Measurement of the Acidity and Fine-control of the Pore-opening Size of Zeolites

Zeolite has the fine property of strong acidity and micro porosity, with which active and selective catalysts are developed. Our studies on zeolites, measurement of the acidity using ammonia temperature programmed desorption and fine control of the pore-opening size by chemical vapor deposition of silica, are reviewed

Methods for Calculating Heat of Adsorption from Temperature-Programmed Desorption Spectrum under Equilibrium Control

Methods for calculation of heat of adsorption from a TPD (temperature-programmed desorption) spectrum are reviewed. Ammonia TPD is well analyzed by these methods to clarify the acidic properties of various solid catalysts

Development of a quantitative prediction model for peripheral blood stem cell collection yield in the plerixafor era

BACKGROUND AIMS: Predicting autologous peripheral blood stem cell (PBSC) collection yield before leukapheresis is important for optimizing PBSC mobilization and autologous stem cell transplantation (ASCT) for treating hematological malignancies. Although guidelines for plerixafor usage based on peripheral blood CD34+ (PB-CD34+) cell count are available, their predictive performance in the real world remains unclear. METHODS: This study retrospectively analyzed 55 mobilization procedures for patients with non-Hodgkin lymphoma or multiple myeloma and developed a novel quantitative prediction model for CD34+ cell collection yield that incorporated four clinical parameters available the day before leukapheresis; namely, PB-CD34+ cell count the day before apheresis (day -1 PB-CD34+), number of prior chemotherapy regimens, disease status at apheresis and mobilization protocol. RESULTS: The effects of PB-CD34+ cell counts on CD34+ cell collection yield varied widely per patient characteristics, and plerixafor usage was recommended in patients with poorly controlled disease or those with a history of heavy pre-treatments even with abundant day -1 PB-CD34+ cell count. This model suggested a more proactive use of plerixafor than that recommended by the guidelines for patients with poor pre-collection condition or those with a higher target number of CD34+ cells. Further, the authors analyzed the clinical outcomes of ASCT and found that plerixafor use for stem cell mobilization did not affect short- or long-term outcomes after ASCT. CONCLUSIONS: Although external validations are necessary, the results can be beneficial for establishing more effective and safer mobilization strategies

Vaughan-Jackson-like syndrome as an unusual presentation of Kienböck's disease: a case report

<p>Abstract</p> <p>Introduction</p> <p>Kienböck's disease is a condition of osteonecrosis of the lunate bone in the hand, and most patients present with a painful and sometimes swollen wrist with a limited range of motion in the affected wrist. Vaughan-Jackson syndrome is characterized by the disruption of the digital extensor tendons, beginning on the ulnar side with the extensor digiti minimi and extensor digitorum communis tendon of the small finger. It is most commonly associated with rheumatoid arthritis. We describe a case of a patient with an unusual presentation of Kienböck's disease with symptoms similar to those of Vaughan-Jackson syndrome.</p> <p>Case presentation</p> <p>A 40-year-old man of Indian ethnic origin with no known history of trauma presented to our clinic with a ten-day history of an inability to extend his right little and ring fingers with associated pain in his right wrist. He was being treated with long-term steroids but had no other significant medical history. His examination revealed an inability to extend the metacarpal and phalangeal joints of the right ring and little fingers with localized tenderness over the lunate bone. Spontaneous disruption of the extensor tendons was diagnosed clinically and, after radiological investigation, was confirmed to be secondary to dorsal extrusion of the fragmented lunate bone. The patient underwent surgical repair of the tendons and had a full recovery afterward.</p> <p>Conclusion</p> <p>Kienböck's disease, though rare, is an important cause of spontaneous extensor tendon rupture. The original description of Vaughan-Jackson syndrome was of rupture of the extensor tendons of the little and ring fingers caused by attrition at an arthritic inferior radioulnar joint. We describe a case of a patient with Kienböck's disease that first appeared to be a Vaughan-Jackson-like syndrome.</p

Signaling mechanisms that regulate actin-based motility processes in the nervous system

Actin-based motility is critical for nervous system development. Both the migration of neurons and the extension of neurites require organized actin polymerization to push the cell membrane forward. Numerous extracellular stimulants of motility and axon guidance cues regulate actin-based motility through the rho GTPases (rho, rac, and cdc42). The rho GTPases reorganize the actin cytoskeleton, leading to stress fiber, filopodium, or lamellipodium formation. The activity of the rho GTPases is regulated by a variety of proteins that either stimulate GTP uptake (activation) or hydrolysis (inactivation). These proteins potentially link extracellular signals to the activation state of rho GTPases. Effectors downstream of the rho GTPases that directly influence actin polymerization have been identified and are involved in neurite development. The Arp2/3 complex nucleates the formation of new actin branches that extend the membrane forward. Ena/VASP proteins can cause the formation of longer actin filaments, characteristic of growth cone actin morphology, by preventing the capping of barbed ends. Actin-depolymerizing factor (ADF)/cofilin depolymerizes and severs actin branches in older parts of the actin meshwork, freeing monomers to be re-incorporated into actively growing filaments. The signaling mechanisms by which extracellular cues that guide axons to their targets lead to direct effects on actin filament dynamics are becoming better understood.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66422/1/j.1471-4159.2002.01185.x.pd

Asymmetric nature of two subunits of RAD18, a RING-type ubiquitin ligase E3, in the human RAD6A–RAD18 ternary complex

RAD18, a RING-type ubiquitin ligase (E3) that plays an essential role in post-replication repair, possesses distinct domains named RING, UBZ, SAP and the RAD6-binding domain (R6BD) and forms a dimer. RAD6, an ubiquitin-conjugating enzyme (E2), stably associates with R6BD in the C-terminal portion. In this study, we established a method to distinguish between the two subunits of RAD18 by introduction of different tags, and analyzed mutant complexes. Our results, surprisingly, demonstrate that RAD6A and RAD18 form a ternary complex, RAD6A–(RAD18)2 and the presence of only one R6BD in the two RAD18 subunits is sufficient for ternary complex formation and the ligase activity. Interestingly, ligase activity of a mutant dimer lacking both R6BDs is not restored even with large amounts of RAD6A added in solution, suggesting a requirement for precise juxtaposition via interaction with R6BD. We further show that mutations in both subunits of either RING or SAP, but not UBZ, strongly reduce ligase activity, although inactivation in only one of two subunits is without effect. These results suggest an asymmetric nature of the two RAD18 subunits in the complex

Properties of resistant cells generated from lung cancer cell lines treated with EGFR inhibitors

<p>Abstract</p> <p>Background</p> <p>Epidermal growth factor receptor (EGFR) signaling plays an important role in non-small cell lung cancer (NSCLC) and therapeutics targeted against EGFR have been effective in treating a subset of patients bearing somatic EFGR mutations. However, the cancer eventually progresses during treatment with EGFR inhibitors, even in the patients who respond to these drugs initially. Recent studies have identified that the acquisition of resistance in approximately 50% of cases is due to generation of a secondary mutation (T790M) in the EGFR kinase domain. In about 20% of the cases, resistance is associated with the amplification of MET kinase. In the remaining 30-40% of the cases, the mechanism underpinning the therapeutic resistance is unknown.</p> <p>Methods</p> <p>An erlotinib resistant subline (H1650-ER1) was generated upon continuous exposure of NSCLC cell line NCI-H1650 to erlotinib. Cancer stem cell like traits including expression of stem cell markers, enhanced ability to self-renew and differentiate, and increased tumorigenicity <it>in vitro </it>were assessed in erlotinib resistant H1650-ER1 cells.</p> <p>Results</p> <p>The erlotinib resistant subline contained a population of cells with properties similar to cancer stem cells. These cells were found to be less sensitive towards erlotinib treatment as measured by cell proliferation and generation of tumor spheres in the presence of erlotinib.</p> <p>Conclusions</p> <p>Our findings suggest that in cases of NSCLC accompanied by mutant EGFR, treatment targeting inhibition of EGFR kinase activity in differentiated cancer cells may generate a population of cancer cells with stem cell properties.</p