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Biomedical subjects

D Tanaka

Publications and source records attributed to D Tanaka.

At least 37 records · Page 2Linked to original sources
PubMed1997

Assessment of cerebral hemispheric symmetry in hatchling chickens exposed in ovo to polychlorinated biphenyl congeners.

Previous investigators have reported that exposure to a mixture of environmental contaminants, including polychlorinated biphenyls, results in morphologic asymmetry of the cerebral hemispheres in hatchling great blue herons (Ardea herodias) and have suggested that this asymmetry may be a useful biomarker for contamination. This study was made to determine whether exposure to PCB congeners 3,3',4,4'-tetrachlorobiphenyl (IUPAC #77) and 3,3',4,4',5-pentachlorobiphenyl (IUPAC #126) causes similar asymmetry in hatchling domestic chickens (Gallus domesticus). Eggs were injected at day 0 of incubation with either a high dose, low dose, or combination of each congener. At hatching, the chicks were perfused with 10% formalin-saline. The brains were removed, sectioned and stained with cresyl violet. Width and height measurements of each hemisphere were taken at eight locations, caudal to rostral, 400 microm apart starting at the level of the anterior commissure (CA) and ending at the lobus paraolfactorius (LPO). The absolute differences between measurements of the left and right sides were used to run a univariate split plot analysis of variance to determine if the amount of asymmetry present was associated with specific congeners or doses. Significant differences in asymmetry were found between noninjected control groups and vehicle-injected control groups (p </= 0.05), but not between noninjected controls and treatment groups. A first degree orthogonal polynomial contrast analysis illustrated a linear trend with asymmetry increasing from the most caudal section at the CA to the most rostral section at the LPO for both non-injected control and treatment groups (p </= 0.05). These data indicate that asymmetry may be normal in avian brains resulting from both intrinsic structural asymmetry and extrinsic molding forces acting on the head during development. Both of these factors should be taken into consideration when assessing the usefulness of cerebral asymmetry as a biomarker.

Abnormalities, Drug-Induced↗
PubMed1997

Serotyping of Streptococcus pyogenes isolated from common and severe invasive infections in Japan, 1990-5: implication of the T3 serotype strain-expansion in TSLS. The Working Group for Group A Streptococci in Japan.

To clarify the relationship between the epidemics of severe invasive group A streptococcal infections (streptococcal Toxic Shock-Like Syndrome: TSLS) and common group A streptococcal infections in Japan, we examined the T serotypes of S. pyogenes strains (group A streptococci) isolated from clinical specimens of the streptococcal infections (17999 cases) in the period 1990-5, including the severe infections (TSLS) (29 cases) in the period 1992-5. Characteristic points of the analyses were: (1) dominant serotypes of the infections in these periods were T12, T4, T1, T28 and TB3264, which were consistently isolated; (2) isolates of T3 rapidly increased through 1990 to 1994 while T6 decreased in the period 1990-3; (3) when Japanese area was divided into three parts, T3 serotype tended to spread out from the north-eastern to the south-western area; (4) strains of T3 and T1 serotypes were dominant in the TSLS. Dominant-serotype strains of streptococcal infections did not always induce severe infections and dominance of T3 serotype in the TSLS seemed to be correlated with the increase of T3 in streptococcal infections. These results may indicate that certain clones of S. pyogenes are involved in the pathogenesis of the TSLS.

Adolescent↗
PubMed1996

Triphenyl phosphite and diisopropylphosphorofluoridate produce separate and distinct axonal degeneration patterns in the central nervous system of the rat.

This study compared the neurotoxic effects of triphenyl phosphite (TPP) in the rat with those seen after exposure to diisopropylphosphorofluoridate (DFP), a compound known to produce organophosphorus-induced delayed neurotoxicity (OPIDN). Animals received either three subcutaneous injections of TPP (1184 mg/kg body wt each dose) administered at 3-day intervals or a single subcutaneous injection of DFP (4 mg/kg body wt). TPP-induced clinical signs were initially observed 2 to 18 days after the last injection and included ataxia, flaccid paresis, stereotyped alternating side-to-side movements, and circling behavior. Axonal and terminal degeneration were present in the cerebellum, vestibular nuclear complex, cochlear nuclei, and superior and inferior colliculi. The subthalamic nucleus, substantia nigra, septal region, hypothalamus, thalamus, hippocampus, and cerebral cortex also contained degenerating axons and terminals. Degeneration was particularly evident in the sensorimotor cerebral cortex, mediodorsal, ventromedial, and medial geniculate thalamic nuclei and in the magnocellular preoptic and medial mammillary nuclei of the hypothalamus. Very light degeneration was present in the gracile fasciculus and nucleus. In contrast, rats injected with DFP showed moderate degeneration in the gracile fasciculus and nucleus but did not display degeneration in any other brain region. Injections of DFP did not produce delayed onset clinical signs. The results indicate that in the rat, different central nervous system cell groups are affected by these two organophosphorus compounds and that TPP affects nuclei and tracts at all levels of the neuraxis, including those associated with higher-order processing and cognitive functions. In addition, the distinct degeneration patterns produced by these two compounds support the view that TPP-induced neurotoxicity should not be considered as a type of OPIDN, but rather as a separate category of organophosphorus-induced neurotoxicity.

Animals↗
PubMed1996

Evaluation of bone density in newborn infants by computed x-ray densitometry.

We evaluated bone density in term and preterm infants using computed x-ray densitometry, which permits measurement of bone density with minimal disturbance to the infants in their incubators. Bone density, bone width, and bone length of the right radius were determined in 155 infants of appropriate weights for their gestational ages (23 to 41 weeks). A curve for intrauterine bone growth was extrapolated from these data. The mean coefficients of variations for variabilities for intra- and interobserver error for all measurements were < 3.5%. In 18 infants, measurements of the right forearm were obtained in two positions to confirm the validity of densitometric measurements. The mean coefficients of variation were 3.42% for bone density, 3.48% for bone width, and 0.21% for bone length. Bone density was significantly correlated with gestational age (r = 0.924) and birth weight (r = 0.921). Bone width and length were also correlated with gestational age (r = 0.866 and 0.937) and birth weight (r = 0.878 and 0.954). Our results suggest that computed x-ray densitometry is a useful method for evaluation of bone density in preterm infants, including those in an intensive care environment.

Absorptiometry, Photon↗
PubMed1996

[Typing of group A streptococci by pulsed field gel electrophoresis].

Restriction endonuclease (Sma I) digestion patterns of chromosomal DNAs of T types 1 and 3 (T1 and T3) group A streptococci (GAS), isolated at two hospitals in Toyama Prefecture from 1983 to 1994, were analysed by pulsed-filed gel electrophoresis (PFGE). One hundred twenty seven isolated of T1 GAS were further divided into 5 PFGE types, which were provisionally designated as T1-1 approximately T1-5. Two epidemics of T1 GAS were observed during the 1983 approximately 1994 period, the first of which (1887 approximately 1988) seemed to be caused by T1-2, and the second (1991 approximately 1993) by T1-5. Some differences in biological characteristics between the two PFGE type strains were also observed. On the other hand, eighty one T3 GAS strains were divided into only two PFGE types, provisionally designated as T3-1 and T3-2, most of which belonged to T3-2. Naturally, both epidemics by T3 GAS, first from 1985 to 1986 and second from 1993 to 1994, seemed to be caused by the same PFGE type, T3-2. No differences in biological characteristics were observed between T3-1 and T3-2 strains.

Electrophoresis, Gel, Pulsed-Field↗
PubMed1995

NAD(+)-glycohydrolase productivity of haemolytic streptococci assayed by a simple fluorescent method and its relation to T serotype.

The ability of haemolytic streptococci to produce NAD(+)-glycohydrolase was investigated by a fluorescent assay. Enzyme production was found in 31 (91%) of 34 group A, 17 (61%) of 28 group C and eight (27%) of 30 group G isolates. The high producers were found in 22 (65%) of group A, one (4%) of group C and none of group G isolates. The high producers of the group A isolates belonged to T-1, T-3, T-4 or T-12 serotype. These results suggest that NAD(+)-glycohydrolase productivity of streptococci is closely related to specific Lancefield's groups or T serotypes.

Cell Division↗
PubMed1995

[Typing of group B streptococci by pulsed-field gel electrophoresis].

Restriction endonuclease (Sma I) digestion patterns of chromosomal DNAs from 459 group B streptococci (GBS) isolated in two hospitals (C and S) in Toyama Prefecture were analysed by pulsed-field gel electrophoresis (PFGE). Results were summarized as follows. 1) One hundred thirty eight isolates of GBS serotype Ia, 174 of serotype III, 102 of serotype JM-9 and 45 of serotype NT-6 were further divided into 56, 41, 36 and 19 PFGE types, respectively. 2) Appreciable differences in the distribution of PFGE types were not observed between C and S hospital isolates, nor among specimens from which GBS strains were isolated. 3) Long-term inspection of 5 patients, from whom the same serotype strains were repeatedly isolated, revealed that some changes in PFGE types were observed in 2 patients, but not in the other 3.

Electrophoresis, Gel, Pulsed-Field↗
PubMed1995

Triphenyl phosphite-induced neuropathy in the avian forebrain: a silver impregnation study of the visual and auditory systems of the Japanese quail.

Single subcutaneous injections of triphenyl phosphite (TPP) (62.5-500 mg/kg body weight) were made in the Japanese quail (Coturnix coturnix japonica). The extent and density of resultant central nervous system degeneration were mapped by using the Fink-Heimer silver impregnation method to selectively impregnate degenerating axons and terminals. In addition to resulting in degeneration in the medulla and cerebellum, exposure to TPP also resulted in axonal and terminal degeneration in specific midbrain and forebrain nuclei and tracts related to the auditory and visual systems. Auditory system nuclei containing axonal and terminal degeneration included the lateral mesencephalic nucleus, pars dorsalis, the nucleus ovoidalis, and area L of Rose in the caudal neostriatum. Anterograde degeneration was also noted in nuclei and tracts related to the visual tectofugal system-the brachium of the superior colliculus, nucleus rotundus, pretectal nuclei, and the ectostriatum. Additional degeneration was noted in the paleostriatum primitivum, dorso-intermediate posterior thalamic nucleus, lateral spiriform nucleus, and the pedunculopontine tegmental nucleus, all of which are related to visuomotor control. These results indicate that in the Japanese quail, exposure to TPP yields anterograde degeneration in nuclei and tracts involved with the transmission and processing of higher order visuomotor, visual sensory, and auditory sensory information.

Animals↗
PubMed1995

Organophosphorus-induced delayed neurotoxicity: a comparative study of the effects of tri-ortho-tolyl phosphate and triphenyl phosphite on the central nervous system of the Japanese quail.

The neurotoxic effects of single oral doses of tri-ortho-tolyl phosphate (TOTP) (500 mg/kg body weight) or single subcutaneous injections of triphenyl phosphite (TPP) (62.5-500 mg/kg body weight) were investigated in the Japanese quail (Coturnix coturnix japonica). Oral doses of TOTP resulted in no detectable clinical signs while injections of TPP resulted in mild ataxia to severe paralysis depending upon the dosage level. At 24 hr postdosing, whole-brain activity of neuropathy target esterase (NTE) was inhibited by 90% in birds exposed to TOTP and by 11-87% in birds injected with TPP. Oral doses of TOTP resulted in only sparse Fink-Heimer silver-impregnated degeneration in the white matter of the cerebellum with no degeneration noted in any other region of the brain. Injections of TPP resulted in widespread degeneration in large numbers of brainstem nuclei and tracts and in all cerebellar foliae and deep nuclei. These results indicate that the Japanese quail responds differentially to exposure to TOTP and TPP. Oral doses of TOTP do not result in clinical signs or in significant amounts of degeneration in the brain even though NTE activity is inhibited by 90%. In contrast, injections of TPP at higher dosage levels yield severe clinical signs, widespread axonal and terminal degeneration in the CNS, and significant inhibition of NTE activity. This sharp dichotomy in relative sensitivity to TOTP and TPP in the Japanese quail suggests that each compound may have its own unique effect on CNS structure and function. In addition, the relationship between levels of NTE inhibition and the onset of clinical signs or neuropathology remains unclear.

Animals↗
PubMed1994

Age-related effects of triphenyl phosphite-induced delayed neuropathy on central visual pathways in the European ferret (Mustela putorius furo).

The objective of this study was to investigate the relationship between the maturation of visual system neurons and the onset of their susceptibility to triphenyl phosphite (TPP)-induced delayed neurotoxicity in the European ferret. We administered single subcutaneous doses of TPP (1184 mg/kg body wt) to 1- to 10-week-old ferret kits to assess the effects on connections and neurons of the developing lateral geniculate thalamic nucleus (LGN) and primary visual cortex. Brains were processed with a modified Fink-Heimer silver-impregnation method. Axonal and terminal degeneration were first noted in the LGN of kits injected at 5 weeks of age. The severity of the degeneration increased in kits injected at later ages and reached adult densities and configurations in ferrets injected at 10 weeks of age. Degenerating neuronal cell bodies were also present in the LGN of kits injected at 7 weeks of age and older. In the visual cortex, axonal and terminal degeneration were consistently present in kits injected at 8 weeks of age and attained adult-like densities in kits injected at 10 weeks of age. Previous studies have reported that the ferret visual system appears to reach anatomical maturity (as defined by mature LGN lamination patterns, the location and density of axon terminals originating from neurons in the retina and LGN, and the migration and synaptic connections of cortical neurons) by 4-5 weeks of age. A temporal comparison of these normal developmental data with the degeneration data obtained in the present study suggests that immature neurons in the visual system of the ferret are not susceptible to TPP-induced delayed neurotoxicity but only become so after they have achieved some degree of maturity. Whether the LGN neurons undergoing degeneration are directly affected by TPP or are showing a transneuronal response to loss of afferent input remains unresolved.

Age Factors↗
PubMed1993

The role of neurotoxic esterase (NTE) in the prevention and potentiation of organophosphorus-induced delayed neurotoxicity (OPIDN).

The first step in the initiation of organophosphorus-induced delayed neuropathy (OPIDN) is proposed to be the phosphorylation of an enzyme found in the nervous system called neurotoxic esterase (neuropathy target esterase, NTE). It has been known for over twenty years that non-neuropathic inhibitors of NTE exist and can actually prevent OPIDN when given before a neuropathic organophosphate (OP). Within the last three years it has become evident that another outcome is possible following in vivo interaction between neuropathic and nonneuropathic NTE inhibitors. When administered after OP exposure, nonneuropathic inhibitors can intensify or potentiate signs of OPIDN in adult chickens. Additionally, whereas developing chickens are typically resistant to the effects of neuropathic OPs, resistant age groups will develop OPIDN when exposure to a neuropathic OP is followed by the non-neuropathic NTE inhibitor phenylmethylsulfonyl fluoride. As in the case of prevention, studies of the potentiation of OPIDN may yield insight into mechanisms involved in the pathogenesis of delayed neurotoxicity. A brief review of current knowledge regarding the role of NTE in both the prevention and potentiation of OPIDN is presented.

Animals↗
PubMed1993

[Anticancer and side effect of arterial subsegmental chemoembolization using cisplatinum/pirarubicin lipiodol suspension (CTLS) for hepatocellular carcinoma].

Twenty patients with unresectable hepatocellular carcinoma were treated by intra-arterial subsegmental injection of Cisplatin/4-0-Tetrahydro-Pyranyl-adriamycin Lipiodol suspension (CTLS). The mean single doses of Lipiodol, cisplatin and THP were 2.3 ml, 85 mg and 8.9 mg, respectively. The therapy was given once in 10 patients, twice in 8 and 3 times in two. Over 25% reduction in tumor size was recognized in 12 patients (60%). Fifty or more % decrease of alfa-feto-protein (AFP) was observed in all of 7 patients (100%) with the initial serum AFP level of more than 200 ng/ml. Although transitional and mild symptoms, such as fever, abdominal pain and vomiting were recognized in some cases, no severe complications were encountered. This method is promising as an excellent procedure for unresectable hepatocellular carcinoma.

Aged↗
PubMed1993

[Hepatocellular carcinoma treated by intraarterial injection of adriamycin/mitomycin C oil suspension alone or combined with cis-diaminodichloroplatinum].

One hundred thirty-five patients with hepatocellular carcinoma (HCC) were treated by intraarterial injection of adriamycin/mitomycin C oil suspension (ADMOS) alone (59 cases) and ADMOS plus cis-diaminodichloroplatinum (CDDP) (76 cases). Tumor size was reduced by over 25% in 13 of 38 patients (35%) in the ADMOS alone group and in 39 of 76 patients (50%) in the ADMOS plus CDDP group. Serum alpha-fetoprotein (AFP) levels decreased by more than 50% in 7/17 (59%) in the ADMOS alone group and in 23/32 (70%) in the ADMOS plus CDDP group. The overall 1- and 2-year survival rates were 68% and 41% by the Kaplan-Meier method. However, no significant difference in the survival rates was observed between the two groups.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1992

A minimal model to account for the response of N-Methyl-D-aspartate receptors expressed in Xenopus oocyte injected with rat brain mRNA.

N-Methyl-D-aspartate (NMDA) receptors were expressed in Xenopus oocytes by injecting rat brain mRNA. NMDA-elicited responses in the oocytes were measured by the voltage-clamping method. The following measurements were made in the presence of 50 microM glycine (Gly) to establish the relationship between the NMDA concentration and the current: (1) the NMDA-induced membrane current before desensitization; (2) the NMDA-induced membrane current after desensitization equilibrium; (3) the fraction of the active form of the receptor after desensitization equilibrium in the presence and absence of 50 microM Gly; (4) the rate of the recovery of desensitized receptors upon removal of NMDA. Gly was essential for not only the activation of NMDA receptors but also their desensitization. These results were analyzed on the basis of a minimal model where one agonist and one Gly binding site were assumed. The equilibrium and rate constants of the model were evaluated for NMDA in the presence of saturating amounts of Gly. This model will be useful for systematically explaining the complicated responses of NMDA receptors.

Animals↗
PubMed1992

Neuropathological effects of triphenyl phosphite on the central nervous system of the hen (Gallus domesticus).

The neurotoxic effects of single subcutaneous injections of 1000 mg triphenyl phosphite (TPP)/kg body weight were investigated in White Leghorn hens. At 7 days postexposure, birds began to show signs of mild to moderate ataxia that progressed to severe ataxia and paralysis at 21 days. Inhibition of whole brain neuropathy target esterase was 85% at 48 hr and 73% by 21 days postexposure. After postexposure periods of 7, 14, and 21 days, hens were killed and their brains and spinal cords were examined for degenerating axons and terminals using the Fink-Heimer silver impregnation method. A small amount of degeneration was noted at 7 days. By 21 days, dense degeneration was noted in the spinal gray matter and funiculi. Degeneration was also present in the granular cell layer of cerebellar folia I-VI and in nuclei and fiber tracts of the medulla. Moderate to dense degeneration was also seen in several forebrain and midbrain areas including the paleostriatum, ansa lenticularis, the dorso-intermediate thalamic nucleus, lateral spiriform, pedunculopontine tegmental, and lateral mesencephalic nuclei and in the deeper layers of the optic tectum. These results indicate that, in addition to affecting the spinal cord and brainstem, exposure to TPP also damages higher order centers responsible for processing and integrating sensorimotor, visual, and auditory information.

Animals↗
PubMed1992

Phenylmethylsulfonyl fluoride alters sensitivity to organophosphorus-induced delayed neurotoxicity in developing animals.

The serine/cysteine hydrolase inhibitor phenylmethylsulfonyl fluoride (PMSF) markedly intensifies the clinical expression of organophosphorus-induced delayed neurotoxicity (OPIDN) in adult chickens when administered after organophosphate exposure. In this study, we have examined the ability of PMSF post-treatment to affect sensitivity to OPIDN in developing animals at ages normally showing resistance. Chickens (35, 49 or 70 days of age) were treated with diisopropylphosphorofluoridate (DFP, 2 mg/kg, sc) and then treated four hours later with PMSF (90 mg/kg, sc) or vehicle only and examined for clinical signs of ataxia and incoordination. Chickens treated with DFP alone showed a marked age-related increase in the severity of motor deficits. Birds treated with DFP followed by PMSF showed more extensive clinical deficits relative to those treated with DFP only, but relatively similar degrees of motor dysfunction among the age groups. Cervical spinal cord samples processed by the Fink-Heimer degeneration method indicated that PMSF post-treatment induced more extensive axonal degeneration in all age groups relative to treatment with DFP only. As the DFP treatment alone caused greater than or equal to 90% inhibition of neurotoxic esterase activity (NTE, the putative molecular target site for OPIDN), interaction with NTE by PMSF does not appear to be involved in potentiation. We hypothesize that PMSF potentiates OPIDN through impairment of a physiological process which normally imparts resistance to young animals and which regresses during development.

Animals↗