Feature coordinate estimation by time differenced vision/GPS/INS

This paper proposes a multi-baseline method to estimate absolute coordinates of point clouds and the camera attitude parameter utilizing feature points in successive images. Conventionally, 3D map generation methodologies have been based on images acquired by aerial or land vehicles. Pixels corresponding to known landmarks are manually identified at first. Next, the coordinates are directly geo-referenced and automatically allocated to pixels with high-quality Global Positioning System (GPS) and Inertial Navigation System (INS). However, it is difficult to obtain accurate coordinates by the conventional methodology with low-cost GPS and INS. With camera positions and attitude parameters, image-based point clouds can be compensated accurately. A simulation was carried out to evaluate the performance of the proposed method

Chfr is linked to tumour metastasis through the downregulation of HDAC1

Chfr is a ubiquitin ligase that functions in the mitotic checkpoint by delaying entry into metaphase in response to mitotic stress. It has been suggested that Chfr is a tumour suppressor as Chfr is frequently silenced in human cancers. To better understand how Chfr activity relates to cell-cycle progression and tumorigenesis, we sought to identify Chfr-interacting proteins using affinity purification combined with mass spectrometry. Histone deacetylase 1 (HDAC1), which represses transcription by deacetylating histones, was newly isolated as a Chfr-interacting protein. Chfr binds and downregulates HDAC1 by inducing its polyubiquitylation, both in vitro and in vivo. Ectopic expression of Chfr in cancer cells that normally do not express it results in downregulation of HDAC1, leading to upregulation of the Cdk inhibitor p21^(CIP1/WAF1) and the metastasis suppressors KAI1 and E-cadherin. Coincident with these changes, cells arrest in the G1 phase of the cell cycle and become less invasive. Collectively, our data suggest that Chfr functions as a tumour suppressor by regulating HDAC1

Changes in the accreditation standards of medical schools by the Korean Institute of Medical Education and Evaluation from 2000 to 2019

This review presents information on changes in the accreditation standards of medical schools in Korea by the Korean Institute of Medical Education and Evaluation (KIMEE) from 2000 to 2019. Specifically, the following aspects are explained: the development process, setting principles and directions, evaluation items, characteristics of the standards, and validity testing over the course of 4 cycles. The first cycle of accreditation (2000–2005) focused on ensuring the minimum requirements for the educational environment. The evaluation criteria emphasized the core elements of medical education, including facilities and human resources. The second cycle of accreditation (2007–2010) emphasized universities’ commitment to social accountability and the pursuit of excellence in medical education. It raised the importance of qualitative standards for judging the content and quality of education. In the post-second accreditation cycle (2012–2018) which means third accreditation cycle, accreditation criteria were developed to standardize the educational environment and programs and to be used for curriculum development in order to continually improve the quality of basic medical education. Most recently, the ASK 2019 (Accreditation Standards of KIMEE 2019) accreditation cycle focused on qualitative evaluations in accordance with the World Federation of Medical Education’s accreditation criteria to reach the international level of basic medical education, which emphasizes the need for a student-centered curriculum, communication with society, and evaluation through a comprehensive basic medical education course. The KIMEE has developed a basic medical education evaluation and accreditation system in a step-by-step manner, as outlined above. Understanding previous processes will be helpful for the future development of accreditation criteria for medical schools in Korea

Differential spatial expression of peripheral olfactory neuron-derived BACE1 induces olfactory impairment by region-specific accumulation of beta-amyloid oligomer

Olfactory dysfunction is a common symptom associated with neurodegenerative diseases including Alzheimer's disease (AD). Although evidence exists to suggest that peripheral olfactory organs are involved in the olfactory dysfunction that accompanies AD pathology, the underlying mechanisms are not fully understood. As confirmed using behavioral tests, transgenic mice overexpressing a Swedish mutant form of human amyloid precursor proteins exhibited olfactory impairments prior to evidence of cognitive impairment. By measuring the expression of tyrosine hydroxylase, we observed that specific regions of the olfactory bulb (OB) in Tg2576 mice, specifically the ventral portion exhibited significant decreases in the number of dopaminergic neurons in the periglomerular regions from the early stage of AD. To confirm the direct linkage between these olfactory impairments and AD-related pathology, beta-site amyloid precursor protein cleaving enzyme 1 (BACE1)-the initiating enzyme in A beta genesis-and beta-amyloid peptide (A beta), hallmarks of AD were analyzed. We found that an increase in BACE1 expression coincided with an elevation of amyloid-beta (A beta) oligomers in the ventral region of OB. Moreover, olfactory epithelium (OE), in particular the ectoturbinate in which axons of olfactory sensory neurons (OSNs) have direct connections with the dendrites of mitral/tufted cells in the ventral part of OB, exhibited significant decreases in both thickness and cell number even at early stages. This result suggests that A beta oligomer toxicity in the OE may have induced a decline in the number of OSNs and functional impairment of the olfactory system. We first demonstrated that disproportionate levels of regional damage in the peripheral olfactory system may be a specific symptom of AD with A beta oligomer accumulation occurring prior to damage within the CNS. This regional damage in the olfactory system early in the progression of AD may be closely related to AD-related pathological abnormality and olfactory dysfunction found in AD patients.1

Imaging of Viral Thymidine Kinase Gene Expression by Replicating Oncolytic Adenovirus and Prediction of Therapeutic Efficacy

PURPOSE: We have used a genetically attenuated adenoviral vector which expresses HSVtk to assess the possible additive role of suicidal gene therapy for enhanced oncolytic effect of the virus. Expression of TK was measured using a radiotracer-based molecular counting and imaging system. MATERIALS AND METHODS: Replication-competent recombinant adenoviral vector (Ad-DeltaE1B19/55) was used in this study, whereas replication-incompetent adenovirus (Ad-DeltaE1A) was generated as a control. Both Ad-DeltaE1B19/55-TK and Ad-DeltaE1A-TK comprise the HSVtk gene inserted into the E3 region of the viruses. YCC-2 cells were infected with the viruses and incubated with 2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl-5-iodouracil (I-131 FIAU) to measure amount of radioactivity. The cytotoxicity of the viruses was determined, and gamma ray imaging of HSVtk gene was performed. MTT assay was also performed after GCV treatment. RESULTS: On gamma counter-analyses, counts/ minute (cpm)/microg of protein showed MOIs dependency with DeltaE1B19/55-TK infection. On MTT assay, Ad-DeltaE1B19/55-TK led to more efficient cell killing than Ad-DeltaE1A-TK. On plate imaging by gamma camera, both Ad-DeltaE1B19/55-TK and Ad-DeltaE1A-TK infected cells showed increased I-131 FIAU uptake in a MOI dependent pattern, and with GCV treatment, cell viability of DeltaE1B19/55-TK infection was remarkably reduced compared to that of Ad-DeltaE1A-TK infection. CONCLUSION: Replicating Ad-DeltaE1B19/55-TK showed more efficient TK expression even in the presence of higher-cancer cell killing effects compared to non-replicating Ad-DeltaE1A-TK. Therefore, GCV treatment still possessed an additive role to oncolytic effect of Ad-DeltaE1B19/55-TK. The expression of TK by oncolytic viruses could rapidly be screened using a radiotracer-based counting and imaging technique.ope

Rapid Identification of Thrombocytopenia-Associated Multiple Organ Failure Using Red Blood Cell Parameters and a Volume/Hemoglobin Concentration Cytogram

Thrombocytopenia-associated multiple organ failure (TAMOF) has a high mortality rate when not treated, and early detection of TAMOF is very important diagnostically and therapeutically. We describe herein our experience of early detection of TAMOF, using an automated hematology analyzer. From 498,390 inpatients, we selected 12 patients suspected of having peripheral schistocytosis, based on the results of red blood cell (RBC) parameters and a volume/hemoglobin concentration (V/HC) cytogram. We promptly evaluated whether the individual patients had clinical manifestations and laboratory findings were consistent with TAMOF. Plasma exchanges were then performed for each patient. All 12 patients had TAMOF. The mean values of RBC parameters were significantly higher in all of the patients than with the reference range, however, 3 patients had % RBC fragments within the reference range. The mean value of ADAMTS-13 activity was slightly lower in patients compared with the reference range. Of the 12 patients, remission was obtained in 9 patients (75%) within 4 to 5 weeks using plasma exchanges. Three patients died. An increased percentage of microcytic hyperchromic cells with anisocytosis and anisochromia indicated the presence of schistocytes, making it an excellent screening marker for TAMOF. Identification of TAMOF with RBC parameters and a V/HC cytogram is a facile and rapid method along with an automated hematology analyzer already in use for routine complete blood cell counting test