Risk factors in community-acquired/onset urinary tract infections due to extended-spectrum beta-lactamase-producing Escherichia coli and Klebsiella pneumoniae.

We investigated the risk factors for community acquired/onset urinary tract infections due to extended spectrum beta-lactamase (ESBL)-positive Escherichia coli or Klebsiella pneumoniae in 62 patients who were followed-up from August 1, 2003 to September 1, 2006. Sixty patients with community-acquired urinary tract infections caused by ESBL-negative E. coli or K. pneumoniae who were followed-up during the same dates were included as a control group. Age (> or =65 or <65 years old), sex, bladder cancer, benign prostate hypertrophy (BPH), prostate cancer, urolithiasis, urethral catheter, previous urological operation, diabetes mellitus, use of antibiotics during the last 3 months and hospitalization during the last 3 months were investigated as risk factors. The presence of previous urological operation and quinolone or cephalosporin use for any infection during the last 3 months were found to be independent risk factors. Knowing the risk factors for community acquired/onset urinary tract infections caused by ESBL-positive E. coli or K. pneumoniae is of great importance in planning empirical antibiotic therapy.

5,6-Diphenylthieno[2,3-d][1,3]dithiole-2-thione.

The title compound, C(17)H(10)S(4), has two independent molecules in the asymmetric unit. In both molecules, the fused heterocycle is almost planar and the phenyl groups make dihedral angles of 42.88 (9) and 52.79 (8) degrees with the fused heterocycle in one molecule, and angles of 40.62 (9) and 52.28 (8) degrees in the other. The crystal packing is governed by short intermolecular S.S interactions, the shortest contact being 3.333 (1) A.

5,6-Diphenyl[1,3]dithiolo[4,5-b]-dithiine-2-thione.

In the title compound, C(17)H(10)S(5), the dithiine ring adopts a boat conformation while the dithiole ring has an envelope conformation. The phenyl groups are planar and make dihedral angles of 40.7 (2) and 59.8 (2) degrees with the best plane of the thiine ring. The shortest intermolecular S...S contact is 3.305 (2) A.

Synthesis of some 1-(2-naphthyl)-2-(imidazole-1-yl)ethanone oxime and oxime ether derivatives and their anticonvulsant and antimicrobial activities.

In this study, oxime and oxime ether derivatives of anticonvulsant nafimidone [1-(2-naphthyl)-2-(imidozole-1-yl)ethanone] were prepared as potential anticonvulsant compounds. Nafimidone oxime was synthesized by the reaction of nafimidone and hydroxylamine hydrochloride. O-Alkylation of the oxime by various alkyl halides gave the oxime ether derivatives. Anticonvulsant activity of the compounds was determined by maximal electroshock (MES) and subcutaneous metrazole (scMet) tests in mice and rats according to procedures of the Antiepileptic Drug Development (ADD) program of the National Institutes of Health (NIH). In addition to anticonvulsant evaluation, compounds were also screened for possible antibacterial and antifungal activities because of the structural resemblance to the azole antifungals, especially to oxiconazole. All compounds were evaluated against three human pathogenic fungi and four bacteria using the microdilution method. Most of the compounds exhibited both anticonvulsant and antimicrobial activities; the O-alkyl substituted compounds (2, 3, 4 and 5) were found to be more active than the O-arylalkyl substituted compounds in both screening paradigms.

5-Benzyl-5-phenyl[1,3]dithiolo[4,5-d]-[1,3]dithiole-2-thione.

In the title compound, C(17)H(12)S(5), the dithiole ring bearing the aryl substituents assumes an envelope conformation with the maximum deviation from planarity being -0.053 A. The phenyl and benzyl rings are twisted by 33.0 (1) and 31.1 (1) degrees, respectively, out of the dithiole plane. The crystal packing is governed by short S...S interactions, with the shortest being 3.550 (2) A.

2-[(4-Hydroxyphenyl)iminomethyl]thiophene.

The molecular structure of the title compound, C(11)H(9)NOS, has three planar moieties, two of which are rings, namely the hydroxyphenyl and the thiophene, with an angle of 20.76 (10) degrees between them. The crystal structure is stabilized by an O-H.N hydrogen bond and by C-H.O intermolecular interactions. The C.O intermolecular contact distance is 3.443 (2) A.

Synthesis and hypnotic activity of new 4-thiazolidinone and 2-thioxo-4,5-imidazolidinedione derivatives.

Conveniently accessible 4-[(2-(3,4-dimethoxyphenyl)ethyl]-3-thiosemicarbazide (2) was converted to new 1-substituted benzylidene/furfurylidene-4- [2-(3,4-dimethoxyphenyl)ethyl]-3-thiosemicarbazides (3) which furnished 2-(substituted benzylidene/furfurylidene) hydrazono-3-[2-(3,4-dimethoxyphenyl)ethyl]thiazolidin-4-ones (4) and 1-(substituted benzylidene/furfurylidene)-amino -3-[2-(3,4-dimethoxyphenyl)ethyl]-2-thioxo-4,5-imidazolidinedio nes (5) on reaction with chloroacetic acid and oxalyl chloride, respectively. The structure of 5 was confirmed by X-ray diffraction studies performed on 5a. 4 and 5 were evaluated for their potentiating effects on pentobarbital induced hypnosis. Most of the compounds caused remarkable increases in pentobarbital sleeping time.

Synthesis and X-ray crystal structure of the calcium channel antagonist: dimethyl 1,4-dihydro-2,6-dimethyl-4-[4'-(4H-4-oxo-1-benzopyran-2-yl)phenyl]- 3,5-pyridine dicarboxylate.

The synthesis of the title compound via the Hantzsch method from 4'-flavone carboxaldehyde is described, and its molecular structure was determined by X-ray crystallography. The 1,4-dihydropyridine (1,4-DHP) ring adopts a boat conformation. The phenyl ring of the flavone is not exactly perpendicular to the DHP ring. Calcium antagonistic activity of this compound was evaluated in vitro by using BaCl2-stimulated rat ileum.

A GLC1A gene Gln368Stop mutation in a patient with normal-tension open-angle glaucoma.

PURPOSE: To present a case involving a patient with normal-tension glaucoma with a Gln368Stop mutation of the myocilin/trabecular meshwork inducible glucocorticoid response protein (MYOC/TIGR) gene. METHODS: Slit-lamp biomicroscopic and gonioscopic examination, morphometry of the optic disc, 24-hour intraocular pressure (IOP) profile, and perimetry were performed to determine the phenotype of the patient. Neurologic examination and a computed tomographic (CT) scan of the brain were performed to rule out a neurologic disorder. Single-strand confirmation polymorphism (SSCP) analysis and subsequent sequence analysis of blood was performed for genotyping of the GLC1A gene. RESULTS: A nonsense codon, namely a Gln368Stop mutation in the third exon of the GLC1A gene, was found in this patient with normal-tension glaucoma. CONCLUSION: In contrast to previous reports, a Gln368Stop mutation of the GLC1A gene need not be confined to patients with glaucomatous optic atrophy due to high IOP. The pathogenesis of glaucoma associated with GLC1A gene mutations might be more complex than expected, and (unknown) suppressor mechanisms have to be considered.

Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies: a SacI polymorphism in the proximal CMT1A-REP elements may lead to genetic misdiagnosis.

A male patient with clinical signs and symptoms of a demyelinating neuropathy was shown to have a duplication of the 1.5-Mb region on chromosome 17p11.2 by means of two-color fluorescence in situ hybridization (FISH). This duplication is typical for the vast majority of Charcot-Marie-Tooth type 1A (CMT1A) cases. Analysis of DNA extracted from peripheral blood used to detect an EcoRI/SacI 3. 2-kb junction fragment with probe pLR7.8 confirmed the CMT1A duplication, but also revealed a 7.8-kb fragment usually observed in patients with a hereditary neuropathy with liability to pressure palsies (HNPP). Both fragments observed in one patient canot result from one unequal crossover. In EcoRI/SacI Southern hybridization experiments with probe pLR7.8 DNA of his healthy parents also revealed a 7.8-kB restriction fragment. A subsequent two-color FISH analysis, however, indicated a normal status for interphase nuclei of the parents. Hence we hypothesize that the 7.8-kb fragment observed in our patient and his parents is not the product of unequal crossover during meiosis but due to a polymorphism of the SacI site in a proximal CMT1A-REP element.