Abstract    The reaction of quinazoline (I) with active methylene compound in the presence of sodium amide were carried out and resulted in the formation of 4, 4'-biquinazoline (III) and 4-substituted quinazoline. Thus reaction with phenylacetonitrile gave III and α-phenyl-4-quinazolineacetonitrile (IV), with ethyl cyanoacetate, III and methyl α-cyano-4-quinazolineacetate (V), with nitromethane, III and 4-(nitromethyl) quinazoline (VI), respectively. But in the case of the reaction with malononitrile, it gave III, 2-amino-3-quinolinecarbonitrile (VII) and 2-amino-6-methoxy-3, 5-pyridinedicarbonitrile (VIII). The reaction of I with active methylene compound without a base catalyst was also carried out and succeeded in finding the transformation of I into quinoline derivatives. Thus, the reaction with malononitrile gave VII, with ethyl cyanoacetate, ethyl 2-amino-3-quinolinecarboxylate (XV) and 2-hydroxy-3-quinolinecarbonitrile (XVI), with phenyl-acetonitrile, 2-amino-3-phenylquinoline, respectively. But in the case of the reaction with diethyl malonate, ethyl 4-quinazolineacetate (XVIII) was obtained.

Abstract    A highly stereoselective, efficient synthetic route to ethyl trans-5-ethyl-2-oxo-4-piperidineacetate (11a) from 1-benzyl-2, 4-dioxo-5-ethylpiperidine (2) is described. The steps involved are conversion of 2 into 1-benzyl-5-ethyl-2-oxo-1, 2, 5, 6-tetrahydropyridine (6) through the lactam alcohol (5), the Michael condensation of 6 with diethyl malonate followed by alkaline hydrolysis, decarboxylation of the resulting trans-lactam dicarboxylic acid (8a) to the trans-lactam acid (9a), and debenzylation of 9a followed by esterification.

Abstract  The pollen beetle, Meligethes aeneus F. (Coleoptera: Nitidulidae) and the cabbage seed weevil, Ceutorhynchus assimilis (Payk.) (Coleoptera: Curculionidae) are two most dangerous winter rape pests in Europe, which frequently co-occur on fields. Difficulties in controlling both pest species stem not only from their resistance to various active ingredients of insecticides, but also from significant differences in their susceptibility to the same active ingredients. The aim of our research was to establish the level of susceptibility of the pests to deltamethrin, a pyrethroid, and indoxacarb, an oxadiazine, and to determine enzymatic mechanisms of resistance to indoxacarb in the cabbage seed weevil, using pesticide synergists that block particular groups of enzymes. The results have shown that the pollen beetle was highly resistant to deltamethrin and highly susceptible to indoxacarb, while the cabbage seed weevil was highly susceptible to deltamethrin and highly resistant to indoxacarb. Studies of resistance mechanisms to indoxacarb in the cabbage seed weevil have not indicated participation of oxidative enzymes blocked by piperonyl butoxide, esterases blocked by S,S,S-tributylphosphorotrithioate or glutathione transferases blocked by diethyl malonate in the metabolism of this substance. Thus, further research on mechanisms behind the resistance of the cabbage seed weevil to indoxacarb is necessary.

Abstract  Carboxylate Gemini surfactants were produced from diethyl malonate which hydrogen was deprived by sodium ethoxide, then connected with alkyl chain and spacer. IR, super(1) HNMR, and MS were used to identify their structures. Their solution properties were characterized by equilibrium surface tension and steady-state fluorescence spectroscopy of pyrene. When the connecting chain carbon number is 6, the hydrophobic chain length of 8, 10, 12, the product cmc are 1.51 x 10 super(-4), 1.05 x 10 super(-4), 9.03 x 10 super(-5) mol/L, and the corresponding surface tensions are 42.09, 36.30, 34.96 mN/m. Results from TEM and DLS suggest that this series of compounds can easily form the vesicles in aqueous solution above cmc.

Abstract    Both the reactions of 3, 4-dihydro-4-quinazolinylmethyl alkyl ketones (4) with active methylene compounds or ketones (NuH) without a catalyst and in the presence of alumina as a catalyst were carried out, and resulted in the transformation of 4 into quinolines (3). Thus 2-(3, 4-dihydro-4-quinazolinyl) acetophenone (4a), 2-(3, 4-dihydro-4-quinazolinyl)-cyclohexanone (4b), and 1-(3, 4-dihydro-4-quinazolinyl)-2-propanone (4c) reacted with diethyl malonate (NuH-2), phenylacetonitrile (NuH-3), acetophenone (NuH-4), cyclopentanone (NuH-5), and cyclohexanone (NuH-6) without catalyst to give 2-phenylquinoline (3b), 1, 2, 3, 4-tetrahydroacridine (3c), and 2-methylquinoline (3d), respectively, together with the dissociation product, quinazoline (1a), although the yield of 3 was very poor. Alumina as a catalyst accelerated these reactions to give 3 in moderate yield. Even the reaction with chloroform (NuH-7) and ethyl orthoformate (NuH-8) gave 3 in good yield. The phenyl and methyl groups substituted at the 2-position prevented 4 from transforming into 3 in both the reactions without a catalyst and in the presence of alumina. A similar transformation was also found between 4, 5-dihydro-5-hydroxy-1-methyl-1H-pyrazolo [3, 4-d] pyrimidine-4-malononitrile (5) and NuH in the presence of alumina, and resulted in the formation of 6-amino-1-methyl-1H-pyrazolo [3, 4-b] pyridine-5-carbonitrile (8). The possible mechanism of the reaction was discussed.

Abstract    A highly enantiospecific, azide-free synthesis of (-)-(R)- and (+)-(S)-piperidin-3-ol in excellent yield was developed. The key step of the synthesis involves the enantiospecific ring openings of enantiomerically pure (R)- and (S)-2-(oxiran-2-ylmethyl)-1H-isoindole-1,3(2H)-diones with the diethyl malonate anion and subsequent decarboxylation.

Abstract  The title compound was synthesized by reacting 2-hydroxy-4-methoxy-benzaldehyde with diethyl malonate in the presence of piperidine catalyst and ethanol as solvent. The chemical structure of the title compound was elucidated by elemental analysis, super(1)H-NMR, and IR. The crystal structure was determined by X-ray diffraction data. It crystallizes in monoclinic crystal system, P2 sub(1)/c space group with unit cell parameters, a = 12.840(2) Aa, b = 24.790(4) Aa, c = 7.8544(13) Aa, beta = 98.035(5) degree , V = 2475.5(7) Aa super(3), and Z = 8. The molecular and crystal structure of the title compound is stabilized by inter- and intramolecular interactions of the type C-H...O. The newly synthesized compound was screened for its antibacterial activity against two gram-positive and two gram-negative bacteria.

Abstract    Water plays an important role in a palladium-catalyzed allenylation of diethyl malonate with 2,3-allenyl acetates to yield centrally chiral allenyl malonates bearing synthetically useful functional groups. The products were formed with 92-96%ee in the presence of a bulky, electron-rich biphenyl ligand at room temperature.

Abstract  Trichoderma harzianum Rifai SKW-36 produced two kinds of D-amino acid oxidizing enzymes. One enzyme was D-aspartate oxidase acting on acidic D-amino acids such as D-aspartate and D-glutamate and another one was D-amino acid oxidase acting on neutral D-amino acid such as D-phenylalanine and D-methionine. These enzymes in the cell-free extract were separated by DEAE-Toyopearl ion-exchange column chromatography. Casamino acids, peptone, and yeast extract as carbon and nitrogen sources were effective for the production of the enzymes. No D-amino acid tested induced the production of the enzymes. Casamino acid (0.33%) as carbon and nitrogen source gave a highest specific activity of D-aspartate oxidase among media tested. D-Aspartate oxidase, which was purified by four-step column chromatography in addition to ammonium sulfate precipitation, exhibited a subunit molecular mass of 40 kDa by SDS-PAGE analysis. D-Aspartate, D-glutamate and N-methyl-D-aspartate were oxidized as substrates with the specific activities of 7.80 U/mg, 4.90 U/mg, and 4.22 U/mg, respectively. D-Asparagine, D-glutamine, D-alanine, and D-valine were slightly oxidized. No other D-amino acids tested were inert. The enzyme exhibited relatively wide substrate specificity compared to D-aspartate oxidases reported so far. The pH and temperature optima were 7.5 - 8.0 and 35 degree C, respectively. The enzyme was stable at pH 6.0 - 9.0. About 75% of the enzyme activity was retained even after treating the enzyme at 50 degree C for 10 min. The enzyme activity was inhibited not by benzoate and tartrate, but 60% and 24% by fumarate and malonate, respectively.

Abstract  There is a substantial body of literature, which has demonstrated that creatine has neuroprotective effects both in vitro and in vivo. Creatine can protect against excitotoxicity as well as against β-amyloid toxicity in vitro. We carried out studies examining the efficacy of creatine as a neuroprotective agent in vivo. We demonstrated that creatine can protect against excitotoxic lesions produced by N-methyl-D: -aspartate. We also showed that creatine is neuroprotective against lesions produced by the toxins malonate and 3-nitropropionic acid (3-NP) which are reversible and irreversible inhibitors of succinate dehydrogenase, respectively. Creatine produced dose-dependent neuroprotective effects against MPTP toxicity reducing the loss of dopamine within the striatum and the loss of dopaminergic neurons in the substantia nigra. We carried out a number of studies of the neuroprotective effects of creatine in transgenic mouse models of neurodegenerative diseases. We demonstrated that creatine produced an extension of survival, improved motor performance, and a reduction in loss of motor neurons in a transgenic mouse model of amyotrophic lateral sclerosis (ALS). Creatine produced an extension of survival, as well as improved motor function, and a reduction in striatal atrophy in the R6/2 and the N-171-82Q transgenic mouse models of Huntington's disease (HD), even when its administration was delayed until the onset of disease symptoms. We recently examined the neuroprotective effects of a combination of coenzyme Q10 (CoQ10) with creatine against both MPTP and 3-NP toxicity. We found that the combination of CoQ and creatine together produced additive neuroprotective effects in a chronic MPTP model, and it blocked the development of alpha-synuclein aggregates. In the 3-NP model of HD, CoQ and creatine produced additive neuroprotective effects against the size of the striatal lesions. In the R6/2 transgenic mouse model of HD, the combination of CoQ and creatine produced additive effects on improving survival. Creatine may stabilize mitochondrial creatine kinase, and prevent activation of the mitochondrial permeability transition. Creatine, however, was still neuroprotective in mice, which were deficient in mitochondrial creatine kinase. Administration of creatine increases the brain levels of creatine and phosphocreatine. Due to its neuroprotective effects, creatine is now in clinical trials for the treatment of Parkinson's disease (PD) and HD. A phase 2 futility trial in PD showed approximately a 50% improvement in Unified Parkinson's Disease Rating Scale at one year, and the compound was judged to be non futile. Creatine is now in a phase III clinical trial being carried out by the NET PD consortium. Creatine reduced plasma levels of 8-hydroxy-2-deoxyguanosine in HD patients phase II trial and was well-tolerated. Creatine is now being studied in a phase III clinical trial in HD, the CREST trial. Creatine, therefore, shows great promise in the treatment of a variety of neurodegenerative diseases.

Abstract  During the period from late September through early October 1973 , an epizootic occurred among mullet populations in a bay in Kochi Prefecture. Dying fish displayed erratic swimming and a more or less whirling motion at the surface. Affected fish had large malodorous abscesses with hemorrhagic borders in the body surface. The etiological agent was isolated from the kidney of diseased mullets. These organisms were gram-negative motile peritrichously flagellated rods, not encapsulated, and measuring about 0.8 x 0.4 u. The bacteria grew slowly on nutrient agar requiring 48 hr of incubation at 25C to form the typical small (0.5 mm in diameter), circular, transparent, slightly raised colonies. They gave negative oxidase reaction, positive catalase reaction, utilized glucose fermentatively and reduced nitrate to nitrite. They did not utilize citrate and malonate as a sole carbon source. No actions on d-tartrate and mucate were exhibited. The organisms were the production of hydrogen sulfide in TSI agar and indole in tryptone water positive to methyl red test, negative to VP reaction, decarboxylation of lysine and ornithine, and utilization of fructose, galactose, mannose and glycerol. They were sensitive to streptomysin, kanamycin, chloramphenol, furazolidon and nalidix acid. (Katz)

Abstract    The effects of α-substituents on sodium-ion selectivities of bis(12-crown-4-methyl) malonates, which are highly selective for sodium ions, were investigated by incorporating various substituents with high lipophilicity, bulkiness, polarity and back strain. The incorporation of geminal substituents such as long alkyl chains and benzyl groups into the α-position of the malonate was found to generally enhance the Na+ selectivity, especially against K+, of the bis(12-crown-4) derivatives. The α, α'-dibenzylmalonate derivative gave the best Na+ selectivity of all the bis(crown ether)s designed here.

Abstract  Coenzyme Q10 (CoQ10) is an essential cofactor of the electron transport gene as well as an important antioxidant, which is particularly effective within mitochondria. A number of prior studies have shown that it can exert efficacy in treating patients with known mitochondrial disorders. We investigated the potential usefulness of coenzyme Q10 in animal models of Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD). It has been demonstrated that CoQ10 can protect against striatal lesions produced by the mitochondrial toxins malonate and 3-nitropropionic acid. These toxins have been utilized to model the striatal pathology, which occurs in HD. It also protects against 1-methyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in mice. CoQ10 significantly extended survival in a transgenic mouse model of ALS. CoQ10 can significantly extend survival, delay motor deficits and delay weight loss and attenuate the development of striatal atrophy in a transgenic mouse model of HD. In this mouse model, it showed additive efficacy when combined with the N-methyl-D-aspartate (NMDA) receptor antagonist, remacemide. CoQ10 is presently being studied as a potential treatment for early PD as well as in combination with remacemide as a potential treatment for HD.

Abstract    Par condensation du bromure d'allyle, puis des halogenures d'alcoyles sur le malonate d'ethyle, nous avons prepare des alcoyl-allyl malonates d'ethyles. L'hydrolyse de ces esters donne des acides alcoyl-2δ4-pentenoiques que I'on transforme, au moyen du bis-(methyl-3 butyl-2) borane, en acides alcoyl-2 hydroxy-5 pentanoiques. La cyclodehydration de ces acides hydroxyles conduit a des alcoyl-3 δ-lactones.

Abstract  The influence of the selective adenosine A(2A) receptor antagonist ZM 241385 on exogenous l-DOPA-derived dopamine (DA) release in intact and dopamine-denervated rats was studied using an in vivo microdialysis in freely moving animals. Local infusion of l-DOPA (2.5 microM) produced a marked increase in striatal extracellular DA level in intact and malonate-lesioned rats. Intrastriatal perfusion of ZM 241385 (50-100 microM) had no effect on basal extracellular DA level, but enhanced dose-dependently the l-DOPA-induced DA release in intact and malonate-lesioned animals. A non-selective adenosine A(2A) receptor antagonist DMPX (100 microM), similarly to ZM 241385, accelerated conversion of l-DOPA in intact and malonate-denervated rats. This effect was not produced by the adenosine A(1) receptor antagonist, CPX (10-50 microM). However, ZM 241385 did not affect the l-DOPA-induced DA release in rats pretreated with reserpine (5 mg/kg i.p.) and alpha-methyl-p-tyrosine (AMPT, 300 mg/kg i.p.). Obtained results indicate that blockade of striatal adenosine A(2A) receptors increases the l-DOPA-derived DA release possibly by indirect mechanism exerted on DA terminals, an effect dependent on striatal tyrosine hydroxylase activity. Selective antagonists of adenosine A(2A) receptors may exert a beneficial effect at early stages of Parkinson's disease by enhancing the therapeutic efficacy of l-DOPA applied exogenously.

Abstract  Water-suppressed chemical shift magnetic resonance imaging was used to detect neurochemical alterations in vivo in neurotoxin-induced rat models of Huntington's and Parkinson's disease. The toxins were: N-methyl-4-phenylpyridinium (MPP+), aminooxyacetic acid (AOAA), 3-nitropropionic acid (3-NP), malonate, and azide. Local or systemic injection of these compounds caused secondary excitotoxic lesions by selective inhibition of mitochondrial respiration that gave rise to elevated lactate concentrations in the striatum. In addition, decreased N-acetylaspartate (NAA) concentrations were noted at the lesion site over time. Measurements of lactate washout kinetics demonstrated that t1/2 followed the order: 3-NP approximately MPP+ >> AOAA approximately malonate, which parallels the expected lifetimes of the neurotoxins based on their mechanisms of action. Further increases in lactate were also caused by intravenous infusion of glucose. At least part of the excitotoxicity is mediated through indirect glutamate pathways because lactate production and lesion size were diminished using unilateral decortectomies (blockade of glutamatergic input) or glutamate antagonists (MK-801). Lesion size and lactate were also diminished by energy repletion with ubiquinone and nicotinamide. Lactate measurements determined by magnetic resonance agreed with biochemical measurements made using freeze clamp techniques. Lesion size as measured with MR, although larger by 30%, agreed well with lesion size determined histologically. These experiments provide evidence for impairment of intracellular energy metabolism leading to indirect excitotoxicity for all the compounds mentioned before and demonstrate the feasibility of small-volume metabolite imaging for in vivo neurochemical analysis.

Abstract  The push-pull activated methyl (3Z)-4,6-O-benzylidene-3-[(methylthio)methylene]-3-deoxy-a-D-eryth ro-hexopy ranosid-2-ulose (1) reacted with dialkyl malonate in the presence of potassium carbonate to give the alkyl (2R,4aR,6S,10bS)-4a,6,8,10b-tetrahydro-6-methoxy-8-oxo-2-phenyl-4H -pyrano[3 ',2':4,5]pyrano[3,2-d][1,3]dioxine-9-carboxylates 2 and 3. Treatment of 1 with 3-oxo-N-phenyl-butyramide, N-(4-methoxy-phenyl)-3-oxo-butyramide, and 3-oxo-N-o-tolyl-butyramide, respectively, in the presence of potassium carbonate and 18-crown-6 yielded the (2R,4aR,6S,10bS)-9-acetyl-7-aryl-4,4a,7,10b-tetrahydro-6-methoxy-2 -phenyl[1 ,3]dioxino-[4',5':5,6]pyrano[3,4-b]pyridin-8(6H)-ones 4-6. (2R,4aR,6S,10bS)-4,4a,8,10b-Tetrahydro-6-methoxy-8-oxo-2-phenyl-4H -pyrano[3 ',2':4,5]pyrano[3,2-d][1,3]dioxine-9-carboxamide (7) was prepared by anellation reactions of 1 either with malononitrile or with cyanoacetamide.

Abstract  A total of 203 Klebsiella strains isolated from patients with acute intestinal diseases were studied. The biochemical variants were determined by taking into account the complex of such signs as the capacity for producing indole, hydrolyzing urea, utilizing sodium malonate, fermenting inositol, dulcitol, sorbose, adonitol, synthesizing acetylmethyl carbinol, reacting with methyl red. The strains under study were found to belong to 36 K-types. Klebsiella strains with K-antigens 20, 2, 62, 60, 21, 40 showed the highest isolation rate.

Abstract  In this study, we exploit the alpha-acidity of saturated fatty acid methyl esters (FAMEs) for the direct conversion of these renewable raw materials to malonate derivatives. After deprotonation with sodium hydride in dimethyl carbonate (DMC) as reactive solvent, the ester enolates react with DMC to give the desired products with up to 80% isolated yield. These malonate derivatives, bearing a long aliphatic chain with chain lengths of C sub(6)-C sub(16), were then polymerized to yield polyesters and polyamides. The polyesters were obtained by copolymerization with 1,6-hexanediol and titanium isopropoxide as a catalyst. For the polyamides, 1,6-hexanediamine was used with 1,5,7-triazabicyclo[4.4.0]dec-5-ene (TBD) as a catalyst. The obtained polyesters are highly viscous and tacky materials with low melting points and a molecular weight range of 9-17 kDa. The polyamides, on the other hand, are high melting polymers with molecular weights from 7-15 kDa.

Abstract  The biogenesis of sorangicin A (1) was studied by feeding experiments with single and doubly labeled ( super(13)C)acetates as well as sodium. ( super(13)C)hydrogencarbonate and (methyl- super(13)C)methionine. Accordingly, 1 is assembled by linear condensation of twenty acetate units onto a malonate starter unit, which is completely preserved in 1. The carboxy group of the malonyl-CoA ester, identical with C-1 in 1, is labeled by ( super(13)C)carbonate or by carbon originating from (1- super(13)C)acetate. The four methyl groups in 1 are derived from methionine.

Abstract  Focal infusions of the succinate dehydrogenase inhibitor, malonate, into the substantia nigra pars compacta (SNc) of adult Sprague-Dawley rats resulted in a substantial depletion of ipsilateral striatal tyrosine hydroxylase (TH) activity. The percentage decrease in striatal TH activity following intranigral malonate (0.5 mumol/0.5 microliter) infusion was similar at 4 (58%) and 7 days (62%) post-infusion. To assess the role of N-methyl-D-aspartate (NMDA) receptor activation in malonate neurotoxicity, animals were pretreated with the NMDA receptor antagonist MK-801 (2 x 5 mg/kg, i.p.). Four days post-infusion of malonate (0.5 mumol/0.5 microliter) into the SNc, striatal TH activity was depleted by 58% in vehicle pretreated animals and 14% in the presence of MK-801 indicating a significant neuroprotective effect of MK-801 on malonate action. To determine the role of nitric oxide (NO) in malonate-induced nigral toxicity, the actions of malonate were evaluated in the presence of the nitric oxide synthase (NOS) inhibitors, 7-nitro indazole (7-NI) and N omega-nitro-L-arginine methyl ester (L- NAME). Systemic injections of 7-NI (20, 30, 40, 50 and 75 mg/kg, i.p.) produced a dose-related inhibition of nigral NOS activity which was maximal at a dose of 40 mg/kg. Intranigral infusion of malonate with 20 and 50 mg/kg 7-NI pretreatment produced a 46 and 31% decrease in striatal TH activity, respectively. Thus, a significant protective effect at the higher but not lower dose of 7-NI was observed. Pretreatment with a L- NAME regimen (2 x 250 mg/kg; i.p.), previously shown to inhibit brain NOS activity by greater than 86%, also produced a significant neuroprotective effect against malonate-induced neurotoxicity (30% decrease). The results of this study suggest that malonate-induced toxicity to the dopaminergic neurons of the nigrostriatal pathway is mediated, at least in part, by NMDA receptor activation and the formation of NO.

Abstract  Methyl 10-undecenoate (2b) has been oxidized with tert-butyl hydroperoxide/selenium dioxide and potassium dichromate to 53% of methyl 9-oxo-10-undecenoate (4). Based on the conversion of 2b, the yield of 4 is 81%. Residual selenium in ester 5 was determined to be less than 1ppm. The electrophilic double bond in enone 4 reacts in good to excellent yield with a variety of nucleophiles. With dimethyl malonate, acetylacetone, and methyl acetoacetate Michael-adducts at C-11 of enone 4 were obtained in 88-99% yield. Corresponding additions were achieved with nitroethane, 1- and 2-nitropropane in 78-89% yield. In a Nef-reaction some nitroalkyl adducts were converted to methyl esters of 9,12-dioxofatty acids in 99% yield. In methanol/sodium methoxide the ester methyl 11-methoxy-9-oxoundecanoate was obtained in 86% yield from enone 4. In a three step reaction with ammonium chloride/sodium cyanide, hydrochloric acid/acetic acid, and methanol/2,2-dimethoxypropane the ester 4 yielded 63% of dimethyl 4-oxo-dodecanedioate. With the cyanide ion the electrophilic carbon atom in aldehydes can be converted into a nucleophile (Stetter-reaction). Catalysed by sodium cyanide in DMF aromatic and heteroaromatic aldehydes RCHO with R=phenyl, 2-thienyl, 2-furyl and 3-pyridyl were added to enone 4 to afford methyl 12-aryl- and methyl 12-heteroaryl-9,12-dioxododecanoates in 54-73% yield. Practical applications: The prepared oleochemicals are useful as precursors for pharmaceuticals and as monomers for polyesters and polyamides. They also may be applied to synthesize fatty acid conjugates by providing suitable connectors for biological active compounds and to attach groups with suitable physical properties for materials. For enone 4 prepared from methyl 10-undecenoate, thirteen Michael additions with 1,3-dicarbonyl and nitro alkyl compounds, hydrocyanic acid and acyl anions are reported.

Abstract    Several bisquarternary ammonium salts were synthesized and tested as to their antitumor activity. However, none of them exhibited any effective activity. Additionally, alkylation of nucleophiles with quarternary ammonium salts, dimethylaminomethyl p-tolyl ether methiodide and ethylene bis (N, N-diethyl-N-methylammonium iodide), was examined. Dimethylaminomethyl p-tolyl ether methiodide reacted successfully with nucleophiles, such as amine, thiol and alcohol, to give the expected compounds in which p-tolyloxymethyl group was introduced to the nucleophilic compounds. On the other hand, ethylene his (N, N-diethyl-N-methylammonium iodide) reacted with thiophenol and diethyl malonate to give the methylated compounds, methyl phenyl sulfide and diethyl malonate respectively.

Abstract  The name Escherichia vulneris sp. nov. (formerly called Alma group 1 and Enteric group 1 by the Centers for Disease Control and API group 2 by Analytab Products, Inc.) is proposed for a group of isolates from the United States and Canada, 74% of which were from human wounds. E. vulneris is a gram-negative, oxidase-negative, fermentative, motile rod with the characteristics of the family Enterobacteriaceae Biochemical reactions characteristic of 61 E. vulneris strains were positive tests for methyl red, malonate, and lysine decarboxylase; a delayed positive test for arginine dihydrolase; acid production from D-mannitol, L-arabinose, raffinose, L-rhamnose, D-xylose, trehalose, cellobiose, and melibiose; negative tests for Voges-Proskauer, indole, urea, H sub(2)S, citrate, ornithine decarboxylase, phenylalanine deaminase, and DNase; and no acid from dulcitol, adonitol, myo-inositol, and D-sorbitol. )E. vulnerisshowed the highest relatedness to species of Escherichia (25 to 39%) and Enterobacter (24 to 35%). On the basis of biochemical similarity, the new species was placed in the genus Escherichia The type strain of E. vulneris is ATCC 33821 (CDC 875-72).

Abstract  Arphamenine A, produced from Chromobacterium violaceum BMG361-CF4 as an amino peptidase B inhibitor, is the first naturally occurring carba analog of peptide and epi-arphamenine A is the artifact from the epimerization at C-2. Here the authors describe the synthesis of optically active arphamenine A and epi-arphamenine A. Since in these compounds epimerization at C-2 should be inevitable, the C-1 similar to C-3 portion was synthesized by "malonic ester synthesis" which gave the diastereomers.