Rapid exploration with multi-rotors: A frontier selection method for high speed flight

Exploring and mapping previously unknown environments while avoiding collisions with obstacles is a fundamental task for autonomous robots. In scenarios where this needs to be done rapidly, multi-rotors are a good choice for the task, as they can cover ground at potentially very high velocities. Flying at high velocities, however, implies the ability to rapidly plan trajectories and to react to new information quickly. In this paper, we propose an extension to classical frontier -based exploration that facilitates exploration at high speeds. The extension consists of a reactive mode in which the multi-rotor rapidly selects a goal frontier from its field of view. The goal frontier is selected in a way that minimizes the change in velocity necessary to reach it. While this approach can increase the total path length, it significantly reduces the exploration time, since the multi-rotor can fly at consistently higher speeds

Analysis of Sequence Variation and Risk Association of Human Papillomavirus 52 Variants Circulating in Korea

<div><p>Introduction</p><p>Human papillomavirus (HPV) 52 is a carcinogenic, high-risk genotype frequently detected in cervical cancer cases from East Asia, including Korea.</p><p>Materials and Methods</p><p>Sequences of HPV52 detected in 91 cervical samples collected from women attending Seoul St. Mary’s Hospital were analyzed. HPV52 genomic sequences were obtained by polymerase chain reaction (PCR)-based sequencing and analyzed using Seq-Scape software, and phylogenetic trees were constructed using MEGA6 software.</p><p>Results</p><p>Of the 91 cervical samples, 40 were normal, 22 were low-grade lesions, 21 were high-grade lesions and 7 were squamous cell carcinomas. Four HPV52 variant lineages (A, B, C and D) were identified. Lineage B was the most frequently detected lineage, followed by lineage C. By analyzing the two most frequently detected lineages (B and C), we found that distinct variations existed in each lineage. We also found that a lineage B-specific mutation K93R (A379G) was associated with an increased risk of cervical neoplasia.</p><p>Conclusions</p><p>To our knowledge, we are the first to reveal the predominance of the HPV52 lineages, B and C, in Korea. We also found these lineages harbored distinct genetic alterations that may affect oncogenicity. Our findings increase our understanding on the heterogeneity of HPV52 variants, and may be useful for the development of new diagnostic assays and therapeutic vaccines.</p></div

HPV52 variant lineage distribution of study samples.

<p>(A) Lineages A (sublineages: A1 and A2), B (sublineage: B2), C (sublineage: C2) and D were detected. (B) A phylogenetic tree was constructed from 57 HPV52 variants using concatenated L1, LCR, E6 and E7. A maximum-likelihood tree was constructed using the program, MEGA6. Bootstrap values of key nodes generated by 1,000 resamplings are shown. The length of the scale bar represents 0.005 substitutions per nucleotide position. To root the tree, HPV67 prototype sequences (NCBI accession no. NC_004710) were set as outgroup. The GenBank accession no. of study samples are KY077824-KY077901.</p

Diabetic (db/db) mice promoted CUP-1 xenograft growth.

<p>CUP-1 cells were injected subcutaneously into the scruff of diabetic db/db mice and non-diabetic control littermates (m+/db) of 10 weeks age. Tumor size was monitored every other day for 2 weeks and tumor volume was calculated as in nude mice. <b>(A)</b> CUP-1 tumor growth in db/db and m+/db mice. Each point represents mean ± S.E.M (n = 10). <b>(B</b>) Representative photographs show db/db (right) and m+/db mice (left) with respective representative excised tumors on day 27 after CUP-1 inoculation. Arrows indicate the site with CUP-1 inoculation. <b>(C)</b> Representative photomicrographs of H&E-stained CUP-1 tumor tissues from db/db (left) and m+/db mice (right) excised on day 27 after CUP-1 inoculation, X400. Atypical cells with large irregular nuclei (stars) and mitotic figures (arrows) were present in CUP-1 tumor tissues. <b>(D)</b> Western blotting confirmed E7 expression in CUP-1 excised xenograft from both db/db and m+/db mice.</p

CUP-1 cells were tumorigenic in athymic (nu/nu) mice.

<p>Ten million CUP-1 cells were injected subcutaneously into the scruff of 10-week-old nude mice and tumour development was monitored for 12 weeks. <b>(A)</b> Representative image of a nude mouse with significant tumor mass growth (arrow) at week 12 upon CUP-1 inoculation. <b>(B)</b> Representative excised tumors at 12 weeks after inoculation. <b>(C)</b> CUP-1 xenograft growth in nude mice. Tumor volumes were monitored every other day over the study period by caliper measurement of the largest dimension of the tumor, “a” and the perpendicular diameter, “b”. Tumor volumes were calculated using the formula (a×b²) × 0.5236. Each point represents mean ± S.E.M (n = 10). <b>(D)</b> (i) and (ii) Representative photomicrographs of H&E-stained CUP-1 tumor tissues excised from nude mice, X200. Tissue sections showed presence of cells with enlarged and pleomorphic nucleus (black arrowhead), mitotic figures (black circle) and infiltration of red blood cells (black arrow).</p

CUP-1 was an immortalized epithelial cell line with functional E7 protein.

<p><b>(A)</b> Phase-contrast micrograph of CUP-1 cells, (i) x40 (ii) x200. <b>(B)</b> Proliferation profile of CUP-1. CUP-1 was plated at a density of 2 × 10⁵ cells in a T25 flask. When they reached 80% confluency, cell number was determined and cells were subcultured. Each sub-culture was counted as one passage. This process was repeated up to 200 days with over 60 passages. Cumulative population doublings was calculated using the equation: 3.32 x [log(the number of cell harvested)–log(the initial number of cells plated) + S, where S is the initial population doubling. Cumulative population doubling was then plotted against days in culture. Each point represents the mean of triplicate determinations. CUP-1 grew in a steady rate without any sign of senescence, indicating that it was immortalized. <b>(C)</b> Cell type of CUP-1 at passage 28 (P28) and 60 (P60) was characterized via (i) Western blotting and (ii) immunofluorescence using keratinocyte marker pan-keratin (green) and fibroblast marker S100A. HaCaT (keratinocytes) and NIH 3T3 (fibroblasts) were included as cell type controls. CUP-1 nuclei was counterstained by DAPI (blue) in immunofluorescence. <b>(D)</b> Western blot analysis of pRb levels in CUP-1. Total cell lysate was collected from non-transfected primary baby mouse kidney (BMK) cells and CUP-1 cells at P28 and P60. CUP-1 expressed E7 and readily degraded pRb in both P28 and P60. β-actin was included as the loading control.</p