abstract: Recent years have seen fin field effect transistors (finFETs) dominate modern complementary metal oxide semiconductor (CMOS) processes, [1][2], e.g., at the sub 20 nm technology nodes, as they alleviate short channel effects, provide lower leakage, and enable some continued VDD scaling. However, a realistic finFET based predictive process design kit (PDK) that supports investigation into both circuit and physical design, encompassing all aspects of digital design, for academic use has been unavailable. While the finFET based FreePDK15 was supplemented with a standard cell library, it lacked full physical verification (LVS) and parasitic extraction at the time [3][4]. Consequently, the only available sub 45 nm educational PDKs are the planar CMOS based Synopsys 32/28 nm and FreePDK45 (45 nm PDK) [5][6]. The cell libraries available for those processes are not realistic since they use large cell heights, in contrast to recent industry trends. Additionally, the SRAM rules and cells provided by these PDKs are not realistic. Because finFETs have a 3D structure, which affects transistor density, using planar libraries scaled to sub 22 nm dimensions for research is likely to give poor accuracy. Commercial libraries and PDKs, especially for advanced nodes, are often difficult to obtain for academic use, and access to the actual physical layouts is even more restricted. Furthermore, the necessary non disclosure agreements (NDAs) are un manageable for large university classes and the plethora of design rules can distract from the key points. NDAs also make it difficult for the publication of physical design as these may disclose proprietary design rules and structures. This work focuses on the development of realistic PDKs for academic use that overcome these limitations. These PDKs, developed for the N7 and N5 nodes, even before 7 nm and 5 nm processes were available in industry, are thus predictive. The predictions have been based on publications of the continually improving lithography, as well as estimates of what would be available at N7 and N5. For the most part, these assumptions have been accurate with regards to N7, except for the expectation that extreme ultraviolet (EUV) lithography would be widely available, which has turned out to be optimistic. / Dissertation/Thesis / Doctoral Dissertation Electrical Engineering 2019

Sections 2(3) and 2A of the Wills Act of 1953 were incorporated into the Wills Act in 1992. The purpose of the two sections was to give the court power to condone a document that did not comply with the formalities for making a will and to empower a court to condone a legally ineffective attempt by a testator to revoke his or her will. By introducing section 2(3) and 2A of the Wills Act, the Legislature intended to eliminate the injustice and inequities which frequently resulted from non-compliance with legal requirements. However, after the implementation of the two sections, problems arose with regard to the interpretation and application thereof. This dissertation identifies and analyses the sections to show the current issues which have been discussed in case law and writings by scholars. They are as follows: <ul> (a) Meaning of the word “document” in section 2(3). (b) Meaning of “drafted” by a person who has died since the……drafting thereof. (c) Meaning of “executed” by a person who has died since the….. execution thereof. (d) Should there already be partial compliance with some of the formalities? (e) How does the court conclude that the deceased intended the document to be his will? (f) When must the intention be present? (g) Is a subsequent change in intention (even though it was present at time of making a document) relevant? (h) Interpretation of section 2A. (i) Interaction between section 2(3) and 2A. </ul> Comparing and analysing section 2(3) with a similar provision in Canada and Australia, gives an insight into the problems they encounter and measures that are implemented to achieve the purpose of the provision. Finally, this dissertation will make recommendations regarding the possible alternative wording of the relevant section(s). / Dissertation (LLM)--University of Pretoria, 2012. / Private Law / unrestricted

Elevers intresse för att läsa är avgörande för hur mycket de läser och hur goda läsförmågor de utvecklar. I Sverige finns en nedåtgående trend bland barn och unga gällande intresset för att läsa och skolan har därför en viktig roll i att främja elevers läslust på alla sätt den kan. Denna systematiska litteraturstudie undersöker hur skolan kan främja läslusten hos elever i årskurs 7–9. Syftet med studien var att undersöka vad forskning säger om hur undervisningen så väl som skolmiljön kan främja elevers läslust. Data samlades in genom att systematiskt söka efter forskning såväl manuellt som i nationella och internationella databaser. Ett urval av forskning gjordes utifrån på förhand bestämda kriterier som motsvarar studiens syfte. Urvalet resulterade i totalt 13 forskningsstudier som sedan analyserades med metoden innehållsanalys. Resultatet av studien är att forskningen visar en mångsidig bild av hur skolan kan verka för att främja elevers läslust. De faktorer som forskningen främst visar ha potential att gynna elevers läslust har i studien sammanfattats i fyra övergripande teman: läsarens relation till texten, sammanhang för läsning, social miljö och materiell miljö. Till de mest avgörande sakerna som skolan kan göra för att främja elevers läslust hör god tillgång till litteratur och att skolan tillhandahåller läsande förebilder, såväl som att elever får möjlighet och hjälp att välja litteratur efter sina egna intressen, ges tillräcklig tid till läsning och tillfällen att samtala kring det lästa.

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No description available.

Macrophage apoptosis is an important process in the pathophysiology of atherosclerosis. Oxidized low-density lipoproteins (OxLDL) are a major component of lesions and potently induce macrophage apoptosis. Cannabinoid receptor 2 (CB2), the predominant macrophage cannabinoid receptor, modulates several macrophage processes associated with ongoing atherosclerosis; however, the role of CB2 in macrophage apoptosis is unknown. To determine if CB2 influences a macrophage apoptotic pathway relevant to atherosclerosis, we examined the effect of CB2 deficiency on OxLDL-induced macrophage apoptosis. In situ terminal transferase-mediated dUTP nick end labeling (TUNEL) analysis of resident peritoneal macrophages detected significantly fewer apoptotic CB2-/- macrophages than CB2+/+ macrophages after incubation with OxLDL (27.9 ± 4.7% vs. 61.9 ± 8.5%, P < 0.001) or 7-ketocholesterol (7KC) (18.9 ± 10.5% vs. 54.1 ± 6.9%, P < 0.001), an oxysterol component of OxLDL. Caspase-3 activity; proteolytic conversion of procaspase-3; and cleavage of a caspase-3 substrate, PARP, were also diminished in 7KC-treated CB2-/-macrophages. Furthermore, the deactivation of the prosurvival kinase, Akt, in response to 7KC was impaired in CB2-/-macrophages. These results suggest that CB2 expression increases the susceptibility of macrophages to OxLDL-induced apoptosis, in part, by modulating the effect of oxysterols on the Akt survival pathway and that CB2 may influence atherosclerosis by modulating lesional macrophage apoptosis.

Repeated treatment in ontogeny with the dopamine (DA) D2/D3 receptor agonist quinpirole is associated with enhanced quinpirole-induced yawning and other behaviors such as vacuous chewing, vertical jumping, and antinociception. To determine if the reputedly DA D3 agonist (±)-2-(dipropylamino)-7-hydroxy-1,2,3,4-tetrahydronaphthalene (7-OH-DPAT) would prime for yawning in a manner analogous to that for quinpirole, rats were treated for the first 11 days after birth with an equimolar dose of either quinpirole or 7-OH-DPAT (195.4 nmol/kg/day) and tested for agonist-induced yawning in adulthood. While enhanced quinpirole-induced and 7-OH-DPAT-induced yawning was observed in quinpirole-primed rats, acute treatments with quinpirole and 7-OH-DPAT did not produce an enhanced yawing response in 7-OH-DPAT-'primed' rats. Our findings indicate that 7-OH-DPAT, unlike quinpirole, does not prime for quinpirole- or 7-OH-DPAT-induced yawning in rats.

Oxysterol-induced macrophage apoptosis may have a role in atherosclerosis. Macrophages lacking the type 2 cannabinoid receptor (CB2) are partially resistant to apoptosis induced by 7-ketocholesterol (7KC). AM-251 and SR144528 are selective antagonists of CB1 and CB2 receptors, respectively. We observed that both compounds reduce 7KC-induced apoptosis in Raw 264.7 macrophages. As oxysterol-induced macrophage apoptosis requires acyl-coenzymeA:cholesterol acyltransferase (ACAT) activity, we tested their affects on ACAT activity. AM-251 and SR144528 both reduced cholesteryl ester synthesis in unstimulated and acetylated LDL-stimulated Raw 264.7 macrophages, CB2+/+ and CB2-/- peritoneal macrophages, as well as in vitro, in mouse liver microsomes. Consistent with inhibition of ACAT, the development of foam cell characteristics in macrophages by treatment with acetylated LDL was reduced by both compounds. This work is the first evidence that AM-251 and SR144528 are inhibitors of ACAT and as a result, might have anti-atherosclerotic activities independent of their affect on cannabinoid signaling.

7-Ketocholesterol (7KC) is a cytotoxic component of oxidized low density lipoproteins (OxLDLs) and induces apoptosis in macrophages by a mechanism involving the activation of cytosolic phospholipase A2 (cPLA 2). In the current study, we examined the role of ACAT in 7KC-induced and OxLDL-induced apoptosis in murine macrophages. An ACAT inhibitor, Sandoz 58-035, suppressed 7KC-induced apoptosis in P388D1 cells and both 7KC-induced and OxLDL-induced apoptosis in mouse peritoneal macrophages (MPMs). Furthermore, compared with wild-type MPMs, ACAT-1-deficient MPMs demonstrated significant resistance to both 7KC-induced and OxLDL-induced apoptosis. Macrophages treated with 7KC accumulated ACAT-derived [14C]cholesteryl and [ 3H]7-ketocholesteryl esters. Tandem LC-MS revealed that the 7KC esters contained primarily saturated and monounsaturated fatty acids. An inhibitor of CPLA2, arachidonyl trifluoromethyl ketone, prevented the accumulation of 7KC esters and inhibited 7KC-induced apoptosis in P388B1 cells. The decrease in 7KC ester accumulation produced by the inhibition of cPLA 2 was reversed by supplementing with either oleic or arachidonic acid (AA); however, only AA supplementation restored the induction of apoptosis by 7KC. These results suggest that 7KC not only initiates the apoptosis pathway by activating cPLA2, as we have reported previously, but also participates in the downstream signaling pathway when esterified by ACAT to form 7KC-arachidonate.

The goal of our research was to find a cancer treatment that was both effective and cancer specific, sparing immune and normal tissues. We evaluated the efficacy of a combinatorial treatment using the glycolytic inhibitor 3-bromopyruvate and the fatty acid metabolism inhibitor fenofibrate in cancer, immune and normal tissue cells lines. Treatment of the human breast cancer MCF-7 with 3-bromopyruvate and fenofibrate resulted in increased cell death and decreased colony formation. In the immune cells known as peripheral blood mononuclear cells our combinatorial treatment displayed less toxicity than the traditional chemotherapy doxorubicin. Our combinatorial treatment displayed greater toxicity than doxorubicin towards an established breast cell line MCF- 10A, described in the literature as representing normal breast cells. We have shown for the first time a synergistic relationship between 3-bromopyruvate and fenofibrate. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2020. / FAU Electronic Theses and Dissertations Collection