Love exists in many forms: love between family members, love between friends and significant others, and generally, love of a person for every entity or object in-between. From love between a man and fish, to the love of alcohol, familial or fraternal relationships, and, finally, romantic love, Raymond Carver and Tobias Wolff depict love in its many forms in their short fiction. This thesis specifically explores the portrayal of romantic love in Carver’s story “Beginners” from the collection Beginners and Wolff’s story “Maiden Voyage” from In the Garden of the North American Martyrs. The characters in these stories form a spectrum of love. From the ideal love of Henry and Anna Gates or the modern, simple love, of Nick and Laura in “Beginners,” to the passionless love of Howard and Nora in “Maiden Voyage,” by analyzing the relationships in these stories this thesis concludes that love does exists differently for every marriage. While all relationships can have love in a broad sense, some of these loves are more powerful and lasting than others.
The chemical properties, namely pK and reactivity, of the N-termini of oxyhaemoglobin and deoxyhaemoglobin toward acetic anhydride and 1-fluoro-2,4-dinitrobenzene (Dnp-F) were determined by the competitive-labelling approach [Kaplan, Stevenson & Hartley, (1971) Biochem. J. 124, 289-229; Duggleby & Kaplan (1975) Biochemistry 14, 5168-5175]. At physiological pH and temperature, the valine-1 alpha and valine-1-beta amino groups had unusually low pK values, but showed only minimal changes in their pK values on deoxygenation. Between pH 7.5 and pH 8.0 a deviation was observed in the pH-reactivity profiles and the apparent pK values became markedly pH-dependent. It was found that Dnp-F, but not acetic anhydride, had an abnormally high reactivity toward the N-termini. It is concluded that the valine-1 alpha and valine-1 beta N-termini make little or no contribution to the alkaline Bohr effect at physiological pH values. The high reactivity toward Dnp-F is attributed to an interaction or binding near the N-terminal region, and the discontinuity in the pH-reactivity profile at moderate alkaline pH values to a conformational change which alters the environment of these groups.
Abstract Glioblastoma is an aggressive form of brain cancer with universally poor prognosis. Even with optimal therapy, the cancer recurs frequently. Phosphatase and tensin homolog (PTEN) is a tumor suppressor gene whose mutations are often found in multiple human cancers. PTEN encodes a lipid phosphatase and serves as a negative regulator of the phosphoinositide 3-kinase (PI3K) pathway. Cumulative evidence suggests that PTEN mutations play significant roles in tumorigenesis of glioblastoma as 60% of glioblastoma patients acquired mutations in this gene. Based on our preliminary data, transcriptomic profiling of primary astrocytes derived from Pten knockout mice revealed an overlapping enrichment of mitotic regulators and cell cycle related pathways with human GBM. 4 genes (RCC1, RCC2, NEK2, and CHK2) were validated to be significantly upregulated in PTEN KO astrocytes by qRT-PCR. Regulator of chromatin condensation 2 (RCC2) has been reported to be guanine-nucleotide exchange factor (GEF) for Rac1 and RalA GTPase and act as a regulator of cell cycle progression. Accumulating evidence revealed a pro-tumorigenic role of RCC2 in multiple cancers such as tumor growth and tumor metastasis. Via siRNA inhibition of RCC2, we demonstrated that knocking down of RCC2 in glioblastoma cell lines suppresses cell growth and RCC2 is essential for both G1-S and G2-M progression. Additionally, RCC2 knocking down and a PI3K inhibitor LY294002 inhibit glioblastoma cell viability in a synergistic manner. In summary, PTEN deficiency leads to the upregulation of RCC2, which may promote tumorigenesis of glioblastoma by dysregulating cell cycle progression.To further explore the RCC2 roles, we will find the potential downstream target of RCC2 in dysregulating cell cycle and its potential therapeutic effect in vivo. Funding: General Research Fund Grant #14113519 from The Research Grants Council of Hong Kong Citation Format: Tian Liu, Penelope Mei-Yu Or, Chi-Wai Wong, Stanley Kwok-Kuen Cheung, Yubing Wang, Yiwei Wang, Andrew M. Chan. Analysis of Pten-null mouse astrocytes revealed overlapping transcribed genes with human glioblastoma transcriptome [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 97.
A promising class of nonlinear multiuser detector is introduced for CDMA systems. These "iterated-decision" multiuser detectors use optimized multipass algorithms to successively cancel multiple-access interference (MAI) from received data and generate symbol decisions whose reliability increases monotonically with each iteration. They significantly outperform decorrelating detectors and linear minimum mean-square error (MMSE) multiuser detectors, but have the same order of computational complexity. When the ratio of the number of users to the spreading factor is below a certain threshold, iterated-decision multiuser detectors asymptotically achieve the performance of the "optimum" multiuser detector, ie, maximum-likelihood (ML) decoding.
We derive the asymptotic signal-to-interference ratio (SIR) of the decorrelator in the large system limit, both for the case in which the number of users exceeds the spreading gain and for the case in which the number of users is less than the spreading gain. We show that, contrary to what is claimed by Tse and Hardy (see ibid., vol.45, p.641-57, Mar. 1999) and by Tse and Zeitouni (see ibid., vol.46, p.171-188, Jan. 2000) when the number of users exceeds the spreading gain and the decorrelator is defined in terms of the Moore-Penrose pseudoinverse, the SIR does not converge to zero.
In this paper, experimental investigation of multiple-input multiple-output (MIMO) channel-probing estimation are reported for outdoor environments near the PCS frequency allocation (1.79 GHz). A simple channel parameterization and channel distance metrics are introduced. Channel complexity and channel stationarity are also investigated. Complexity is associated with channel-matrix singular value distributions. Stationarity is associated with the stability of channel singular value and singular vector structure over time.
Sphere decoding for multiple antenna systems has been shown to achieve near-ML performance with low complexity. However, the achievement of such an excellent performance-complexity tradeoff is highly dependent on the initial choice of sphere radius. We present a new sphere decoding algorithm which is even less computationally complex than the original sphere decoder. Moreover, the complexity of the new sphere decoder is relatively insensitive to the initial choice of sphere radius. Thus, by making the choice of radius sufficiently large, the ML solution is guaranteed with low complexity, even for large constellations. In our simulations, we show that with 4 transmit and 4 receive antennas and 64-QAM, our new sphere decoding algorithm achieves the exact ML solution with approximately a factor of 3.5 reduction in complexity when compared to the original sphere decoder, and a factor of 10/sup 5/ reduction when compared to brute-force ML decoding.
Abstract Regulator of chromatin condensation 2 (RCC2), also known as telophase disk protein of 60 kDa (TD-60), has been previously identified as a component of the chromosome passenger complex. Accumulating evidence suggested that RCC2 plays a vital role in the mitotic process and abnormal RCC2 expression is essential for cancer development including Glioblastoma Multiforme (GBM). GBM is the most lethal and frequent brain tumor. Even with the optimal therapy, the 5-year survival rate of GBM remains poor. TCGA data revealed an upregulation of RCC2 in human GBM. Our preliminary data showed that RCC2 was upregulated in PTEN knockout mice primary astrocytes, and loss of function of PTEN has been found in nearly 95% GBM patients. This indicated that RCC2 might act as a PTEN downstream regulator and promote glioblastoma progression. RCC2 has been reported to be essential for tumorigenesis which may act as a GEF for Rac1 or RalA GTPase. Coincidently, our study showed that silencing RCC2 could suppress GBM cell proliferation. Using RNA-seq, we identified 737 DEGs between control siRNA- and RCC2 siRNA-treated A1172 cells. GSEA analysis delineated G2-M progression as the most notably altered pathway by silencing RCC2. Indeed, we observed a G2-M arrest in cells with RCC2 silenced, suggesting that RCC2 is essential for G2-M progression. Additionally, the connectivity map (C-map) analysis was conducted and identified LY294002 and cephaeline as promising inhibitors for RCC2-associated gene signatures. Both LY294002 and cephaeline can synergistically inhibit glioblastoma cell viability with RCC2 silencing. In summary, our study demonstrated that RCC2 signaling is essential for GBM development. We provided evidence that RCC2 exerts a positive effect on G2-M progression. These findings may shed light on anti-RCC2 targeted therapy in GBM treatment. Funding: This work is supported by a General Research Fund grant (#14113519) from the University Grants Committee of Hong Kong. Citation Format: Tian Liu, Penelope Mei-Yu Or, Chi-Wai Wong, Wayne Lut-Heng Ho, Stanley Kwok-Kuen Cheung, Yubing Wang, Andrew M. Chan. RCC2 promotes glioblastoma through regulation of G2-M progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1971.
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