNF-stimulated glutamate transport in HUVECs requires do novo protein synthesis, possibly of the System xAG- transporter protein itself. Accelerated glutamate transport provides a precursor for the biosynthesis of macromolecules and glutamine.

Biological Transport↗
PubMed1995

Balloon-expandable stent repair of severe coarctation of aorta.

Experimental studies have shown that stents implanted at the aorta become incorporated within the aortic wall and can be further expanded in growing animals. This study evaluates the feasibility and immediate results of balloon-expandable stent implantation in 10 patients with severe coarctation of aorta. The ages of the patients ranged from 1 month to 43 years; 1 was an infant, 8 were children (mean age 5.3 +/- 4 years), and 1 was an adult. All had an unfavorable anatomy for balloon angioplasty; 9 had isthmus hypoplasia. Balloon predilation was first performed and its immediate effect evaluated. Then a balloon-expandable stent that was 30 mm long and covered the isthmus and coarctation levels was deployed, and it was further expanded to the preselected final diameter (12 +/- 4 mm). A final hemodynamic and angiographic evaluation was then obtained. Full deployment of an incompletely expanded and distally displaced stent in the infant led to aortic disruption that was controlled by a second stent covering the disrupted zone and the isthmus. After balloon angioplasty alone was done, the mean gradient (43 +/- 12 vs 31 +/- 10 mm Hg) and the percentage stenosis (72% +/- 11% vs 54% +/- 11%) had an insufficient decrease. However, after stent implantation was done, the gradient almost disappeared (mean 2 +/- 3 mm Hg). The angiographic stenosis disappeared in 7 patients and was markedly reduced in 3. The ratio of isthmus/descending aorta changed from 0.65 +/- 0.14 to 1 +/- 0.08 (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1995

Follow-up patency of side branches covered by intracoronary Palmaz-Schatz stent.

To assess the risk of late side branch occlusion after Palmaz-Schatz stent deployment, we analyzed the angiographic evolution of 62 patients treated by successful stent implantation who had a total of 85 side branches starting from the stented segment. Side branches were considered minor (n = 39) when the diameter was < 1 mm and intermediate (n = 46) when the vessel had > or = 1 mm diameter. One angiographic follow-up study was available in all patients at 8 +/- 5 months. Eight minor branches presented some degree of stenosis at origin before stent deployment (4 totally occluded). After stent deployment, 32 (82%) of 39 remained unchanged and 3 became occluded. Late progression at origin occurred in 4 of 34 (3 occluded). Before stent deployment, 48% of the intermediate branches had some compromise degree at their starting point (1 totally occluded). Eight of 45 intermediate branches became occluded after stent implantation. Late progression at origin happened in 5 of 32 branches (2 occluded). Some degree of follow-up stenosis regression at the origin was observed in 22 (26%) of 85 arteries. Neither clinical nor angiographic factors could be identified as predictors of late side branch occlusion or stenosis progression at its origin. Later occlusion or progression at origin of a side branch covered by a Palmaz-Schatz stent seems to be an uncommon occurrence (7% and 12% respectively) that cannot be predicted by angiographic or clinical factors. On the contrary, regression at follow-up of a side branch-origin stenosis can also come about.

Adult↗
PubMed1995

TNF-stimulated arginine transport by human vascular endothelium requires activation of protein kinase C.

OBJECTIVE: The authors determined the endothelial arginine transport mechanism and the potential role of a tumor necrosis factor (TNF)-alpha-mediated signal transduction pathway involving protein kinase C (PKC) in regulating this transport in cultured endothelial cells. SUMMARY BACKGROUND DATA: The vascular endothelium metabolizes arginine to generate nitric oxide (NO), and an increase in NO production can be stimulated by several cytokines. The mechanism(s) responsible for the accelerated arginine transport are poorly understood. METHODS: Arginine transport was assayed in confluent human umbilical vein endothelial cells in the presence of TNF +/- the PKC inhibitor chelerythrine chloride. RESULTS: Carrier-mediated arginine transport was accomplished by two Na(+)-independent transporters, System y+ (80% of total transport) and System b0,+ (20% of transport). Tumor necrosis factor (0.1-2 ng/mL) increased System y(+)-mediated arginine transport in a time- and dose-dependent manner by augmenting System y+ transport maximal capacity (control Vmax = 1325 +/- 60 pmol/mg protein/minute vs. TNF Vmax = 3015 +/- 110 pmol/mg protein/minute, p < 0.01) without affecting transporter affinity (control Km = 30 +/- 1.4 microM vs. 34 +/- 1.3 microM arginine, p = NS). Stimulation was maximal at the 8-hour time point and was inhibited by both actinomycin D and cycloheximide. In addition, inhibition of PKC with chelerythrine abrogated the TNF-augmented arginine transport. Similarly, incubation of cells with the direct PKC activator TPA (phorbol ester 12-myristate 13-acetate) stimulated System y(+)-mediated arginine transport nearly fivefold, secondary to an increase in transporter Vmax (TPA Vmax = 5349 +/- 310 pmol/mg protein/minute, p < 0.001 vs. control), with no change in Km. This TPA-induced stimulation of arginine transport also was blocked by chelerythrine CI, actinomycin D, and cycloheximide. Incubation of TNF-stimulated cells with two NO synthase inhibitors did not reduce transport activity, suggesting that the arginine transporter and the NO synthase enzyme may, in part, be independently regulated.

Alkaloids↗
PubMed1995

Amino acid metabolism and the vascular endothelium: regulation and disease implications.

Amino acid metabolism by the vascular endothelium is a complex process that often begins with the carrier-mediated uptake of circulating amino acids into the endothelial cytoplasm. Amino acids are essential for maintaining intact endothelial functions, which include cell proliferation, regulation of blood flow and vascular tone, coagulation and fibrinolysis, and metabolism of a variety of macromolecules. The disturbances in endothelial amino acid transport and metabolism that occur during infection and inflammation are due, in part, to changes in substrate availability and to the local and/or systemic elaboration of specific mediators. An improved understanding of endothelial amino acid metabolism will not only provide new knowledge regarding disease mechanisms and regulation, but may also lead to new treatment strategies that may include the clinical use of specific nutritional formulas.

Amino Acid Sequence↗
PubMed1995

Regulation of system y+ arginine transport capacity in differentiating human intestinal Caco-2 cells.

This study describes the ability of passaged human intestinal Caco-2 cells to regulate transport of L-arginine via system y+. Subconfluent and confluent cells possessed system y+ activity, as determined by the sodium independence of uptake and the pattern of inhibition by amino acid analogues or N-ethylmaleimide. Initial rates of arginine uptake via system y+ decreased as the cells advanced from the undifferentiated to the differentiated state following culture passaging. Furthermore, kinetic analysis of the leucine-insensitive portion of uptake indicated that the Caco-2 system y+ transport capacity decreased with cell age, dropping from a maximal velocity (Vmax) = 1,094 pmol.mg-1.min-1 [Michaelis constant (Km) = 41 microM] in undifferentiated cells 2 days postseeding to Vmax = 320 pmol.mg-1.min-1 (Km = 37 microM) in confluent cells 9 days postseeding (from cells of the same passage). Northern analysis indicated that the levels of a single 7.9-kb mCAT-1 mRNA species were relatively constant over the course of Caco-2 differentiation and therefore were unsynchronized with the system y+ relative transport activities. It is concluded that the Caco-2 capacity to transport arginine via system y+ may be downregulated by posttransitional modifications in confluent cells compared with newly passaged undifferentiated cells. These data serve as a well-defined in vitro model for further studies regarding regulation of arginine transport in epithelial cells.

Amino Acids↗
PubMed1994

[Registry of activities of the Hemodynamics and Interventional Cardiology Section in 1993].

Results of the Spanish Registry for Interventional Cardiology 1993 are presented, as previous years, by the Section of Haemodinamics and Interventional Cardiology of Sociedad Española de Cardiología. There are 72 participating cardiac catheterization laboratories. That represents 100% of those laboratories who had activity in 1993, Public medicine (51 centers) and Private practice (21 centers). From those, 8 laboratories exclusively performed pediatric cases. There have been performed 47353 diagnostic procedures and 2647 endomiocardial biopsies. In diagnostic cases greater proportion corresponds to coronariography (37591, 75.2%). Therapeutic interventionalism is also accomplished in 61 laboratories, on which 7807 balloon PTCA, 535 coronary atherectomies, 825 mitral valvotomies were performed, and 503 endocoronary prostheses were implanted. Mean rate of coronary interventionalism was 222 procedures by a million of inhabitants. This activity represents approximately a 17% increase from 1992, in diagnostic as well interventional procedures. Results of therapeutic cases did not show any significant changes, balloon PTCA primary success rate is 91.5%, with an incidence of 4.2% of complications that includes 0.7% mortality rate.

Adult↗
PubMed1993

Factors determining late success after mitral balloon valvulotomy.

Mitral balloon valvulotomy (MBV) has proved to be an effective method in the treatment of patients with mitral stenosis. Although several factors determining an optimal immediate result have been described, there is little information regarding long-term follow-up, as well as factors influencing late success after MBV. This study analyzes 350 patients (mean age 46 +/- 12 years) treated by MBV who were clinically followed up between 6 months and 6 years. At least 1 echo-Doppler follow-up study was obtained in 298 patients 28 +/- 14 months after MBV; hemodynamic reevaluations were performed in 66 patients after 23 +/- months. Late success was considered if the patient was in functional class I to II and free of major events (death, restenosis and valve surgery). Restenosis was defined as a 50% loss of initial gain with regard to valve area by echocardiography, which was confirmed hemodynamically. After a mean follow-up of 38 +/- 15 months, 296 patients (84%) remained in functional class I to II, without surgery or the need for an increase in medical treatment. The 5-year Kaplan-Meier survival rate was 94 +/- 1%, whereas restenosis, valve surgery and major event-free probability were 90 +/- 3%, 91 +/- 2% and 85 +/- 2%, respectively. Multivariate study (Cox regression model) identified the presence of sinus rhythm (p < 0.001) and the absence of calcium at fluoroscopy (p < 0.003) as the only independent factors of late success.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Serial angiographic observations after successful directional coronary atherectomy.

This study focuses on the early and late angiographic evolution observed in 82 patients with coronary artery disease who were successfully treated by directional coronary atherectomy (DCA) without adjunctive balloon angioplasty. Qualitative inspections and quantitative measurements were obtained from a selected angled-view projection in the following conditions: (1) before treatment; (2) immediately after treatment; (3) the day after atherectomy; (4) 1 month after; and (5) 6 months after. The appearance of the treated segment 24 hours after the procedure did not differ in 79 patients from that observed immediately after DCA; silent total occlusion occurred in two patients, and one had an aneurysm at the site of resection (all three patients were excluded from the analysis). At the 1-month study restenosis developed in 3 (3.6%) patients; the remaining 76 had identical appearances, with no evidence of renarrowing of the lumen. However, from 1 to 6 months after the procedure restenosis developed in 35 of the remaining 76 (46%) patients, and 41 patients were free of restenosis and symptoms. These findings, which show that early elastic recoil does not occur after successful DCA, are different from the changes observed after balloon angioplasty. At the 1-month observation restenosis is an infrequent but possible phenomenon (3.8%). From this point the healing of the arterial wall leads to no or mild renarrowing (late success); an exaggerated proliferative response produces restenosis.

Adult↗
PubMed1993

Intracoronary ultrasound assessment of directional coronary atherectomy: immediate and follow-up findings.

OBJECTIVES: This study was conducted to assess the relations among intracoronary ultrasound, angiographic and histologic data obtained from patients with coronary artery disease successfully treated by directional coronary atherectomy. In addition, it was designed to elucidate whether some aspects of intravascular ultrasound or pathologic findings could predict a propensity to restenosis. BACKGROUND: Intracoronary ultrasound is a useful technique in guiding and assessing atherectomy. However, there is little information about the characterization of the different types of coronary plaques and the changes observed in them after resection. Furthermore, the follow-up ultrasound appearance of previously treated lesions remains undepicted. METHODS: Fifty-two patients (54 +/- 10 years old) were studied. All were successfully treated by atherectomy with the aid of intracoronary ultrasound guidance. Qualitative and quantitative ultrasound and angiographic variables were derived before and after resection. Quantitative histologic morphometric information was also obtained from the specimens. In 22 patients, a follow-up echoangiographic reevaluation was performed 6 +/- 4 months later. RESULTS: Echogenic plaques had a higher collagen and calcium content, whereas echolucent plaques had an increased level of fibrin, nuclei and lipids. Ultrasound plaque reduction after atherectomy was greater in echolucent (76 +/- 21%) than in echogenic plaques (60 +/- 18%; p < 0.05). That reduction correlated with the weight of the resected material (r = 0.62; p < 0.01). At follow-up study, 13 of 22 patients had angiographic and ultrasound evidence of restenosis. Most recurrent lesions had a stenotic three-layer appearance. The incidence of restenosis of primary lesions treated with atherectomy was higher in echolucent (100%) than in echogenic (33%) plaques. Similarly, a higher proportion of nuclear content in the resected material was observed in patients who developed restenosis (2.1 +/- 0.7%) than in patients who had late success after atherectomy (1.2 +/- 0.6%). CONCLUSIONS: Our findings suggest that echolucent plaques are easier to resect than are echogenic plaques but frequently develop restenosis. In contrast, the resection of echogenic plaques, although often incomplete, is associated with better long-term results.

Atherectomy, Coronary↗