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This paper describes the cutting process of a 0.5mm thickness polycarbonate (PC) worksheet stacked on another 0.5mm thickness PC underlay by an adhesive tape layer. As the first investigation, the cutting line force of the two-line blade (90/30deg.) on the laminated PC sheet was measured with a load cell and the sheared profile of the worksheet was observed by a CCD camera in order to reveal the effect of the time delay of the ultrasonic blade excitation on the deformation flow of the worksheet. The profile parameters such as the inclination angle, elevation angle and necked height of sheared section were observed with respect to the blade excitation patterns by varying the delayed time. Secondarily, in order to investigate the effect of the excitation-duty rate on the profile parameters of the sheared zone, two kinds of ultrasonic-excitement patterns were applied to the laminated PC sheet by varying the duty rate. Through the two experiments, it was revealed that both, the positioning control in the case of the time delay and the power density control in the case of the duty ratio were superior for varying the profile parameters of sheared zone.

Designs and test results for a single-flux-quantum(SFQ) eight-bit shift register circuit operating at frequencies above 100GHz are described. Thehigh-speed performance was realized by introducing a planarized 10kAcm−2 Nb fabrication process as an advanced process and by adopting middle-damped junctions with McCumber parameters βc of 1.8–2.9 in the circuit. The middle-damped junctions were used to reduce the repulsion between SFQ pulses and to adjust the timing. The circuit was designed using a cell-based design method and was tested by constructing an on-chip test system with a ladder-type four-bit high-frequency clock generator. We confirmed its correct operations up to 120 GHz.

Designs and test results for a single-flux-quantum (SFQ) eight-bit shift register circuit operating at frequencies above 100 GHz are described. The high-speed performance was realized by introducing a planarized 10 kA cm?2Nb fabrication process as an advanced process and by adopting middle-damped junctions with McCumber parameters ?cof 1.8-2.9 in the circuit. The middle-damped junctions were used to reduce the repulsion between SFQ pulses and to adjust the timing. The circuit was designed using a cell-based design method and was tested by constructing an on-chip test system with a ladder-type four-bit high-frequency clock generator. We confirmed its correct operations up to 120 GHz.

The Superconductivity Research Laboratory has successfully fabricated large quantities of single flux quantum (SFQ) large scale integrated circuits, including several thousands of Josephson junctions (JJs). Using a Jc= 2.5 kA cm?2process in which the number of Nb layers was four and the minimum JJ size was 2 µm square. We developed a new advanced fabrication process that produced a Jc= 10 kA cm?2, nine Nb layers and a minimum JJ size of 1 µm square. The increase in the number of Nb layers was achieved by using a planarization technique. The target of our next generation process is a Jc= 40 kA cm?2with a 0.5 µm square for the minimum junction size. This specification will be achieved by using advanced semiconductor technologies. This process will enable SFQ circuits to be produced with one million JJs on a chip and achieve a clock frequency greater than 100 GHz.

There have been few reports of stenting in the intracranial arteries. We used coronary stents in the chronically occluded intracranial vertebral artery and stenosis of internal carotid artery by the external force, and good blood flow were resumed. Stenosis in the intracranial arteries is also a good indication for stent placement when it is due to chronic total occlusion or artery compression by external force. But stent placement in the intracranial arteries has some problems. Stent placement in the intracranial artery is indicated only when the site of stent placement has a diameter of 3 mm or more, is a relatively linear portion of the vertebrobasilar artery or the internal carotid artery proximal to the C3 segment, and does not branch off perforating arteries or is already completely occluded.

The transmembrane tyrosine phosphatase CD45 regulates the activity of src family protein tyrosine kinases (PTK) and thereby influences the signaling via such receptors as T and B cell antigen receptors associated with these PTK. However, its implication in signaling through the mast cell receptor with high affinity for IgE (FcεRI) is less clear, although Lyn, a member of the src family, plays an important role in FcεRI-mediated signaling. To define a role for CD45 in FcεRI signal transduction, we established CD45 high expressing rat basophilic leukemia cell lines (RBL-CD45H) and cell lines expressing trace amounts of CD45 (RBL-CD45L). We demonstrate that although all RBL-CD45L cell lines degranulate following IgE- and antigen-induced FcεRI aggregation, the response is significantly reduced at a low dose of antigen. The cells show a delayed and slowed Ca²⁺ mobilization even though at a higher dose where the cells degranulate to a similar extent as RBL-CD45H. This diminished Ca²⁺ response is restored by reconstitution of RBL-CD45L with a chimeric molecule containing the cytoplasmic phosphatase domains of rat CD45. Furthermore, tyrosine phosphorylation of FcεRI, association of FcεRI with Lyn and PTK activity associated with FcεRI, all of which are enhanced upon FcεRI aggregation in RBL-CD45H, are impaired in RBL-CD45L. Finally, we show that FcεRI is physically associated with CD45 in RBL-CD45H prior to receptor aggregation. Thus, we propose that, although not indispensable in mast cell degranulation, CD45 positively regulates the signaling through FcεRI by promoting the activation of FcεRI-associated Lyn.

The transmembrane tyrosine phosphatase CD45 regulates the activity of src family protein tyrosine kinases (PTK) and thereby influences the signaling via such receptors as T and B cell antigen receptors associated with these PTK. However, its implication in signaling through the mast cell receptor with high affinity for IgE (FcepsilonRI) is less clear, although Lyn, a member of the src family, plays an important role in FcepsilonRI-mediated signaling. To define a role for CD45 in FcepsilonRI signal transduction, we established CD45 high expressing rat basophilic leukemia cell lines (RBL-CD45H) and cell lines expressing trace amounts of CD45 (RBL-CD45L). We demonstrate that although all RBL-CD45L cell lines degranulate following IgE- and antigen-induced FcepsilonRI aggregation, the response is significantly reduced at a low dose of antigen. The cells show a delayed and slowed Ca(2+) mobilization even though at a higher dose where the cells degranulate to a similar extent as RBL-CD45H. This diminished Ca(2+) response is restored by reconstitution of RBL-CD45L with a chimeric molecule containing the cytoplasmic phosphatase domains of rat CD45. Furthermore, tyrosine phosphorylation of FcepsilonRI, association of FcepsilonRI with Lyn and PTK activity associated with FcepsilonRI, all of which are enhanced upon FcepsilonRI aggregation in RBL-CD45H, are impaired in RBL-CD45L. Finally, we show that FcepsilonRI is physically associated with CD45 in RBL-CD45H prior to receptor aggregation. Thus, we propose that, although not indispensable in mast cell degranulation, CD45 positively regulates the signaling through FcepsilonRI by promoting the activation of FcepsilonRI-associated Lyn.

This case illustrates the usefulness of an endovascular stent to treat a pseudoaneurysm of the cervical internal carotid artery. A 46-year-old male patient presented with a spontaneous dissection of the cervical internal carotid artery. After failing conservative therapy, he was treated by endovascular placement of a Palmaz stent at level of the pseudoaneurysm and dissection.Immediate obliteration of pseudoaneurysm was achieved, and patency of the internal carotid artery was maintained. The patient sustained no neurological complications and the stenosis of treated carotid artery did not occur during the 6-month follow-up period.For internal carotid artery dissection, stent placement seems to be a reasonable therapeutic alternative to direct surgery.

The osmoregulatory expression of ompC and ompF in Escherichia coli is mediated by a pair of bacterial signal transduction proteins, EnvZ (sensory kinase) and OmpR (response regulator). We isolated previously multicopy suppressors which can complement a defect in the phosphotransfer signal transduction caused by an envZ deletion mutation. Among such suppressors, arcB and barA are of particular interest because these gene products are unique in the sense that they contain both an autophosphorylated histidine site (or transmitter module) and a phospho‐accepting aspartate site (or receiver module) in their primary amino acid sequences. Here we report that ArcB and BarA possess in the C‐terminal region a phosphorylated histidine site which has never been noticed, in addition to the authentic one identified previously. This newly identified histidine in ArcB and BarA was demonstrated to play a crucial role in the observed multicopy suppression. Furthermore, it was demonstrated in vivo and in vitro for ArcB that the C‐terminal domain containing the histidine can function as an alternative phosphodonor (or transmitter). This novel type of sensory kinase was therefore revealed to contain two independent phosphodonor sites, together with a phospho‐accepting site. These findings suggest that this unique feature of ArcB and BarA, in terms of the signaling modules, make it possible for these sensory kinases to function as dual‐signaling transducers.

Two different, hitherto unknown, diseases occurred in two specimens ofSagitta crassa which were individually isolated and maintained in the laboratory. One specimen survived for 24 days, producing a total of 343 eggs and suddenly died without showing any prior symptoms, and upon death had a grotesque appearance. The other had ciliary sense organs the hairs of which became stuck to one another. Ciliary sense organs are important for feeding of chaetognaths; once they become abnormal, the chaetognath may die of starvation. Specimens suffering from X-diseases have not been obtained from field samples so far. Chaetognaths which remained transparent at the time of death included specimens whose ciliary sense organs were attacked by bacteria, those slightly infected by bacteria on their body surface and those with abnormally rough body surfaces. Although the reasons for the development of the abnormality of the ciliary sense organs and body surfaces as well as the mechanism of bacterial infection remain obscure, bacterial infection and abnormalities of the body surface are often observed not only in the laboratory but also in the sea.

Clinical resistance to thyroid hormone (RTH) has been classified into generalized resistance to thyroid hormone (GRTH) and pituitary resistance to thyroid hormone (PRTH) types. Since similar mutations have been identified in tri-iodothyronine (T3) receptor (TR) β gene in GRTH and PRTH, and since considerable overlap has been seen in the clinical manifestations in patients with GRTH and PRTH, two subtypes of RTH are now considered to be a continuous spectrum with the same genetic defect. A point mutation at amino acid Arg 338 to Trp (R338W) which we identified in a patient with PRTH is very interesting, since R338W has been found in several other patients with PRTH, raising the possibility that this mutation may tend to associate with a phenotype of PRTH.In our previous study, we found that R338W had relatively less impaired transcriptional potency, weaker dominant negative activity on various T3response elements and poor homodimer formation, as compared with another GRTH mutant. In this study, to investigate the functional properties of R338W further, especially in terms of the relation between transcriptional activity and dimer formations, we introduced the R338W mutation into the mutant receptors, K443E and F451X, constructing the double mutants, R338W/K443E and R338W/F451X. Both R338W/K443E and R338W/F451X showed negligible T3binding and transcriptional activities. The dominant negative activities of K443E and F451X were, however, significantly weakened by introducing the R338W mutation. As a control, a double mutant G345R/K443E was constructed by introducing a point mutation, G345R, located in the same exon 9 as R338W, into the K443E mutant. Dominant negative activity did not differ between G345R/K443E and K443E. Homodimer formation was significantly reduced in the double mutants containing R338W, but not G345R.In summary, introducing the R338W mutation, but not G345R, into the mutant TR significantly weakened the dominant negative activity, despite further impairment of the T3binding and transcriptional activities.Journal of Endocrinology(1996) 151,293–300

Three major membrane cofactor protein (MCP) phenotypes with different serine-threonine (ST)-rich regions, namely STc (L-phenotype), STBC (H or U phenotype) and STABC, and the MCP without the ST domain (delta ST) were expressed in Chinese hamster ovary (CHO) cells by transfecting the respective cDNAs. The expressed molecules migrated with a larger molecular mass on SDS/PAGE than those expected from their amino acid sequences. O-Glycanase digestion showed that this was due to O-linked sugar chains. The apparent sugar contents in each ST segment were compatible with their serine and threonine contents in the ST regions. The functional properties of these phenotypes as inhibitors of human complement (C) and receptors of measles virus (MV) were compared. The classical pathway-dependent CHO cell lysis by human C was more effectively suppressed by the expressed delta ST and STC than by the STABC and STBC phenotypes, although the difference was not so prominent. In contrast, alternative C pathway-dependent CHO-cell lysis was most effectively suppressed by the STABC phenotype and was only slightly blocked by the ST-deleted mutant. MV infection occurred with all of the phenotypes, but the infectious dose required to cause the same level of syncytium formation was 100-times higher in large ST (STABC and STBC) than in small ST (STC and delta ST) phenotypes. Thus, the ST domain serves as a functional modulator in MCP: MCP with a large ST domain having high O-linked sugar contents is favourable to the effective suppression of both the alternative C pathway-mediated cytolysis and MV infection, whereas MCP with a small ST domain is favourable to the suppression of the classical C pathway.

Treatment of complement component C4 with C1(-)s and methylamine induces a series of conformation changes such as to generate functional binding sites. A monoclonal antibody (mAb), Al 121/6, which does not inhibit the haemolytic activity of C4 was found to bind to native C4 and C4d, but not to C4b and methylamine-treated C4, unless these C4 derivatives were denatured. These results suggested that a linear epitope for mAb Al 121/6 in the C4d domain is originally located at the surface of C4 and becomes hidden as a result of conformational changes induced by C1(-)s or methylamine treatment. The hidden linear epitope was exposed again upon further cleavage of C4b into C4c and C4d. Trypsin digestion of C4d and its chemical modification with phthalic anhydride suggested that the epitope is located at the C-terminal 13 kDa region of C4d and that lysine residues are involved in the epitope. There is a single lysine residue at 1259 in the 13 kDa C-terminal side of C4d and the synthetic undecapeptide Leu1254-Asp1264 was found to inhibit the binding of C4 to mAb Al 121/6, suggesting that the epitope for mAb Al 121/6 is involved in the sequence. The N-terminal portion of the peptide is partly overlapping, with a highly hydrophobic amino acid sequence spanning residues Ala1249-Leu-Leu-His-Leu-Leu-Leu1255. The surface hydrophobicity of C4 has been reported to decrease upon treatment with C1(-)s and methylamine. So it appears that the hydrophobic sequence spanning Ala1249-Leu1255 may be hidden, together with the linear epitope, into the inner region of C4 upon treatment with C1s and methylamine.

The assembly of the classical-pathway C3 convertase from C4 and I2-treated C2 by the action of C1s is an Mg2(+)-dependent reaction. The Mg2+ concentration necessary for the assembly of C3 convertase in the fluid phase was found to be dependent on NaCl concentration. In the absence of NaCl more than 5 mM-MgCl2 was found to be required, whereas 0.5 mM-MgCl2 was adequate for the assembly of C3 convertase in the presence of 150 mM-NaCl. The C3 convertase assembled in a low-ionic-strength buffer was extremely labile compared with that assembled in buffer of physiological ionic strength, and the stability of C3 convertase was improved with the increase in NaCl concentration. It was found that the stabilizing effect of NaCl on C3 convertase was due to inhibition of the dissociating activity of C2b, which was formed during the assembly of C3 convertase. In addition to the dissociation-accelerating effect, C2b inhibited the assembly of C3 convertase in low-ionic-strength buffer, and this effect also was diminished with increase in NaCl concentration. An increase in NaCl concentration to more than 200 mM resulted in a decrease in the assembly of C3 convertase. This effect was not due to the lability of the assembled C3 convertase but due rather to the inhibition of C2 cleavage by C1s. Purified C3 convertase itself is stable in dilute medium or high-ionic-strength medium such as 500 mM-NaCl, suggesting that the interactions between C4b and C2a are hydrophobic. In these respects C2b seemed to be functionally similar to C4bp, but C2b failed to act as a cofactor for the Factor I-catalysed C4b cleavage.

The osmoregulatory expression of ompC and ompF in Escherichia coli is mediated by a pair of bacterial signal transduction proteins, EnvZ (sensory kinase) and OmpR (response regulator). We isolated previously multicopy suppressors which can complement a defect in the phosphotransfer signal transduction caused by an envZ deletion mutation. Among such suppressors, arcB and barA are of particular interest because these gene products are unique in the sense that they contain both an autophosphorylated histidine site (or transmitter module) and a phospho‐accepting aspartate site (or receiver module) in their primary amino acid sequences. Here we report that ArcB and BarA possess in the C‐terminal region a phosphorylated histidine site which has never been noticed, in addition to the authentic one identified previously. This newly identified histidine in ArcB and BarA was demonstrated to play a crucial role in the observed multicopy suppression. Furthermore, it was demonstrated in vivo and in vitro for ArcB that the C‐terminal domain containing the histidine can function as an alternative phosphodonor (or transmitter). This novel type of sensory kinase was therefore revealed to contain two independent phosphodonor sites, together with a phospho‐accepting site. These findings suggest that this unique feature of ArcB and BarA, in terms of the signaling modules, make it possible for these sensory kinases to function as dual‐signaling transducers.

Summary A hydraulic vascular model of the vertebrobasilar artery with an autoregulatory mechanism was constructed. The haemodynamic effect of superficial temporal artery (STA)-posterior cerebral artery (PCA) bypass was investigated in cases of bilateral vertebral artery (VA) occlusion and basilar artery (BA) occlusion. Assuming therapeutic BA occlusion for basilar bifurcation aneurysms, the flow volume through the P 1 segment of the PCA was determined in relation to diameters of the posterior communicating artery (PCom).

Human malignant cells are targeted by homologous complement C3b if they express M161Ag, a 43-kDa protein with C3-activating property. cDNA of M161Ag cloned from human leukemia cell lines predicted M161Ag as a novel secretory protein comprised of 428 amino acids including 5 amino acids encoded by TGA codons (Matsumoto M., Takeda, J., Inoue, N., Hara, T., Hatanaka, M., Takahashi, K., Nagasawa, S., Akedo, H., and Seya, T. (1997) Nat. Med. 3, 1266-1270), although the origin of this gene was obscure. Here we clarified this point through genomic and biochemical analysis: 1) 5'-UT and genomic sequences represented the prokaryote promoter and ribosomal binding site; 2) the TGA codons in M161Ag cDNA were translated not into selenocysteines but into tryptophans; 3) M161Ag anchored onto the membrane secondary to its N-terminal palmitoylation like prokaryote lipoproteins; 4) genomic and cDNA clones of M161Ag were highly homologous to Mycoplasma fermentans gene encoding P48, a monocytic differentiation/activation factor, recently released in the data base, although the resultant proteins were different in the amino acid sequences. Additionally, purified soluble M161Ag efficiently provoked IL-1beta, tumor necrosis factor alpha, and IL-6 like P48, and further IL-10 and IL-12 in human peripheral blood monocytes. Thus, M161Ag originates from M. fermentans, and latently infected M. fermentans allows human cells to produce M161Ag. The liberated protein serves as a potent modulator of innate and cellular immune responses via its complement-activating and cytokine-producing activities.

We have isolated two cDNA clones encoding the guinea pig receptor for the Fc portion of IgG2 (Fc gamma 2R) from a guinea pig peritoneal macrophage cDNA library. Analysis of the predicted amino acid sequence of the one cDNA clone indicated that the guinea pig Fc gamma 2R is a type I transmembrane protein and has approximately 72% DNA sequence homology and approximately 57% protein sequence homology with the human Fc gamma RIII. Therefore, we propose that the guinea pig Fc gamma 2R is referred to as guinea pig Fc gamma RIII. The most important finding in this report is that the obtained cDNA directed the cell surface expression of the Fc gamma 2R on COS-7 cells without association with the gamma chain of the high-affinity IgE receptor (Fc epsilon RI gamma) which is required for human and mouse Fc gamma RIII to be expressed on the cell surface. Furthermore, we demonstrated that the endocytosis activity of Fc gamma RIII is dependent upon the association with Fc epsilon RI gamma, suggesting that Fc epsilon RI gamma is involved in the functions of guinea pig Fc gamma RIII. The other clone was found to lack the sequence encoding transmembrane and cytoplasmic domains, suggesting the presence of a soluble form of guinea pig Fc gamma RIII. Northern blot analysis and RT-PCR showed that a transmembrane form of guinea pig Fc gamma RIII was expressed in peritoneal macrophages, but not in neutrophils in spite of the fact that they express Fc gamma 2R, indicating that the Fc gamma 2R on neutrophils is a product of a distinct gene.

Monkey cells persistently infected by measles virus (MV) Biken strain (Biken-CV-1 cells) showed no cytopathic effects and lacked surface expression of a homolog of human cell receptor, membrane cofactor protein CD46. Transfection of a human CD46 gene into these cells induced extensive cell fusion, indicating that down regulation of the endogenous CD46 homolog was essential for the maintenance of a noncytopathic mode of infection. Surface expression of the exogenously introduced human CD46 was also drastically down regulated in the persistently infected cells compared with uninfected cells. The down regulation was specific for CD46 and did not affect surface expression of exogenously introduced CD4. Exogenous human CD46 was synthesized efficiently in the persistently infected cells, but it did not accumulate on the cell surface. Fusion of Biken-CV-1 cells required the extracellular hemagglutinin (H-protein)-binding domain but not the cytoplasmic domain. Replacing the transmembrane and cytoplasmic domains of CD46 with a glycosylphosphatidylinositol anchor did not prevent cell fusion but completely alleviated down regulation of the glycosylphosphatidylinositol-anchored CD46 in Biken-CV-1 cells. Deletion analyses revealed that the membrane-distal sequences of the CD46 cytoplasmic domain were not only unnecessary but also inhibitory for CD46 down regulation. By contrast, the six amino acid residues proximal to the membrane contained a sequence required for CD46 down regulation in the persistently infected cells. These results indicate that CD46 is down regulated in the persistently infected cells by a mechanism that recognizes a membrane-proximal sequence in the CD46 cytoplasmic domain.

Human granulocytes (polymorphonuclear leucocytes, PMN) possess a membrane cofactor protein (MCP, CD46), which is structurally and functionally distinct from the MCPs of other cell types: it shows a single broad band of 56-80 kDa (without the doublet pattern characteristic of MCP) on SDS/PAGE and has less affinity for complement component C3b. We purified PMN MCP using monoclonal antibodies in order to study the molecular differences between it and other MCPs. Several forms of PMN MCP with size heterogeneity were noted on SDS/PAGE and by immunoblotting. O-Glycanase treatment decreased this heterogeneity, yielding a fast-migrating component identical in position on SDS/PAGE to the O-glycanase-treated MCP of other cells. The cell-specific variation of MCP, therefore, arises from post-translational glycosylation and not from a difference in primary structure. The Factor I cofactor activity of PMN MCP was more efficient in cleaving the methylamine-treated complement components C4/C3 than was MCP from other cells, which shared a similar potency of cofactor activity on a weight basis. Two types of small-form PMN MCP were identified during purification. These were 42 kDa and 30 kDa in size; the former was recognized by M177 (a monoclonal antibody against the active site marker), possessed N-linked sugars [located on the short consensus repeats (SCRs)] but not O-linked ones (on the Ser/Thr-rich region), and retained cofactor activity for C3b/C4b cleavage, similar in potency to that of other MCPs. The functionally active soluble form of MCP was observed specifically in PMN. Protease inhibitors did not inhibit liberation of the fragments, although the generated fragments became susceptible to serine proteases. The findings show that the SCRs are the functional domain of MCP and that the MCP proteolysis found only in PMN may modulate the properties of PMN MCP. In conclusion, the structural features of PMN MCP largely reflect a variability in the O-linked sugars, and the decreased affinity for C3b may be in part attributable to proteolysis.

Background: A good knowledge of acquired morphologic changes and congenital anomalies requires precise understanding of pathologic conditions of the visceral organs. The aim of the present study was to systematically investigate the types and frequencies of laparoscopically observed congenital anomalies of the liver. Methods: We studied congenital anomalies observed laparoscopically in 1802 consecutive patients who underwent laparoscopy from 1981 to 1994. Results: Congenital anomalies observed laparoscopically were as follows: ape's (monkey's) fissure (6.8%), fissure formation with anomalous lobation (4.3%), left deviation of the round ligament (3.6%), high insertion of the round ligament (2.8%), ectopic liver and accessory lobe of the liver (0.7%), lobar fusion (0.5%), partial defect of the falciform ligament (0.3%), and situs inversus totalis (0.1%). None of these anomalies except situs inversus totalis were diagnosed by imaging techniques other than laparoscopy. Conclusion: Congenital anomalies of the liver are unexpectedly frequent (19.3% of patients) at laparoscopy, which seems to be the most useful method for finding such anomalies. (Gastrointest Endosc 1998;47:136-40.)

OBJECTIVE Although abnormalities of the humoral immune system, such as increased immunoglobulin production, are known in sarcoidosis, the relationship between sarcoidosis and autoimmune disorders is uncertain. We studied the incidence of thyroid autoantibodies and the prevalence of Hashimoto's thyroiditis in patients with sarcoidosis.
PATIENTS AND MEASUREMENTS Sixty-two patients with pulmonary sarcoidosis, diagnosed by a combination of clinical, radiographic and histological findings, were studied. As controls, three groups of subjects aged 40 and over without a known history of thyroid disease (60 patients with pulmonary diseases other than sarcoidosis, 88 hospital employees and 82 company workers), were also analysed. Antibodies against thyroid peroxidase (TPO-Ab) and purified thyroglobulin (Tg-Ab) were measured by radioimmunoassay and antibodies against microsomal antigen (MCHA) and thyroglobulin (TGHA), by haemagglutination.
RESULTS Seventeen of 62 patients (27.4%) had either positive TPO-Ab or Tg-Ab or both. All the patients with positive thyroid autoantibodies were of middle or advanced age, and the incidence of positive TPO-Ab/Tg-Ab in patients with sarcoidosis aged 40 and over was 54.5% in males, 32.4% in females and 37.8% overall. The prevalence was significantly higher in males compared to age-matched control males (0-7.7% in the controls), and in female patients was twice that found in controls (11.8-16.3%). Seven patients had Hashimoto's thyroiditis, indicating that the prevalence was 11.3%, and much higher than that previously reported.
CONCLUSIONS The data show a remarkably high incidence of thyroid autoantibodies in patients of middle or advanced age with sarcoidosis, especially in males, and a higher prevalence of Hashimoto's thyroiditis than in previous reports.

The complement system membrane cofactor protein (MCP) CD46 serves as a C3b/C4b inactivating factor for the protection of host cells from autologous complement attack and as a receptor for measles virus (MV). MCP consists of four short consensus repeats (SCR) which are the predominant extracellular structural motif. In the present study, we determined which of the four SCR of MCP contribute to its function using Chinese hamster ovary cell clones expressing each SCR deletion mutants. The results were as follows: 1) SCR1 and SCR2 are mainly involved in MV binding and infection; 2) SCR2, SCR3, and SCR4 contribute to protect Chinese hamster ovary cells from human alternative complement pathway-mediated cytolysis; and 3) SCR2 and SCR3 are essential for protection of host cells from the classical complement pathway. These results on cell protective activity of the mutants against the human classical and the alternative complement pathways were compatible with factor I-mediated inactivation profiles of C4b and C3b, respectively, in the fluid-phase assay using solubilized mutants and factor I; the results were mostly consistent with those reported by Adams et al. (Adams, E. M., Brown, M. C., Nunge, M., Krych, M., and Atkinson, J. P. (1991) J. Immunol. 147, 3005-3011). SCR2 and SCR3 were required for C3b and C4b inactivation, and SCR4-deleted MCP showed weak cofactor activity for C4b cleavage but virtually no cofactor activity for C3b cleavage. The functional domains of MCP for the three natural ligands C3b, C4b, and MV, therefore, map to different, although partly overlapping, SCR domains.

AbstractLittle has been reported on the flow volume of cortical arteries in the posterior circulation. During craniotomy in 28 patients, we measured the flow velocity of the arteries using microvascular Doppler sonography and recorded their arterial radii and the insonation angle. The flow velocities and radii were 25.7 cm sec–1and 0.11 cm for the posterior cerebral artery (PCA), 19.5 cm sec–1and 0.07 cm for the superior cerebellar artery (SCA), 19.6 cm sec–1and 0.04 cm for the anterior inferior cerebellar artery (AICA), 14.9 cm sec–1and 0.05 cm for the posterior inferior cerebellar artery (PICA), 28.3 cm sec–1and 0.18 cm for the basilar artery, and 18.5 cm sec–1and 0.16 cm for the vertebral artery, respectively. Since the flow velocities of these arteries were confined in a narrow range compared to the cross-sectional areas, the latter was considered to be the primary determinant for flow volume in these arteries. Based on certain assumptions, we estimated the flow volume of the PCA, SCA, AICA and ICA to be 60, 20, 10 and 10 ml min–1, respectively, which could be regarded as the current reference values for the arterial flow volumes. [Neurol Res 2000; 22: 194-196]

Summary We report an unusual case of exostosis arising from the lateral aspect of the posterior clinoid process. Its presence should be considered in approaching the parasellar regions.

New demountable single-fibre and multifibre connectors have been constructed whose plugs include a precision multi-glass-rod arrangement, made by drawing, for locating the fibres and aligning pairs of plugs. The single-fibre and 6-fibre connectors exhibit an average insertion loss of 0.2 dB with index matching and an average off-axis of 3.5 μm. The connectors are potentially cost-effective and reliable.

Low-loss interchangable multifibre connectors have been developed using plugs consisting of large guiding grooved and fibre-fixing V-grooved silicon chips. Guiding grooves etched on silicon chips accomplish extremely small average fibre offset less than 2 μm. A 6-fibre connector plug pair selected from the same wafer exhibits 0.14 dB average connection loss. Connector plugs from different wafers exhibit 0.17 dB and 0.24 dB average connection losses.

New splicers for optical fibres have been fabricated in a process in which arrayed glass rods are heated and drawn together. The splicers exhibit low average splicing loss of less than 0.1 dB, slight loss fluctuation of less than 0.05 dB in the temperature range −20°C∼ +60°C, and are potentially low in cost.

Abstract: We evaluated the usefulness of magnetic resonance angiography (MRA) for showing the topography of paraclinoid carotid artery aneurysms in 27 patients with 30 paraclinoid aneurysms undergoing conventional angiography, three-dimensional time-of-flight MRA and surgery. The anatomy shown on the axial MRA source images was consistent with that found at surgery. The neck of the aneurysm could always be identified on the source images, while it could not be analysed exactly on conventional angiography in 3 cases (10 %). The optic nerves, including those displaced by the aneurysm, were recognised in all patients. The anterior clinoid process was shown as a low-intensity rim or area contiguous with the cortical bone. The source images were of great value in understanding the topography of paraclinoid carotid artery aneurysms.