Thin Film Thermal Deposition at Various Pressures

This research was to verify the hypothesis that resistivity of metal\u27s thin film deposited in a low-pressure environment is the same as its solid material. Thermal Evaporation is a thin film deposition technique in which metal inside a vacuum is evaporated, then deposited onto a surface. Higher quality metal films are deposited when the vacuum pressure is lower. At higher pressures, more air molecules are trapped within the layers of metal, thus increasing scattering sites and increasing the resistance. However, reaching a lower pressure requires more time and effort. In this research, films were deposited at various pressures and resistivities were calculated for each film to determine an ideal pressure range that creates the least resistivity

What is the Point: Will Screening Mammography Save my Life?

Background: We analyzed the claim mammography saves lives by calculating the life-saving absolute benefit of screening mammography in reducing breast cancer mortality in women ages 40 to 65. Methods: To calculate the absolute benefit, we first estimated the screen-free absolute death risk from breast cancer by adjusting the Surveillance, Epidemiology and End Results Program 15-year cumulative breast cancer mortality to account for the separate effects of screening mammography and improved therapy. We calculated the absolute risk reduction (reduction in absolute death risk), the number needed to screen assuming repeated screening, and the survival percentages without and with screening. We varied the relative risk reduction from 10%–30% based on the randomized trials of screening mammography. We developed additional variations of the absolute risk reduction for a screening intervention, including the average benefit of a single screen, as well as the life-saving proportion among patients with earlier cancer detection. Results: Because the screen-free absolute death risk is approximately 1% overall but rises with age, the relative risk reduction from repeated screening mammography is about 100 times the absolute risk reduction between the starting ages of 50 and 60. Assuming a base case 20% relative risk reduction, repeated screening starting at age 50 saves about 1.8 (overall range, 0.9–2.7) lives over 15 years for every 1000 women screened. The number needed to screen repeatedly is 1000/ 1.8, or 570. The survival percentage is 99.12% without and 99.29% with screening. The average benefit of a single screening mammogram is 0.034%, or 2970 women must be screened once to save one life. Mammography saves 4.3% of screen-detectable cancer patients\u27 lives starting at age 50. This means 23 cancers must be found starting at age 50, or 27 cancers at age 40 and 21 cancers at age 65, to save one life. Conclusion: The life-saving absolute benefit of screening mammography increases with age as the absolute death risk increases. The number of events needed to save one life varies depending on the prospective screening subset or reference class. Less than 5% of women with screen-detectable cancers have their lives saved

Quantitative analysis of approaches to group marking

Group work, where students work on projects to overcome challenges together, has numerous advantages, including learning of important transferable skills, better learning experience and increased motivation. However, in many academic systems the advantages of group projects clash with the need to assign individualised marks to students. A number of different schemes have been proposed to individualise group project marks, these include marking of individual reflexive accounts of the group work and peer assessment. Here we explore a number of these schemes in computational experiments with an artificial student population. Our analysis highlights the advantages and disadvantages of each scheme and particularly reveals the power of a new scheme proposed here that we call pseudoinverse marking.Comment: 13 pages, 1 table, 4 figure

How does age affect baseline screening mammography performance measures? A decision model

Background: In order to promote consumer-oriented informed medical decision-making regarding screening mammography, we created a decision model to predict the age dependence of the cancer detection rate, the recall rate and the secondary performance measures (positive predictive values, total intervention rate, and positive biopsy fraction) for a baseline mammogram. Methods: We constructed a decision tree to model the possible outcomes of a baseline screening mammogram in women ages 35 to 65. We compared the single baseline screening mammogram decision with the no screening alternative. We used the Surveillance Epidemiology and End Results national cancer database as the primary input to estimate cancer prevalence. For other probabilities, the model used population-based estimates for screening mammography accuracy and diagnostic mammography outcomes specific to baseline exams. We varied radiologist performance for screening accuracy. Results: The cancer detection rate increases from 1.9/1000 at age 40 to 7.2/1000 at age 50 to 15.1/ 1000 at age 60. The recall rate remains relatively stable at 142–157/1000, which varies from 73– 236/1000 at age 50 depending on radiologist performance. The positive predictive value of a screening mammogram increases from 1.3% at age 40 to 9.8% at age 60, while the positive predictive value of a diagnostic mammogram varies from 2.9% at age 40 to 19.2% at age 60. The model predicts the total intervention rate = 0.013*AGE2 - 0.67*AGE + 40, or 34/1000 at age 40 to 47/1000 at age 60. Therefore, the positive biopsy (intervention) fraction varies from 6% at age 40 to 32% at age 60. Conclusion: Breast cancer prevalence, the cancer detection rate, and all secondary screening mammography performance measures increase substantially with age

A unique role for clathrin light chain A in cell spreading and migration.

Clathrin heavy chain is the structural component of the clathrin triskelion, but unique functions for the two distinct and highly conserved clathrin light chains (CLCa and CLCb, also known as CLTA and CLTB, respectively) have been elusive. Here, we show that following detachment and replating, CLCa is uniquely responsible for promoting efficient cell spreading and migration. Selective depletion of CLCa, but not of CLCb, reduced the initial phase of isotropic spreading of HeLa, H1299 and HEK293 cells by 60-80% compared to siRNA controls, and wound closure and motility by ∼50%. Surface levels of β1-integrins were unaffected by CLCa depletion. However, CLCa was required for effective targeting of FAK (also known as PTK2) and paxillin to the adherent surface of spreading cells, for integrin-mediated activation of Src, FAK and paxillin, and for maturation of focal adhesions, but not their microtubule-based turnover. Depletion of CLCa also blocked the interaction of clathrin with the nucleation-promoting factor WAVE complex, and altered actin distribution. Furthermore, preferential recruitment of CLCa to budding protrusions was also observed. These results comprise the first identification of CLCa-specific functions, with implications for normal and neoplastic integrin-based signaling and cell migration

Exosome-mediated Transfer of αvβ3 Integrin from Tumorigenic to Nontumorigenic Cells Promotes a Migratory Phenotype.

The αvβ3 integrin is known to be highly upregulated during cancer progression and promotes a migratory and metastatic phenotype in many types of tumors. We hypothesized that the αvβ3 integrin is transferred through exosomes and, upon transfer, has the ability to support functional aberrations in recipient cells. Here, for the first time, it is demonstrated that αvβ3 is present in exosomes released from metastatic PC3 and CWR22Pc prostate cancer cells. Exosomal β3 is transferred as a protein from donor to nontumorigenic and tumorigenic cells as β3 protein or mRNA levels remain unaffected upon transcription or translation inhibition in recipient cells. Furthermore, it is shown that upon exosome uptake, de novo expression of an αvβ3 increases adhesion and migration of recipient cells on an αvβ3 ligand, vitronectin. To evaluate the relevance of these findings, exosomes were purified from the blood of TRAMP mice carrying tumors where the expression of αvβ3 is found higher than in exosomes from wild-type mice. In addition, it is demonstrated that αvβ3 is coexpressed with synaptophysin, a biomarker for aggressive neuroendocrine prostate cancer. IMPLICATIONS: Overall this study reveals that the αvβ3 integrin is transferred from tumorigenic to nontumorigenic cells via exosomes, and its de novo expression in recipient cells promotes cell migration on its ligand. The increased expression of αvβ3 in exosomes from mice bearing tumors points to its clinical relevance and potential use as a biomarker. Mol Cancer Res; 14(11); 1136-46. ©2016 AACR

Characterisation and simulation of InAs/InAsSb structures for mid-infrared LEDs

This work reports research on InAs/InAsSb structures focusing on their photoluminescence and electroluminescence spectra over the 4 – 300 K temperature range. The purpose was to gain an insight into developing mid – infrared light – emitting diodes (LEDs) operating with sufficiently high power and efficiency for room temperature gas sensing applications. InAs/InAsSb strained – layer superlattice (SLS) and multiple quantum well (MQW) structures of low antimony content (Sb = 3.7 – 13.5 %) grown by MBE on InAs substrates were compared. These structures were characterised by XRD and TEM imaging. Band structure simulations highlighted the effects of changing QW antimony content and layer thicknesses on the emission properties. Mid – infrared 4 – 300 K photoluminescence showed peak shifting to longer wavelengths and intensity reduction for structures with increased QW antimony content. Excitonic emission identified in the photoluminescence spectra under low excitation power was investigated. Temperature quenching was attributed to competing radiative and non – radiative free carrier recombination processes. At higher temperatures, MQW photoluminescence was dominated by emission from electron – hole recombination in the InAs barrier layers. This was not observed for the SLS, with holes strongly confined in the QWs up to room temperature. The dominant Auger process was identified to differ between the MQW and SLS structures, with larger experimental values for these processes compared to theory indicating some degree of suppression due to the type II band alignment of the structures. All these findings highlighted the superiority of the SLS and its attractiveness for use in the active region of MIR LEDs. Two prototype SLS LEDs were fabricated. Mid – infrared 7 – 300 K electroluminescence was obtained, with the 4.2 µm CO2 absorption fingerprint identifiable. The electroluminescence spectra displayed similar behaviour to the PL spectra. Microwatt output powers were produced by the devices at room temperature. Approaches to improve device performance are considered, as it is of interest to further develop SLS LEDs for mid – infrared applications

G protein–coupled receptor/arrestin3 modulation of the endocytic machinery

Nonvisual arrestins (arr) modulate G protein–coupled receptor (GPCR) desensitization and internalization and bind to both clathrin (CL) and AP-2 components of the endocytic coated pit (CP). This raises the possibility that endocytosis of some GPCRs may be a consequence of arr-induced de novo CP formation. To directly test this hypothesis, we examined the behavior of green fluorescent protein (GFP)-arr3 in live cells expressing β2-adrenergic receptors and fluorescent CL. After agonist stimulation, the diffuse GFP-arr3 signal rapidly became punctate and colocalized virtually completely with preexisting CP spots, demonstrating that activated complexes accumulate in previously formed CPs rather than nucleating new CP formation. After arr3 recruitment, CP appeared larger: electron microscopy analysis revealed an increase in both CP number and in the occurrence of clustered CPs. Mutant arr3 proteins with impaired binding to CL or AP-2 displayed reduced recruitment to CPs, but were still capable of inducing CP clustering. In contrast, though constitutively present in CPs, the COOH-terminal moiety of arr3, which contains CP binding sites but lacks receptor binding, did not induce CP clustering. Together, these results indicate that recruitment of functional arr3–GPCR complexes to CP is necessary to induce clustering. Latrunculin B or 16°C blocked CP rearrangements without affecting arr3 recruitment to CP. These results and earlier studies suggest that discrete CP zones exist on cell surfaces, each capable of supporting adjacent CPs, and that the cortical actin membrane skeleton is intimately involved with both the maintenance of existing CPs and the generation of new structures