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Monitoring image data at a field site provides important and useful information concerning plant and environmental conditions for agricultural users. We propose an image monitoring system that makes it possible to work in harsh areas, collect large amounts of data in real time, and analyze the data according to users’ requests. The system is constructed for use via the Internet with Web-based sensor nodes, an agent program, and Web analysis applications. Web-based sensor nodes such as Field Servers allow the monitoring of various types of sensor data, including image data, via the Internet. The agent program performs complicated operations on the sensor nodes from a remote site via the Internet; it can also analyze monitoring data easily using Web applications. To evaluate the effectiveness of the image monitoring system, we executed a long-term field experiment at a grape farm in Obuse-town, Nagano, Japan. Four types of sensor data concerning environmental condition and 2 types of image data concerning plant detail and field overview were collected and stored at a remote site via the Internet. The image data were analyzed using a filtering approach operated by the agent program and Web applications which were used for calculations in a background subtraction model. The proposed system has worked stably since May 2006 and provided results in which approximately 84% of unnecessary image data were filtered. Due to its construction with a distributed architecture based on the Internet, this system has the advantage that non-expert users can easily obtain the monitoring data on the Web and image processing can be provided for users without changing the system architecture.

Field Server is composed of durable casing, Web-server, multiple sensors, network-camera, wireless LAN card, high intensity LED lighting etc. The most important part in Field Server is a core card, Field Server Engine (FSE). The FSE functions as Web server, advanced data acquisition system (16ch), signal generator, remote controller for external devices and RS-S23C serial interface. Field Server equipped with FSE is a multi-functional sensor node, which can measure 3-dimentionalwind velocity, EC and so on. Prototype of advanced FSE, which has FPAA (Field Programmable Analog Array), also has been developed. All functions of the FSE are operated on Web pages of FSE using Web-browser manually, or Agent program operates automatically FSE by HTTP. Field Servers with FSE can realize multifunctional sensor networks.

The effects of platelet-activating factor (PAF) antagonists on the agonist-induced increase in cytosolic free calcium concentration, [Ca2+]i, in human vascular endothelial cells grown in monolayer were investigated by a continuous superfusion technique using a calcium fluorescent probe, fura-2. PAF caused a small but dose-dependent increase in [Ca2+]i. Seven structurally dissimilar PAF antagonists dose-dependently suppressed the peak response, among which WEB 2086 was the most potent, followed by WEB 2170 greater than FR 900452 not equal to ONO 6240 greater than BN 52021 not equal to kadsurenone not equal to CV 3988. These antagonists except for CV 3988 were specific for PAF, since they had no effects on calcium mobilization induced by thrombin or histamine, while CV 3988 had a non-specific effect. PAF in the same range of concentration increased prostacyclin release from human endothelial cells. WEB 2086 also inhibited the PAF-induced prostacyclin release, while it had not effect on the release induced by histamine and thrombin. These results demonstrate the specificity and dose-response characteristics of PAF antagonists in cultured human endothelial cells and suggest that a PAF antagonist could be a valuable therapeutic agent in certain human diseases where PAF activation of endothelial cells may have a critical role.

A continuous-time quantitative plant growth model is proposed. The model is implemented as a neural network, which is a three layers neural network and has mutual connections on the middle layer. The neural network is derived from Lotka-Volterra equations which describe mechanism of physiological interference between organs. The plant growth model includes the specific organ growth models which are represented by units which have same functions as neurons. It is shown with computer simulation that solutions of the plant growth model implemented as a neural network are approximated to that of Lotka-Volterra equations. The relation between the Lotka-Volterra system and neural networks is discussed and an algorithm to estimate unknown parameters in the models is proposed.

A new agricultural farming and management system is proposed, which is based on real time field monitoring of agricultural related information using a Field Server. The Field Server monitoring network system was developed at a vine yard at Obuse-town in Nagano, Japan. Data of environmental condition (solar-radiation, temperature, relative humidity, and soil moisture) and growth information (leaf and branch shapes, blooming, fruiting and size) were automatically collected by the Field Server and transferred to a personal computer inside a house through a wireless LAN which could connect the two places at a distance of about 300 m. These information are used not only for farming, but also for agri-tourism that will be one of strategies for the Obuse's agricultural industry with sustainable development. Some ideas are also proposed for the data use.

In order to elucidate 5-HT release influenced by PGE2 in the background of the anticancer drug-induced emesis, the effect of nabumetone, a COX-2 inhibitor, on the release of 5-HT from the isolated rat ileum was investigated. PGE2 produced a concentration-dependent increase (10(-9) to 10 M) and decrease (10(-8) to 10(-6) M) in 5-HT release. Arachidonic acid also demonstrated a similar bell-shaped 5-HT release. The arachidonic acid-induced 5-HT release at 3 x 10(-6) M (313.04 +/- 25.90%) was significantly inhibited by the concomitant perfusion with BRL10720 (10(-6) M) (161.98 +/- 19.4%, p0.01), an active metabolite of nabumetone, or indomethacin (3 x 10(-7) M)(190.01 +/- 16.19%, p0.05). BRL10720 (10(-6) M)(428.57 +/- 51.72%, p0.05) significantly inhibited the increase in 5-HT release induced by cisplatin (10(-6) M)(748.56 +/- 136.31%), suggesting that PGE2would be involved in cisplatin-induced 5-HT release. The increase in 5-HT release from the isolated ileum 72 hrs after cisplatin administration, in a delayed-emesis animal model, was significantly inhibited by the in vivo 3-day administration of nabumetone or BRL10720, but was not affected by the 3-day administration of dexamethasone. After 72 hours, however, the in vivo 3-days administration of nabumetone, BRL10720 or dexamethasone had no effect on the increase in ileal 5-HT levels induced by cisplatin. The use of COX-2 inhibitors to ameliorate delayed emesis induced by cisplatin-based anticancer chemotherapy has been proposed. On the other hand, there is a possibility that dexamethasone works through a mechanism other than 5-HT release in delayed emesis.

In order to elucidate the precise mechanism of ipecac syrup (TJN-119) on the occurrence of vomiting, we examined the effects of ipecac syrup on the abdominal afferent nerve activity as well as on the 5-HT levels of the ileum and area postrema in ferrets. Oral administration of TJN-119 (0.5 mg/kg) produced a significant increase in afferent abdominal vagus nerve activity which lasted approximately 1 hour. The maximum response induced by TJN-119 was estimated to be 219 +/- 18% of the pre-injection level. Cephaeline or emetine, the main alkaloids of ipecac syrup, also demonstrated similar effects on afferent vagus nerve activity. TJN-119 increased the 5-HT content in the ileum but not in the area postrema. These observations illustrate possible mechanisms that may act at peripheral sites. It was recently reported that TJN-119 has a high affinity to 5-HT4 receptors (Hasegawa et al., unpublished data). These results suggest that 5-HT4 receptors may be involved in the emetic action of TJN-119.

We have previously reported that diesel exhaust particles (DEP) caused a negative inotropic effect that was followed by cardiac arrest in the isolated atrial preparation of guinea pigs. The purpose of this study was to examine the systemic effects of DEP on electrocardiographic (ECG) changes using guinea-pigs. We found that intravenously administered dimethyl sulfoxide (DMSO) extract of DEP solution induced arrhythmias and deaths via complete atrioventricular (AV) block in guinea pigs. The LD of DEP solution was 132.0 +/- 7.2 mg/kg. The coefficient of variance (CV) of LD measured by the modified Hatcher-Magnus method was relatively small (5.5%). Fractions of DEP extracted by hexane, ethanol or methanol, 4-hydroxyphthalic acid 2-methyl ester, a compound isolated from methanol extract of DEP did not induce significant ECG changes in guinea pigs. As compared with fresh DEP solution, the DMSO/DEP solution used in the present study induced similar cardiac toxicity after being stored in a freezer at 4 degrees C for 3 days. These results suggest that stable and water-soluble fractions of DEP may be responsible for cardiotoxicity.

The object of this study was to evaluate the involvement of 5-HT3 receptors in the regulation of 5-HT release from the small intestine using ferrets, an animal model of emesis. 2-Methyl-5-HT, a 5-HT3 receptor agonist, produced a concentration-dependent increase of 5-HT from the ferret ileum. This increase in 5-HT release was significantly inhibited by granisetron (10(-7) and 10(-6) M) or azasetron (10(-7) and 10(-6) M) in a concentration-dependent manner. Ondansetron (10(-7) M) and ramosetron (10(-6) M) also significantly inhibited the 2-methyl-5-HT-induced increase in 5-HT release. When the concentration of ondansetron was increased from 10(-7) M to 10(-6) M, inhibition of 5-HT release was reduced. Ramosetron, for which 5-HT3 receptor binding of the rat brain is remarkably stronger than for any other 5-HT3 receptor antagonists, inhibited the 5-HT release at only the highest concentration of 10(-6) M. Based on these observations that the mode of action on the 2-methyl-5-HT induced 5-HT release is different among 5-HT3 receptor antagonists, it is suggested that there is a possibility that the neuronal 5-HT3 receptors and the 5-HT3 receptors on the EC cells may represent two distinct subtypes.

In order to elucidate the role of emetic action, the effects of talipexole and bromocriptine, two antiparkinsonian dopamine receptor agonists, on serotonin (5-HT) release from enterochromaffin (EC) cells were studied by measuring 5-HT concentrations in the perfusate of the isolated rat ileum. Bromocriptine (10(-8)-10(-6) M), which exerts agonistic effects on D1 and D2 receptors, increased 5-HT release in a concentration-dependent manner. No significant increase in 5-HT release was seen after addition of talipexole, which selectively stimulates D2 receptors and blocks 5-HT3 receptors, even at 10(-6) M. The increase in 5-HT release caused by bromocriptine at 10(-6) M was inhibited by administration of 10(-6) M of D1 receptor antagonist SCH 23390, D2 receptor antagonist spiperone, 5-HT3 receptor antagonist granisetron or tetrodotoxin (TTX). These results showed the involvement of both dopaminergic and serotonergic mechanisms in the 5-HT release from EC cells following the administration of dopamine receptor agonists. Bromocriptine might induce 5-HT release by stimulating D1, D2 and 5-HT3 receptors and depolarizing neurons in the ileum. On the other hand, talipexole might weaken 5-HT release from EC cells elicited by D2 receptor stimulation with its 5-HT3 receptor blocking property. It is suggested that the emetic effect of dopamine receptor agonists involves the peripheral gastrointestinal tract as their site of action.

The effects of DHA treatment on intracellular Ca2+ dynamics in aortic smooth muscle cells isolated from young stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched normotensive Wistar Kyoto rats (WKY) were investigated. The resting intracellular Ca2+ concentration ([Ca2+]i) before stimulation and the peak [Ca2+]i induced by 5-HT, angiotensin II and depolarizing concentration of KC1 were higher in SHRSP than in WKY. When added to the culture medium for 2 days, DHA at a concentration of 30 microM significantly suppressed the peak [Ca2+]i induced by these stimulants in aortic smooth muscle cells isolated from WKY, whereas smooth muscle cells of SHRSP were refractory to the suppression. DHA had no suppressive effect on the 5-HT-induced increase in the inositol triphosphate production. The present study indicates that DHA can suppress receptor-mediated Ca2+ influx, at least, through the voltage-dependent channel, in vascular smooth muscle cells. Since the intracellular Ca2+ plays an important role in regulating vascular tone, the suppressive effect of DHA on [Ca2+]i in vascular smooth muscle cells may be contributed to the beneficial properties of DHA on cardiovascular disorders. The precise mechanisms of action remain to be elucidated.

We investigated the influence of granisetron, a 5-HT3 receptor antagonist, on the increase in 5-hydroxytryptamine (5-HT) release induced by cisplatin from the isolated ileum of the ferret, a species known to vomit in response to cisplatin. 2-Methyl-5-HT, a selective 5-HT3 receptor agonist, increased the release of 5-HT from the ferret ileum in a concentration-dependent manner within the range of 10(-7) to 10(-6)M. The 5-HT release induced by 2-methyl-5-HT was significantly inhibited by a concomitant perfusion with granisetron (10(-6)M). Cisplatin also increased the 5-HT release from the ferret ileum within the range of 10(-8) to 10(-6)M, in a concentration-dependent manner. Granisetron (10(-6)M) also significantly inhibited the cisplatin-induced 5-HT release. Since the cisplatin-induced 5-HT release was significantly inhibited by tetrodotoxin, the possible involvement of an interneuron pathway in the cisplatin-induced 5-HT release mechanism was suggested in the ileal tissue. It is likely that granisetron inhibited the cisplatin-induced 5-HT release from the gut EC cells by producing blockade of an EC cell 5-HT3 receptor.

The present study elucidated the precise mechanism of 5-hydroxytryptamine (5-HT)-induced increase of intracellular Ca2+ concentration ([Ca2+]i) in cultured vascular smooth muscle cells isolated from rat aortic media. [Ca2+]i was measured using fluorescent Ca2+ indicator, fura-2. 5-HT caused a dose-dependent increase in [Ca2+]i, which was completely inhibited by ketanserin. alpha-Methyl-5-HT had an equipotent effect to 5-HT. Diltiazem at 10 microM partially suppressed the 5-HT-induced increase in [Ca2+]i. 5-HT also augmented Mn2+ influx, when monitored by Mn2+ quenching of fura-2 fluorescence. When extracellular Ca2+ (1.3 mM) was removed, a decrease in resting level and a small, transient increase in [Ca2+]i were observed. 5-HT stimulation also induced an increase in the production of inositol triphosphate. 5-HT-induced increase in [Ca2+]i was significantly, but partially inhibited by staurosporin and H-7. Phorbol 12-myristate 13-acetate induced an increase in [Ca2+]i, which was abolished by removal of extracellular Ca2+. 5-HT-induced increase in [Ca2+]i was not affected by the pretreatment with pertussis toxin (PTX), and was not accompanied by a change in cyclic AMP content. These results suggest that, in cultured rat aortic smooth muscle cells, 5-HT increases [Ca2+]i via 5-HT2 receptor subtype by inducing influx of extracellular Ca2+ partially through L-type voltage-dependent Ca2+ channel, as well as by mobilizing Ca2+ from its intracellular stores. Activation of protein kinase C may be positively involved in the regulatory mechanism of Ca2+ influx, but PTX-sensitive G protein and cyclic AMP seem to be not involved.

We recently reported that chronic administration of cyclophosphamide significantly increased urinary 5-hydroxyindole acetic acid (5-HIAA) excretion in rats indicative of a release of 5-hydroxytryptamine (5-HT) from intestinal enterochromaffin (EC) cells. Cyclophosphamide is considered to be an inactive prodrug and require conversion to active emetic metabolities (e.g. phosphoramide mustard) by hepatic metabolism. However the presence of cytochrome P450 in the intestine raises the possibility of cyclophosphamide metabolism in the wall of the intestine, a site which would have considerable significance for 5-HT release and the emetic effects of cyclophosphamide. The aim of this study was to investigate whether cyclophosphamide could induce the release of 5-HT from the isolated ileum and to examine its mechanism of action. Cyclophosphamide (10(-6)M and 10(-7)M) induced a concentration dependent increase of 5-HT from rat isolated ileum. This cyclophosphamide-induced 5-HT release was significantly reduced by granisetron (10(-6)M and 10(-7)M) or atropine (10(-7)M and 10(-6)M). Tetrodotoxin (10(-6)M completely inhibited the increased 5-HT release induced by cyclophosphamide. These results suggest that cyclophosphamide has the capacity to induce 5-HT release via activation of enteric cholinergic neurons. In addition the in vitro study demonstrate for the first time that cyclophosphamide may be activated to emetic metabolites at extra-hepatic sites (e.g. intestine) and that conversion at these sites could contribute to the mechanism of cyclophosphamide induced emesis.

The effects of 3 bisphosphonates, AHBuBP, AHPrBP, and Cl2MBP on cell growth, alkaline phosphatase (ALP) activity, mineralization, and prostaglandin E2 (PGE2) synthesis in the clonal osteoblast-like cell line MC3T3-E1 were studied. These bisphosphonates had essentially similar effects on growth and the osteoblastic functions of the cells, i.e., they had no inhibitory effects on cell growth except at higher concentrations, they increased ALP activity, and inhibited PGE2 production. In the presence of AHBuBP, ALP activity was higher than that in the control after day 6 of culture. Lower concentrations of AHBuBP slightly facilitated mineralization by the cells. It is probable that bisphosphonates enhance the functions of osteoblasts in certain concentration and that the inhibition of endogenous PGE2 production may be involved in the mechanism of action of bisphosphonates.

Diesel engine-powered vehicles emit some 30 to 100 times more particles than do gasoline engine cars. We previously reported that diesel exhaust particles (DEP) instilled intratracheally into mouse caused lung edema accompanying endothelial cell damage. In order to clarify further the biological effects of DEP on the respiratory system, the primary target of DEP instillation, we examined the direct action of DEP on isolated tissues and the cytotoxicity of DEP on cultured cells of respiratory tracts in guinea pigs. DEP were collected on glass fiber filters from a light-duty (2730 cc), four cylinder diesel engine. DEP induced a dose-dependent relaxation in tracheal smooth muscle and lung parenchymal preparations from guinea pigs. Neither propranolol nor ranitidine inhibited the relaxing effect of DEP on tracheal preparations. DEP also exhibited concentration- and time-dependent cytotoxicity on cultured tracheal smooth muscle cells and lung fibroblasts from guinea pigs, as assessed by specific [51Cr] release. These cytotoxicities induced by DEP were significantly inhibited by catalase, deferoxamine and MK-447, whereas SOD and mannitol had little effect. These inhibitory effects were blunted by the higher concentration of DEP. These results suggest that the cytotoxicity of DEP may cause dysfunction of respiratory tissues, which are mediated via oxygen radicals, probably hydroxyl radicals or hydrogen peroxides.

In species which vomit, elevated intestinal serotonin (5-hydroxytryptamine, 5-HT) may stimulate abdominal vagal afferent fibers, which in turn evoke the vomiting reflex. The release of 5-HT from intestinal enterochromaffin (EC) cells is regulated by polymodal mechanisms. The object of this study was to evaluate the involvement of 5-HT autoreceptors in the regulation of 5-HT release from the small intestine. Functional studies were carried out using 5-HT3 receptor agonist and antagonists, and 5-HT4 receptor agonist. Ferret and rat ileal tissue were isolated and 5-HT released into the bathing solution was determined using HPLC with an electrochemical detector (ECD). We previously reported that cisplatin produced a significant increase in cumulative 5-HT release and that ondansetron, a selective 5-HT3 receptor antagonist, did not alter the 5-HT release from the ferret ileum. In this study, a selective 5-HT3 agonist, 2-methyl-5-HT, induced a dose-dependent increase of 5-HT from the rat ileum. This release of 5-HT was significantly reduced by granisetron, a selective 5-HT3 receptor antagonist. Furthermore, a selective 5-HT4 receptor agonist, 5-methoxytryptamine induced a concentration-dependent increase of 5-HT in the rat ileum. These results suggest that both 5-HT3 and 5-HT4 receptors may be involved in intestinal 5-HT release.

Diesel engine-powered vehicles emit some 30 to 100 times more particles than do gasoline engine cars. We previously reported that diesel exhaust particles (DEP) could produce superoxide anions in an in vitro study. Furthermore, mice instilled intratracheally with DEP showed high mortality at low doses. The cause of death was lung edema with damage to the lung endothelial cells. In order to elucidate the mechanism of the onset of mortality induced by DEP, we examined the direct action of DEP on the isolated atrium of guinea pigs. A light-duty (2740cc), four cylinder diesel engine was used. The DEP were collected on fiberglass filter. DEP caused a negative inotropic action that was followed by the cardiac arrest of the isolated left atrium. These actions were not inhibited by propranolol, atropine, verapamil, diltiazem, diphenhydramine, indomethacin, superoxide dismutase or catalase. The precise mechanism of cardiac arrest is unknown. However, these results suggest that cardiac toxicity induced by DEP might be involved in lung edema.

MC3T3-E1 cells actively synthesized and released prostaglandin E 2 (PGE 2 ) during culture. PGE 2 release was minimal on day 9 and gradually increased with culture up to day 27. DNA content gradually increased until day 27. Alkaline phosphatase (ALP) activity increased up to day 15 and decreased thereafter. In contrast to the decrease in ALP activity, calcium accumulation increased rapidly after day 21, possibly due to mineralization by the cells. Indomethacin, a cyclooxygenase inhibitor, blocked PGE 2 production completely at concentrations higher than 0.3 μmol/L. In the presence of indomethacin (3 μmol/L), DNA content was slightly decreased on day 27. Furthermore, ALP activity on day 15 was greater than that of the control and this high activity was maintained until day 27. However, calcium accumulation was not affected by the addition of indomethacin. These results suggest that endogenous PGE 2 down-regulates ALP activity and slightly stimulates the proliferation of MC3T3-E1 cells as an autocrine mediator, although it does not directly influence the cells' mineralizing activity.

The effect of activin (activin A/EDF) on osteoclast formation was investigated. In mouse bone marrow cell cultures, activin enhanced the formation of tartrate-resistant acid phosphatase (TRACP)-positive multinucleated cells (MNC) in a dose-dependent manner, either in the presence or absence of 1,25-(OH)2D3 or PTH. In organ cultures of neonatal mouse calvaria, activin also enhanced the generation of TRACP-positive giant cells in the endosteal periosteum and increased the TRACP staining of whole calvaria, but did not exhibit bone resorbing activity. These results indicate that activin stimulates the formation of osteoclasts, but not osteoclast activation. Activin is produced by bone marrow cells and might be involved in the local process of osteoclast differentiation.

N-formyl-methionyl-leucyl-phenylalanine (FMLP), but not leukotriene B4 (LTB4), induced a significant platelet adhesion to endothelial cell monolayer when polymorphonuclear leukocytes (PMNs) were present in vitro. Neither of FMLP and LTB4 had an effect on the platelet adhesion in the absence of PMNs. An antagonist of platelet-activating factor (PAF), WEB 2086 completely inhibited the platelet adhesion induced by FMLP, while indomethacin and AA-861 had no effect. These results suggest that PMN-dependent platelet adhesion to endothelial cells induced by FMLP is mediated by PAF, and that PAF plays an important role during cell-cell interactions among platelets, PMNs and endothelial cells.

One of the recent developments which made great contribution to the progress in biology and medicine is the discovery of a family of arachidonic acid metabolites such as prostaglandins (PGs) and leukotrienes (LTs). These metabolites, known as a family of ‘eicosanoids’, are formed in a variety of cells and tissues in response to specific or nonspecific stimuli, and have a number of potent biological activities which affect cardiovascular, renal, pulmonary, gastrointestinal and eye functions, platelet aggregation, peripheral and central nervous systems, and the reproductive system. Furthermore, these eicosanoids have been implicated in many aspects of the inflammatory process, including vasodilation, increased vascular permeability, pain, leukocyte migration and bone resorption.

1. Intact platelets and confluent human umbilical vein endothelial cells bound [3H]-Paf-acether (platelet activating factor, [3H]-Paf) at 20 degrees C in the presence of 0.25% (w/v) bovine serum albumin (BSA). 2. [3H]-Paf binding to platelets was inhibited in a concentration-dependent manner by WEB 2086. An excess of WEB 2086 indicated the presence of specific, saturable Paf binding which reached a maximum of 28.3 +/- 3.7 fmol [3H]-Paf per 5 x 10(7) platelets. In platelets, different hetrazepines (WEB 2098, 2105, but not 2118) also inhibited [3H]-Paf binding in a concentration-dependent manner. 3. WEB 2086 partially displaced platelet-bound [3H]-Paf in a concentration-dependent manner reaching a plateau at 400 nM WEB 2086. No further displacement was observed when WEB 2086 and an excess of unlabelled Paf were added together. 4. The hetrazepines inhibited platelet aggregation. Platelet aggregation IC50 values correlated well with the IC50 values of the hetrazepines against [3H]-Paf binding (r2 = 0.99). WEB 2086 shifted the Paf dose-response curve rightwards in a parallel manner. Tested against platelet aggregation the pA2 obtained for WEB 2086 was 7.9. 5. WEB 2086 inhibited [3H]-Paf binding to endothelial cells in a concentration-dependent manner. WEB 2086 also inhibited the Paf-mediated cytosolic calcium increase in endothelial cells with an IC50 value of 23.1 +/- 10.4 nM as compared with an IC50 of 21.6 +/- 10.4 nM WEB 2086 for platelet aggregation. 6. These results demonstrate an inhibition of [3H]-Paf binding to platelets and endothelial cells by different hetrazepines, most probably at the Paf receptor level.

In rat basophilic leukemia cells (2 H3-RBL) stimulated with the calcium ionophore A 23187, a rapid build-up of PAF-acether was observed within 5 minutes. Thereafter, a slow and complete catabolism was observed within the next 55 minutes. Accumulation of PAF-acether required calcium in the medium and was increased in the presence of acetyl-CoA. Phenyl methyl sulfonyl fluoride, a serine hydrolase inhibitor active on 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetyl hydrolase also produced an increased accumulation of PAF-acether in ionophore-stimulated cells. Quinacrine, a non specific inhibitor of phospholipase A2 impaired PAF-acether formation in a dose-dependent manner. The time-course of PAF-acether formation was compared with the ionophore-induced release of arachidonic acid from these cells.

When prostaglandin E (PGE) contents in kidney medullary tissue were determined, we found that the PGE level was significantly higher in the male rats. The activity of PG synthetase in kidney medullary microsomes to synthesize PGE2 and the effect of treatment with sex hormones on the activity were also investigated. There was no significant difference in PG synthetase activity between male and female intact rats. Subsequently, ovariectomy and orchidectomy wee carried out and corn oil (control group), testosterone (2.0 mg/kg) or estradiol (0.2 mg/kg) were given subcutaneously every other day for 2 weeks. Testosterone treatment produced a significant increase in the activity of PG synthetase in males, but not in females, when compared with control values. In contrast, estradiol treatment produced a significant decrease in PG synthetase activity in both sexes. These results suggest that sex hormones may play an important role in the regulation of PG biosynthesis in kidney.

Paf-acether (paf, formerly platelet-activating factor) (Benveniste et al., 1972), with the structure 1-0-alkyl-2-acetyl-sn-glycero-3-phosphocholine (Benveniste et al., 1979; Demopoulos et al., 1979; Blank et al., 1979), is a biologically active phospholipid which is released by several cell types upon stimulation (for review Pinckard et al., 1982; Vargaftig et al., 1981). The mediator activates platelets, polymorphonuclear neutrophils, macrophages and endothelial cells most probably via a receptor-dependent pathway (Valone et al., 1982; Valone and Goetzl 1983; Lambrecht and Parnham, 1986; Korth et al., 1987; Valone, 1988). Serum albumin acts as a necessary phospholipid carrier for both paf release (Benveniste, J. et al., 1972; Benveniste, J., 1974) and specific paf binding (Korth and Benveniste, 1987) and seems to inhibit the pafdegrading enzyme, acetylhydrolase (Wardlow et al., 1986). Different specific antagonists, such as the paf analogue CV 3988 (Terashita et al., 1983), the naturally occurring kad-surenone (Shen et al., 1985) and Ginkgolides (Nunez et al., 1986; Korth and Benveniste, 1987; Korth et al., 1988 c; Braquet and Godfroid, 1987), as well as synthetic hetrazepines and calcium-blocking agents, inhibited platelet activation and paf binding (Casals-Stenzel and Weber, 1987; Korth et al., 1987 and 1988 b; Wade et al., 1986). Binding studies with radiolabeled antagonists supported the existence of paf receptors in platelets (Hwang et al., 1986 a). A close correlation between inhibition of paf-induced platelet aggregation and binding of labelled paf suggested the importance of the putative paf receptor for platelet activation (Korth et al., 1988 c). Paf receptors were coupled with modulation of phospholipase C activity (Morrison and Shukla, 1988).