The effect of the oil resin on the properties of solution of the petroleum wax treated in an ultrasonic field

It was found that the complex treatment of ultrasonic followed by the addition of 0.3% by weight. petroleum resins, a more efficient method of inhibiting sedimentation processes than just ultrasonic or addition of 0,3% by weight. petroleum resins. According to the obtained data, fragments of aliphatic petroleum resins are adsorbed on the high molecular hydrocarbons of normal structure and prevent their aggregation thus the inhibition of sedimentation occurs

Enzymology of dicarboxylic acid metabolism in Corynebacterium sp. strain 7E1C

1.Dicarboxylic acid metabolism was investigated in the alkane-utilizing bacterium Corynebacterium 7E1C.2.The best yields of dicarboxylic acid were obtained during growth on dodecane although significant amounts of tetradecanedioic acid were produced during growth on methyl myristate. No dicarboxylic acid was produced during growth on hexadecane, methyl palmitate or 16-hydroxypalmitate.3.Corynebacterium 7E1C possesses constitutive NAD+-dependent and NADP+-dependent alcohol dehydrogenases active with mono-ol, a, w-diol and (L)-hydroxyfatty acids. Additional NADP+-dependent octanol dehydrogenase activity was detected after growth on alkyl-containing substrates.4.Corynebacterium 7E1C possesses a constitutive acyl-CoA thioesterase active with monocarboxyl-, w-hydroxymonocarboxyl- and dicarboxyl-CoA esters. Long chain-length acyl-CoAs are the preferred substrates.5.Corynebacterium 7E1C possesses constitutive acyl-Con synthetase(s) active with monocarboxylic, w-hydroxymonocarboxylic and dicarboxylic-acids.6.Corynebacterium 7E1C possesses a constitutive ß-oxidation system. Long chain monocarboxyl-CoA esters and 16-hydroxypalmitoyl-CoA are good ß-oxidation substrates whereas short chain monocarboxyl-CoAs, long chain dicarboxyl-CoAs and 12-hydroxylauroyl-CoA are poor 5-oxidation substrates. Significant accumulation of saturated ß-oxidation intermediates occurred during the 9-oxidation of palmitate by cell-free extracts. When hydroxyacyl-CoA dehydrogenase was inhibited, hexadecenoyl-CoA and 3-hydroxypalmitoyl-CoA accumulated.7. The specificities of these enzyme systems are consistent with the range of dicarboxylic acids accumulated by this organism

The liver isoform of carnitine palmitoyltransferase 1 is not targeted to the endoplasmic reticulum.

Liver microsomal fractions contain a malonyl-CoA-inhibitable carnitine acyltransferase (CAT) activity. It has been proposed [Fraser, Corstorphine, Price and Zammit (1999) FEBS Lett. 446, 69-74] that this microsomal CAT activity is due to the liver form of carnitine palmitoyltransferase 1 (L-CPT1) being targeted to the endoplasmic reticulum (ER) membrane as well as to mitochondria, possibly by an N-terminal signal sequence [Cohen, Guillerault, Girard and Prip-Buus (2001) J. Biol. Chem. 276, 5403-5411]. COS-1 cells were transiently transfected to express a fusion protein in which enhanced green fluorescent protein was fused to the C-terminus of L-CPT1. Confocal microscopy showed that this fusion protein was localized to mitochondria, and possibly to peroxisomes, but not to the ER. cDNAs corresponding to truncated (amino acids 1-328) or full-length L-CPT1 were transcribed and translated in the presence of canine pancreatic microsomes. However, there was no evidence of authentic insertion of CPT1 into the ER membrane. Rat liver microsomal fractions purified by sucrose-density-gradient centrifugation contained an 88 kDa protein (p88) which was recognized by an anti-L-CPT1 antibody and by 2,4-dinitrophenol-etomoxiryl-CoA, a covalent inhibitor of L-CPT1. Abundance of p88 and malonyl-CoA-inhibitable CAT activity were increased approx. 3-fold by starvation for 24 h. Deoxycholate solubilized p88 and malonyl-CoA-inhibitable CAT activity from microsomes to approximately the same extent. The microsomal fraction contained porin, which, relative to total protein, was as abundant as in crude mitochondrial outer membranes fractions. It is concluded that L-CPT1 is not targeted to the ER membrane and that malonyl-CoA CAT in microsomal fractions is L-CPT1 that is derived from mitochondria, possibly from membrane contact sites

A new mouse mutant, skijumper

Low blood sugar levels are a well-known cause of severe illness and often death in newborn humans, especially those that are small for age. Few of the causes of neonatal hypoglycemia are known, and many remain to be found. We describe a novel mouse mutant, skijumper (skimp), in which pups, despite feeding well, have low levels of glucose and develop opisthotonos, followed by death typically within a few days after birth. Genetic mapping studies have localized the lesion to a approximately 1 cM interval on mouse Chromosome (Chr) 7 between D7Mit318 and D7Mit93. We have carried out extensive analysis to define the phenotype and its likely cause. In addition to low blood glucose, affected skijumper mice have lowglycogen and ketone levels. Mass spectrometric analysis of blood samples has excluded major defects in amino acid metabolism. Initial biochemical analyses suggested a defect in ketogenesis as one possible cause of this phenotype. However, measurements of levels and activities of carnitine, carnitine palmitoyl transferases, and other enzymes involved in ketogenesis, along with studies of mitochondrial structure and function, did not demonstrate significant differences between skijumper, unaffected littermates, and control wild-type mice. These results indicate that abnormal enzyme activity in known pathways does not appear to be the primary biochemical lesion in skijumper. The skijumper may be a new valuable model for studying and understanding one type of neonatal morbidity and death

A Schlemm Canal Microstent for Intraocular Pressure Reduction in Primary Open-Angle Glaucoma and Cataract: The HORIZON Study

Objective: To compare cataract surgery with implantation of a Schlemm canal microstent with cataract surgery alone for the reduction of intraocular pressure (IOP) and medication use after 24 months. Design: Prospective, multicenter, single-masked, randomized controlled trial. Participants: Subjects with concomitant primary open-angle glaucoma (POAG), visually significant cataract, and washed-out modified diurnal IOP (MDIOP) between 22 and 34 mmHg. Methods: Subjects were randomized 2:1 to receive a single Hydrus Microstent (Ivantis, Inc, Irvine, CA) in the Schlemm canal or no stent after uncomplicated phacoemulsification. Comprehensive eye examinations were conducted 1 day, 1 week, and 1, 3, 6, 12, 18, and 24 months postoperatively. Medication washout and MDIOP measurement were repeated at 12 and 24 months. Main Outcome Measures: The primary and secondary effectiveness end points were the proportion of subjects demonstrating a 20% or greater reduction in unmedicated MDIOP and change in mean MDIOP from baseline at 24 months, respectively. Hypotensive medication use was tracked throughout the course of follow-up. Safety measures included the frequency of surgical complications and adverse events. Results: A total of 369 eyes were randomized after phacoemulsification to Hydrus Microstent (HMS) and 187 to no microstent (NMS). At 24 months, unmedicated MDIOP was reduced by ≥20% in 77.3% of HMS group eyes and in 57.8% of NMS group eyes (difference = 19.5%, 95% confidence interval [CI] 11.2%–27.8%, P < 0.001). The mean reduction in 24-month unmedicated MDIOP was −7.6±4.1 mmHg (mean ± standard deviation) in the HMS group and −5.3±3.9 mmHg in the NMS group (difference = −2.3 mmHg; 95% CI, −3.0 to −1.6; P < 0.001). The mean number of medications was reduced from 1.7±0.9 at baseline to 0.3±0.8 at 24 months in the HMS group and from 1.7±0.9 to 0.7±0.9 in the NMS group (difference = −0.4 medications; P < 0.001). There were no serious ocular adverse events related to the microstent, and no significant differences in safety parameters between the 2 groups. Conclusions: This 24-month multicenter randomized controlled trial demonstrated superior reduction in MDIOP and medication use among subjects with mild-to-moderate POAG who received a Schlemm canal microstent combined with phacoemulsification compared with phacoemulsification alone