Testicular torsion before 6 hours. I

BACKGROUND: Following the crash of a Boeing 737-400 aircraft on the M1 motorway at Kegworth, near Nottingham, England, on January 8, 1989, it became apparent that a large number of pelvic and lower limb injuries had been sustained by the survivors. Had there been a fire, these injuries would have severely hindered the ability of the occupants to escape. The mechanism of pelvic and lower limb injuries in impact accidents previously has been related to flailing of the limbs and axial loading of the femur as in automobile accidents. HYPOTHESIS: A bending load is the primary mechanism of femoral fracture in an impact aircraft accident rather than an axial load. METHODS: Two methods of study have been used to investigate the impact biomechanics of the pelvis and lower limb: a) clinical review of the injuries sustained in the M1 Kegworth accident; and b) impact testing. RESULTS: A clinical review of the M1 aircrash survivors suggested that axial loading was not the primary mechanism causing femoral fractures and suggested that a bending load might be applied to the femur. Impact testing confirmed that axial loading of the femur did not appear to be significant. CONCLUSIONS: Our study suggests that in the presence of intact occupant protection systems, a femoral bending mechanism involving the front seat spar of passenger seats is a primary cause of femoral fracture in an impact aircraft accident.     

蜡助剂在水性镶木地板漆和印墨中的应用

重点讨论了通过在水性镶木地板漆和水性印墨中正确地使用蜡助剂,以得到最有效的表面保护,如耐细微划伤性、耐擦洗性和耐磨性的可能性.由于在干燥期间,蜡粒子聚集在涂层表面,对最终涂层的性质而言,选择合适的碱性蜡或其组合物是最重要的依据.除了表面保护外,蜡助剂还会影响其他性质,如表面滑爽性和抗粘连性.     

The Vibrio cholerae mannose-sensitive hemagglutinin is the receptor for a filamentous bacteriophage from V. cholerae O139

We previously isolated from a 1994 isolate of Vibrio cholerae O139 a filamentous lysogenic bacteriophage, choleraphage 493, which inhibits pre-O139 but not post-O139 El Tor biotype V. cholerae strains in plaque assays. We investigated the role of the mannose-sensitive hemagglutinin (MSHA) type IV pilus as a receptor in phage 493 infection. Spontaneous, Tn5 insertion, and mshA deletion mutants are resistant to 493 infection. Susceptibility is restored by mshA complementation of deletion mutants. Additionally, the 493 phage titer is reduced by adsorption with MSHA-positive strains but not with a DeltamshA1 strain. Monoclonal antibody against MSHA inhibits plaque formation. We conclude that MSHA is the receptor for phage 493. The emergence and decline of O139 in India and Bangladesh are correlated with the susceptibility and resistance of El Tor strains to 493. However, mshA gene sequences of post-O139 strains are identical to those of susceptible pre-O139 isolates, indicating that phage resistance of El Tor is not due to a change in mshA. Classical biotype strains are (with rare exceptions) hemagglutinin negative and resistant to 493 in plaque assays. Nevertheless, they express the mshA pilin gene. They can be infected with 493 and produce low levels of phage DNA, like post-O139 El Tor strains. Resistance to 493 in plaque assays is thus not equivalent to resistance to infection. The ability of filamentous phages, such as 493, to transfer large amounts of DNA provides them, additionally, with the potential for quantum leaps in both identity and pathogenicity, such as the conversion of El Tor to O139.     

A lactulose sensor based on coupled enzyme reactions with a ring electrode fabricated from tetrathiafulvalen-tetracyanoquinodimetane

A dual enzyme electrode is explored for measuring lactulose in milk. A ring electrode (diameter = 3 mm; ring width = 10-20 microns) is proposed onto which tetrathiafulvalen-tetracyanoquinodimetane (TTF-TCNQ) salt was physically packed. The electrode is a band electrode with dimensions approaching those for micro electrodes, so that the improved faradaic current/charging current ratio lead to improved detection limits. Fructose dehydrogenase (FDH) and beta-galactosidase (beta-gal) were immobilized by covering the electrode surface with a dialysis membrane. Lactulose was hydrolyzed to D-fructose and D-galactose by beta-gal. The hydrolyzed D-fructose was oxidized by FDH which was simultaneously reduced to the reduced form (FDH-PQQH2). The FDH-PQQH2 was directly reoxidized by TTF-TCNQ on the ring electrode, whose current was monitored at 200 mV vs Ag/AgCl. The detection limit of the lactulose sensor was 1.0 microM and the selectivity for lactulose was at least 1000 times higher than that for lactose. Pasteurized, UHT and sterilized milks were applied to the lactulose sensor, showing good accuracy and precision and, furthermore, good correlation to a reference photometric method, even though no rigorous procedure for the electrode fabrication has presently been addressed.     

N-(2-Benzoylphenyl)-L-tyrosine PPARgamma agonists. 2. Structure-activity relationship and optimization of the phenyl alkyl ether moiety

We previously reported the identification of (2S)-((2-benzoylphenyl)amino)-3-?4-[2-(5-methyl-2-phenyloxazol-4-y l)e thoxy]phenyl?propanoic acid (2) (PPARgamma pKi = 8.94, PPARgamma pEC50 = 9.47) as a potent and selective PPARgamma agonist. We now report the expanded structure-activity relationship around the phenyl alkyl ether moiety by pursuing both a classical medicinal chemistry approach and a solid-phase chemistry approach for analogue synthesis. The solution-phase strategy focused on evaluating the effects of oxazole and phenyl ring replacements of the 2-(5-methyl-2-phenyloxazol-4-yl)ethyl side chain of 2 with several replacements providing potent and selective PPARgamma agonists with improved aqueous solubility. Specifically, replacement of the phenyl ring of the phenyloxazole moiety with a 4-pyridyl group to give 2(S)-((2-benzoylphenyl)amino)-3-?4-[2-(5-methyl-2-pyridin-4-yloxazol+ ++- 4-yl)ethoxy]phenyl?propionic acid (16) (PPARgamma pKi = 8.85, PPARgamma pEC50 = 8.74) or a 4-methylpiperazine to give 2(S)-((2-benzoylphenyl)amino)-3-(4-?2-[5-methyl-2-(4-methylpiperazin+ ++- 1-yl)thiazol-4-yl]ethoxy?phenyl)propionic acid (24) (PPARgamma pKi = 8.66, PPARgamma pEC50 = 8.89) provided two potent and selective PPARgamma agonists with increased solubility in pH 7.4 phosphate buffer and simulated gastric fluid as compared to 2. The second strategy took advantage of the speed and ease of parallel solid-phase analogue synthesis to generate a more diverse set of phenyl alkyl ethers which led to the identification of a number of novel, high-affinity PPARgamma ligands (PPARgamma pKi's 6.98-8.03). The combined structure-activity data derived from the two strategies provide valuable insight on the requirements for PPARgamma binding, functional activity, selectivity, and aqueous solubility.     

Myocardial morphology in fibrillation and defibrillation of the heart ventricles

The morphology of the contractile myocardium was studied experimentally in fibrillation and defibrillation of the ventricles on 30 rabbits. Morphology of the contractile myocardium appears as vacuolated dystrophy of the cardiomyocytes, destruction of mitochondria and contracture lesions of the myofibrils. The latter with progressing fibrillation become irreversible. Myocardial changes are related both to the mechanical lesions of cardiomyocytes and the haemodynamic disorders, developing as a result of ventricular fibrillation, which leads to marked myocardial hypoxia. The changes in the microcirculatory bed contribute to the development of the latter. Hyperfunction of the intracellular structures, especially of mitochondria and myofibrils, taking place under unfavourable conditions leads to a rapid energy depletion, which is one of the main causes of development of the acute cardiac insufficiency in this type of arrhythmias. Studies of cardiac defibrillation enabled one to elicit the dynamics of morphological changes, appearing in the myocardium as related to the duration of ventricular fibrillation.