Collaboration of local government and experts responding to increase in environmental radiation level due to the nuclear disaster: focusing on their activities and latest radiological discussion.

Activities were introduced in Kashiwa city in the Tokyo metropolitan area to correspond to the elevated environmental radiation level after the disaster of the Fukushima Daiichi nuclear power plant. These were based on a strong cooperation between local governments and experts. Ambient dose rate and radioactivity of foodstuff produced inside of the city have been monitored. Representative ambient dose rates around living environments have almost already become their original levels of the pre-accident because of the decontamination activity, natural washout and effective half-lives of radioactivity. The internal annual dose due to radioactive cesium under the policy of 'Local Production for Local Consumption' is estimated as extremely low comparing the variation range due to natural radioactivity. Systematic survey around a retention basin has been started. All of these latest monitoring data would be one of the core information for the policy making as well as a cost-benefit discussion and risk communication.

Collaboration of local governments and experts responding to the increase of the environmental radiation level secondary to the nuclear accident: a unique activity to relieve residents' anxiety.

After the Fukushima nuclear power plant accident, 'hot spots' were found in Tokatsu area in Chiba prefecture. Although ambient radiation dose in this area was too low to harm residents' health, local residents were particularly worried about possible adverse effects from exposure to radiation. To avoid unnecessary panic reactions in the public, local governments in Tokatsu area collaborated with radiation specialists and conducted activities to provide local residents with accurate information on health effects from radiation. In addition to these activities, the authors offered one-to-one consultations with a radiologist for parents of small children and expecting mothers. They herein report this unique attempt, focusing on parents' anxiety and the age of their children. Taken together, this unique collaborative activity between local government and experts would be one of the procedures to relieve residents' anxiety.

Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging.

Mutations in mitochondrial DNA (mtDNA) accumulate in tissues of mammalian species and have been hypothesized to contribute to aging. We show that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mtDNA mutations and display features of accelerated aging. Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.

HNS-32, a novel azulene-1-carboxamidine derivative, inhibits nifedipine-sensitive and -insensitive contraction of the isolated rabbit aorta.

The vasorelaxant profile of a novel azulene-1-carboxamidine derivative, HNS-32 [N1,N1-dimethyl-N2-(2-pyridylmethyl)-5-isopropyl-3,8-dimethyl-azulene-1-carboxamidine, CAS 186086-10-2], was investigated in the isolated rabbit aorta precontracted with high KCl, noradrenaline (NA) or phorbol 12, 13-dibutyrate (PDBu) and compared with those of nifedipine and nitroglycerin. In preparations without endothelium, HNS-32 elicited concentration-dependent, full inhibition of contractions elicited by high KCI (80 mM), NA (3x10(-6) M) or PDBu (10(-6) M). In contrast, nifedipine inhibited only the contraction elicited by membrane depolarization with high KCl. Nitroglycerin also attenuated high-KCl-, NA- and PDBu-elicited contractions effectively, although full suppression was obtained only for NA-elicited contraction. Whilst the relaxant effect of HNS-32 was not affected by the presence of endothelium, the relaxant response to acetylcholine was endothelium dependent. Addition of excess Ca2+ restored both the HNS-32-reduced tension in muscle precontracted with high KCI and the nifedipine-mediated tension decrease. Relaxation elicited by HNS-32 was not affected by the adenylate cyclase inhibitor, 9-(tetrahydro-2'-furyl)adenine (SQ 22,536, 10(-4) M), the soluble guanylate cyclase inhibitor, 1H-(1,2,4)-oxadiazolo-(4,3-a)-quinoxalin-1-one (ODQ, 10(-5) M) or a cocktail of K+ channel blockers (glybenclamide 10(-6) M, tetraethylammonium 2x10(-3) M, apamin 10(-7) M, 4-aminopyridine 10(-4) M and Ba2+ 10(-5) M). These findings indicate that HNS-32 inhibits both L-type Ca2+ channel-dependent and -independent vascular contraction. Blockade of Ca2+ entry through L-type Ca2+ channels may be involved in the inhibitory effect of HNS-32 on the contraction due to membrane depolarization with high KCl. On the other hand, HNS-32 seems to inhibit Ca2+ channel-independent contraction via mechanism(s) other than elevation of cyclic nucleotides (cAMP and cGMP) and opening of K+ channels.

Potentiation of stretch-induced tone in the rabbit facial vein by an isoquinoline derivative, LOE 908.

The rabbit facial vein exhibits extracellular Ca2+- and temperature-dependent spontaneous myogenic tone in response to stretch. The present study aimed to elucidate pharmacological characteristics of Ca2+ entry mechanisms responsible for the stretch-induced tension development of the rabbit facial vein. Ca2+- and temperature-sensitive vascular tone in response to stretch was refractory to L-type Ca2+ channel blockers such as nifedipine and diltiazem but was abolished by papaverine or SK&F 96365 which blocks both receptor- and store-operated Ca2+ channels. Interestingly, LOE 908, another type of voltage-independent Ca2+-permeable channel blocker, showed augmentation of the stretch-induced vascular tone instead of inhibition. Potentiation by LOE 908 of stretch-induced vascular tone was also extracellular Ca2+-dependent and counteracted by SK&F 96365. Membrane stretch-activated Ca2+ channels in the rabbit facial vein smooth muscle cells may have a unique characteristic that their opening is stimulated by LOE 908 and thus is distinguishable from other voltage-independent Ca2+-permeable channels.

[Case of the maxillofacial defect patient. Prosthetic treatment after reconstruction of the palate and face using deltopectral flap].

The patient, a 72-year-old edentulous man, had an extensive maxillofacial defect caused by treatment of the maxillary cartinoma. As his left maxillary and zygomatic bone, a portion of the soft palate, orbital cavity contents and soft tissues of the cheek had been excised, his face was ugly, and his speech and eating were extremely poor. For this patient, first of all, plastic surgeons reconstructed the cheek and palate using deltopectral flap. Secondly, dentists prepared a facial prosthesis and a set of complete dentures. Four months after prosthetic treatment, plastic surgeons corrected the left corner of the mouth using temporal muscle flap and fascia lata, and strengthened infraorbial region of deltopectral flap by grafting the left 5th rib. Lastly, dentists remade the facial prosthesis. As a result, the patient had great improvement in his face, speech and eating. Periodic examination of the surgical site can be practiced through the remaining facial defect. The advantages of the surgical reconstruction in this case were as follows. (1) As reconstruction of the cheek narrowed a facial defect, it was easy to improve patient's appearance by a small facial prosthesis. (2) The closure of the palate was effective to improve hypernasal speech, to prevent fluid leakage into the nasal cavity and to improve the retention and stability of the upper complete denture.

Depolarizing afterpotentials in myelinated axons of mammalian spinal cord.

Microelectrode recordings were made from 5-10 micron dia axons of adult rat spinal cord in vitro. Action potentials in response to electrical stimulation were recorded intracellularly and electrical characteristics of the axons were examined by injecting current pulses through a bridge circuit. All action potentials larger in amplitude than 80 mV were followed by depolarizing afterpotentials, similar to those recorded in peripheral axons [Barrett and Barrett (1982) J. Physiol., Lond. 323, 117-144]. The afterpotential could be described as the sum of three exponential components, the time constants of which (tau 1, tau 2 and tau 3) were 25.2 +/- 5.6, 3.1 +/- 0.8 and 0.8 +/0 0.3 ms, respectively, at 25 degrees C and a membrane potential of -80 mV. The maximal amplitudes of the afterpotential components, obtained by extrapolating to the peak of the action potential, were 3.8 +/- 1.0, 6.4 +/- 5.2 and 21.7 +/- 9.8 mV, for action potential amplitudes of 102 +/- 11 mV. The amplitude of the longest component of the afterpotential decreased with depolarization and increased with hyperpolarization at the recording site. The amplitude decreased markedly with increase of temperature to physiological levels, in conjunction with the expected decrease in action potential duration. Similar afterpotential components were present in the response of the axon to injected hyperpolarizing current pulses. The observations are consistent with the suggestion [Barrett and Barrett (1982) J. Physiol., Lond. 323, 117-144] that the afterpotential results from charging of the axolemmal capacitance by current passing through the myelin sheath during the action potential. They are inconsistent with a number of calculations of electrical characteristics of peripheral axons derived from voltage clamp experiments in isolated fibers. It is argued that the electrical resistance of the myelin lamellae is relatively low, though within the range calculated for other glial membranes. This suggestion is found more compatible with the available morphological data than the alternative proposal that a leakage pathway under the myelin sheath might be responsible for the afterpotential [Barrett and Barrett (1982) J. Physiol., Lond. 323, 117-144]. The significance of this organization for the function of myelinated axons and the electrical basis of the afterpotential are examined further in the accompanying paper [Blight (1985) Neuroscience 15, 13-31].

[Intrathecal administration of amikacin in postoperative refractory meningitis].

The intrathecal administration of amikacin (AMK) (50--100 mg/day) was effective for 3 cases of postoperative refractory meningitis caused by gentamicin (GM) resistant organisms. The infecting pathogen of case 1 was K. pneumoniae and that of case 2 was S. epidermidis, while no pathogen was cultured in case 3. The causative pathogens in the former were eradicated only with AMK. No therapeutic response was gained with GM, but with AMK in the latter. High tone hearing impairment was observed in case 1 and transient vomiting was observed in case 3. However, these side effects were trivial for the severity of disease. It is suggested in these 3 cases that the high dose intrathecal administration of AMK may be extremely useful in the treatment of postoperative refractory meningitis which has shown no response to GM.