Coral communities of the remote atoll reefs in the Nansha Islands, southern South China Sea.

During the months of May and June in the year 2007, a survey was conducted regarding coral reef communities in the remote atolls (Zhubi Reef and Meiji Reef) of Nansha Islands, southern South China Sea. The goals of the survey were to: (1) for the first time, compile a scleractinian coral check-list; (2) estimate the total richness, coral cover, and growth forms of the community; and (3) describe preliminary patterns of community structure according to geomorphological units. Findings of this survey revealed a total of 120 species of scleractinia belonging to 40 genera, while the average coral cover was 21 %, ranging from less than 10 % to higher than 50 %. Branching and massive corals were also found to be the most important growth forms of the whole coral community, while Acropora, Montipora, and Porites were the three dominant genera in the overall region, with their contributions to total coral cover measuring 21, 22, and 23 %, respectively. Overall, coral communities of the Nansha Islands were in a relative healthy condition with high species diversity and coral cover. Spatial pattern of coral communities existed among various geomorphological units. Mean coral cover was highest in the patch reef within the lagoon, followed by the fore reef slope, reef flat, and lagoon slope. The greatest contributors to total coral cover were branching Acropora (45 %) in the lagoon slope, branching Montipora (44 %) in the reef flat, and massive Porites (51 %) in the patch reef. Coral cover in the fore reef revealed a greater range of genera than in other habitats. The leeward fore reef slope had higher coral cover (> 50 %) when compared with the windward slope (< 10 %). The coral communities of the inner reef flat were characterized by higher coral cover (27 %) and dominant branching Montipora corals, while lower coral cover (4 %) was dominated by Psammocora with massive growth forms on the outer reef flat. Destructive fishing and coral bleaching were two major threats to coral communities in the study area.

Effects of tumour necrosis factor-alpha on activity and nitric oxide synthase of endothelial progenitor cells from peripheral blood.

The aim of this investigation was to determine whether tumour necrosis factor-alpha (TNF-α) has any effect on endothelial progenitor cells (EPCs). Total mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days culture, attached cells were stimulated with tumour necrosis factor-α (final concentrations: 0, 10, 20, 50 and 100 mg/l) for 0, 6, 12, 24 and 48 h. EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding, by direct fluorescence staining. EPC proliferation and migration were assayed using the MTT assay and modified Boyden chamber assay, respectively. EPC adhesion assay was performed by re-plating those cells on fibronectin-coated dishes, and adherent cells were counted. Tube formation activity was assayed using a tube formation kit. Levels of apoptosis were revealed using an annexin V apoptosis detection kit. Vascular endothelial growth factor Receptor-1 (VEGF-R1) and stromal derived factor-1 (SDF-1) mRNA, assessed by real-time RT-PCR inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) were assayed by western blot analysis. Incubation of EPCs with tumour necrosis factor-α reduced EPC proliferation, migration, adhesion, tube formation capacity, iNOS and eNOS in concentration- and time-dependent manners. Tumour necrosis factor-α reduced proliferation, migration, adhesion and tube formation capacity of EPCs. TNF-α increased EPC apoptosis level, reduced VEGF-R1 and SDF-1 mRNA expression; tumour necrosis factor-α also reduced iNOS and eNOS in the EPCs.

Effects of rapamycin on number activity and eNOS of endothelial progenitor cells from peripheral blood.

The aim of this investigation is to determine whether rapamycin treatment has any effect on endothelial progenitor cells (EPCs). Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7 days in culture, attached cells were stimulated with rapamycin (in a series of final concentrations: 0.1, 1.0, 2.0 and 5.0 g/ml) for 6, 12, 24 and 48 h. EPCs were characterized as adherent cells, double positive for DiLDL uptake and lectin binding by direct fluorescence staining. EPC proliferation and migration were determined using the MTT assay and a modified version of the Boyden chamber assay, respectively. An EPC adhesion assay was performed by replating the cells on fibronectin-coated dishes; adherent cells were then counted. Tube formation activity was assayed by using a tube formation assay kit and endothelial nitric oxide synthase (eNOS) was assayed by Western blot analysis. Incubation of isolated human MNCs with rapamycin decreased the number of EPCs present; rapamycin also decreased EPCs proliferative, migratory, adhesive, tube formation capacity and eNOS production in a concentration- and time-dependent manner. Rapamycin was found to decrease the number, proliferative, migratory, adhesive and tube formation capacities of the EPCs, and also was found to decreases eNOS in the EPCs.

Modulation of cytochrome P-450 dependent monooxygenases in streptozotocin-induced diabetic hamster: I. Effects of propofol on defluorination and cytochrome P-450 activities.

BACKGROUND: Diabetes mellitus could induce polymorphic alterations of metabolic activities of cytochrome P-450 dependent monooxygenases in chemical-induced diabetic animals. The purpose of this study is to define the functional impact of clinical concentrations of propofol on the metabolic activities of cytochrome P-450 in the diabetic animals. METHODS: In order to validate the effect of propofol on cytochrome P-450 activities, especially the cytochrome P-450 2E1 and its defluorination activity, we applied NADPH-generating system to measure the metabolizing activities of cytochrome P-450 isozymes of streptozotocin-induced diabetic hamsters within the microsomes preincubated with various concentrations of propofol. The extent of defluorination and activity of cytochrome P-450 2E1 were assessed by reacting the propofol-treated microsomes in NADPH-generating system with enflurane and aniline as substrates respectively. Drug metabolizing activities of cytochrome 1A1, 2B1, and 3A4 were evaluated by metabolizing specific substrates, benzo(a)pyrene, pentoxyresorufin and erythromycin, within the microsomes of diabetic hamsters preincubated with various concentrations of propofol. RESULTS: The hepatic and renal defluorination of enflurane was significantly inhibited by 0.05 and 0.10 mM propofol in the microsomes of diabetic hamster (P < 0.05). The activities of aniline hydroxylase (cytochrome 2E1), pentoxyresorufin O-dealkylase (cytochrome 2B1) and benzo(a)pyrene hydroxylase (cytochrome 1A1) were inhibited by propofol in a concentration-dependent manner from 0.05 to 0.10 mM. However, propofol showed no significant effect to the erythromycin N-demethylase (cytochrome 3A4) at its concentration of 0.05-0.10 mM in the diabetic hamsters. CONCLUSIONS: Our data demonstrated that propofol in therapeutic concentrations of 0.05 and 0.10 mM, could inhibit both liver and kidney defluorination and cytochrome P-450's activities of the diabetic hamsters in vitro of different extent. This should remind clinicians of propofol's potential drug-to-drug interactions in the diabetic patients.

Modulation of cytochrome P450-dependent monooxygenases in streptozotocin-induced diabetic hamster: II. Reverse role of insulin in P450 activity and defluorination.

BACKGROUND: Metabolic activities of cytochrome (cyt) P450-dependent monooxygenase could be modulated by diabetic state in experimental diabetic animals. The purpose of this study is to validate the effect of insulin on the modulation of the metabolic activity of cyt P450 and the defluorination ability to inhalational anesthetics in diabetic animals. METHODS: Diabetic state in golden Syrian hamsters was achieved by intraperitoneal injection of streptozotocin 40 mg/kg once a day for 4 days. After stabilization of diabetic state for 6 weeks, a regimen of insulin treatment given subcutaneously was carried out. Metabolic activities of cyt P450 were assessed by the reaction with benzo(a) pyrene, pentoxyresorufin, aniline and erythromycin (specific substrates). The metabolic activities of cyt 1A1, 2B1, 2E1 and 3A4 respectively in a NADPH-generating system in microsomal preparations of the diabetic hamsters were observed before and after insulin treatment, and were compared with the control group. The ability of defluorination was evaluated by measuring the free fluoride metabolites after incubating the microsomes with enflurane in diabetic and insulin-treated hamsters. Contents of cyt P450 isozymes were measured by electrophoresis and immunoblotting before and after insulin treatment. Pathological features of hepatocytes in diabetic hamsters were evaluated microscopically before and after insulin treatment. RESULTS: The defluorination of enflurane and activity of aniline hydroxylase (cyt 2E1) were successfully induced by diabetic state (P < 0.01). The pentoxyresorufin O-dealkylase (cyt 2B1) was inhibited nearly 50% in the diabetic hamster liver when compared with that of control (P < 0.01). While the activities of benzo(a)pyrene hydroxylase (cyt 1A1) and the erythromycin N-demethylase (cyt 3A4) were basically unaffected by diabetes, alterations in content of cyt P450 were parallel to the alterations in enzyme activities. Microscopically, diabetes induced vacuolization with fatty droplets in the hepatocytes. After treatment with insulin injection, the enzyme activities, protein content and pathologic features returned to the baseline similar to the control. CONCLUSIONS: Our data demonstrated that under diabetic state, metabolic activities of cyt P450 and its extent of defluorination would be polymorphically modulated. After administration of insulin, the activities of cyt P450 and defluorination of enflurane returned to baseline as the blood sugar level had been normalized. This could remind the clinicians of the importance of insulin treatment in the potential drug-to-drug interactions in the diabetic patients.

Propofol inhibits renal cytochrome P450 activity and enflurane defluorination in vitro in hamsters.

PURPOSE: To determine the effect of propofol on renal cytochrome P450 activity and defluorination of enflurane. METHODS: Renal microsomes were prepared by homogenization and differential centrifugation from pooled hamster kidneys. Defluorination of enflurane was assessed by measuring free fluoride metabolites after reacting enflurane with renal microsomes incubated with various concentrations, 0.05 - 1.0 mmol x L(-1) propofol in the NADPH-generating system. Drug metabolizing activities of renal cytochrome P450 mono-oxygenase enzymes were evaluated within microsomes preincubated with propofol and reacted with the specific marker substrates, aniline, benzo(a)pyrene, erythromycin and pentoxyresorufin, for cytochrome P450 2E1, 1A1, 3A4 and 2B1, respectively. RESULTS: Renal defluorination of enflurane was inhibited by clinical concentrations, 0.05 mmol x L(-1) of propofol (P < 0.05). Dose-dependent inhibition of defluorination, aniline and benzo(a)pyrene hydroxylase within kidney microsomes was related to propofol concentration. Propofol demonstrated a profound inhibition of renal pentoxyresorufin dealkylase activity even at low concentrations, 0.05 mmol x L(-1) (P < 0.01). Propofol did not exhibit inhibition of erythromycin N-demethylation of kidney microsomes except at high concentration, 1.0 mmol x L(-1). Spectral analyses of key coenzymes of renal cytochrome P450 monooxygenase, cytochrome b5 and cytochrome c reductase, demonstrated an inhibition when incubated with high concentrations of propofol (P < 0.05). CONCLUSION: In an in vitro study in an NADPH-generating system of hamster kidney microsomes, propofol, in clinical concentrations, exhibited a broad-spectrum of inhibition to renal monooxygenase activities and enflurane defluorination.

Effects of propofol on functional activities of hepatic and extrahepatic conjugation enzyme systems.

The effect of propofol on the hepatic and extrahepatic conjugation enzyme systems was assessed in vitro using microsomal and cytosolic preparations of human liver, hamster kidney, lung and gut. The functional activities of phase-II enzymes, including uridine diphosphate-glucuronosyltransferase (UDPGT), glutathione S-transferase (GST) and N-acetyltransferase (NAT) were evaluated in the presence of various concentrations of propofol (0.05-1.0 mmol litre-1), using 1-naphthol, 1-chloro-2,4-dinitrobenzene and p-aminobenzoic acid as substrates respectively. Propofol produced concentration-dependent inhibition of UDPGT activity in human liver microsomes. Propofol did not produce significant inhibition of human hepatic GST activity at concentrations below 1.0 mmol litre-1. In contrast, NAT activity was unaffected by propofol 0.05-1.0 mmol litre-1 in human liver cytosolic preparations. In extrahepatic tissues, hamster renal and intestinal UDPGT activities were significantly inhibited by propofol at 0.25-1.0 mmol litre-1. In these tissues, GST and NAT were unaffected by propofol at 1.0 mmol litre-1. Propofol produced differential inhibition of human liver and hamster extrahepatic conjugation enzymes as a result of different substrate and tissue specificities. The potential interference of the metabolic profile of phase-II enzymes as a result of inhibition by propofol (especially of UDPGT and GST) should be considered when using propofol with other drugs for anaesthesia.

Study of propofol in bovine aortic endothelium: I. Inhibitory effect on bradykinin-induced intracellular calcium immobilization.

BACKGROUND: Propofol has been found to affect the intracellular calcium concentration with clinical manifestations of hypotension and bradycardia. The purpose of this study is to examine the effect of propofol on intracellular calcium immobilization in bovine aortic endothelium under the stimulation of bradykinin. METHODS: In order to validate the effect of propofol on the alteration of intracellular calcium concentration, we used the cultured bovine endothelial cells (Gm 7372a) to measure the calcium immobilization within the cells preincubated with or without propofol of clinical concentration. Using Fluo-3 staining and a fluorescence spectrophotometer (confocal microscope), intracellular calcium immobilization was demonstrated by the appearance of "hot spots" within the cytoplasm and perinuclear regions after addition of bradykinin to the cells. The changes of fluorescence density measured within these areas versus the effect of time were analyzed and compared with the cells in control group. RESULTS: After addition of bradykinin, intracellular calcium hot spots increased dramatically within seconds and reached a maximal level within 20 seconds. The concentrations of calcium gradually decreased to a constant level after about 3 min following the addition of bradykinin to the cells. With pretreatment of propofol at 0.01 mM and 37 degrees C for 30 min, the immobilization of intracellular calcium from the intracellular stores were significantly inhibited that was demonstrated by the decreased appearance of hot spots when compared with control. CONCLUSIONS: Our data demonstrated that under the stimulation of bradykinin, propofol at 0.01 mM, could inhibit intracellular calcium release from the intracellular stores in bovine aortic endothelial cells. This phenomenon might explain the possible mechanism for the clinical manifestations of hypotension and/or bradycardia associated with propofol.

HELLP syndrome with antepartum pulmonary edema--a case report.

A 44-year-old pregnant female with a gestation of 29 weeks suddenly developed abdominal pain, nausea, vomiting, and laboratory study showed anemia, elevated liver enzymes, and lower platelets. HELLP syndrome was diagnosed and urgent delivery was needed. In order to correct the plasma volume and platelet deficiency, 6 units of both fresh frozen plasma and platelets, were given before operation. However, acute pulmonary edema was noted in the antepartum period. After vigorous treatment, she gave birth to a male infant. The postoperative course was smooth and she and her baby were discharged eleven days later. This case reminded us once again of the importance and necessity of invasive monitoring in fluid management of these patients.

The effect of cerebrospinal fluid dilution of isobaric 0.5% bupivacaine used for spinal anaesthesia.

A prospective study was conducted to see the effect on spinal anaesthesia of the dilution of isobaric 0.5% bupivacaine with cerebrospinal fluid. Sixty patients were randomly allocated to three groups. In group 1, patients received 3 ml isobaric 0.5% bupivacaine intrathecally without aspirating cerebrospinal fluid. In groups 2 and 3, cerebrospinal fluid 1 ml and 2 ml was aspirated respectively and mixed with 3 ml isobaric 0.5% bupivacaine. A total volume of 4 ml in group 2 and 5 ml in group 3 was administered. Thus, the volume of cerebrospinal fluid remained unchanged. Pinprick analgesia and motor block was evaluated from induction until recovery. No differences in onset time, duration and 'two segments regression' were noticed. The only statistical difference was the time to reach complete motor block, which was shorter in group 1 as compared to groups 2 and 3 (6.9 SD 1.4 min versus 11.3 SD 3.0 and 13.5 SD 3.9 min respectively). The mean value of maximum decrease in systolic blood pressure was small, being less than 15% of the pre-operative value for each group. In conclusion, the effect of diluting isobaric 0.5% bupivacaine with cerebrospinal fluid, 1 ml and 2 ml, is minimal and it is an unnecessary procedure with limited clinical effect.

Cardiac tamponade in an infant. A rare complication of central venous catheterisation.

A 2994 g infant suffered cardiac tamponade from an infusion of total parenteral nutrition through an indwelling central venous catheter. The infant survived as a result of early diagnosis and aggressive therapeutic intervention. Cardiac tamponade secondary to central venous catheterisation is rare, but potentially lethal. Possible mechanisms are direct puncture by the catheter tip, or osmotic injury from the use of hypertonic solutions. To avoid this complication, the catheter tip should be prevented from entering the right atrium and its position should be checked periodically by chest X ray. Cardiac tamponade should be considered in any patient with a central venous catheter whose clinical condition deteriorates suddenly. Diagnostic or therapeutic pericardiocentesis should be employed as the first measure and time should not be wasted on other diagnostic procedures.

Holographic real-time three-slit interferometer.

A new and highly sensitive system, based on the three-slit interferometer, is described for the scanning measurement of optical path length differences over large objects. The system relieves the positional constraints of previous systems by separating the two lateral slits from the central slit using a double-exposure hologram. The lateral slit wavefronts are holographically reconstructed from an off-axis reference beam and added to light from the central slit to form a live intensity distribution pattern. Optical path length measurements can be made by comparing the magnitude of adjacent maxima as an object is translated across the central slit. The apparatus can be used for a number of practical applications including the measurement of flatness for an optical flat, thickness for transmissive or reflective films, and refractive-index differences of materials.