Role of colchicine to reduce NLRP3 marker in STEMI patients undergo primary PCI: A randomised controlled clinical trial.

INTRODUCTION: ST-segment elevation myocardial infarction (STEMI) is a fatal disease with significant burden worldwide. Despite advanced medical treatment performed, STEMIrelated morbidity and mortality remains high due to ischemia reperfusion injury after primary angioplasty mediated by NLRP3 inflammasome. Adding colchicine expected to reduce inflammation both in vitro and in vivo. We want to evaluate the effect of colchicine administration on the NLRP3 level of STEMI patient who undergo primary cutaneous intervention (PCI). MATERIALS AND METHODS: Randomised controlled trial was conducted on STEMI patients who undergo PCI in two hospitals in Jakarta, 104 patients enrolled to this study, and 77 patients completed the trial. 37 patients were randomly assigned to receive colchicines (2 mg loading dose; 0.5 mg thereafter every 12 hour for 48 hours) while 40 patients received placebo. NLRP3 level was measured from venous blood at baseline (BL), after procedure (AP), dan 24-hour post procedure (24H). RESULTS: No NLRP3 difference was observed initially between colchicine arm and placebo arm 38,69 and 39,0138, respectively (p >0.05). Measurement conducted at 24H, patients received colchicine demonstrate reduction in NLRP3 level (37.67), while placebo arm results increase in NLRP3 level (42.89) despite not statistically significant (p >0,05). CONCLUSION: Colchicine addition to standard treatment of STEMI patients undergo PCI reduce NLRP3 level despite statistically insignificant.

The Role of Acute Hyperglycemia on the Risk of Malignant Arrhythmia in Acute Myocardial Infarction Patients: A Study of Myocardial Damage, Ion Channel Changes and Inflammatory Factors.

BACKGROUND: acute myocardial infarction (AMI) is often followed by hyperglycemia. To date, there is no study that examine the role of myocardial damage, ion channel changes and increased inflammatory response as a pathomechanism of malignant arrhythmias due to hyperglycemia in AMI patients. The aim of this study is to determine the effect of acute hyperglycemia on the occurence of malignant arrhythmias, troponin I, VLP, echocardiographic strain, ion channel changes (CaMKII) and hsCRP. This study also aims to assess the effect of troponin I, VLP, GLS, CaMKII and hsCRP on the occurence of malignant arrhythmias in AMI patients with acute hyperglycemia. METHODS: a cross-sectional study followed by a cohort study was conducted on AMI patients treated at ICCU Cipto Mangunkusumo Hospital Jakarta during November 2018 to May 2019 period. Patients with severe infections and who had experienced malignant arrhythmias at admission were excluded from the study. The occurence of malignant arrhythmias as the main outcome of this study and CaMKII level were assessed on the fifth day of treatment. Patients who died before the fifth day of treatment due to causes other than malignant arrhythmias were excluded from analysis. The association between acute hyperglycemia with VLP and the occurence of malignant arrhythmias was analyzed through a chi-square test, whereas the differences between troponin I, GLS, CaMKII and hsCRP, based on the hyperglycemia status of the patient, were analyzed by Mann-Whitney U test. RESULTS: a total of 110 patients were included in the study. Two patients died on the third day of observation due to malignant arrhythmias. No significant relationship was found between acute hyperglycemia in AMI and malignant arrhythmias (RR = 1,38, 95%CI 0.50-3.77). There were differences of CaMKII level on day-1 and day-5 between those who were experienced malignant arrhytmia and those who were not (p-value for differences are 0,03 and 0,01, respectively. In the acute hyperglycemia group, there was difference of CaMKII day-5 levels between positive and negative VLP (p = 0.03). CONCLUSION: it was concluded that the inititial stage of AMI causes more dominant myocardial damage, as compared to metabolic factors. In the next stage of AMI, acute hyperglycemia increases ROS and the activation of ion channel changes described by CaMKII. This change results in electrophysiological remodeling of the heart, as seen in the VLP image on SA-ECG.

[Clinical results and prospects for the use of phenosanic acid in patients with focal epilepsy]. / Klinicheskie rezul'taty i perspektivy primeneniya fenozanovoi kisloty u vzroslykh patsientov s fokal'noi epilepsiei.

OBJECTIVE: To study the efficacy and safety of using a new original synthetic antioxidant - phenosanic acid as an adjunct therapy in patients with focal epilepsy. MATERIAL AND METHODS: A randomized, double-blind, placebo-controlled, parallel-group study evaluated the efficacy and safety of phenosanic acid as an adjunct therapy to basic antiepileptic drugs in 120 patients with focal epilepsy. Primary purpose: to study the dynamic of seizure frequency. Secondary purposes: to study the dynamic of seizure-free days, the dynamics of bilateral tonic-clonic seizures, the results of questionnaires and scales (General Dynamics Assessment, Visual Analogue Scale (VAS), Quality of Life in Epilepsy (QOLIE-31-P), European Quality of Life Questionnaire (EQ-5D), Hospital Anxiety and Depression Scale (HADS), Frontal Asstssment Battery (FAB), Mini-Mental State Examination (MMSE)). RESULTS: Phenosanic acid (Dibufelon) showed statistically significant benefit over placebo in the primary indicator of efficacy (reduction in the frequency of epileptic seizures by at least 50%) and in the secondary indicators. The drug was safe and well tolerated by the patients. CONCLUSION: The addition of phenosanic acid (Dibufelon) to base antiepileptic drugs seems to be perspective because of its positive effect on reducing the number of epileptic seizures, as well as on comorbid disorders in the emotional and cognitive spheres.

ATP reactivation of the rotary axostyle in termite flagellates: effects of dynein ATPase inhibitors.

The anterior end or head of a devescovinid flagellate from termites continually rotates in a clockwise direction relative to the rest of the cell. Previous laser microbeam experiments showed that rotational motility is caused by a noncontractile axostyle complex which runs from the head through the cell body and generates torque along its length. We report here success in obtaining glycerinated cell models of the rotary axostyle which, upon addition of ATP, undergo reactivation and exhibit rotational movements similar to those observed in vivo. Reactivation of rotational motility and flagellar beating of the models requires ATP or ADP and is competitively inhibited by nonhydrolyzable ATP analogs (AMP-PNP and ATP-gamma-S). N-ethylmaleimide, p-hydroxymercuribenzoate, and mersalyl acid also blocked reactivation of both the rotary axostyle and flagella. Vanadate and erythro-9-[3-(2-hydroxynonyl)]-adenine (EHNA) selectively inhibited flagellar reactivation without effecting rotational motility. These results, together with previous ultrastructural findings, suggest that the rotary axostyle does not operate by a dynein-based mechanism but may be driven by an actomyosin system with a circular arrangement of interacting elements.

Cellulose metabolism by the flagellate trichonympha from a termite is independent of endosymbiotic bacteria.

Continuous axenic cultures were established of Trichonympha sphaerica, a cellulose-digesting symbiotic protozoon in the gut of a termite. The cultured flagellates harbored no endosymbiotic bacteria and metabolized cellulose to acetate, carbon dioxide, and hydrogen. Thus, the cellulolytic activity of this flagellate is an inherent property and is not dependent on endosymbiotic bacteria.

Cloning, characterization, and expression of a human calcitonin receptor from an ovarian carcinoma cell line.

A human ovarian small cell carcinoma line (BIN-67) expresses abundant calcitonin (CT) receptors (CTR) (143,000 per cell) that are coupled, to adenylate cyclase. The dissociation constants (Kd) for the CTRs on these BIN-67 cells is approximately 0.42 nM for salmon CT and approximately 4.6 nM for human CT. To clone a human CTR (hCTR), a BIN-67 cDNA library was screened using a cDNA probe from a porcine renal CTR (pCTR) that we recently cloned. One positive clone of 3,588 bp was identified. Transfection of this cDNA into COS cells resulted in expression of receptors with high affinity for salmon CT (Kd = approximately 0.44 nM) and for human CT (Kd = approximately 5.4 nM). The expressed hCTR was coupled to adenylate cyclase. Northern analysis with the hCTR cDNA probe indicated a single transcript of approximately 4.2 kb. The cloned cDNA encodes a putative peptide of 490 amino acids with seven potential transmembrane domains. The amino acid sequence of the hCTR is 73% identical to the pCTR, although the hCTR contains an insert of 16 amino acids between transmembrane domain I and II. The structural differences may account for observed differences in binding affinity between the porcine renal and human ovarian CTRs. The CTRs are closely related to the receptors for parathyroid hormone-parathyroid hormone-related peptide and secretin; these receptors comprise a distinct family of G protein-coupled seven transmembrane domain receptors. Interestingly, the hCTR sequence is remotely related to the cAMP receptor of Dictyostelium discoideum (21% identical), but is not significantly related to other G protein-coupled receptor sequences now in the data bases.

Wolf-parkinson-white syndrome presented with broad QRS complex tachycardia.

Broad QRS complex tachycardia is tachycardia with widened QRS complex more than 12 s and caused by various mechanisms, either supraventricular or ventricular. It is important to differentiate between ventricular and supraventricular because it will determine treatment and prognosis of patients. We report a case which was referred to us and first diagnosed as ventricular tachycardia but happened to be atrial fibrillation with RBBB. On ECG examination we found irregular broad complex of tachycardia, RBBB, extreme right axis and heart rate 170-180 beat/minute. Intravenous bolus of 300 mg amiodarone was administered within 30 minutes and continued with 900 mg/24 hours. During administration of amiodarone, heart rhythm was converted to sinus rhythm with short PR interval (0.09 s), left axis deviation, and positive delta wave at lead V1. The final diagnosis of wolf-parkinson-white (WPW) syndrome was then confirmed.

L-glutamine therapy reduces endothelial adhesion of sickle red blood cells to human umbilical vein endothelial cells.

BACKGROUND: We have previously demonstrated that therapy with orally administered L-glutamine improves nicotinamide adenosine dinucleotide (NAD) redox potential of sickle red blood cells (RBC). On further analysis of L-glutamine therapy for sickle cell anemia patients, the effect of L-glutamine on adhesion of sickle RBC to human umbilical vein endothelial cells (HUVEC) was examined. METHODS: The first part of the experiment was conducted with the blood samples of the 5 adult sickle cell anemia patients who had been on L-glutamine therapy for at least 4 weeks on a dosage of 30 grams per day compared to those of patient control group. In the second part of the experiment 6 patients with sickle cell anemia were studied longitudinally. Five of these patients were treated with oral L-glutamine 30 grams daily and one was observed without treatment as the control. t-test and paired t-test were used for determination of statistical significance in cross-sectional and longitudinal studies respectively. RESULTS: In the first study, the mean adhesion to endothelial cells with the autologous plasma incubated cells were 0.97 +/- 0.45 for the treated group and 1.91 +/- 0.53 for the nontreated group (p < 0.02). Similarly with lipopolysaccharide (LPS) incubated cells the mean adhesion to endothelial cells were 1.39 +/- 0.33 for the treated group and 2.80 +/- 0.47 for the untreated group (p < 0.001). With the longitudinal experiment, mean decrease in the adhesion to endothelial cells was 1.13 +/- 0.21 (p < 0.001) for the 5 treated patients whereas the control patient had slight increase in the adhesion to endothelial cells. CONCLUSION: In these studies, oral L-glutamine administration consistently resulted in improvement of sickle RBC adhesion to HUVEC. These data suggest positive physiological effects of L-glutamine in sickle cell disease.

Murine osteoclasts and spleen cell polykaryons are distinguished by mRNA phenotyping.

To probe osteoclast gene expression, we combined the techniques of cell microisolation and RT-PCR to develop a novel and sensitive method for the isolation and mRNA phenotyping of small numbers of authentic osteoclasts and spleen cell polykaryons. Using this method we report (1) direct evidence for the presence of calcitonin receptor mRNA in osteoclasts, (2) confirmation of the recent finding of osteopontin mRNA in osteoclasts, and (3) demonstration that the specific expression of mRNA for tartrate-resistant acid phosphatase, carbonic anhydrase II, calcitonin receptor, and osteopontin enable one to distinguish the osteoclast from the morphologically similar and developmentally related spleen cell polykaryon. We also show that mRNA associated with the osteoblast phenotype, such as alkaline phosphatase, osteocalcin, and type I collagen, are absent in osteoclasts. This is the first report in which such an approach has been used successfully to distinguish the mRNA expression pattern of an authentic osteoclast from a macrophage polykaryon, and as such it should provide an important new tool for evaluating the results of various cell culture model systems designed to examine the origin and ontogeny of osteoclasts. Our results also indicate that these procedures can be used as an alternative to in situ hybridization methods for the cell-specific localization of specific mRNA in a mixed cell preparation and for colocalization of multiple mRNA species to a single cell type.

Cloning and characterization of a mouse brain calcitonin receptor complementary deoxyribonucleic acid and mapping of the calcitonin receptor gene.

We have identified and characterized a mouse brain calcitonin receptor (CTR) complementary DNA (cDNA). This cDNA encodes a receptor protein that, after expression, has high affinity binding for salmon calcitonin (Kd approximately, 12.5 nM) and is coupled to adenylate cyclase. The binding affinity of this expressed receptor for salmon calcitonin is lower than that described for the previously cloned porcine renal and human ovarian CTRs, but is similar to that of the recently described rat brain CTR, designated the C1b form of the receptor. Analysis of the deduced structure of the mouse brain CTR reveals that it is highly related to the other CTR cDNAs that belong to a distinct family of G-protein-coupled receptors with seven transmembrane-spanning domains. The major structural feature that distinguishes the mouse cDNA clone from the other CTRs is the presence of a consecutive 111-basepair nucleotide sequence that encodes a 37-amino acid sequence which is predicted to localize to the first extracellular loop between the second and third transmembrane-spanning domains. We have mapped the CTR gene in the mouse to the proximal region of chromosome 6, which is homologous to the 7q region of human chromosome 7; only a single CTR gene was identified. Preliminary analysis of the mouse CTR gene reveals that it is complex, consisting of multiple exons separated by lengthy introns that would allow for splice variants consistent with the existence of multiple CTR isoforms predicted from the CTR cDNA clones. The differential cellular and tissue distribution of these functionally distinct CTR isoforms provides the molecular basis for the previously reported widespread distribution and functional heterogeneity of the CTR.

[Results and complications after deep sclerectomy]. / Ergebnisse und Komplikationen nach tiefer Sklerektomie.

BACKGROUND: As nonperforating glaucoma surgery, deep sclerectomy seems to offer the advantage of fewer complications than the classic trabeculectomy during the first weeks after surgery. PATIENTS AND METHODS: In this prospective study, 74 eyes of 56 patients received deep sclerectomy. The mean follow-up time was 9.5 +/- 5.8 months. Twelve eyes were treated intraoperatively with additional mitomycin C and 11 eyes had combined cataract procedures. The deep sclerectomies were performed without using material of high viscosity or a collagen implant. RESULTS: The mean preoperative pressure of 24.8 +/- 9 mmHg could be lowered to 16.1 +/- 5.9 mmHg (P < 0.0001). The number of glaucoma medications was reduced from 2.2 +/- 1.1 to 0.6 +/- 1.0 substances. Thirty-eight percent of the eyes needed glaucoma medication again. Complications included chorioidal detachment (n = 9), temporary hyphema (n = 6), and delayed pressure reduction (n = 2). CONCLUSIONS: Deep sclerectomy as nonpenetrating glaucoma surgery lowers the intraocular pressure as well as standard trabeculectomy. Its complication rate is very low during the early postoperative weeks. The number of patients who still need glaucoma medication seems to be higher than after trabeculectomy.

[Persistent neutrophilic meningitis in a patient with the acquired immunodeficiency syndrome]. / Meningite neutrofílica persistente em paciente com síndrome de imunodeficiência adquirida.

Persistent neutrophilic meningitis is rarely found and it is characterized by predominance of the number of neutrophils in samples of C SF (cerebrospinal fluid) from the patient after seven days of treatment. The above patient in HIV positive; he has developed fever and mental disorder for 4 months and has presented neutrophilic pleocytosis in analysis of CSF for more than 5 months. Since the beginning or the treatment he has taken antituberculous drugs and corticosteroids. For 3 months, the serologic evaluation, smears and cultures were negative. On the 60th day in hospital, the investigation of acid-fast bacilli in CSF was positive and culture confirmed the presence of Mycobacterium tuberculosis resistant to isoniazid. Several factors that may have caused this uncommon development were discussed: the disturbance of cell-mediated immunity, mainly in release of IL 8 and TNF, the simultaneous use of medicines that could alter the CSF concentration of antituberculous drugs, and the increasing number of multiresistant strains.

Cellulose Metabolism by the Termite Flagellate Trichomitopsis termopsidis.

The end products of cellulose metabolism by the trichomonad flagellate Trichomitopsis termopsidis from the termite Zootermopsis sp. were investigated by growing axenic flagellates on [C]cellulose. The growth of T. termopsidis resulted in the release of label into the supernatant fraction of the culture fluid, and > 75% was volatile under acid conditions. The label was analyzed for CO(2) and for [C]volatile compounds by vacuum distillation under acid and alkaline conditions in disposable micro-distillation vessels. The distillate and undistilled culture supernatant fluid were chromatographed on cellulose thin layers to identify the labeled end product. T. termopsidis produced CO(2) and [C]acetate which accounted for 25 to 30% and 55 to 60% of the labeled end products, respectively. The ratio of label in CO(2) to acetate suggests that they are produced in equimolar amounts. No neutral volatile compounds were produced. The remaining unidentified end product (10 to 20%) was not volatile nor extractable into ether. Hydrogen was produced by T. termopsidis, and the cells were killed by the drug metronidazole. Enzymatic activities were found which account for these end products: pyruvate:ferredoxin oxidoreductase and hydrogenase. The results indicate that acetate is the end product of T. termopsidis cellulose metabolism and is available to the termite for energy metabolism and biosynthesis.

Characterization of the structural and functional properties of cloned calcitonin receptor cDNAs.

We have recently cloned CTRs from cDNA libraries prepared from porcine renal and human ovarian cell lines. In situ hybridization and Northern analysis confirm the widespread distribution of CTR mRNA in numerous tissues. Hydropathy plots of the predicted amino acid sequence of the receptors demonstrate multiple hydrophobic regions that could generate 7 transmembrane spanning domains, similar to other G protein-coupled receptors. Searches of databanks for proteins with related amino acid sequences reveals that the CTRs are closely related to the receptors for parathyroid hormone/parathyroid hormone related peptide, secretin, vasoactive intestinal peptide, growth hormone releasing hormone, glucagon-like peptide-1 and glucagon. These receptors have no significant sequence homology to other G protein-coupled receptors, and therefore, appear to comprise a distinct receptor family. Expression of the hCTR or pCTR in COS cells results in expression of high affinity CTRs which are coupled to adenylate cyclase (AC). The hCTR, however, demonstrates higher affinity for human and salmon CT compared to the pCTR. Both CTRs demonstrate low affinity binding and AC activation in response to calcitonin gene related peptide, amylin or secretin, providing a possible explanation for the cross-reactivity among these peptides in vivo. Stable transfectants expressing the pCTR increase cAMP levels and increases in cytosolic free Ca2+ concentration consistent with dual coupling to AC and phospholipase C. Additional studies will help to establish the structural basis for this functional property as well as the evolutionary relationship of the members of this newly identified family of receptors.

IL-1 production by T6 (CD1a) positive cord blood mononuclear cells (Langerhan's cell precursors?).

Human cord blood (CB) mononuclear cells were fractionated into peanut agglutinin positive (PNA+) and PNA negative (PNA-) subsets. The PNA+ subset was enriched for T6+(CD1a)Ia+ cells, which we have previously shown to resemble the Langerhans cells (LCs) of the skin, and therefore described as circulating LCs precursors. Supernatants of PNA+ and PNA- cells, and of FACS purified populations of T6+ CB cells, cultured with and without LPS, were tested for IL-1 activity. It was found that cord blood PNA+ mononuclear cells as well as purified populations of T6+ CB cells produce significant amounts of, both extracellular and cell associated, IL-1 as compared to PNA- and T6- cells, and comparable to those produced by macrophages. LPS stimulation mainly affected T6+ cells. It can be concluded that cord blood T6+ cells, presumably LCs precursors, are capable of IL-1 production.

Anti-RMA, a murine monoclonal antibody, activates rat macrophages: II. Induction of DNA synthesis and formation of multinucleated giant cells.

Anti-RMA is a murine anti-rat monoclonal antibody that binds to a 120-kD surface membrane antigen expressed primarily by alveolar macrophages. Saline-lavaged alveolar macrophages (AM) formed clusters after incubation with anti-RMA. Anti-RMA produced multinucleated giant cells (MGC) in approximately 15% of adherent AM, and the F (ab')2 fragment of anti-RMA yielded MGC in approximately 9% of AM. The Fab fragment of anti-RMA did not promote MGC formation, nor did the murine anti-rat monoclonal antibodies OX41 and W3/25 (anti-CD4). Although anti-RMA produced a tenfold increase in [3H]thymidine incorporation by AM, it yielded a minimal increase in the number of AM. Autoradiography of AM stimulated with anti-RMA showed heterogeneous labeling of nuclei in MGC, suggesting that 3H-labeled AM may fuse with AM that are not actively synthesizing DNA. These findings suggest that binding of anti-RMA to AM may activate DNA synthesis, and promote clustering and fusion of AM, leading to MGC formation.

Anti-RMA: a murine monoclonal antibody that activates rat macrophages. I. Distribution and characterization of the RMA antigen.

Activated macrophages participate in inflammation by eliminating foreign cells, promoting wound healing, and modulating the immune response. A murine monoclonal antibody, designated anti-rat macrophage activator (RMA), was raised against alveolar macrophages (AM) activated with interferon-gamma (IFN-gamma) and phorbol myristate acetate (PMA). The RMA antigen is expressed by resident macrophages but not by other cells. Binding to AM by anti-RMA is not competitively inhibited by the murine monoclonal antibodies MRC OX-41, OX-42, and OX-43. Surface membrane expression of RMA antigens is upregulated by lipopolysaccharide, PMA, and tumor necrosis factor-alpha but not by IFN-gamma. Stimulation of AM with anti-RMA yields distinct ultrastructural alterations, as well as de novo protein and DNA synthesis. Immunoprecipitation of [35S]methionine metabolically labeled AM yields a 120 kD protein by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) that is not altered by chemical reduction. We conclude that the RMA antigen is macrophage specific and that binding of anti-RMA to AM promotes functional activities in a subset of these cells.

Detection of different interleukin-1 activities in human monocytes and monocytic cell lines.

Culture supernatants from normal human monocytes, monocyte hybrid cell lines, and myelomonoblastic cell lines were tested for human interleukin-1 (IL-1) activity. In the present study, we report the detection of IL-1 secreted by several cell lines of monocyte origin and compare their biological and biochemical characteristics. IL-1 activity was tested by the regular assay of phytohemagglutinin (PHA) response of mouse thymus cells. IL-1 was found to be constitutively secreted by U937 and the M20 cell lines, as well as by three of the monocyte hybrid cell lines. The activity was always augmented following dialysis and did not require the presence of serum for its secretion. We compared the IL-1 activity of the myelomonoblastic M20 and hybrid 1C4 cell lines to that of normal monocytes. We found differences in the kinetics of IL-1 secretion, the pattern of activity following dilution of concentrated supernatants, and augmentation of activity by various inducers. The differences described may be explained by concomitant secretion of IL-1 inhibitory factors, as well as the secretion of activities other than IL-1. Preliminary biochemical analysis showed that all three cell sources tested shared some species of molecules characterized by gel filtration and ion-exchange chromatography. However, some species of molecules expressing IL-1 activity were unique to the cell lines and were not found in normal monocytes.

A cloned porcine renal calcitonin receptor couples to adenylyl cyclase and phospholipase C.

The signal transduction pathways of the recently cloned porcine kidney calcitonin (CT) receptor were evaluated. This receptor, when stably transfected into MC-3T3 cells, avidly bound salmon CT (SCT) [dissociation constant (Kd) = 4 nM]. Incubation with SCT resulted in a dose-dependent accumulation of adenosine 3',5'-cyclic monophosphate (cAMP) [50% effective concentration (EC50) = 0.02 nM] in transfected cells (referred to as PC-1 cells). Binding kinetics and cAMP dose response relationships were similar to those of the native receptor in LLC-PK1 cells. PC-1 cells also responded to calcitonin gene-related peptide (CGRP), but the EC50 value for cAMP accumulation was more than three orders of magnitude higher than for SCT. Exposure of PC-1 cells to SCT (5 nM to 1 microM) produced a dose-dependent rise in cytosolic free Ca2+ concentration ([Ca2+]i), whereas CGRP did not. The initial rise in [Ca2+]i was not dependent on extracellular Ca2+, suggesting that SCT induced release of Ca2+ from intracellular stores. SCT also increased inositol trisphosphate production in PC-1 cells. In conclusion, the cloned, transfected porcine CT receptor functionally couples to and activates both adenylyl cyclase and phospholipase C. This dual coupling is also a characteristic of the parathyroid hormone receptor, which has significant homology in amino acid sequence with the CT receptor.