Modeling the Influence of Land Use Developments on Transportation System Performance

The growth in the urban population has influenced urban sprawl, congestion, and subsequently, delays on the existing road infrastructure. New land use developments occur in every part of the city due to rapid economic development and to meet the demand for better living standards. The induced traffic volume generated from such land use developments often results in increased congestion and vehicular delay on the existing roads. With recent advancements in the technology, it is possible to capture continuous, and comprehensive travel time data for every major corridor in a city. Therefore, the goal of this research is to model the influence of land use developments on travel time variations to improve the mobility of people and goods. Data for 259 road links were selected within the city of Charlotte, North Carolina (NC). Three years of travel time data, from the year 2013 to the year 2015, were collected from the private agency. Thirty-five different types of land use developments were considered in this research. The spatial dependency was incorporated by considering the land use developments within 0.5 miles, 1 mile, 2 miles, and 3 miles of the selected road link. Forty-eight statistical models were developed. The results obtained indicate that land use developments have a significant influence on travel times. Different land use categories contribute to the average travel time based on the buffer width, area type, and the link speed limit. Developing the models by classifying the links based on the speed limit (\u3c 45 mph, 45 to 50 mph, and \u3e 50 mph) was observed to be the best approach to examine the relationship between land use developments and the average travel time. Also, typically travel time on a selected road link is higher during the evening peak period compared to the morning peak and the afternoon off-peak period. Further, the results obtained indicate that the number of lanes and the posted speed limit are negatively associated with the travel time of the selected link

Odontogenic tumors: a review of 60 cases

Objective: Studies on odontogenic tumors published from many parts of the world show a distinct geographic va- riation; however, there is little information available in the English-language literature on the relative frequency of odontogenic tumors in India. This retrospective study was designed to determine the relative frequency of odonto- genic tumors in an Indian population and compare them with various reports from other parts of the world. Study design: The histopathology records of the Department of Oral pathology and Microbiology of Government Dental College and Hospital, Mumbai were retrieved retrospectively within the period of January 2001 to March 2010. A total of 60 lesions classified as odontogenic tumors were reviewed. These were analyzed for age, gender, site of tumor and histopathologic typing. Criteria used were World Health Organization (WHO) classification 2005. The controversy still exists regarding the nature of odontogenic keratocyst or tumor, so it has not been included in this study. Results: A total of 60 cases of odontogenic tumors were reported in this period. The most frequent histological type was ameloblastoma (66.67%), followed by odontome (20%), adenomatoid odontogenic tumor (10%). In general, the odontogenic tumors showed a predilection for the mandible and the posterior regions of the jaws. Ameloblastomas occurred with a marked predilection for the mandible, while adenomatoid odontogenic tumor showed predi- lection for the maxilla, anterior regions of the jaws, and young females. Conclusion: Odontogenic tumors show a definite geographic variation. In our study, ameloblastomas were the most frequent odontogenic tumors, with distinct anatomic predilection

Plexiform ameloblastoma of mandible: case report

Ameloblastoma, a benign epithelial odontogenic tumor, is locally aggressive. This tumor comprises about 1% of tumors and cysts arising in the jaws. It appears most commonly in the third to fifth decades and with equal frequency between sexes. Ameloblastoma prevalently occurs in the mandibular molar and the ramus areas. Recurrence frequently appears after inadequate treatment. They are usually benign in growth pattern but frequently invade locally and occasionally metastasize. In the present study, a case of unusually large plexiform ameloblastoma was presented with its clinical, radiological, histological features and treatment modalities, and this is the addition of one more case in the literature

Interplay between Artemis and TDP1 in sensitivity to radiomimetic agents

DNA double-strand breaks containing unligatable termini are potent cytotoxic lesions leading to cell death or growth arrest. Artemis, which is associated with the Non-Homologous End Joining (NHEJ) pathway, is the major end processing nuclease that resolves unligatable termini, especially the 3′ blocks, by nucleolytic trimming. Tyrosyl-DNA Phosphodiesterase 1 (TDP1) is an enzyme which is biochemically competent in 3′-phosphoglycolate processing. The purpose of this study is to investigate if TDP1 is an end-processing enzyme involved in the NHEJ pathway. Clonogenic Survival assays using shRNA-mediated TDP1 knockdown and Artemis knockout (Artemis-/-) in HCT116 cells showed increased sensitivity to Neocarzinostatin (NCS) and Calicheamicin, radiomimetic drugs that produce 3′-phosphoglycolate-terminated double-strand breaks. Thus, a cell line with combined deficiency in Artemis and TDP1 was generated by infecting Artemis-/- single mutants with a lentivirus expressing a TDP1 shRNA. Positive clones were screened for maximum TDP1 knockdown which was found to be 10X. Clonogenic survival assays carried out on shTDP1 & Artemis-/- single mutants and the Artemis-/-.shTDP1 double mutants showed similar sensitivity to Calicheamicin and NCS. Immunofluorescence studies on Art-/- and Art-/-.shTDP1 mutants also showed a similar increase in persistent 53BP1 foci, a measure of DNA damage, after treatment with NCS. Cell cycle analysis studies showed all these mutants arrest in G1 phase of the cell cycle after treatment with NCS. Thus, taken all together, surprisingly, these experiments suggest that TDP1 functions are epistatic with Artemis in the NHEJ pathway for repair of Calicheamicin- and NCS-mediated DNA damage

Application or Tab Switching via Mouse Hover and Scroll

Many computer users use several applications simultaneously for various tasks. Switching between applications or browser tabs is cumbersome and requires the user to lift their fingers off the keyboard, move the cursor to the target application via a pointing device, and click the pointing device. This disclosure describes techniques that enable a user to rapidly switch between applications or browser tabs using the scroll of a mouse or a trackpad. The user can simply hover the mouse pointer over the system taskbar or browser tab-bar and scroll the mouse or trackpad to switch between apps or tabs

Updating the Taskbar with Contextual Actions Relevant to the Application in Focus

Users perform a variety of actions when interacting with a software application via various user interface (UI) controls provided by the application to perform operations corresponding to the actions. Differences in user interfaces across applications and the requirement to perform complex actions such as multi-click can be confusing and cumbersome. Users benefit from quick and easy access to high-priority contextual actions. This disclosure describes a dynamically updating taskbar provided by a device operating system. With user permission, the taskbar changes dynamically based on the currently active application as the user switches between applications. The taskbar provides quick access to the most important interactive elements within the application in focus (and optionally, the specific task being performed), such as specific buttons or controls. When the user switches to a different application, the interactive elements shown on the taskbar are updated with the appropriate interactive elements corresponding to the new application in focus

Fabrication of Nonplanar Surfaces Via 5-Axis 3D Printing

The advancements in manufacturing have always played a vital role in human life. One of the most recent and growing manufacturing methods is additive manufacturing (AM). AM has been in focus for its ability to manufacture intricate parts with internal features which are not possible with traditional manufacturing processes. Making parts lighter and stronger has been the goal for most AM processes. The advancements in AM have made it possible to produce parts with high strength internal structures. The overall strength of the manufactured plastic parts depends on several variables. The part’s strength is determined by the material, the build direction, the infill settings, and the printing parameters. Optimization of each of these variables is critical for obtaining the desired result for the intended application of the printed part. One of the major drawbacks of these parts is the weak interlayer bonding within parts which are susceptible to failure under high loads. Similarly, the stair stepping effect compromises the surface finish of a part. This is prominently seen when the angle of inclination is less than 30 degrees. Previous research shows that the mixture of non-planar and planar layers in a 3DP part can improve its surface finish. Non-Planar 3D printing done using a 3-axis machine is limited by the angle of the nozzle with respect to the previously printed layers. This study will focus on incorporating 5-axis 3D printer toolpath motions to print nonplanar surfaces. It will also shed some light on the enhanced mechanical properties of the parts which have non-planar layers as compared to conventionally 3D printed parts

PROCESSING OF 3′-BLOCKED DNA DOUBLE-STRAND BREAKS BY TYROSYL-DNA PHOSPHODIESTERASE 1, ARTEMIS AND POLYNUCLEOTIDE KINASE/ PHOSPHATASE

DNA double-strand breaks (DSBs) containing unligatable termini are potent cytotoxic lesions leading to growth arrest or cell death. The Artemis nuclease and tyrosyl-DNA phosphodiesterase (TDP1) are each capable of resolving protruding 3′-phosphoglycolate (PG) termini of DNA double-strand breaks (DSBs). Consequently, a knockout of Artemis and a knockout/knockdown of TDP1 rendered cells sensitive to the radiomimetic agent neocarzinostatin (NCS), which induces 3′-PG-terminated DSBs. Unexpectedly, however, a knockdown or knockout of TDP1 in Artemis-null cells did not confer any greater sensitivity than either deficiency alone, indicating a strict epistasis between TDP1 and Artemis. Moreover, a deficiency in Artemis, but not TDP1, resulted in a fraction of unrepaired DSBs, which were assessed as 53BP1 foci. Conversely, a deficiency in TDP1, but not Artemis, resulted in a dramatic increase in dicentric chromosomes following NCS treatment. An inhibitor of DNA-dependent protein kinase, a key regulator of the classical nonhomologous end joining (C-NHEJ) pathway sensitized cells to NCS but eliminated the sensitizing effects of both TDP1 and Artemis deficiencies. Moreover, Polynucleotide Kinase/ Phosphatase (PNKP) is known to process 3′-phosphates and 5′-hydroxyls during DSB repair. PNKP-deficiency sensitized both HCT116 and HeLa cells to 3′-phosphate ended DSBs formed upon radiation and radiomimetic drug treatment. The increased cytotoxicity in the absence of PNKP was synonymous with persistent, un-rejoined 3′-phosphate-ended DSBs. However, DNA-PK deficiency sensitized PNKP-/- cells to low doses of NCS suggesting that, in the absence of PNKP, alternative enzyme(s) can remove 3′-phosphates in a DNA-PK-dependent manner. These results suggest that TDP1 and Artemis perform different functions in the repair of terminally blocked DSBs by the C-NHEJ pathway, and that whereas an Artemis deficiency prevents end joining of some DSBs, a TDP1 deficiency tends to promote DSB mis-joining. In addition, loss of PNKP significantly sensitizes cells to 3′-phosphate-ended DSBs due to a defect in 3′-dephosphorylation