Oligosaccharide dehydrogenase-modified graphite electrodes for the amperometric determination of sugars in a flow injection system

Enzyme electrodes for the determination of sugars based on solid graphite electrodes modified with oligosaccharide dehydrogenase "wired" with an osmium-based one-electron (no proton) acceptor redox hydrogel were studied as sensors in a flow injection system. The enzyme and a poly(1-vinylimidazole) (PVI) where every tenth mer is complexed with osmium (4,4'-dimethylbpy)(2)Cl, (denoted PVI(10)dmeOs) were cross-linked with poly(ethylene glycol) (diglycidyl) ether. The electrodes were active for l-arabinose, d-xylose, d-galactose, d-fructose, d-glucose, d-mannose, cellobiose, lactose, maltose, and maltooligosaccharides up to a degree of polymerization of 7. The highest relative response found was for glucose (100%) followed by maltose (40.6%) and lactose (40.6%). Fructose and isomaltotriose gave the lowest responses (<1%). Calibration curves for glucose were strictly linear in the range between 30 and 500 μM with sensitivity and apparent Michaelis-Menten constant (K(m)(app)) of 23.0 ± 1.4 μA mM(-)(1)cm(-)(2) and 4.26 ± 0.95 mM, respectively.     

Replantation of multi-level hand severances

Since 1990, the replantation of hands severed at multiple levels has been carried out successfully for 22 patients. In each case the motor and sensory functions of the hand were recovered satisfactorily. We suggest that such wounds should be named 'multi-level severances' and should be classified into five groups according to the wound localities. In order to shorten ischaemic time, debridement should be carried out simultaneously by several groups. The main technical points of the operation are: (1) The order of replantation for multiply severed fingers is that the most distant section should be reattached first, and then the more proximal part. (2) High quality blood vessel anastomosis must be ensured. (3) Avoid taking the blood vessels, nerves and tendons from severed region. (4) During the operation, care should be taken to ensure that the replanted fingers' segments are protected from collision and stretching. In the early stages following the operation correct functional exercise is very important.     

Measurement of Prepl Pwall factors in electron beams and in a 60Co beam for plane-parallel chambers

This paper describes a method to measure the product of Prepl Pwall correction factors for ionization chambers and presents our measured values of Prepl Pwall for Markus plane-parallel chambers in electron beams. It is shown that the measured values of Prepl Pwall can be fitted to an equation, Prepl Pwall = c1 + c2 R50 + c3 (R50)2, for Markus chambers at the new reference depth for electron beams (6 MeV < or = nominal energy E < or = 20 MeV). We also present our measured values of Prepl Pwall for NACP and Markus chambers in a water phantom irradiated in a 60Co beam.     

Relationship between decreased function and O2 consumption caused by cyclic GMP in cardiac myocytes and L-type calcium channels

We tested the hypothesis that part of the decreased function and metabolism caused by cyclic guanosine monophosphate (GMP) in beating cardiac myocytes is related to inhibition of L-type calcium channels. The steady state oxygen consumption (VO2) of a suspension of ventricular myocytes isolated from hearts of New Zealand white rabbits was measured using oxygen electrodes. Cellular cyclic GMP levels were determined by radioimmunoassay. Cell shortening was measured with a video edge detector. The VO2 was obtained after: (1) adding sodium nitroprusside (NP 10(-8),(-6),(-4) M), (2) pretreatment by BAY K8644 10(-5) M (BAY, L-type calcium channel activator), nifedipine 10(-4) M (NF, L-type calcium channel blocker) or forskolin 10(-7) M (FK, adenylate cyclase activator), then adding NP 10(-8),(-6),(-4) M, (3) pretreatment with both FK 10(-7) M and NF 10(-4) M and subsequently adding NP 10(-8),(-6),(-4) M. NP 10(-4) M decreased VO2 from 707 +/- 34 to 410 +/- 13 (nl O2/min per 10(5) myocytes), decreased the percentage of shortening (Pcs) from 5.7 +/- 0.6 to 3.7 +/- 0.5 and the rate of shortening (Rs) from 65.5 +/- 4.5 (microns/s) to 46.2 +/- 5.5. NP 10(-4) M also increased cyclic GMP from 264 +/- 70 (fmol/10(5) myocytes) to 760 +/- 283. Both BAY and FK increased VO2, Pcs and Rs without changing cyclic GMP. NF decreased Pcs, Rs and VO2. Similar metabolic and functional effects of NP were observed with pretreatment with these agents separately, compared to NP alone, and the elevation of cyclic GMP level was not different from the control group. With FK alone, NP 10(-4) M decreased VO2 by 51%, Pcs by 44% and Rs by 39%. In the presence of both FK and NF, the negative effects of NP were diminished significantly. NP 10(-4) M decreased VO2 by 37%, Pcs by 25% and Rs 20%. Thus, in beating cardiac myocytes, the negative metabolic and functional effects of cyclic GMP were related to inhibition on L-type calcium channels only when adenylate cyclase was stimulated.     

Negative metabolic effects of cyclic GMP in quiescent cardiomyocytes are not related to L-type calcium channel activity

Evidence of immune system abnormalities in adult schizophrenia has prompted examination of the human leukocyte antigen (HLA) system. Childhood onset schizophrenia offers a unique opportunity to test neurodevelopmental hypotheses of schizophrenia, including those which implicate components of the immune system. In the present study, class I and II HLA antigens were typed using sequence-specific primers and the polymerase chain reaction in 28 childhood onset schizophrenics and 51 ethnically matched healthy subjects. Groups were compared for frequencies of HLA antigens reported to be associated with schizophrenia and/or autoimmune disorders. We hypothesized that antigen frequencies would differ between schizophrenic and healthy children, suggesting that some dimension of the neurodevelopmental disturbance experienced by these children may be mediated by subtle abnormalities of immune function. There were no significant differences between schizophrenic and healthy subjects in the frequency of any antigen tested. These findings do not support HLA-associated pathology in childhood onset schizophrenia.