In vivo and cellular antiarrhythmic and cardiac electrophysiological effects of desethylamiodarone in dog cardiac preparations.

BACKGROUND AND PURPOSE: The aim of the present study was to study the antiarrhythmic effects and cellular mechanisms of desethylamiodarone (DEA), the main metabolite of amiodarone (AMIO), following acute and chronic 4-week oral treatments (25-50 mg·kg-1 ·day-1 ). EXPERIMENTAL APPROACH: The antiarrhythmic effects of acute iv. (10 mg·kg-1 ) and chronic oral (4 weeks, 25 mg·kg-1 ·day-1 ) administration of DEA were assessed in carbachol and tachypacing-induced dog atrial fibrillation models. Action potentials were recorded from atrial and right ventricular tissue following acute (10 µM) and chronic (p.o. 4 weeks, 50 mg·kg-1 ·day-1 ) DEA application using the conventional microelectrode technique. Ionic currents were measured by the whole cell configuration of the patch clamp technique in isolated left ventricular myocytes. Pharmacokinetic studies were performed following a single intravenous dose (25 mg·kg-1 ) of AMIO and DEA intravenously and orally. In chronic (91-day) toxicological investigations, DEA and AMIO were administered in the oral dose of 25 mg·kg-1 ·day-1 ). KEY RESULTS: DEA exerted marked antiarrhythmic effects in both canine atrial fibrillation models. Both acute and chronic DEA administration prolonged action potential duration in atrial and ventricular muscle without any changes detected in Purkinje fibres. DEA decreased the amplitude of several outward potassium currents such as IKr , IKs , IK1 , Ito , and IKACh , while the ICaL and late INa inward currents were also significantly depressed. Better drug bioavailability and higher volume of distribution for DEA were observed compared to AMIO. No neutropenia and less severe pulmonary fibrosis was found following DEA compared to that of AMIO administration. CONCLUSION AND IMPLICATIONS: Chronic DEA treatment in animal experiments has marked antiarrhythmic and electrophysiological effects with better pharmacokinetics and lower toxicity than its parent compound. These results suggest that the active metabolite, DEA, should be considered for clinical trials as a possible new, more favourable option for the treatment of cardiac arrhythmias including atrial fibrillation.

Mexiletine-like cellular electrophysiological effects of GS967 in canine ventricular myocardium.

Enhancement of the late Na+ current (INaL) increases arrhythmia propensity in the heart, while suppression of the current is antiarrhythmic. GS967 is an agent considered as a selective blocker of INaL. In the present study, effects of GS967 on INaL and action potential (AP) morphology were studied in canine ventricular myocytes by using conventional voltage clamp, action potential voltage clamp and sharp microelectrode techniques. The effects of GS967 (1 µM) were compared to those of the class I/B antiarrhythmic compound mexiletine (40 µM). Under conventional voltage clamp conditions, INaL was significantly suppressed by GS967 and mexiletine, causing 80.4 ± 2.2% and 59.1 ± 1.8% reduction of the densities of INaL measured at 50 ms of depolarization, and 79.0 ± 3.1% and 63.3 ± 2.7% reduction of the corresponding current integrals, respectively. Both drugs shifted the voltage dependence of the steady-state inactivation curve of INaL towards negative potentials. GS967 and mexiletine dissected inward INaL profiles under AP voltage clamp conditions having densities, measured at 50% of AP duration (APD), of -0.37 ± 0.07 and -0.28 ± 0.03 A/F, and current integrals of -56.7 ± 9.1 and -46.6 ± 5.5 mC/F, respectively. Drug effects on peak Na+ current (INaP) were assessed by recording the maximum velocity of AP upstroke (V+max) in multicellular preparations. The offset time constant was threefold faster for GS967 than mexiletine (110 ms versus 289 ms), while the onset of the rate-dependent block was slower in the case of GS967. Effects on beat-to-beat variability of APD was studied in isolated myocytes. Beat-to-beat variability was significantly decreased by both GS967 and mexiletine (reduction of 42.1 ± 6.5% and 24.6 ± 12.8%, respectively) while their shortening effect on APD was comparable. It is concluded that the electrophysiological effects of GS967 are similar to those of mexiletine, but with somewhat faster offset kinetics of V+max block. However, since GS967 depressed V+max and INaL at the same concentration, the current view that GS967 represents a new class of drugs that selectively block INaL has to be questioned and it is suggested that GS967 should be classified as a class I/B antiarrhythmic agent.

Antiarrhythmic and cardiac electrophysiological effects of SZV-270, a novel compound with combined Class I/B and Class III effects, in rabbits and dogs.

Cardiovascular diseases are the leading causes of mortality. Sudden cardiac death is most commonly caused by ventricular fibrillation (VF). Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and a major cause of stroke and heart failure. Pharmacological management of VF and AF remains suboptimal due to limited efficacy of antiarrhythmic drugs and their ventricular proarrhythmic adverse effects. In this study, the antiarrhythmic and cardiac cellular electrophysiological effects of SZV-270, a novel compound, were investigated in rabbit and canine models. SZV-270 significantly reduced the incidence of VF in rabbits subjected to coronary artery occlusion/reperfusion and reduced the incidence of burst-induced AF in a tachypaced conscious canine model of AF. SZV-270 prolonged the frequency-corrected QT interval, lengthened action potential duration and effective refractory period in ventricular and atrial preparations, blocked I Kr in isolated cardiomyocytes (Class III effects), and reduced the maximum rate of depolarization (V max) at cycle lengths smaller than 1000 ms in ventricular preparations (Class I/B effect). Importantly, SZV-270 did not provoke Torsades de Pointes arrhythmia in an anesthetized rabbit proarrhythmia model characterized by impaired repolarization reserve. In conclusion, SZV-270 with its combined Class I/B and III effects can prevent reentry arrhythmias with reduced risk of provoking drug-induced Torsades de Pointes.

Hidden Cardiotoxicity of Rofecoxib Can be Revealed in Experimental Models of Ischemia/Reperfusion.

Cardiac adverse effects are among the leading causes of the discontinuation of clinical trials and the withdrawal of drugs from the market. The novel concept of 'hidden cardiotoxicity' is defined as cardiotoxicity of a drug that manifests in the diseased (e.g. ischemic/reperfused), but not in the healthy heart or as a drug-induced deterioration of cardiac stress adaptation (e.g. ischemic conditioning). Here, we aimed to test if the cardiotoxicity of a selective COX-2 inhibitor rofecoxib that was revealed during its clinical use, i.e., increased occurrence of proarrhythmic and thrombotic events, could have been revealed in early phases of drug development by using preclinical models of ischemia/reperfusion (I/R) injury. Rats that were treated with rofecoxib or vehicle for four weeks were subjected to 30 min. coronary artery occlusion and 120 min. reperfusion with or without cardioprotection that is induced by ischemic preconditioning (IPC). Rofecoxib increased overall the arrhythmias including ventricular fibrillation (VF) during I/R. The proarrhythmic effect of rofecoxib during I/R was not observed in the IPC group. Rofecoxib prolonged the action potential duration (APD) in isolated papillary muscles, which was not seen in the simulated IPC group. Interestingly, while showing hidden cardiotoxicity manifested as a proarrhythmic effect during I/R, rofecoxib decreased the infarct size and increased the survival of adult rat cardiac myocytes that were subjected to simulated I/R injury. This is the first demonstration that rofecoxib increased acute mortality due to its proarrhythmic effect via increased APD during I/R. Rofecoxib did not interfere with the cardiprotective effect of IPC; moreover, IPC was able to protect against rofecoxib-induced hidden cardiotoxicity. These results show that cardiac safety testing with simple preclinical models of I/R injury uncovers hidden cardiotoxicity of rofecoxib and might reveal the hidden cardiotoxicity of other drugs.

Late sodium current in human, canine and guinea pig ventricular myocardium.

Although late sodium current (INa-late) has long been known to contribute to plateau formation of mammalian cardiac action potentials, lately it was considered as possible target for antiarrhythmic drugs. However, many aspects of this current are still poorly understood. The present work was designed to study the true profile of INa-late in canine and guinea pig ventricular cells and compare them to INa-late recorded in undiseased human hearts. INa-late was defined as a tetrodotoxin-sensitive current, recorded under action potential voltage clamp conditions using either canonic- or self-action potentials as command signals. Under action potential voltage clamp conditions the amplitude of canine and human INa-late monotonically decreased during the plateau (decrescendo-profile), in contrast to guinea pig, where its amplitude increased during the plateau (crescendo profile). The decrescendo-profile of canine INa-late could not be converted to a crescendo-morphology by application of ramp-like command voltages or command action potentials recorded from guinea pig cells. Conventional voltage clamp experiments revealed that the crescendo INa-late profile in guinea pig was due to the slower decay of INa-late in this species. When action potentials were recorded from multicellular ventricular preparations with sharp microelectrode, action potentials were shortened by tetrodotoxin, which effect was the largest in human, while smaller in canine, and the smallest in guinea pig preparations. It is concluded that important interspecies differences exist in the behavior of INa-late. At present canine myocytes seem to represent the best model of human ventricular cells regarding the properties of INa-late. These results should be taken into account when pharmacological studies with INa-late are interpreted and extrapolated to human. Accordingly, canine ventricular tissues or myocytes are suggested for pharmacological studies with INa-late inhibitors or modifiers. Incorporation of present data to human action potential models may yield a better understanding of the role of INa-late in action potential morphology, arrhythmogenesis, and intracellular calcium dynamics.

Novel mono- and bimetallic organotin(iv) compounds as potential linkers for coordination polymers.

The reaction of [2-(O[double bond, length as m-dash]CH)C6H4]Me2SnCl (2), obtained by the hydrolysis of [2-{(CH2O)2CH}C6H4]Me2SnCl (1), with the appropriate diamine, in a 2 : 1 molar ratio, in the absence of a solvent or catalyst, resulted in the bimetallic species ClSnMe2[2-C6H4(4-CH[double bond, length as m-dash]N-1,1'-C6H4C6H4-4'-N[double bond, length as m-dash]CH)-2'-C6H4]Me2SnCl (4) and ClSnMe2[2-C6H4(CH[double bond, length as m-dash]NCH2CH2N[double bond, length as m-dash]CH)-2'-C6H4]Me2SnCl (5). The reaction of 2 and 5 with KSCN gave the corresponding isothiocyanates [2-(O[double bond, length as m-dash]CH)C6H4]Me2Sn(NCS) (3) and (SCN)SnMe2[2-C6H4(CH[double bond, length as m-dash]NCH2CH2N[double bond, length as m-dash]CH)-2'-C6H4]Me2Sn(NCS) (6). Treating 3 with H2NCH2CH2NH2 also resulted in the corresponding bimetallic compound 6. The reaction of 2 with sodium isonicotinate gave [2-(O[double bond, length as m-dash]CH)C6H4]Me2SnO(O)CC5H4N-4 (7) and the subsequent treatment with ZnTPP (TPP = tetraphenylporphyrinate) led to the isolation of the heterobimetallic complex [{2-(O[double bond, length as m-dash]CH)C6H4}Me2SnO(O)CC5H4N-4]ZnTPP (8). The compounds were characterized by multinuclear NMR spectroscopy and mass spectrometry in solution and IR spectroscopy in the solid state. The molecular structures for compounds 1-6 and 8 were established by single-crystal X-ray diffraction. For all compounds intramolecular O→Sn or Nimine→Sn coordination results in hypercoordinated species with a distorted trigonal bipyramidal (C,E)C2SnX core (E = O, Nimine; X = Cl, Nisothiocyanato, Oisonicotinato). In the heterobimetallic complex 8 the zinc atom has a distorted square pyramidal geometry with the Npyridyl atom at the apical position.

The Effect of a Novel Highly Selective Inhibitor of the Sodium/Calcium Exchanger (NCX) on Cardiac Arrhythmias in In Vitro and In Vivo Experiments.

BACKGROUND: In this study the effects of a new, highly selective sodium-calcium exchanger (NCX) inhibitor, ORM-10962 were investigated on cardiac NCX current, Ca2+ transients, cell shortening and in experimental arrhythmias. The level of selectivity of the novel inhibitor on several major transmembrane ion currents (L-type Ca2+ current, major repolarizing K+ currents, late Na+ current, Na+/K+ pump current) was also determined. METHODS: Ion currents in single dog ventricular cells (cardiac myocytes; CM), and action potentials in dog cardiac multicellular preparations were recorded utilizing the whole-cell patch clamp and standard microelectrode techniques, respectively. Ca2+ transients and cell shortening were measured in fluorescent dye loaded isolated dog myocytes. Antiarrhythmic effects of ORM-10962 were studied in anesthetized ouabain (10 µg/kg/min i.v.) pretreated guinea pigs and in ischemia-reperfusion models (I/R) of anesthetized coronary artery occluded rats and Langendorff perfused guinea pigs hearts. RESULTS: ORM-10962 significantly reduced the inward/outward NCX currents with estimated EC50 values of 55/67 nM, respectively. The compound, even at a high concentration of 1 µM, did not modify significantly the magnitude of ICaL in CMs, neither had any apparent influence on the inward rectifier, transient outward, the rapid and slow components of the delayed rectifier potassium currents, the late and peak sodium and Na+/K+ pump currents. NCX inhibition exerted moderate positive inotropic effect under normal condition, negative inotropy when reverse, and further positive inotropic effect when forward mode was facilitated. In dog Purkinje fibres 1 µM ORM-10962 decreased the amplitude of digoxin induced delayed afterdepolarizations (DADs). Pre-treatment with 0.3 mg/kg ORM-10962 (i.v.) 10 min before starting ouabain infusion significantly delayed the development and recurrence of ventricular extrasystoles (by about 50%) or ventricular tachycardia (by about 30%) in anesthetized guinea pigs. On the contrary, ORM-10962 pre-treatment had no apparent influence on the time of onset or the severity of I/R induced arrhythmias in anesthetized rats and in Langendorff perfused guinea-pig hearts. CONCLUSIONS: The present study provides strong evidence for a high efficacy and selectivity of the NCX-inhibitory effect of ORM-10962. Selective NCX inhibition can exert positive as well as negative inotropic effect depending on the actual operation mode of NCX. Selective NCX blockade may contribute to the prevention of DAD based arrhythmogenesis, in vivo, however, its effect on I/R induced arrhythmias is still uncertain.

Supramolecular anion recognition by ß-HCH.

The formation of highly ordered supramolecular architectures via cooperative C(aliphatic)-H·anion contacts between ß-HCH and various anions (Cl-, Br-, I- and HSO4-) was investigated by single crystal X-ray diffractometry, molecular modelling, ESI-MS and 1H-NMR titrations.

Di(imino)aryltin(IV) dichlorides as tectons for heterometallic coordination compounds.

Hydrolysis of [2-{(CH2O)2CH}C6H4]2SnCl2 (1) [prepared from 2-[(CH2O)2CH]C6H4MgBr and SnCl4, in 2 : 1 molar ratio] gave [2-(O=CH)C6H4]2SnCl2 (2). Treatment of with the appropriate amine, in the absence of a solvent or catalyst, resulted in the isolation in high yields of [2-(RN[double bond, length as m-dash]CH)C6H4]2SnCl2 [R = 2'-C10H7 (3), 2',4',6'-Me3C6H2 (4), PhCH2 (5), Me2NCH2CH2 (6), 2'-PyCH2 (7)]. The reaction of with [Pd(COD)Cl2] provided the heterometallic species [Cl2Pd{2-(2'-PyCH2N[double bond, length as m-dash]CH)C6H4}2SnCl2] (8). The compounds were characterised by multinuclear NMR spectroscopy in solution, and mass spectrometry and IR spectroscopy in the solid state. The molecular structures of 1, 2, 4-7 and 8·CH3CN were established by single-crystal X-ray diffraction. For all diorganotin(IV) dichlorides intramolecular O→Sn or Nimine→Sn coordination results in hypercoordinated species with a distorted octahedral (C,E)2SnCl2 core (E = O, N). The presence of intramolecular N→Sn interactions in solution, responsible for the restriction of free rotation of mesityl groups around the C-N(=C) single bonds, is suggested by (1)H and (13)C NMR data. In the heterometallic dinuclear complex 8 the octahedral coordination around tin is preserved as in 7 and the nitrogen atoms from the pyridyl groups in the pendant arms are coordinated to palladium, leading to a trans-square planar PdCl2N2 core.

[Anthropometric data, fetal and neonatal complications in infants of diabetic mothers. Results of a 10-year retrospective study]. / Antropometriai jellemzok, foetalis és perinatalis szövodmények diabeteses anyák újszülötteiben. Tízéves retrospektív vizsgálat eredményei.

INTRODUCTION: Disturbances in carbohydrate metabolism during pregnancy may result in harmful fetal and neonatal consequences. OBJECTIVES: To assess the fetal and neonatal complications of pregnancy in mothers with gestational and pregestational diabetes during a 10-year period in a county hospital in Hungary. METHODS: Retrospective analysis of infants of diabetic mothers admitted to the neonatal unit between 2001 and 2010. RESULTS: 32% of the infants were transferred to the neonatal unit. Neonatal macrosomia (birth weight >90 centile) was observed in one quarter of the infants. 39% of the infants developed hypoglycemia (blood glucose <2.6 mmol/l), in the majority of the cases within the first 8 hours. Hypoglycaemia was symptomatic in 55% of the infants. Hypocalcemia was observed in 17%, hyperviscosity in 23%, hyperbilirubinaemia in 32%, respiratory distress syndrome and/or transient tachypnoe in 22% and cardiac complications in 13% of the infants. 10% of the inafnts were affected with birth injuries. Congenital anomalies were seen in 17% of the cases, and severe malformations were present in 4% of the infants. CONCLUSIONS: Despite modern diabetes management, there is still a higher incidence of fetal macrosomia, adverse neonatal outcomes and a higher rate of severe congenital malformations in neonates of diabetic mothers.

The ring-chain tautomeric equilibria of selenium macrocyclic compounds: the isolation of the ring tautomer.

A broadening of the investigation of the ring-chain tautomeric process of N-substituted 1,3-X,N-heterocycles (X = O, S, NR) to Se containing macrocyclic compounds allowed the isolation and structurally solid state characterization of the cyclic tautomer 7, which due to the length of the aliphatic chain, is able to form a stable six-membered ring (6-endo-trig). The theoretical calculations based on the DFT method (Gaussian 03 software package) also support the fact that tautomer 7 is more stable than the chain tautomer 6. Thus, based on the ring-chain tautomerism of the macrocycles that contain alkyl chains with amino-imino, imino-alcohol or sulphur-imino groups, combined with a strategy that allows the formation of a stable six-membered ring, the main reaction products will be the cyclic tautomers. The ring-chain equilibria of these macrocycles could be exploited advantageously in different areas of macrocyclic, physical and medicinal chemistry in order to obtain compounds with practical applications.

(3-Chloro-phen-yl){2-eth-oxy-5-[(Z)-hydroxy(phen-yl)methyl-idene]cyclo-penta-1,3-dien-1-yl}methanone.

The title compound, C(21)H(17)ClO(3), which crystallizes as one of two possible oxo/hy-droxy-fulvene prototropic tautomers, possesses a strong intra-molecular O-H⋯O hydrogen bond that closes a seven-membered ring. The dihedral angles between the central five-membered ring and two pendant rings are 55.05 (9) and 44.51 (10)°. The crystal packing is characterized by weak inter-molecular C-H⋯O inter-actions between an H atom of the oxymethyl-ene unit and the carbonyl group of an adjacent mol-ecule, resulting in formation of chains of mol-ecules along the a axis.

Di-µ-chlorido-bis[chloridobis(dimethyl sulfoxide-κO)tin(II)].

The structure of the title compound, [Sn(2)Cl(4)(C(2)H(6)OS)(4)], contains dimers formed through weak Sn⋯Cl [3.691 (2) Å] inter-actions, resulting in a planar Sn(2)Cl(2) core with an inversion center at the centre of the four-membered ring. The Sn(II) atoms are penta-coordinated and have a distorted octa-hedral Ψ-SnCl(3)O(2) coordination geometry. The O atoms from the dimethyl sulfoxide mol-ecules occupy trans positions, while the Cl atoms exhibit a meridional arrangement.

A new ortho-rhom-bic polymorph of 1,1'-seleno-bis-(N,N-diethyl-sulfanecarbothio-amide).

THE TITLE COMPOUND [SYSTEMATIC NAME: N,N-dieth-yl({[(diethyl-carbamothio-yl)sulfan-yl]selan-yl}sulfan-yl)carbothio-amide], C(10)H(20)N(2)S(4)Se, crystallizes in a new form in the space group Pca2(1): the previously reported polymorph crystallizes in the space group P2(1)2(1)2(1). The new phase contains two independent mol-ecules in the asymmetric unit. The Se atoms are tetra-coordinated, with a distorted square-planar geometry. The ligands coordinate asymmetrically to the Se atoms, with one strong Se-S bond [range 2.2833 (13)-2.3041 (15) Å] and one weaker bond [range 2.7318 (14)-2.7873 (12) Å].

Geometric enantiomerism in cyclic compounds: chiral dibrominated 1,3-dioxanes.

The first geometric enantiomers in the cyclic compounds series are reported. The investigated compounds are 2,2-disubstituted-5-methyl-1,3-dioxane derivatives in which the substituents at position 2 bear chiral centers with identical substituents but with opposite configurations. The structure of the unlike isomers was determined from the solid state molecular structure of the compounds obtained by single crystal X-ray diffractometry and the enantiomers of these diastereoisomers were observed by chiral column HPLC base-line separation. The investigated compounds were obtained by a diastereoselective bromination reaction of the corresponding 2,2-dialkyl and 2,2-dibenzyl-5-methyl-1,3-dioxanes.

[Antidiabetic therapy--a new possibility in the complex therapy of cancer?]. / Antidiabetikus kezelés, mint újabb lehetoség a daganatok komplex terápiájában.

Nowadays the lack of exercise and improper eating habits are main characteristics of modern life style. This favors not only formation of type 2 diabetes or cardiovascular diseases, but also increaseas the incidence and prevalence of malignant tumors. Today there are many epidemiologic trials that demonstrate the connection between type 2 diabetes and formation of several malignomas. Its cause should be searched in common paths of pathologic processes. One of this is the birth of hyperinsulinsulinemia, which accompanies insulin resistance. Hyperinsulinemia of the host leads to increased glucose uptake in the highly insuline sensitive tumor cells which supports tumor growth. This makes type 2 diabetes a metabolic state favoring tumor formation, suggesting a potential application of oral insulin sensitizers in cancer therapy. Currently several international trials are testing the anti-tumor activity of metformin and thiazolidinedions (TZD). Besides this, encouraging results were obtained with the use of anti-IGFR antibodies in the treatment of tumors. A common therapy of diabetes and tumor may lead to new possibilities in the treatment of malignant tumor diseases. By doing this we could be able to weaken the tumor and strengthen the body, enabling it to fight against cancer. Bánhegyi RJ, Rus-Gal PO, Nagy AK, Martyin T, Varga R, Pikó B. Correlation between type 2 diabetes and malignant tumors - new possibilities in the complex therapy of cancers?

Organobismuth compounds with the pincer ligand 2,6-(Me2NCH2)2C6H3: monoorganobismuth(III) carbonate, sulfate, nitrate, and a diorganobismuthenium(III) salt.

The reaction of RBiCl(2) (1) [R = 2,6-(Me(2)NCH(2))(2)C(6)H(3)] with Na(2)CO(3) or Ag(2)SO(4) (1 : 1 molar ratio) gave RBiCO(3) (2) and RBiSO(4) (3), respectively. RBi(NO(3))(2) (4) was obtained from RBiCl(2) and AgNO(3) (1 : 2 molar ratio). The ionic complex [R(2)Bi][W(CO)(5)Cl] (6) was obtained from R(2)BiCl (5) and W(CO)(5)(THF), following an unusual chlorine transfer from bismuth to tungsten. Compounds 2-4 are partially soluble in water. The molecular structures of 2·0.5CH(2)Cl(2), 3, 4·H(2)O and 6 were established by single-crystal X-ray diffraction. The carbonate 2 and the sulfate 3 exhibit a polymeric structure based on bridging oxo anions, while for the compound 4 dimer associations are formed, with both bridging and terminal nitrate anions. Dimer associations, based on weak Cl···H interactions between the cation and the anion, were found in the crystal of 6.

[2,6-Bis(dimethyl-amino-meth-yl)phen-yl]selenium bromide monohydrate.

In the title hydrated molecular salt, C(12)H(19)N(2)Se(+)·Br(-)·H(2)O, the two independent bromide anions lie on a twofold rotation axis. Strong intra-molecular N→Se inter-actions [2.185 (3) and 2.181 (3) Å] are established by both N atoms of the organic group in the cation, in trans positions to each other, with an N-Se-N angle of 161.6 (1)°, resulting in a T-shaped (C,N,N')Se core. In the crystal, dimeric associations are formed by Br⋯Se [3.662 (2) Å] and Br⋯H inter-actions [2.56 (6) and 2.63 (7) Å] involving two bromide anions, two cations and two water mol-ecules.

3,9-Diisopropyl-2,4,8,10-tetra-thia-spiro-[5.5]undeca-ne.

The mol-ecule of the title compound, C(13)H(24)S(4), has C2 symmetry and it crystallizes as a racemate. The structure displays two six-membered rings exhibiting chair conformations, with the isopropyl substituents in equatorial positions. In the crystal structure, weak inter-molecular C-H⋯S inter-actions are observed, leading to a channel-like arrangement along the c axis.

2,6-Dichloro-pyridine-3,5-dicarbonitrile.

In the crystal, essentially planar (r.m.s. deviation = 0.003 Å) mol-ecules of the title compound, C(7)HCl(2)N(3), form chains along the b axis by means of C-H⋯N inter-actions. These chains are further linked into layers parallel to the ab plane by C-Cl⋯N inter-actions.