Biomedical subjects

H Namba

Publications and source records attributed to H Namba.

At least 109 records · Page 6Linked to original sources

PubMed1996

Quantifying brain tumor blood flow by the microsphere model with N-isopropyl-p-[123I]iodoamphetamine super-early SPECT.

Regional cerebral blood flow was quantitatively measured in 6 patients with brain tumor by the microsphere model with N-isopropyl-p-[123I]iodoamphetamine (IMP) "super-early" single photon emission computed tomography (SPECT) images obtained 4-6 min after IMP injection with a three-head rotating gamma camera. The ratio of radioactivities (counts/pixel/min) in the "early" SPECT images (taken 25-55 min after IMP injection) to the "super-early" images of the brain tumors was 1.47 +/- 0.13 (mean +/- SD, n = 6), which was significantly lower than the ratio in the normal cerebral cortices (1.93 +/- 0.25) (p < 0.01). This indicates faster clearance of IMP from the tumor tissue than that from the normal brain tissue. Blood flow values for the brain tumors obtained by the microsphere model based on the "super-early" SPECT images were 39.3 +/- 12.4 ml/100 g/ min, which was similar to the blood flow values for normal gray matter and in agreement with previous studies with positron emission tomography.

Adult↗

PubMed1996

Time courses of changes in cerebral blood flow and blood-brain barrier integrity by focal proton radiation in the rat.

In order to know the pathophysiological mechanisms underlying radiation brain injury, cerebral blood flow and blood-brain barrier integrity were studied using N-isopropyl-p-[123l]iodoamphetamine (IMP) and [14C]-alpha-aminoisobutyric acid (AIB), respectively, in the rat focal proton radiation model (a single dose of 30 or 60 Gy radiation with 70 MeV proton beams). One, 2, 4, and 5.5 months after irradiation, [123l]IMP and [14C]AIB were intravenously injected and uptake of IMP and AIB in the cerebral cortex, striatum, hippocampus, and thalamus was measured. Significant decreases in IMP uptake were observed in the cerebral cortex and thalamus of the irradiated side at 4 and 5.5 months after 60 Gy irradiation; the effects at 5.5 months were more prominent than those at 4 months. AIB uptake markedly increased in all the brain regions of the irradiated side at 5.5 months after 60 Gy irradiation, and at 4 months, only in the hippocampus. The results suggest that there are dose- and time-dependent responses in radiation effects and regional differences in tissue vulnerability to radiation. Proton focal radiation model appears to be a useful model for studies of radiation brain injury in small animals such as rats.

Aminoisobutyric Acids↗

PubMed1996

Low incidence of the stimulatory G protein alpha-subunit mutations in autonomously functioning thyroid adenomas in Japan.

Point mutations of the alpha-subunit of the stimulatory G protein (Gs alpha) (termed gsp) and the TSH receptor, leading to constitutive elevation of intracellular cAMP contents, have recently been described in autonomously functioning thyroid adenomas. Since we have recently found a clear difference in the incidence of such gain-of-function mutations of the TSH receptor between Japan and Europe, the present study was designed to evaluate the incidence of gsp mutations in a series of autonomously functioning thyroid adenomas in a Japanese population. Thirty-eight autonomously functioning thyroid adenomas were employed in the present study. Genomic DNA was extracted from archival formalin-fixed, paraffin-embedded tissue specimens. Exons 8 and 9 of the Gs alpha gene were examined for activating mutations at codons 201 and 227 by single-strand conformation polymorphism (SSCP) and nucleotide sequencing. Both exons 8 and 9 were successfully amplified in 28 of 38 samples by polymerase chain reaction. Of these only one sample for exon 9 displayed a distinct migration pattern in SSCP analysis, in which a point mutation of a G to C transversion was identified by nucleotide sequencing, resulting in substitution of His (CAC) for Gln (CAG) at codon 227. The wild-type sequence of exon 9 in 10 randomly selected samples with an identical migration pattern in SSCP analysis suggests that underestimation of the incidence of gsp mutations is unlikely in our work. In conclusion, the present data, together with our previous data on the TSH receptor, suggest that oncogenic mutations of the Gs alpha as well as the TSH receptor do not seem to play a major role in tumorigenesis of autonomously functioning thyroid adenomas in Japan.

Adenoma↗

PubMed1996

Expression and regulation of G protein-coupled receptor kinase 5 and beta-arrestin-1 in rat thyroid FRTL5 cells.

G protein-coupled receptor kinases (GRKs) and arrestins are implicated in homologous desensitization of G protein-coupled receptors. We have recently demonstrated that among six GRKs so far identified, GRK5 is the isoform predominantly expressed in the thyroid and appears to be mainly involved in homologous desensitization of thyrotropin receptor (TSHR) in FRTL5 cells. To further understand the molecular mechanisms of the TSHR desensitization, the expression and regulation of GRKs and arrestins together with those of the TSHR were examined in FRTL5 cells. Northern blot analysis of total RNA from FRTL5 cells with the available rat GRK cDNAs (GRK4, 5, and 6) as probes showed that only GRK5 mRNAs of approximately 3, 8, and 10 kilo bases (kb) in length were detectable. When probed with rat beta-arrestin-1 and beta-arrestin-2 cDNAs, beta-arrestin-1 mRNAs of approximately 7.5 and 2.5 kb long, but no (or possibly faint) approximately 2.4 kb beta-arrestin-2 mRNA, were observed, suggesting that in the thyroid, beta-arrestins appear to be predominantly of beta-arrestin-1 isoform. In studies on TSH-regulation of GRK5, beta-arrestin-1 and TSHR mRNAs, steady-state levels of GRK5 and TSHR mRNAs were 3- to 4-fold lower in the cells grown in the medium with TSH than in those without TSH, while betaarrestin-1 mRNA levels were unchanged. Downregulation of GRK5 and TSHR mRNAs by TSH was further confirmed by dose- and time-dependent experiments. Incubation with 1mM 8BrcAMP, a cAMP analog, for 24h fully reproduced this TSH inhibitory effect. A decrease in GRK5 protein by TSH was also confirmed with Western blot analysis. In summary, these data together with our previous data suggested that GRK5 and beta-arrestin-1 seem to be the isoforms predominantly expressed in the thyroid, and they appear to play a pivotal role in TSHR homologous desensitization. We also demonstrated TSH downregulation of GRKS, but not beta-arrestin-1, expression. Further studies will be necessary to elucidate how these phenomena are linked to thyroid pathophysiology.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1996

Parathyroid hormone-related peptide in synovial fluid and disease activity of rheumatoid arthritis.

To understand the clinical role of parathyroid hormone-related peptide (PTHrP) in rheumatoid arthritis (RA), we analysed the circulatory and synovial fluid (SF) concentrations of the N- and C-terminal regions of PTHrP (N- and C-PTHrP) in RA (n = 38), osteoarthritis (OA, n = 45) and control (n = 11) subjects. The SF level of C-PTHrP was markedly higher in RA compared with control and OA groups, while no differences in circulatory C-PTHrP were present among the three groups. In contrast, the SF level of N-PTHrP was marginally higher in OA patients. C-PTHrP levels in SF correlated significantly with CRP, ESR and SF IL-1 receptor antagonist. To identify the mechanism of elevated PTHrP levels in SF, immunohistochemistry and in situ hybridization of synovial membrane (SM) were performed in each subject. Overexpression of PTHrP was identified in the sublining cells within papillary proliferated SM of RA patients only. Our results indicate that C-PTHrP produced from SM into SF reflects the disease activity in RA.

Adult↗

PubMed1996

Effect of volatile anesthetics with and without verapamil on intracellular activity in vascular smooth muscle.

BACKGROUND: Although halothane and isoflurane inhibit receptor agonist-induced smooth muscle contraction by inhibiting Ca2+ influx via the L-type voltage-dependent Ca2+ channels, their effects on pharmacomechanical coupling remained to be clarified. The intracellular action of both anesthetics was studied during agonist-induced contractions using the Ca2+ channel blocker verapamil. METHODS: Isolated spiral strips of rat thoracic aorta with endothelium removed were suspended for isometric tension recordings in physiologic salt solution. Cytosolic concentration of Ca2+ ([Ca2+]i) was measured concomitantly using fura-2-Ca2+ fluorescence. Muscle contraction was evoked by the receptor agonists with 30 nm norepinephrine or 10 microM prostaglandin F2 alpha (PGF2 alpha), followed by exposure to halothane, at 0%, 1%, 2%, and 3% or isoflurane, at 2% and 4%. The effects of the anesthetics were compared with those of 0.1-1 microM verapamil (n = 8 for each condition). To clarify the intracellular action of the volatile anesthetics on agonist-induced contractions, this procedure was repeated for the anesthetics only in the presence of 1 microM verapamil (n = 8 for each condition). The effects of both anesthetics were also examined in nonreceptor-mediated contractions evoked with a 1-microM dose of the protein kinase C activator, 12-deoxyphorbol 13-isobutylate, which increases the Ca2+ sensitivity of the contractile elements (n = 8 for each). RESULTS: Halothane, isoflurane, and verapamil suppressed norepinephrine-and PGF2 alpha-induced increases in muscle tension and [Ca2+]i in a concentration-dependent manner. The Ca2+-tension regression lines suggested that the volatile anesthetics reduced Ca2+ sensitivity of the contractile elements during PGF2 alpha-induced contraction. Pretreatment of the muscle strip with verapamil revealed that halothane and isoflurane released Ca2+ during norepinephrine-induced contraction and that [Ca2+]i-tension relationship was modulated during PGF2 alpha-induced contractions. Halothane at 2% and 3% and isoflurane at 4% suppressed 12-deoxyphorbol 13-isobutylate-induced increases in muscle tension, whereas they enhanced increases in [Ca2+]i, indicating that both anesthetics suppressed Ca2+ sensitivity during 12-deoxyphorbol 13-isobutylate-induced contraction. CONCLUSIONS: Verapamil pretreatment unmasked the intracellular action of the anesthetics. Halothane and isoflurane influenced pharmacomechanical coupling during agonist-induced contraction.

Anesthetics, Inhalation↗

PubMed1996

Osteogenic action of parathyroid hormone-related peptide (1-141) in rat ROS cells.

To examine the autocrine/paracrine effect of parathyroid hormone-related peptide (PTHrP) on osteoblast function, the entire coding region of rat PTHrP (1-141) cDNA inserted into the expression vector was stably transfected into the rat clonal strain of the osteoblast-like cell, ROS 17/2.8, and established stable transfectants. Using the PTHrP-overexpressing ROS cells (ROS/PLP/6), we analyzed in vitro cell characterization and in vivo osteogenic properties. As expected, overexpression of endogenous PTHrP in vitro induced PTH/PTHrP receptor down-regulation confirmed by Northern blots, receptor binding assays, and functional analysis. The established transfectants indicated a decreased growth rate compared with the original non-transfected ROS 17/2.8. Although cAMP production induced by exogenous PTH was suppressed in ROS/PLP/6, the stimulatory effects of forskolin and chorela toxin showed no significant difference between the original ROS 17/2.8 and transfected cells, but the in vivo osteogenic properties were histologically potentiated in transfectants with increased bone matrix and acceleration of mineralization within tumors. The levels of osteocalcin and osteopontin mRNAs were also increased in transfectants. The down-regulated in vitro PTH/PTHrP receptor mRNA was restored in in vivo tumor tissues. Our study provides clear evidence that the in vivo osteogenic function in ROS cells is potentiated by PTHrP, through an autocrine/paracrine mode of action.

Animals↗

PubMed1996

Parathyroid hormone-related protein (PTHrP) action in rat articular chondrocytes: comparison of PTH(1-34), PTHrP(1-34), PTHrP(1-141), PTHrP(100-114) and antisense oligonucleotides against PTHrP.

Parathyroid hormone-related protein (PTHrP) is thought to be an important autocrine/paracrine factor for chondrocyte metabolism since mice lacking the PTHrP gene exhibit abnormal cartilage development. To determine the biological role of PTHrP in chondrocytes, we first compared the agonist potency of human (h) PTHrP(1-34) with hPTH(1-34) in cultured rat articular chondrocytes. Neither hPTHrP(1-34) nor hPTH(1-34) altered basal DNA synthesis, but attenuated the stimulatory effect of transforming growth factor beta (TGF-beta). Both agents suppressed the expression of alpha(1) type II collagen mRNA in a dose-response fashion with the same potency. In addition, the action of exogenously added hPTHrP(1-34) and hPTH(1-34) on intracellular cAMP and [Ca2+]i levels was similar. We next compared the effect of PTHrP within its entire amino acid sequence (1-141). With regard to thymidine incorporation, alpha(1) type II collagen gene expression and accumulation of cAMP and [Ca2+]i level, there was no significant difference between hPTHrP(1-34) and hPTHrP(1-141). PTHrP C-terminal (100-114) did not show any function. To further investigate PTHrP function, intracellular PTHrP translation was inhibited by a transgene of antisense oligonucleotides against PTHrP. Antisense oligonucleotides decreased PTHrP mRNA translation, specifically inhibited DNA synthesis in control as well as TGF-beta-treated chondrocytes and enhanced alpha(1) type II collagen mRNA expression in TGF-beta-treated chondrocytes. These results suggest that there is no significant difference between exogenously added hPTH(1-34), hPTHrP(1-34) and PTHrP(1-141) with regard to the biological action of these agents, including cell growth, differentiation and second messenger pathway. However, the result of DNA synthesis in the antisense PTHrP-inhibition study suggests that intracellular PTHrP may have an as yet unknown biological role, in addition to a classical PTH/PTHrP receptor-mediated function in the rat articular chondrocyte.

Animals↗

PubMed1996

Brain acetylcholinesterase activity: validation of a PET tracer in a rat model of Alzheimer's disease.

UNLABELLED: We developed three radioactive acetylcholine analogs--N[14C]methyl-4-piperidyl acetate ([14C]MP4A), propionate ([14C]MP4P) and isobutyrate ([14C]MP4IB)--as radiotracers for measuring brain acetylcholinesterase (AchE) activity in vivo. The principle of our method is that the lipophilic analog diffuses into the brain where it is metabolized by AchE to produce a hydrophilic metabolite, which is trapped at the site of its production. The purpose of this study was to examine whether the tracers would have the sensitivity needed for early diagnosis of Alzheimer' disease using rats with a unilateral lesion in the nucleus basalis magnocellularis (NBM), an animal model of the cholinergic deficit in Alzheimer's disease. METHODS: Rats with a unilateral NBM lesion were prepared, and the N[14C]methyl-4-piperidyl esters and N-Isopropyl-p-[123I]iodoamphetamine([123I]IMP were injected intravenously 30 and 2 min, respectively, before the rats were killed. Uptake of 14C and 123I and AchE activity in the lesioned and unlesioned (control) sides of the cortex were measured simultaneously. RESULTS: The NBM lesion showed reduced cortical AchE activity by 30%-50%, with no side-to-side differences in [123I]MP uptake. Autoradiographic studies showed that uptake of 14C from [14C]MP4A and [14C]MP4P was significantly lower in the lesioned than unlesioned side of the cortex, which agreed well with the AchE histochemical staining patterns. Tissue dissection studies showed different uptake changes for the three compounds when AchE activity in the lesioned side of the cortex was reduced by 50%: 14C uptake from [14C]MP4P, [14C]MP4A and [14C]MP4IB was reduced by 27%, 21% and 7.3%, respectively. Theoretical analysis of the observed sensitivities of the tracers in relation to their in vitro enzymatic properties indicated that tracer sensitivity was highly dependent on the enzymatic hydrolysis rate of the tracer. CONCLUSION: The [14C]MP4A and [14C]MP4P esters had sufficient sensitivity to enable AchE activity changes in the rat cortex of less than 50% to be detected, indicating that the present method is applicable to PET diagnosis of Alzheimer's disease.

Acetates↗

PubMed1996

IGF-I receptor signalling: lessons from the somatotroph.

Insulin-like growth factor 1 (IGF-I) is a major feedback regulator of pituitary GH secretion, with defined actions occurring at both the hypothalamus and pituitary. The IGF-I gene is expressed in the anterior pituitary in a GH-dependent manner thus providing for both endocrine-as well as autocrine-mediated GH regulation. In turn, IGF-I selectively and specifically inhibits GH gene transcription and secretion, its attenuating effects on nascent GH mRNA synthesis being demonstrable within 1 h. Binding of IGF-I to its pituitary cell surface receptor is followed by rapid activation of the intrinsic tyrosine kinase activity of the receptor beta-subunit and phosphorylation of insulin receptor substrate 1 (IRS-1). Structure-function studies of the human IGF-I receptor were performed in stable, GH-secreting transfectants expressing either the cDNA encoding the wild-type (WT) human IGF receptor and exhibiting enhanced IGF-I responsiveness, or cDNAs encoding IGF-I receptor mutants and a truncated, kinase-deficient receptor (952STOP). 950Tyr situated on the submembrane receptor domain was found to be critical for transducing the IGF-I signal to the GH gene. IGF-I failed to suppress GH secretion by signalling endogenous rat IGF-I receptors when hybrid receptors were formed with kinase-deficient human receptors and rat hemi-receptors. This dominant negative effect on hormone secretion was also evidenced when mitogenic IGF-I signals were blocked in vitro and in vivo by these hybrid receptors. Using similar doses of IGF-I, the IGF-I receptor cell transfectants also demonstrated ligand-dependent activation of ERKs in pituitary cells. In conclusion, the pituitary IGF-I receptor mediates the negative feedback regulation of GH. Thus, IGF-I receptor mass may determine GH responses to malnutrition, pregnancy, and refeeding. IGF-I receptor mutations may also prove useful to abrogate the growth of IGF-I-dependent tumors. These structure-function studies of the human IGF-I receptor provide mechanistic insights into both metabolic control of the GH axis, as well as target tissue proliferative characteristics.

Animals↗

PubMed1996

[Epidural buprenorphine does not improve diaphragmatic function after upper abdominal surgery].

We investigated the effect of epidural buprenorphine on diaphragmatic function using respiratory inductive plethysmography (RIP) in seven healthy patients after upper abdominal surgery. After surgery, changes of rib cage contribution to tidal volume (%RC) increased significantly from 25.3 +/- 7.3 (mean +/- SD) to 50.7 +/- 14.8% (P < 0.05). After the injection of epidural buprenorphine, visual analogue scale (VAS) score decreased significantly from 8.3 to 3.3 (P < 0.05). But, %RC was unchanged compared to the value before the injection. These results indicate that pain relief by epidural buprenorphine does not improve diaphragmatic function after upper abdominal surgery.

Abdomen↗

PubMed1995

Adaptation to high-salt stress in Saccharomyces cerevisiae is regulated by Ca2+/calmodulin-dependent phosphoprotein phosphatase (calcineurin) and cAMP-dependent protein kinase.

Ca2+/calmodulin-dependent phosphoprotein phosphatase (calcineurin, PP2B) of Saccharomyces cerevisiae is implicated in adaptation to high-salt conditions. Calcineurin mediates high salt-induced expression of the ENA1/PMR2 gene encoding the P-type ATPase, which is suggested to be involved in Na+ efflux. We identified the PDE1 gene encoding the low-affinity cAMP phosphodiesterase as a multicopy suppressor of the Li(+)- and Na(+)-sensitive calcineurin null mutant, suggesting that cAMP is a negative regulator of adaptation to high-salt stress. Genetic analysis indicated that calcineurin and cAMP act antagonistically in a common pathway for adaptation. The bcy1 disruption, which leads to constitutive cAMP-dependent protein kinase (PKA) activity inhibited high NaCl-induced expression of the ENA1/PMR2 gene, caused an elevation of the intracellular Na+ level and a growth defect in high-NaCl medium, all of which were analogous to the defects of a calcineurin mutant. A reduced cAMP level resulting from multiple copies of the PDE1 gene caused increased expression of the ENA1/PMR2 gene in response to high NaCl. We propose a model for the regulation of cation homeostasis, in which calcineurin antagonizes PKA to activate transcription of the ENA1/PMR2 gene in response to high-salt conditions.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1995

Cloning and characterization of the Saccharomyces cerevisiae SVS1 gene which encodes a serine- and threonine-rich protein required for vanadate resistance.

A novel Saccharomyces cerevisiae (Sc) SVS1 gene was cloned as a multicopy suppressor of vanadate (Vn) sensitivity (VnS) due to a calcineurin (CaN) null mutation. SVS1 encoded a 260-amino-acid protein abundant in Ser and Thr residues, with a putative signal sequence at the N terminus. Deletion of SVS1 resulted in increased sensitivity to Vn, but not to other metallic ions or drugs. Northern analysis of the SVS1 mRNA indicated that the induction of the gene occurred specifically in the response to Vn. These results suggested that Sc has a mechanism to enhance the tolerance to Vn by increasing the expression of SVS1. The results of genetic experiments suggested that CaN and the Svs1 proteins act in separate pathways to enhance the tolerance to Vn.

Amino Acid Sequence↗

PubMed1995

Radiation-induced G1 arrest is selectively mediated by the p53-WAF1/Cip1 pathway in human thyroid cells.

We investigated the sensitivity and sequential events that take place in thyroid epithelial cells after irradiation. Cell survival ratios at a dose of 2 Gy were 18 +/- 2.5%, 58 +/- 1.0%, 59 +/- 1.5%, and 98 +/- 1.8% in primary thyroid cells, papillary thyroid carcinoma cells, follicular thyroid carcinoma cells, and anaplastic thyroid carcinoma cells, respectively. Thyroid carcinoma cell lines carrying mutations in the p53 gene were resistant to ionizing radiation. Although irradiated cells were accumulated at G1 in primary thyroid cells even after low-dose irradiation (0.2 Gy), this phenomenon was not observed in the thyroid carcinoma cell lines. Wild-type p53 expression in primary thyroid cell was increased following irradiation, but mutated p53 in the thyroid carcinoma cell lines was unchanged. To clarify the signal transduction in the G1 arrest following irradiation, levels of expression of the p53 putative downstream effectors GADD45 and WAF1/Cip1 were examined. Despite the consistent level of GADD45 mRNA, the level of WAF1/Cip1 transcripts was increased in a radiation dose-dependent manner in primary thyroid cells. This increase in the WAF1/Cip1 mRNA level was observed 30 min after irradiation and continued for at least 48 h. A mobility shift assay performed using the sequence of the putative p53 DNA binding site on the WAF1/Cip1 and GADD45 genes as a probe showed that nuclear protein extracted from primary thyroid cells, anti-p53 antibody, and probe oligonucleotide-bound complex was clearly shifted. An increase in binding activity of the p53/antibody/DNA complex was observed following irradiation. In contrast, the nuclear extract from thyroid carcinoma cells could not bind the specific DNA site, suggesting that mutant p53 has lost its binding ability. Actinomycin D inhibited WAF1/Cip1 and GADD45 mRNA levels and cycloheximide stimulated up-regulation of both basal mRNA levels, but an additional increase of the mRNA expression following irradiation was observed only in the WAF1/Cip1 gene. These data suggest that p53 in postradiation acts at a transcriptional level on WAF1/Cip1 gene expression and that de novo protein synthesis is not required for this effect. These results suggest that the p53-WAF1/Cip1 pathway may play a central role in induction of G1 arrest following irradiation in human thyroid epithelial cells.

Base Sequence↗

PubMed1995

Expression of parathyroid hormone-related protein in rat articular cartilage.

Expression and localization of parathyroid hormone-related protein (PTHrP) in rat articular cartilage during fetal and postnatal periods were investigated by immunohistochemistry and in situ hybridization. PHTrP displayed distinct distribution and intensity of staining at different ages. In fetal (18-day-old) and young (3-week-old) rats, articular chondrocytes expressed abundant PTHrP throughout the entire thickness of cartilage. In contrast, in 60-week-old rats, PTHrP was expressed in a few articular chondrocytes of superficial and middle layers. Regulation of PTHrP and PTH/PTHrP receptor mRNA was also studied in cultured rat articular chondrocytes. Northern blot analysis revealed that both transforming growth factor-beta (TGF-beta), an important stimulator for chondrocyte proliferation and differentiation, and 10% fetal bovine serum (FBS) stimulated the expression of PTHrP mRNA with down-regulation of its receptor mRNA. In contrast, 12-O-tetradecanoylphorbol-13-acetate (TPA) down-regulated the expression of receptor without changes of PTHrP mRNA level. These results suggest that the changes in abundance and localization of PTHrP and its receptor may be directly involved in the cell growth and differentiation of articular cartilage.

Animals↗

PubMed1995

Childhood thyroid diseases around Chernobyl evaluated by ultrasound examination and fine needle aspiration cytology.

Screening by ultrasound examination and fine-needle aspiration cytological biopsy (FNA) was conducted in five regions in Belarus, Ukraine, and Russia to investigate the prevalence of childhood thyroid diseases around Chernobyl. Gomel, Zhitomir, Kiev, and the western area of Bryansk are the administrative regions where severe radioactive contamination occurred. The subjects from Mogilev, where contamination was relatively low, served as controls. Among 55,054 subjects (26,406 boys and 28,648 girls), the prevalence of ultrasonographic thyroid abnormalities such as nodule, cyst, and abnormal echogenity was significantly higher in the regions with severe contamination than in Mogilev. Of the 1,396 children showing echographic thyroid abnormalities 197 were selected for FNA, and a sample was successfully obtained for diagnosis from 171 (51 boys and 120 girls) of the 197 subjects. The aspirate was insufficient for diagnosis in the remaining 26 subjects. Thyroid cancer was encountered in four children (2.3%) from the contaminated regions, two children being from Gomel. The other thyroid diseases were follicular neoplasm, 6.4%; adenomatous goiter, 18.7%; chronic thyroiditis, 31.0%; and cyst, 24.0%, suggesting that a major cause of thyroid nodularity is nonneoplastic changes, mainly chronic thyroiditis and cysts. These results will serve as an important data base for further analyses and suggest that childhood thyroid diseases, including both neoplasms and immunological disorders, are consequences of radioactive fallout.

Adenocarcinoma, Follicular↗

PubMed1995

Effect of hemidiaphragmatic paresis caused by interscalene brachial plexus block on breathing pattern, chest wall mechanics, and arterial blood gases.

We investigated the effects of hemidiaphragmatic paresis caused by interscalene brachial plexus block on breathing patterns, chest wall mechanics, and arterial blood gas tensions using respiratory inductive plethysmography. Ten healthy patients received interscalene block with 20-40 mL 1.5% lidocaine with epinephrine. Rib cage contribution to tidal volume (%RC) increased from 28.9% +/- 9.7% to 50.0% +/- 8.3% (P < 0.01), respiratory frequency (f) increased from 14.6 +/- 3.2/min to 16.3 +/- 2.4/min (P < 0.05), and PaO2 decreased from 84.7 +/- 7.3 mm Hg to 78.0 +/- 9.5 mm Hg (P < 0.05). No significant changes were observed in tidal volume (VT), minute volume (VE), or PaCO2. These results indicated that VT, VE, and PaCO2 were maintained after interscalene block, apparently by increases in f and %RC to compensate for hemidiaphragmatic paresis caused by interscalene block. Nevertheless, PaO2 was reduced, presumably due to increased ventilation-perfusion mismatching. Recognizing that we studied healthy patients, the decrease in PaO2 may be more in patients with cardiopulmonary disease.

Adult↗

PubMed1995

Preparation and biological activity of 24-epi-26,26,26,27,27,27-hexafluoro- 1 alpha,25-dihydroxyvitamin D2.

A new fluorinated analog of vitamin D2, 24-epi-26,26,26,27,27,27-hexafluoro- 1 alpha,25-dihydroxyvitamin D2, was efficiently synthesized starting from (R)-4-isopropyl-3-propionyl-2- oxazolidinone with high stereochemical control. In all four physiological test systems, the fluorinate vitamin D2 analog was found to be slightly less active than 1 alpha,25-dihydroxyvitamin D3.

Animals↗