Role of KIFC3 motor protein in Golgi positioning and integration

KIFC3, a microtubule (MT) minus end–directed kinesin superfamily protein, is expressed abundantly and is associated with the Golgi apparatus in adrenocortical cells. We report here that disruption of the kifC3 gene induced fragmentation of the Golgi apparatus when cholesterol was depleted. Analysis of the reassembly process of the Golgi apparatus revealed bidirectional movement of the Golgi fragments in both wild-type and kifC3−/− cells. However, we observed a markedly reduced inwardly directed motility of the Golgi fragments in cholesterol-depleted kifC3−/− cells compared with either cholesterol-depleted wild-type cells or cholesterol-replenished kifC3−/− cells. These results suggest that (a) under the cholesterol-depleted condition, reduced inwardly directed motility of the Golgi apparatus results in the observed Golgi scattering phenotype in kifC3−/− cells, and (b) cholesterol is necessary for the Golgi fragments to attain sufficient inwardly directed motility by MT minus end–directed motors other than KIFC3, such as dynein, in kifC3−/− cells. Furthermore, we showed that Golgi scattering was much more drastic in kifC3−/− cells than in wild-type cells to the exogenous dynamitin expression even in the presence of cholesterol. These results collectively demonstrate that KIFC3 plays a complementary role in Golgi positioning and integration with cytoplasmic dynein

Non-contact detection of nanoscale structures using optical nanofiber

The detection of nanoscale structure/material property in a wide observation area is becoming very important in various application fields. However, it is difficult to utilize current optical technologies. Toward the realization of novel alternative, we have investigated a new optical sensing method using an optical nanofiber. When the nanofiber vertically approached a glass prism with a partial gold film, the material differences between the glass and the gold were detected as a transmittance difference of 6% with a vertical resolution of 9.6 nm. The nanofiber was also scanned 100 nm above an artificial small protruding object with a width of 240 nm. The object was detected with a horizontal resolution of 630 nm, which was less than the wavelength of the probe light

函館の育児規程について : 開拓使管内窮民賑恤規則再考

戦前の函館には、明治、大正、昭和と続いた育児規程があった。規程は、「育児講」に起源をもち、函館の行政の形態が、区から市になっても継続した。これは、父母らの手による養育が困難な子どもたちを救済した規程である。規程を守り続けた函館と吏員の努力を軽視してはならない。しかし、函館独自の育児規程の展開と意義が、社会福祉の観点をもって論じられたことはない。Prewar Hakodate had regulations concerning child rearing that continued throughout the Meiji, Taisho and Showa eras. The regulations derived from「Ikujiko」and continued even after incorporation of area communities as Hakodate city and the subsequent administrative reforms. The regulations helped children whose parents experienced difficulties in raising them. We must not undervalue the efforts of Hakodate and its local officials to maintain these regulations through the years. To date,however, no-one has ever discussed the development or the significance of these regulations unique to Hakodate from the perspective of social work

Sputum cytology of a metastatic postradiation sarcoma (malignant fibrous histiocytoma).

&lt;p&gt;A female patient who died of apparent postradiation sarcoma in the inguinal region after irradiating a metastatic squamous cell carcinoma of the same site was reported. For approximately 20 months, the patient had received a total of 6,600 and 9,600 Roentgen to the right para-aortic and inguinal areas, respectively. About 10 years later, she developed a sarcoma, namely a malignant fibrous histiocytoma. Sputum cytology demonstrated numerous giant cells with bizarre nuclei; subsequent chest films also presented apparent metastatic tumor shadows. The cellular characteristics and also rather low incidence of detection of nonepithelial malignant tumor by sputum cytology were briefly discussed, and ways of enhancing cytodiagnostic accuracy were proposed.&lt;/p&gt;</p

The role of a group III AQP, AQP11 in intracellular organelle homeostasis

AQP11 is a member of a new aquaporin subfamily which includes many aquaporin homologs with low amino acid identities, around 20% of previously identified AQPs. Although these AQPs have unusual NPA sequences, these AQPs have a completely conserved and functionally indispensable cysteine residue downstream of the second NPA box, suggesting that they belong to a specific AQP subfamily, which we propose to name the group III AQPs. On the other hand, the NPA boxes are highly conserved in previous AQP subfamilies : the group I AQPs, original water-selective aquaporin family and the group II AQPs, aquaglyceroporin family. Currently the roles of the group III AQPs are only known with AQP11 as the disruption of intracellularly located AQP11 in mice produced huge vacuoles in the proximal tubule leading to fatal polycystic kidneys at one month old. This review focused on the classification of AQPs based on primary structures to obtain insights into the function and the role of AQPs. With the accumulation of new AQP-like sequences through genome projects, this classification will be useful to predict their functions as each group may have specific characteristics in its function, distribution and regulation

Gene Expression and Localization of High-mobility Group Box Chromosomal Protein-1 (HMGB-1) in Human Osteoarthritic Cartilage

We investigated the expression and localization of high-mobility group box chromosomal protein-1 (HMGB-1) in human osteoarthritic (OA) cartilage in relation to the histopathological grade of cartilage destruction, and examined the role of HMGB-1 in the regulation of proinflammatory cytokine expression in chondrocytes. An immunohistochemical study demonstrated that total HMGB-1-positive cell ratios increase as the Osteoarthritis Research Society International (OARSI) histological grade increased. The population of cytoplasmic HMGB-1-positive chondrocytes was especially increased in the deep layers of higher-grade cartilage. The ratios and localization of receptors for advanced glycation end products (RAGE) expression by chondrocytes in Grade 2, 3, and 4 were significantly higher than those in Grade 1. In vitro stimulation with IL-1β, but not TNFα, significantly upregulated the expression of HMGB-1 mRNA by human OA chondrocytes. Both IL-1β and TNFα promoted the translocation of HMGB-1 from nuclei to cytoplasm. IL-1β and TNFα secretions were stimulated at higher levels of HMGB-1. The results of our study suggest the involvement of HMGB-1 in the pathogenesis of cartilage destruction in OA