Biomedical subjects

K Wada

Publications and source records attributed to K Wada.

At least 37 records · Page 2Linked to original sources

PubMed2003

MRI analysis of hydrocephalus associated with acoustic neurinoma.

We investigated the hydrocephalus in 24 patients associated with acoustic neurinoma. We found the high incidence of homo-lateral ventricular dilatation to the side of the acoustic neurinoma. Utilizing magnetic resonance imaging, the diameter of the tumor parallel to the pyramidal bone, diameter of the tumor perpendicular to the pyramidal bone, grade of the 4th ventricle deviation, and the shape of the tumor (round or oval) were analyzed. Ten (42%) of the 24 patients with acoustic neurinoma were found to have hydrocephalus. Seven (70%) of the 10 patients with hydrocephalus exhibited asymmetrical lateral ventricle dilatation: in all cases the lateral ventricle in the hemisphere homolateral to the acoustic neurinoma was larger than that of the contralateral side. The hydrocephalus was not related to the grade of the 4th ventricle deviation but rather to the diameter of the tumor parallel to the pyramidal bone (p < 0.01). The diameter of the tumor parallel to the pyramidal bone was also related to the asymmetrical lateral ventricular dilatation (p < 0.05).

Adult↗

PubMed2003

Potential role of glial cell line-derived neurotrophic factor receptors in Müller glial cells during light-induced retinal degeneration.

Glial cell line-derived neurotrophic factor (GDNF), neurturin (NTN) and their receptors (GFRalpha1, GFRalpha2 and Ret) play an important role in the survival of neurons in the central and peripheral nervous system. For example, GDNF as well as other trophic factors promotes photoreceptor survival during retinal degeneration. Recent studies have proposed that part of neurotophic rescue of photoreceptors may be indirect, mediated by interaction of the neurotrophic factors with other cell types, that in turn release secondary factors that act directly on photoreceptors. In the present study, we examined the GDNF receptor expression in control and light-damaged retina, and found that GFRalpha2 protein is upregulated in retina-specific Müller glial cells during photoreceptor degeneration. We also examined the effect of GDNF or NTN on cultured Müller cells. Exogenous GDNF increased brain-derived neurotrophic factor, basic fibroblast growth factor and GDNF, but not NTN mRNA production. On the other hand, NTN increased NTN, but not GDNF mRNA production in cultured Müller cells. These observations suggest that GDNF, NTN and their receptors are involved in the regulation of trophic factor production in retinal glial cells, and that functional glia-neuron network may utilize GDNF family for the protection of neural cells during retinal degeneration.

Animals↗

PubMed2003

Axonal and demyelinating forms of the MPZ Thr124Met mutation.

OBJECTIVE: We report on a Japanese family with Charcot Marie Tooth disease (CMT) with the Thr124Met mutation in the peripheral myelin protein zero (MPZ) gene. MATERIAL AND METHODS: Based on the clinical study, we investigated MPZ gene by direct sequence analysis and polymerase chain reaction restriction fragment length polymorphism analysis. RESULTS: Genotyping of four symptomatic family members showed that one family member with severe disease symptoms was homozygous, while the other three were heterozygous. The heterozygous cases were clinicopathologically determined to be the axonal type, which is characterized by late-onset and slow progression associated with Adie's pupil and deafness. The homozygous case was the demyelinating type, which showed earlier onset, rapid progression, sural nerve demyelination, and cranial nerve demyelination at autopsy. CONCLUSIONS: We suggest that axonal and demyelinating forms of CMT are not two distinct classes, but rather parts of a spectrum of genotypically related conditions, particularly with some MPZ mutations.

Adult↗

PubMed2003

Monocyte chemoattractant protein 1 (MCP-1) released from Helicobacter pylori stimulated gastric epithelial cells induces cyclooxygenase 2 expression and activation in T cells.

BACKGROUND: and aims: To clarify the interaction between gastric epithelial and mucosal T cells, we examined the role of cytokines released from epithelial cells in response to Helicobacter pylori water extract protein (HPWEP) in regulating T cell cyclooxygenase 2 (COX-2) expression and activation. METHODS: Media from MKN-28 cells incubated with HPWEP for 48 hours were added to Jurkat T cells and human peripheral T cells. C-C and CXC chemokine concentrations in MKN-28 cell media, and COX-2 expression, interferon gamma (IFN-gamma), and interleukin (IL)-4 secretions in T cells were determined by western blot analysis and ELISA methods. Distributions of COX-2 positive T cells and monocyte chemoattractant protein 1 (MCP-1) in tissue specimens with H pylori associated gastritis were determined as single or double labelling by immunohistochemistry. RESULTS: MCP-1, IL-7, IL-8, and RANTES were detected in media from MKN-28 cells incubated with HPWEP. Media as a whole, and MCP-1 alone, stimulated COX-2 expression and peripheral T cell proliferation. Anti-MCP-1 antibody inhibited media stimulated COX-2 mRNA expression in Jurkat T cells. Media stimulated IFN-gamma but not IL-4 secretion from peripheral T cells, while MCP-1 stimulated IL-4 but not IFN-gamma secretion. Both stimulated cytokine release, and peripheral T cell proliferation was partially inhibited by NS-398, a specific COX-2 inhibitor. In mucosa with gastritis, COX-2 was expressed in T cells and MCP-1 was localised mainly in epithelial and mononuclear cells. MCP-1 levels and the intensity of COX-2 expression in tissue samples were closely related. CONCLUSIONS: Cytokines such as MCP-1, released from gastric epithelial cells in response to HPWEP, seem to modulate T cell immune responses, at least in part via COX-2 expression.

Blotting, Western↗

PubMed2002

A framework for integrating the songbird brain.

Biological systems by default involve complex components with complex relationships. To decipher how biological systems work, we assume that one needs to integrate information over multiple levels of complexity. The songbird vocal communication system is ideal for such integration due to many years of ethological investigation and a discreet dedicated brain network. Here we announce the beginnings of a songbird brain integrative project that involves high-throughput, molecular, anatomical, electrophysiological and behavioral levels of analysis. We first formed a rationale for inclusion of specific biological levels of analysis, then developed high-throughput molecular technologies on songbird brains, developed technologies for combined analysis of electrophysiological activity and gene regulation in awake behaving animals, and developed bioinformatic tools that predict causal interactions within and between biological levels of organization. This integrative brain project is fitting for the interdisciplinary approaches taken in the current songbird issue of the Journal of Comparative Physiology A and is expected to be conducive to deciphering how brains generate and perceive complex behaviors.

Animals↗

PubMed2002

Prenatal ultrasonographic appearance of type IIId (uncorrectable type with cystic dilatation) biliary atresia.

Although prenatal ultrasonographic (US) diagnosis has been reported in biliary atresia (BA), most cases are type I (correctable with cystic dilatation). We report three prenatal cases of type IIId BA (uncorrectable with cystic dilatation). Routine fetal US at 22 to 24 weeks of gestation showed two communicating cystic lesions 12 to 16 mm in diameter. On color Doppler US, the lesions were separate from the portal vein or hepatic artery. The size did not change during the prenatal period in any case. Choledochal cyst (CC) was considered the most likely diagnosis, although BA with cystic lesions was also considered. After birth, the patients developed acholic stools and prolonged neonatal jaundice. Hepatobiliary scintigraphy showed negative passage. Duodenal fluid showed a negative or slightly positive Gmelin test. The neonates underwent laparotomy at the age of 36, 46, and 32 days, respectively. Intraoperative cholangiography showed the gallbladder and slightly-dilated common-bile duct without entering the proximal or distal bile ducts in all cases. They were classified as type IIId BA and underwent excision of the cystic lesions and dissection of the portal bile-duct remnants, followed by hepatic portoenterostomy. Case 1 showed persistent jaundice and finally underwent liver transplantation (LTx), case 2 became anicteric. Case 3 remained jaundiced and is to undergo LTx. In conclusion, type IIId BA may be one of the differential diagnoses when a cystic lesion is detected under the hepatic hilum by fetal US. However, prenatal diagnosis of BA is still difficult with respect to differentiation from a CC or type I BA. Early postnatal diagnosis followed by immediate treatment is important, especially in type IIId BA.

Bile Ducts↗

PubMed2002

Autosomal dominant epilepsy with febrile seizures plus with missense mutations of the (Na+)-channel alpha 1 subunit gene, SCN1A.

Evidence that febrile seizures have a strong genetic predisposition has been well documented. In families of probands with multiple febrile convulsions, an autosomal dominant inheritance with reduced penetrance is suspected. Four candidate loci for febrile seizures have been suggested to date; FEB1 on 8q13-q21, FEB2 on 19p, FEB3 on 2q23-q24, and FEB4 on 5q14-15. A missense mutation was identified in the voltage-gated sodium (Na(+))-channel beta 1 subunit gene, SCN1B at chromosome 19p13.1 in generalized epilepsy with the febrile seizures plus type 1 (GEFS+1) family. Several missense mutations of the (Na(+))-channel alpha 1 subunit (Nav1.1) gene, SCN1A were also identified in GEFS+2 families at chromosome 2q23-q24.3. The aim of this report is precisely to describe the phenotypes of Japanese patients with novel SCN1A mutations and to reevaluate the entity of GEFS+. Four family members over three generations and one isolated (phenotypically sporadic) case with SCN1A mutations were clinically investigated. The common seizure type in these patients was febrile and afebrile generalized tonic-clonic seizures (FS+). In addition to FS+, partial epilepsy phenotypes were suspected in all affected family members and electroencephalographically confirmed in three patients of two families. GEFS+ is genetically and clinically heterogeneous, and associated with generalized epilepsy and partial epilepsy as well. The spectrum of GEFS+ should be expanded to include partial epilepsies and better to be termed autosomal dominant epilepsy with febrile seizures plus (ADEFS+).

Adult↗

PubMed2002

Role of bombesin (BN)-like peptides/receptors in emotional behavior by comparison of three strains of BN-like peptide receptor knockout mice.

Bombesin (BN)-like peptides are involved in the regulation of a wide variety of behaviors, such as spontaneous activity and feeding. We assessed the role of BN-like peptides/receptors in emotional and/or anxiety-related behavior using three strains of knockout mice, each deficient in a single BN-like peptide receptor (gastrin-releasing peptide receptor, bombesin receptor subtype-3, or neuromedin B receptor). Two representative behavioral paradigms, the light-dark (L-D) box test and the elevated plus maze test, were chosen for this purpose. In these two tests, the level of anxiety can be measured as the preference for exploring the light box, or the length of time spent in the open arms, respectively. By conventional parameters, the only significant finding was that BRS-3-deficient mice exhibited a longer duration of remaining in the open arms compared to the wild-type cohort (P < 0.01). However, analyses of risk assessment behavior revealed that BRS-3-deficient mice exhibited increased 'stretched attend posture' behavior (P < 0.01, compared to wild-type mice in both the L-D box and elevated plus maze tests) while NMB-R-deficient mice exhibited decreased behavior (P < 0.05, compared to wild-type mice in both tests). These results suggest that BN-like peptides/receptors may play a role in modulating emotion including some forms of anxiety (e.g., risk assessment behavior). Further, we found that the type of emotional behavior to which each of the peptide/receptor pathways contributes can be clearly specified.

Animals↗

PubMed2002

Effect of acid suppression therapy on development of gastric erosions after cure of Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori eradication markedly improves histological inflammation and decreases peptic ulcer recurrence, but little is known about the subsequent development of gastric mucosal injury. AIM: To investigate whether acid suppression treatment after eradication influences the development of gastric erosions. METHODS: Eighty-one patients (gastritis or peptic ulcer) after successful H. pylori eradication were divided into two groups: 40 received an H2-blocker for 6 months (H2-blocker-positive) and 41 received no treatment (H2-blocker-negative). Endoscopy was performed before, and at 3 and 6 months after completion of eradication. RESULTS: Cumulative prevalence of gastric erosions in the H2-blocker-positive group was significantly lower than in the H2-blocker-negative group, 25% vs. 42%, respectively. In the H2-blocker-negative group but not the H2-blocker-positive group, the cumulative prevalence of gastric erosions after eradication was higher in patients with less severe corpus atrophy or more severe corpus gastritis. CONCLUSIONS: Development of gastric erosions after H. pylori eradication may be controlled by acid suppression treatment. Less severe atrophy or more severe gastritis in oxyntic glands before eradication may be involved in the development of gastric erosions. These results support the idea that recovery of acid secretion may be one of factors for development of gastric mucosal erosions after successful eradication.

Biopsy↗

PubMed2002

Inhibition of Helicobacter pylori-induced cyclo-oxygenase-2 aggravates NSAID-caused gastric damage in Mongolian gerbils.

BACKGROUND: The effect of Helicobacter pylori infection on non-steroidal anti-inflammatory drug-induced gastric mucosal injury is controversial. AIM: To examine the effect of the interaction between H. pylori and non-steroidal anti-inflammatory drugs on gastric mucosal injury. METHODS: Mongolian gerbils infected with H. pylori were treated with indometacin at 8 mg/kg for 2 days or 7 days. Mucosal damage was assessed by macroscopic and histological examination, and myeloperoxidase activity was measured as an index of neutrophil infiltration. The expression levels of cyclo-oxygenase proteins were determined by Western blot analysis and cyclo-oxygenase activity. RESULTS: A 2-day course of indometacin did not cause an increase in gastric damage in H. pylori-infected Mongolian gerbils compared to uninfected gerbils, while a 7-day course of indometacin caused additive gastric damage in H. pylori-infected animals. H. pylori infection induced cyclo-oxygenase-2 expression in the stomach. Treatment with indometacin for 2 days did not significantly affect cyclo-oxygenase activity in H. pylori-infected animals, while treatment for 7 days inhibited both cyclo-oxygenase-1 and cyclo-oxygenase-2 activities. Pre-treatment with a selective cyclo-oxygenase-2 inhibitor aggravated mucosal injury in H. pylori-infected animals treated or not treated with indometacin for 2 days. CONCLUSIONS: Our results suggest that cyclo-oxygenase-2 protein induced by H. pylori infection may be involved in the defence of the gastric mucosa against damage caused by non-steroidal anti-inflammatory drugs. Therefore, inhibition of cyclo-oxygenase-2 activity may enhance non-steroidal anti-inflammatory drug-caused gastric damage in H. pylori-infected animals.

Animals↗

PubMed2002

A case of primary cutaneous CD30+ T-cell lymphoproliferative disorder with features of granulomatous slack skin disease.

We present a patient with primary CD30+ cutaneous T-cell lymphoma whose histological and clinical features overlapped with those of granulomatous slack skin disease (GSSD). A 26-year-old woman had infiltrative erythema on the abdominal wall and an incurable ulcerative lesion on the left knee. Her skin progressively became atrophic and pendulous, showing a hyperpigmented appearance over almost the whole body. Histopathologically, a dense lymphoid cell infiltrate accompanying numerous macrophages and multinucleated giant cells (MGC) extended into the subcutaneous tissue. Most lymphoid cells were small and positive for T-cell markers. Some relatively large atypical cells were scattered in the lesion, most of which (60%) were positive for CD30. T-cell receptor-beta gene rearrangement was confirmed in the abdominal lesion. MGC infiltrated more dominantly into a deeeper layer of the skin with the elastic fibres there almost completely disappearing. Immunoreactivity for CD30 of MGC was negative and overexpression of elastolytic metalloproteinases was observed. The association between primary cutaneous CD30+ lym- phoproliferative disorders and GSSD has not previously been reported. Overexpression of elastolytic metalloproteinases in MGC contributes to the disappearance of the elastic fibres and enhances the severity of the clinical course.

Adult↗

PubMed2002

Potential role of phosphodiesterase 7 in human T cell function: comparative effects of two phosphodiesterase inhibitors.

Even though the existence of phosphodiesterase (PDE) 7 in T cells has been proved, the lack of a selective PDE7 inhibitor has confounded an accurate assessment of PDE7 function in such cells. In order to elucidate the role of PDE7 in human T cell function, the effects of two PDE inhibitors on PDE7A activity, cytokine synthesis, proliferation and CD25 expression of human peripheral blood mononuclear cells (PBMC) were determined. Recombinant human PDE7A was obtained and subjected to cyclic AMP-hydrolysis assay. PBMC of Dermatophagoides farinae mite extract (Df)-sensitive donors were stimulated with the relevant antigen or an anti-CD3 monoclonal antibody (MoAb). PBMC produced IL-5 and proliferated in response to stimulation with Df, while stimulation with anti-CD3 MoAb induced CD25 expression and messenger RNA (mRNA) synthesis of IL-2, IL-4 and IL-5 in peripheral T cells. A PDE inhibitor, T-2585, which suppressed PDE4 isoenzyme with high potency (IC50 = 0.00013 microM) and PDE7A with low potency (IC50 = 1.7 microM) inhibited cytokine synthesis, proliferation and CD25 expression in the dose range at which the drug suppressed PDE7A activity. A potent selective inhibitor of PDE4 (IC50 = 0.00031 microM), RP 73401, which did not effectively suppress PDE7A (IC50 > 10 microM), inhibited the Df- and anti-CD3 MoAb-stimulated responses only weakly, even at 10 microM. PDE7 may play a critical role in the regulation of human T cell function, and thereby selective PDE7 inhibitors have the potential to be used to treat immunological and inflammatory disorders.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2002

Potential impact of global warming on deciduous oak dieback caused by ambrosia fungus Raffaelea sp. carried by ambrosia beetle Platypus quercivorus (Coleoptera: Platypodidae) in Japan.

Deciduous oak dieback in Japan has been known since the 1930s, but in the last ten years epidemics have intensified and spread to the island's western coastal areas. The symbiotic ambrosia fungus Raffaelea sp. is the causal agent of oak dieback, and is vectored by Platypus quercivorus (Murayama). This is the first example of an ambrosia beetle fungus that kills vigorous trees. Mortality of Quercus crispula was approximately 40% but much lower for associated species of Fagaceae, even though each species had a similar number of beetle attacks. It is likely that other oaks resistant to the fungus evolved under a stable relationship between the tree, fungus and beetle during a long evolutionary process. Quercus crispula was probably not part of this coevolution. This hypothesis was supported by the fact that P. quercivorus showed the least preference for Q. crispula yet exhibited highest reproductive success in this species. Therefore, P. quercivorus could spread more rapidly in stands with a high composition of Q. crispula. The present oak dieback epidemic in Japan probably resulted from the warmer climate that occurred from the late 1980s which made possible the fateful encounter of P. quercivorus with Q. cripsula by allowing the beetle to extend its distribution to more northerly latitudes and higher altitudes. Future global warming will possibly accelerate the overlapping of the distributions of P. quercivorus and Q. crispula with the result that oak dieback in Q. crispula will become more prevalent in Japan.

Animals↗

PubMed2001

Involvement of corticotropin-releasing factor receptor subtype 1 in morphine withdrawal regulation of the brain noradrenergic system.

Effects of pretreatment with the selective corticotropin-releasing factor (CRF) subtype 1 (CRF(1)) receptor antagonist, 2-(N-(2-methylthio-4-isopropylphenyl)-N-ethyl-amino-4-(4-(3-fluorophenyl)-1,2,3,6-tetrahydropyridin-1-yl)-6-methylpyrimidine (CRA1000) on the behavioral and biochemical changes after naloxone-precipitated morphine withdrawal were examined in ICR mice. Mice were chronically treated with morphine (8-45 mg/kg) for 5 days. Naloxone (3 mg/kg, s.c.) precipitated jumping, diarrhea, and body weight loss in morphine-dependent mice. In addition, 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) and noradrenaline turnover (MHPG/noradrenaline) levels in the cerebral cortex were increased following naloxone challenge in morphine-dependent mice. However, 5-hydroxytriptamine turnover did not alter the increase following naloxone challenge in morphine-dependent mice. Pretreatment with CRA1000 (20 mg/kg, i.p.) attenuated the incidence of withdrawal signs and naloxone-precipitated increases in noradrenaline turnover. These results suggest that the activation of CRF(1) receptor may play an important role in the elevation of noradrenaline transmission, but not in 5-hydroxytriptamine transmission, in the cerebral cortex, which projects from the locus coeruleus during morphine withdrawal.

Animals↗

PubMed2001

Mouse neurotensin receptor 2 gene (Ntsr2): genomic organization, transcriptional regulation and genetic mapping on chromosome 12.

We earlier isolated and characterized the mouse neurotensin receptor 1 (Ntsr1) gene and developed Ntsr1 null mice. In the present study, we isolated the mouse neurotensin receptor 2 gene (Ntsr2) and characterized the structure. The gene fragments available to us have 1.1 kb of 5' upstream promoter region and a 7 kb coding region composed of four exons. Transcription initiation sites, determined by primer extension analysis, are located at 286 and 303 bp upstream from initiation of the ATG codon. The promoter region contains a TATA-like box, a typical CAAT box and putative GATA-2, CREB, Oct-2 and Ikarous 2 binding elements. We also found novel splice donor-acceptor sites for alternative splicing, which could generate a short form of mRNA encoding a truncate-type receptor. In addition, we determined the chromosomal location of the Ntsr2 gene and mapped it at 6 cM from the centromere on chromosome 12.

Alternative Splicing↗

PubMed2001

Aspirin-triggered lipoxin A4 and lipoxin A4 up-regulate transcriptional corepressor NAB1 in human neutrophils.

Aspirin-triggered 15-epi-lipoxin A4 (ATL) is an endogenous lipid mediator that mimics the actions of native lipoxin A4, a putative "stop signal" involved in regulating resolution of inflammation. A metabolically more stable analog of ATL, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 analog (ATLa), inhibits neutrophil recruitment in vitro and in vivo and displays potent anti-inflammatory actions. ATLa binds with high affinity to the lipoxin A4 receptor, a G protein-coupled receptor on the surface of leukocytes. In this study, we used freshly isolated human neutrophils to examine ATLa's potential for initiating rapid nuclear responses. Using differential display reverse transcription polymerase chain reaction, we identified a subset of genes that was selectively up-regulated upon short exposure of polymorphonuclear leukocytes to ATLa but not to the chemoattractant leukotriene B4 or vehicle alone. We further investigated ATLa regulation of one of the genes, NAB1, a transcriptional corepressor identified previously as a glucocorticoid-responsive gene in hamster smooth muscle cells. Treatment of human neutrophils with pertussis toxin blocked ATLa up-regulation of NAB1. In addition, ATLa stimulated NAB1 gene expression in murine lung vascular smooth muscle in vivo. These findings provide evidence for rapid transcriptional induction of a cassette of genes via an ATLa-stimulated G protein-coupled receptor pathway that is potentially protective and overlaps with the anti-inflammatory glucocorticoid regulatory circuit.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2001

Improvement of some pharmaceutical properties of DY-9760e by sulfobutyl ether beta-cyclodextrin.

The interaction of DY-9760e, a novel cytoprotective agent, with sulfobutyl ether beta-cyclodextrin (SBE-beta-CyD) in phosphate buffered saline (PBS) at various pH and ionic-strengths was studied by spectroscopic methods and the solubility method, and the results were compared with that of 2-hydroxypropyl-beta-cyclodextrin (HP-beta-CyD). The circular dichroism (CD) spectroscopic studies suggested that both beta-CyDs form the inclusion complexes with DY-9760e in a molar ratio of 1:1, and the interaction of DY-9760e with SBE-beta-CyD is much stronger than that with HP-beta-CyD at any pH studied, in terms of a synergetic effect of hydrophobic and electrostatic interactions. The different intermolecular interaction between the SBE-and HP-beta-CyD complexes was clearly reflected in the stability constant (K'), e.g. the different dependence of K' value on pH and ionic strength of solutions. 1H- and 13C-NMR studies suggested that HP-beta-CyD interacts preferably with the benzene ring of DY-9760e, whereas SBE-beta-CyD interacts not only with the benzene ring via hydrophobic interaction but also with the piperazine ring of the drug via electrostatic interaction. The solubilizing ability of SBE-beta-CyD against DY-9760e was much greater than that of HP-beta-CyD at any pH studied. Furthermore, SBE-beta-CyD markedly suppressed the photo-degradation of DY-9760e in aqueous solution and reduced the adsorption of DY-9760e from PBS to polyvinyl chloride (PVC) tubes after incubation. The results suggest that SBE-beta-CyD is useful in preparing parenteral solutions of poorly water-soluble drugs with positive charge such as DY-9760e.

Adsorption↗

PubMed2001

Synthesis of alkenylene-bridged macrocyclic silsesquioxanes by ruthenium or rhodium-catalyzed ring-closing reactions of bis(allyldimethylsilyl) groups.

Novel alkenylene-bridged oligosilsesquioxanes composed of half-caged structures with 16- or 17-membered rings as well as a titanium-containing molecule with a twisted 21-membered macrocycle have been synthesized by ruthenium or rhodium-catalyzed ring-closing reactions of silsesquioxanes with bis(allyldimethylsilyl) groups.

Journal Article↗