Sacral neuromodulation treatment for urinary voiding dysfunctions: Results of treatment with the largest single-center series in a tertiary referral center in Turkey.

Background/aim: Sacral neuromodulation (SNM) is a minimally invasive treatment that modulates spinal reflexes to regulate bladder, urinary sphincter, and pelvic floor and has successfully been used in the treatment of refractory voiding dysfunctions. The aim of this study was to present our experience with SNM in a tertiary referral center with the largest number of patients and review the safety and efficacy of the procedure. Materials and methods: A total of 42 patients with refractory lower urinary tract symptoms were included into the study.

Novel indole hydrazide derivatives: Synthesis and their antiproliferative activities through inducing apoptosis and DNA damage.

A series of novel indole hydrazide derivatives was synthesized and evaluated for their anticancer activities. Compound 12 exhibited the highest antiproliferative activity against the MCF-7 cell line, with an IC value of 3.01 µM.

Role of cytochrome P4503A in cysteine S-conjugates sulfoxidation and the nephrotoxicity of the sevoflurane degradation product fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (compound A) in rats.

The volatile anesthetic sevoflurane is degraded to fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (FDVE) in anesthesia machines. FDVE is nephrotoxic in rats. FDVE undergoes glutathione conjugation, subsequent conversion to cysteine and mercapturic acid conjugates, and cysteine conjugate metabolism by renal beta-lyase, which is a bioactivation pathway mediating nephrotoxicity in rats.

Comparison of derivative spectrophotometric and liquid chromatographic methods for the determination of rofecoxib.

Two different UV spectrophotometric methods were developed for the determination of rofecoxib in bulk form and in pharmaceutical formulations. The first method, an UV spectrophotometric procedure, was based on the linear relationship between the rofecoxib concentration and the lambdamax amplitude at 279 nm. The second one, the first derivative spectrophotometry, was based on the linear relationship between the rofecoxib concentration and the first derivative amplitude at 228, 256 and 308 nm.

Sulfoxidation of cysteine and mercapturic acid conjugates of the sevoflurane degradation product fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (compound A).

The volatile anesthetic sevoflurane is degraded in anesthesia machines to the haloalkene fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (FDVE), which can cause renal and hepatic toxicity in rats. FDVE is metabolized to S-[1,1-difluoro-2-fluoromethoxy-2-(trifluoromethyl)ethyl]-L-cysteine (DFEC) and (E) and (Z)-S-[1-fluoro-2-fluoromethoxy-2-(trifluoromethyl)vinyl]-L-cysteine [(E,Z)-FFVC], which are N-acetylated to N-Ac-DFEC and (E,Z)-N-Ac-FFVC S-conjugates. Some haloalkene S-conjugates undergo sulfoxidation.

Quinidine as a probe for the role of p-glycoprotein in the intestinal absorption and clinical effects of fentanyl.

The mechanism of individual variability in the fentanyl dose-effect relationship is unknown. The efflux pump P-glycoprotein (P-gp) regulates brain access and intestinal absorption of numerous drugs. Evidence exists that fentanyl is a P-gp substrate in vitro, and P-gp affects fentanyl analgesia in animals.

A study on the interaction between p60 c-Src receptor tyrosine kinase and arylcarboxylic and arylacetic acid derivatives based on docking modes and in vitro activity.

The fundamental role that receptor tyrosine kinases play in cancer and other proliferative diseases has provided the impetus for an extensive effort on the part of both academic and pharmaceutical laboratories to develop highly specific inhibitors. In this study, inhibitory activity of previously synthesized arylacetic and arylcarboxylic acid derivatives were examined against substrate of tyrosine kinase. It can be assumed that the activity of compounds becomes higher when the -CH(2) linkage exist between aromatic ring and the amide group of the side chain.

Cytotoxicity of S-conjugates of the sevoflurane degradation product fluoromethyl-2,2-difluoro-1-(trifluoromethyl) vinyl ether (Compound A) in a human proximal tubular cell line.

Fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (FDVE) is a fluorinated alkene formed by degradation of the volatile anesthetic sevoflurane in anesthesia machines. FDVE is nephrotoxic in rats but not humans. Rat FDVE nephrotoxicity is attributed to FDVE glutathione conjugation and bioactivation of subsequent FDVE-cysteine S-conjugates, in part by renal beta-lyase.

Glutathione S-conjugation of the sevoflurane degradation product, fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (compound A) in human liver, kidney, and blood in vitro.

Fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether (FDVE) is a fluorinated alkene formed by degradation of the volatile anesthetic sevoflurane in anesthesia machines. FDVE is nephrotoxic in rats and undergoes glutathione-dependent conjugation to form two alkane (G1, G2) and two alkene glutathione S-conjugates (G3, G4), cleavage to cysteine S-conjugates, and beta-lyase-catalyzed metabolism to reactive thionoacyl fluorides, which may react with cellular macromolecules to cause nephrotoxicity. Although similar metabolites have been identified in human urine in vivo, little is known about sites and mechanisms of GSH conjugation in humans.

Determination of tetrahydrozoline hydrochloride and fluorometholone in pharmaceutical formulations by HPLC and derivative UV spectrophotometry.

Two methods for the quantitative determination of tetrahydrozoline hydrochloride (1) and fluorometholone (2) in pharmaceutical eye drops (Efemoline) are described. The procedures are based on derivative UV spectrophotometry and HPLC. In the former method, d2A/d lambda 2 values were measured in methanol at 226 and 282 nm for 1 and 2, respectively.

Quantitative determination of acrivastine and pseudoephedrine hydrochloride in pharmaceutical formulation by high performance liquid chromatography and derivative spectrophotometry.

In this study, fourth derivative spectrophotometry and high performance liquid chromatography (HPLC) have been used and described for the quantitative determination of acrivastine (I) and pseudoephedrine hydrochloride (II) in their pharmaceutical capsules form (Duact). In the former method, d4A/d gamma 4 values were measured in methanol at 315 and 269 nm for (I) and (II) respectively. The relative standard deviations (RSD) for the method were found to be 1.

Comutagenesis--V: rapid conversion of 2-hydroxyl-amino-3-methylpyridineto 2-amino-3-methylpyridine by a hepatic S9 preparation.

The in vitro metabolism of 2-hydroxylamino-3-methylpyridine has been investigated using arochlor 1254 pretreated rat S9 mixtures. 2-Hydroxylamino-3-methylpyridine is rapidly converted to the parent amine 2-amino-3-methylpyridine. No further oxidation products of 2-hydroxylamino-3-methylpyridine (i.

Comutagenesis-IV in vitro metabolism of the comutagen 2-amino-3-methylpyridine: species differences and metabolic interaction with norharman.

The metabolism of 2-amino-3-methylpyridine (2A3MP) in vitro has been investigated using the rat, rabbit, dog, marmoset, guinea pig and hamster hepatic microsomes and S9 supernatants (10,000 g fraction). Species differences were observed in the in vitro formation of 2-amino-3-methylpyridine-N-oxide (2A3MPNO), 2-amino-3-hydroxymethylpyridine (2A3HMP) and 2-amino-3-methyl-5-hydroxypyridine (2A3M5HP). The order of activity for 2A3MPNO using hepatic microsomes was dog > rat > rabbit > guinea pig > marmoset > hamster, for 2A3HMP dog > hamster > guinea pig > rat > rabbit > marmoset, for 2A3M5HP rabbit > hamster > dog > rat > guinea pig > marmoset.

Comutagenesis-III. In vitro metabolism of 2-amino-3-methylpyridine: the effect of various potential inhibitors, activators and inducers.

1. The effects of various potential inhibitors, activators and inducers on the metabolism of the comutagen 2-amino-3-methylpyridine (2A3MP) by rabbit hepatic microsomes and S9 supernatants have been studied. 2.

Comutagenesis-I: the in vitro metabolism of 2-amino-3-methylpyridine.

The metabolism of the comutagen 2-amino-3-methylpyridine has been studied in vitro using rat and rabbit hepatic preparations. 2-Amino-3-methylpyridine-N-oxide, 2-amino-3-hydroxymethylpyridine and 2-amino-5-hydroxy-3-methylpyridine were formed by both rat and rabbit hepatic preparations. No evidence was obtained for the formation of the corresponding 2-hydroxylamine, 2-nitroso, 2-nitro-3-methyl-pyridine or their condensation products i.

Comutagenesis-II. Some factors influencing the in vitro metabolism of 2-amino-3-methylpyridine.

Factors affecting the metabolism of 2-amino-3-methylpyridine (2A3MP) in vitro have been studied and the conditions which allow maximal metabolism established. Ring nuclear and methyl hydroxylation, and 1-N-oxidation of 2A3MP were linear with respect to arochlor 1254 induced rat S9 supernatant (10,000 g fraction) up to 4.86 mg per ml.

Effect of various potential inhibitors, activators and inducers on the N-oxidation of isomeric aromatic diazines in vitro using rabbit liver microsomal preparations.

1. The effects of various potential inhibitors, activators and inducers on the N-oxidation of isomeric aromatic diazines (pyrazine, pyrimidine and pyridazine) by rabbit liver microsomes have been studied. 2.

Factors involved in the N-oxidation of isomeric aromatic diazines by microsomal preparations.

Factors affecting the metabolism of isomeric aromatic diazines in vitro were studied and the conditions which allow maximal metabolism established. The N-oxidation of isomeric diazines was linear with respect to microsomal concentration up to 0.5 g original liver weight per ml using a rabbit microsomal suspension.

In vitro tuberculostatic activities of some 2-benzylbenzimidazole and 2-phenoxymethylbenzimidazole derivatives.

Some 2-benzylbenzimidazole and 2-phenoxymethylbenzimidazole derivatives were synthesized and tested for in vitro tuberculostatic activity against Mycobacterium tuberculosis H 37 Rv. and human type wild strain (protocol n degrees.4186).