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Journal articles on the topic 'Amlwch'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Chen, Lei Lei, Tanya Reddick Rodgers, Marsha L. Chaffins, and Koichi Maeda. "Acute Monocytic Leukemia With Cutaneous Manifestation." Archives of Pathology & Laboratory Medicine 129, no. 3 (March 1, 2005): 425–26. http://dx.doi.org/10.5858/2005-129-425-amlwcm.

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2

Wood, Andrew, Fiona Young, and Marie O'Donnell. "Angiomyolipoma with Epithelial Cysts Masquerading as a Cystic Renal Cell Carcinoma." Current Urology 9, no. 4 (2015): 209–11. http://dx.doi.org/10.1159/000447142.

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Angiomyolipoma with epithelial cysts (AMLEC) is a very uncommon renal tumor. AMLEC has a characteristic histological appearance and immunohistochemical staining pattern, knowledge of which should preclude misdiagnosis by pathologists. We present a rare case of an AMLEC which was suspected to be a cystic renal cell carcinoma radiologically. We describe the characteristic immunological staining pattern and ultrastructural features of this lesion and discuss the potential differential diagnoses.

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3

Bin Belaisha, Belaisha, and Graham Brooks. "Money laundering in Dubai: strategies and future directions." Journal of Money Laundering Control 17, no. 3 (July 8, 2014): 343–54. http://dx.doi.org/10.1108/jmlc-10-2013-0038.

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Purpose – This paper aims to highlight present strategies to prevent money laundering in Dubai. Design/methodology/approach – Thirty semi-structured interviews were conducted with Anti Money Laundering Suspicion Cases Unit (AMLSCU), Anti Organized Crime Department (AOCD) and Central Bank employees. Findings – This paper shows that AMLSCU, AOCD and Central Bank employees are aware that future strategies to prevent money laundering are needed. Research limitations/implications – Limited available secondary data and cases of money laundering. Originality/value – Interviews with key personnel in main organisations tasked with preventing money laundering in Dubai.

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Zhong, Rui-kun, Thomas A. Lane, and Edward D. Ball. "Generation of Acute Myeloid Leukemia (AML)-Specific Autologous CD4 and CD8 T Cell Lines by Limiting Dilution AML Dendritic Cell Culture." Blood 108, no. 11 (November 1, 2006): 2018. http://dx.doi.org/10.1182/blood.v108.11.2018.2018.

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Naturally occurring cytotoxic T cells directed against various leukemia associated antigens (LAA) expressed by acute myeloid leukemia (AML) cells have been described. However, these LAA-specific T cells are rare and obviously unable to initiate effective anti-leukemia responses. The challenge is how to investigate, select, activate and expand the rare LAA-specific T cells from the vast population of blood cells in patients with AML for immunotherapy. Based on our studies of inducing AML dendritic cell (AMLDC) differentiation and priming in situ AML-reactive T cells, we have developed a novel method of generating multiple autologous AML reactive T cell lines by limiting dilution AMLDC (LD-AMLDC) culture. The principle of LD-AMLDC is based on the assumption that autologous AML-reactive T cells or precursors are randomly distributed in the AML PBMC suspension, and that each one has an equal opportunity to respond to AML cells in the 96-well plates under optimized culture condition. By culturing AML PBMC (>90% blasts) in culture medium supplemented with GM-CSF/IL4/IL2/IL7/IL12 to induce AML DC differentiation and activate in situ autologous T cells, highly reactive anti-AML T cell lines (both CD4+ and CD8+ lines) were selected and expanded from LD-AMLDC culture using the appropriate numbers of AML PBMC in each culture well by the criterion of release of IFN-gamma in response to autologous AML blasts. By maximum likelihood solution, the estimated average frequency of AML reactive T cells or precursors is 6±3/1,000,000 AML PBMC (n=8). Strong intracellular IFN-gamma release of T cell lines obtained in LD-AMLDC was demonstrated by flow cytometry analysis after stimulation by autologous AML cells but not autologous B-lymphoblastoid cell line (LCL) (Figure). Effective specific lysis (up to 70% at E:T=20:1) of autologous AML cells but not autologous LCL or allogeneic AML cells by these T cell lines was observed. Two PR1 specific T cell lines were obtained by screening 39 AML reactive HLA-A2+ CD8+ T cell lines generated from 5 LD-AMLDC cultures, suggesting that other unidentified CD4 or CD8 lines with strong autologous AML responses may be reactive to known or unknown LAAs. These results encourage continued efforts to induce, activate and select T cells lines with high autologous AML reactivity using LD-AMLDC culture and to expand multi-LAA reactive T cell lines acquired from limiting dilution AML-DC culture for AML immunotherapy. Figure Figure

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5

Post, David L., and William F. Reinhart. "Image Quality of Two-Primary Color Active-Matrix Liquid-Crystal Displays." Human Factors: The Journal of the Human Factors and Ergonomics Society 39, no. 4 (December 1997): 618–41. http://dx.doi.org/10.1518/001872097778667951.

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The demand for color head- and helmet-mounted displays (HMDs) is growing. Interest focuses on full-color systems, but a limited color repertoire is sufficient for some applications and can reduce cost and complexity significantly, especially when subtractive-color active-matrix liquid-crystal display (AMLCD) technology is used. We report a series of experiments that investigated important questions about the design and merits of two-primary color AMLCDs for HMD applications. Our main conclusion is that the image quality of a subtractive-color AMLCD with high (≥70%) aperture ratio is superior to a comparable, conventional color AMLCD. Evidence regarding requirements for resolution, aperture ratio, and gray scale is also provided.

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6

Zhong, Ruikun, Thomas A. Lane, and Edward D. Ball. "Approach to Establish Long Term Anti-Acute Myeloid Leukemia (AML) Immune Responses by Inducing Central Memory AML Specific CD4 T Cells." Blood 112, no. 11 (November 16, 2008): 1956. http://dx.doi.org/10.1182/blood.v112.11.1956.1956.

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Abstract The efficacy of adoptive cell therapy of cancer and leukemia is often limited by the failure of cultured T cells, particularly cloned CD8+ T cells, to persist in vivo, and insight into the basis for the poor survival of the transferred cells is lacking. We previously reported a novel culture method that induces AML dendritic cell differentiation and primes in situ AML-reactive T cells (AMLDC culture) (Zhong et al. Exp Hematol2008, 36:486). Highly reactive anti-AML T-cell lines were generated. These T-cell lines caused specific lysis of autologous AML cells, but not autologous LCL or allogeneic AML cells, and they depleted autologous AML colony-forming cells (CFC), but not normal CFC. The culture procedure has been further optimized in this study. We found that by the addition of the TLR-4 agonist LPS,(1–100 ng/ml) in the last 24 hours of AMLDC culture (day 6), CD80, CD86, CD53, CD83 or HLA-Dr expression of AML cells pre-induced by cytokine combination GM-CSF/IL-4 or GM-CSF/IL4/IL2/IL7/IL12 could be significantly enhanced (n=6, P<0.005–0.04; n=8, P<0.0001–0.005 respectively). Addition of LPS increased the IFN-gamma secretion by T cells generated from AMLDC culture in response to autologous AML cells 4–10 fold (3 of 3; P<0.001). Addition of TNF-alpha, (10–20 ng/ml) in the last 24 hours of culture could also significantly enhance the expression of above surface molecules. However, LPS induced significantly higher expression of CD80 and CD86 on AMLDC compared with TNF-alpha. T cells generated from AMLDC culture with TNF-alpha led to differential effects on autologous AML reactivity. IFN-gamma secretion was enhanced in 4 of 7 studies and suppressed in 3 of 7. The significantly enhanced AML cell reactivity of autologous T cells generated from AMLDC culture by adding LPS was also demonstrated in limiting dilution AMLDC culture in 96 well plates. The majority of T cell lines selected and expanded from AMLDC culture with LPS were CD3+CD4+ (12 of 18), and 18 T cell lines tested expressed moderate to high level of CD62L, implying the central memory phenotype. Conclusions: Timely exposure of AMLDC culture to TLR-4 agonists, followed by T cell expansion, may promote the generation of AML-reactive T cells and differentiation toward the central memory phenotype. Theoretically, this should promote long-term maintenance and potential of regulation of both humoral and cellular immune responses against AML upon infusion of AML reactive autologous T cells derived from such cultures and may therefore enhance the therapeutic efficacy of these cells.

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7

Sandoe, J. N. "AMLCD on plastic substrates." SID Symposium Digest of Technical Papers 29, no. 1 (1998): 293. http://dx.doi.org/10.1889/1.1833750.

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8

Kim, I. G., H. H. Lee, D. H. Kim, W. Y. Park, B. H. Min, J. H. Souk, and B. H. Jung. "53.3: Multisync Poly-Si AMLCD." SID Symposium Digest of Technical Papers 31, no. 1 (2000): 1199. http://dx.doi.org/10.1889/1.1832879.

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Fine, Samson W., Victor E. Reuter, Jonathan I. Epstein, and Pedram Argani. "Angiomyolipoma With Epithelial Cysts (AMLEC)." American Journal of Surgical Pathology 30, no. 5 (May 2006): 593–99. http://dx.doi.org/10.1097/01.pas.0000194298.19839.b4.

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10

Jung-kook Paik. "Traces of Amleth Saga Embedded in Shakespeare’s Hamlet." Medieval and Early Modern English Studies 23, no. 2 (August 2015): 75–96. http://dx.doi.org/10.17054/memes.2015.23.2.75.

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Ono, Toshihiko, and Yoko Ishida. "6.1: Cuttability of AMLCD Glass Substrates." SID Symposium Digest of Technical Papers 33, no. 1 (2002): 45. http://dx.doi.org/10.1889/1.1830830.

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Stan, Corneliu S., Petronela Horlescu, Marcel Popa, Adina Coroaba, and Laura E. Ursu. "Photoluminescent polymer composites with R, G, B emission and their potential applications in LCD displays." New Journal of Chemistry 40, no. 7 (2016): 6505–12. http://dx.doi.org/10.1039/c6nj00386a.

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13

Office, Editorial. "Exploring an unconventional approach to cancer." Advances in Modern Oncology Research 2, no. 4 (August 30, 2016): 186. http://dx.doi.org/10.18282/amor.v2.i4.159.

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<p><em>In this issue of AMOR, we introduce Dr. Asma Amleh, our Editorial Board Member and discuss her role in improving our understanding of cancer.</em></p><p><em><br /></em></p><p>According to Dr. Asma Amleh, her curiosity of science began when she was a child.<strong> </strong>“My fascination with science, and particularly applying the scientific method in research, started at a very young age while learning about the contributions of a famous Persian polymath and an important figure in the history of medicine, Abu Bakr Muhammad ibn Zakariyya al-Razi, to the medical field through his observations and discoveries. I was also inspired by the laboratory techniques and experimental methods described by Jabir ibn Hayyan, a prominent Islamic alchemist and physicist,” she says.</p><p><strong> </strong></p><p>For Dr. Amleh, developmental biology is a field that specifically fascinates her like no other. “Cancer itself, being development ‘gone wrong’, is equally as captivating as developmental biology itself,” says Dr. Amleh in an exclusive interview with AMOR. The Associate Professor of Biology at The American University of Cairo (AUC), Egypt, who now has a long-standing experience in the field of developmental biology, credits her supportive parents for her achievements in medical research. “I was constantly inspired by my father as a living example of how to seek knowledge and achieve my goals. My mother’s unconditional support and encouragement paved the path in my journey,” she says.</p><p> </p><p>Motivated by her interest in science and research, Dr. Amleh began her journey in this challenging field by enrolling to study BSc in Biology and Chemistry at The American University of Beirut (AUB), Lebanon, which is ranked first among the universities in Lebanon and is among the top 250 universities in the world by the QS World University Rankings. She then pursued her PhD in Biology at McGill University, Montreal, Canada, where she came under the tutelage of a renowned McGill University researcher and a celebrated developmental biologist, Dr. Paul Lasko. “I learned how to think and design experimental approaches through the Developmental Biology classes offered by Dr. Lasko,” says Dr. Amleh appreciatively of her professor, the recipient of 2014 <em>Prix du Québec</em>,<em> </em>which is the most prestigious award attributed by the Government of Quebec in all fields of culture and science.</p><img align="middle" src="/public/site/images/admin/Untitled.png" alt="" align="middle" /><p><em>Views of a Fetus in the Womb</em>, Leonardo da Vinci, ca. 1510 - 1512. The subject of prenatal development is a major subset of developmental biology.</p><p> </p><p>Upon completing her doctoral degree, Dr. Amleh went on to further her career at various institutions. She became a research fellow at the Laboratory of Cellular and Developmental Biology at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) in Bethesda, Maryland, as well as a research associate at the National Institutes of Health, also in Bethesda. Additional experience in the field also boosted her expertise when she worked as an instructor at the Department of Molecular Medicine, Institute of Biotechnology, at the University of Texas Health Science Center in Houston, and a senior research scientist at the Developmental Biology Program, Memorial Sloan-Kettering Cancer Center in NY.</p><p> </p><p>Reflecting upon her experiences throughout her doctoral and postdoctoral research, Dr. Amleh says, “I have addressed fundamental questions related to mammalian embryonic development through a variety of projects including molecular genetics and cell culture systems.” She adds, “My ongoing and future research work plans will continue to pursue questions related to the molecular/cellular/developmental and differentiation processes.” Dr. Amleh’s research interests are focused on understand- ing the genetic control of normal and abnormal development in the mammalian system including the incidence of cancer. When discussing about the current trends in cancer research, she opined that developing rational personal/targeted therapy is very promising to develop new approaches that deal with the devastating disorder in a more effective way. “It has been suggested that personalized medicine is the right way to conquer cancer. With the fact that environmental factors play a significant role in cancer development and we are moving towards producing medication tailored to the individual patient based on the predicted response, complementary treatment becomes essential,” says Dr. Amleh.</p><p> </p><p>She further adds, “Complementary/alternative treatment such as following a special diet or using acupuncture may help in reducing the side effects of cancer treatment among other forms of treatment.” Dr. Amleh is currently focusing on exploring a novel non-conventional approach to reduce platinum-based drug resistance, which aims to improve the survival of cancer patients. “In my effort to tackle the shortfall of cancer chemotherapy treatment modality, I am also involved in a collaborative study with the metagenomic research team at AUC” says Dr. Amleh. “The collaborative project is aimed at identifying candidate sequences with potential anticancer activity by screening</p><p> </p><p>a metagenomic dataset, established at AUC and derived from the microbial community in several brine pools of the central Red Sea,” she adds.“Another area of study I’m working on is a collaborative effort with Canada’s Ryerson University, which is focused on characterizing the bioactivity of newly synthesized biomaterial intended for developing implants. This research puts my group at the interface with chemistry, physics, materials science, and medical science,” says the scientist.</p><p> </p><p>As a researcher with almost 20 years of experience in medical research, Dr. Amleh urged researchers to continually aim just beyond their current range. “I would recommend that researchers spend more time in exploring unconventional complementary or alternative approached in cancer treatments. There are no downsides to working in the research field. I just wish that the developing countries would allocate more money for research,” she concludes.</p><p> </p><p>Dr. Asma Amleh publishes her work entitled “The potential involvement of the cofactor of BRCA1 in hepatocellular carcinoma pathogenesis” in this issue of AMOR (page 224–235). </p>

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Hamoudi, Walid H., L. Jeffrey, Gault Townsend, Armand B. Glassman, and Carlos E. Bueso-Ramos. "Acute Myelomonocytic Leukemia With Histologic Features Resembling Sarcomatoid Carcinoma in Bone Marrow." Archives of Pathology & Laboratory Medicine 124, no. 2 (February 1, 2000): 315–18. http://dx.doi.org/10.5858/2000-124-0315-amlwhf.

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Abstract We report a case of primary acute myelomonocytic leukemia involving the bone marrow that resembled sarcomatoid carcinoma. The neoplastic cells in bone marrow biopsy specimens formed cohesive-appearing clusters and cords separated by an immature fibroblastic proliferation and myxoid stroma. Blasts in the bone marrow aspirate smears formed clusters and sheets, and a subset of blasts exhibited erythrophagocytosis. Dysgranulopoiesis was also present. Lineage was confirmed by immunohistochemical analysis of formalin-fixed, paraffin-embedded tissue. The tumor cells showed strong reactivity for lysozyme, myeloperoxidase, CD45, and CD68 and were negative for keratin, S100, CD20, and CD3. The serum lysozyme concentration (110 μg/mL) was 13 times greater than the normal value (8 μg/mL). Cytogenetic studies performed on bone marrow aspirate material revealed a complex karyotype, including trisomy 8 and abnormalities of chromosome 11q. We report this case of acute myelomonocytic leukemia because the neoplastic cells appeared cohesive and spindled, resembling sarcomatoid carcinoma, and therefore caused diagnostic difficulty. Other monocytic neoplasms with similar resemblance to carcinoma or sarcoma have been reported in the literature, suggesting that the tendency to appear cohesive may be an inherent characteristic of neoplastic cells with monocytic differentiation.

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15

Rahmdel, Mansour. "FATF and money laundering in Iran." Journal of Money Laundering Control 21, no. 3 (July 2, 2018): 314–27. http://dx.doi.org/10.1108/jmlc-07-2017-0033.

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Purpose The aim of this paper is considering that obtaining illegitimate property and obtaining property illegally is morally outrageous. The law also condemns it as a crime. The act of those who launder the proceeds of crime is also condemned. This condemnation is almost universal. So, money laundering as a way of diversion of the origin of the illegal gains into legitimate currency or other assets has been criminalized in most of the countries, including in Iran. Before criminalization of money laundering, there were different laws which referred to the case without referring to the term of money laundry. According to Article 49 of the Iranian Constitution “all proceeds of illegal sources like embezzlement, bribery, gambling and other ways should be confiscated.” Design/methodology/approach Article 662 of the Islamic Penal Code (IPC) ratified in 1996 criminalized dealing with the proceeds of theft and Note 2 of Article 119 of the Penal Code of the Armed Forces criminalized obtaining the proceeds of embezzlement. But, in 2008, to follow the international conventions, especially Article 3 of the psychotropic substances 1988 in Vienna and also Financial Action Task Force (FATF) recommendations on Money Laundering and Terrorism Financing, the legislator ratified the anti-money laundering code (AMLC). The methodology is an analytical one. The author using an analytical method, has analyzed the subject with consideration of Iran’s situation, as well as international documents and FATF’s recommendations. Findings The author has studied the issue, believing that domestic regulations of Iran comply with international regulations and FATF recommendations. The current paper considers the different aspects of the AMLCs in Iran in relation to FATF recommendations. Originality/value The author confirms the originality of the paper and declares that he has referred all the other materials.

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Schindler, Axel, Achim Pross, Holger Baur, and Norbert Fruehauf. "62.2: AMLCD with Carbon-Nanotube Pixel Electrodes." SID Symposium Digest of Technical Papers 39, no. 1 (2008): 947. http://dx.doi.org/10.1889/1.3069835.

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Westbrook, Jamie T., John F. Bayne, Tim A. Roe, Jum S. Kim, Po-Hua Su, Toshihiko Ono, and Suresh T. Gulati. "72.2: Strength Measurements of Thin AMLCD Panels." SID Symposium Digest of Technical Papers 41, no. 1 (2010): 1073. http://dx.doi.org/10.1889/1.3499838.

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Destura, G. J. A., J. T. M. Osenga, S. J. van der Hoef, and A. D. Pearson. "3.5: Novel Touch Sensitive In-Cell AMLCD." SID Symposium Digest of Technical Papers 35, no. 1 (2004): 22. http://dx.doi.org/10.1889/1.1811447.

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Muravski, A. A., S. Ye Yakovenko, C. Crell, and A. D. Wieck. "24.3: In-Plane-Gate Transistors for AMLCD." SID Symposium Digest of Technical Papers 31, no. 1 (2000): 360. http://dx.doi.org/10.1889/1.1832957.

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Gulati, S. T., J. D. Helfinstine, J. F. Bayne, and J. C. Lapp. "6.5: Mechanical Integrity of an AMLCD Panel." SID Symposium Digest of Technical Papers 36, no. 1 (2005): 81. http://dx.doi.org/10.1889/1.2036572.

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Choi, Jae Beom, Young Jin Chang, Cheol Ho Park, Beom Rak Choi, Hyo Seok Kim, and Kee Chan Park. "TFT Backplane Technologies for AMLCD and AMOLED Applications." Journal of the Korean Physical Society 54, no. 9(5) (January 15, 2009): 549–53. http://dx.doi.org/10.3938/jkps.54.549.

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Hirakata, Yoshiharu, Daisuke Kubota, Akio Yamashita, Tetsuji Ishitani, Takeshi Nishi, Hiroyuki Miyake, Hidekazu Miyairi, et al. "A novel field-sequential blue-phase-mode AMLCD." Journal of the Society for Information Display 20, no. 1 (2012): 38. http://dx.doi.org/10.1889/jsid20.1.38.

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Petrov, V. F. "Liquid crystals for AMLCD and TFT-PDLCD applications." Liquid Crystals 19, no. 6 (December 1995): 729–41. http://dx.doi.org/10.1080/02678299508031092.

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PENNISI, SALVATORE, SALVATORE DI FAZIO, TIZIANA SIGNORELLI, and FRANCESCO PULVIRENTI. "670-nA CMOS OTA FOR AMLCD COLUMN DRIVER." Journal of Circuits, Systems and Computers 18, no. 02 (April 2009): 339–50. http://dx.doi.org/10.1142/s0218126609005101.

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A transconductance operational amplifier specifically optimized for a switched-capacitor LCD column driver is presented. It exploits MOS transistors in subthreshold region and dissipates 670 nA at DC. Despite this extremely low quiescent current value, the amplifier exhibits a DC gain of about 80 dB, and a gain-bandwidth product and phase margin around 2 MHz and 70°, with a load capacitance of 500 fF. Besides, working in class AB, the solution provides a slew rate equal to 27 V/μs. With exception of the DC gain, these performances represent an improvement with respect to comparable solutions, and are obtained while halving the area occupation.

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Ayres, J. R., M. J. Edwards, M. J. Trainor, N. D. Young, R. Pook, A. D. Pearson, and A. V. Henzen. "A highly integrated AMLCD with low-voltage operation." Journal of the Society for Information Display 10, no. 4 (2002): 305. http://dx.doi.org/10.1889/1.1827882.

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Gulati, S. T., J. D. Helfinstine, T. A. Roe, M. L. Hillman, and J. C. Lapp. "6.2: Biaxial Strength of Ultrathin AMLCD Glass Substrates." SID Symposium Digest of Technical Papers 33, no. 1 (2002): 49. http://dx.doi.org/10.1889/1.1830842.

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Maeda, Kazuhiro, Sachio Tsujino, Keiji Takahasi, Yasushi Kubota, Shigeki Imai, Hirohide Nakagawa, and Mikio Katayama. "22.2: Multi-Resolution for Low Power Mobile AMLCD." SID Symposium Digest of Technical Papers 33, no. 1 (2002): 794. http://dx.doi.org/10.1889/1.1830902.

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Senda, M., Y. Tsutsui, A. Sasaki, S. Matsumoto, R. Yokoyama, and K. Yoneda. "Ultra-low-power polysilicon AMLCD with full integration." Journal of the Society for Information Display 11, no. 1 (2003): 121. http://dx.doi.org/10.1889/1.1831694.

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Weindorf, P., and E. Lee. "P-38: LED Parallel Drive for AMLCD Backlighting." SID Symposium Digest of Technical Papers 32, no. 1 (2001): 694. http://dx.doi.org/10.1889/1.1831957.

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Tannas, Lawrence E. "50.1: Invited Paper: AMLCD: The Ultimate Avionics Display." SID Symposium Digest of Technical Papers 31, no. 1 (2000): 1145. http://dx.doi.org/10.1889/1.1832867.

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Brinkley, Rick, Gang Xu, Adi Abileah, and John Vanderploeg. "Wide Viewing AMLCD Optimized for Gray Scale Operation." SID Symposium Digest of Technical Papers 29, no. 1 (1998): 471. http://dx.doi.org/10.1889/1.1833794.

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Tomita, Satoru, Steven Jurichich, and Krishna C. Saraswat. "Transistor sizing for AMLCD integrated TFT drive circuits." Journal of the Society for Information Display 5, no. 4 (1997): 399. http://dx.doi.org/10.1889/1.1985187.

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Cho, Woo Cheal, Katrina Collins, Laila Mnayer, Richard W. Cartun, and Jonathan S. Earle. "Concurrent Eosinophilic Solid and Cystic Renal Cell Carcinoma and Angiomyolipoma With Epithelial Cysts in the Setting of Tuberous Sclerosis Complex: A Rare Synchronous Occurrence of 2 Distinct Entities." International Journal of Surgical Pathology 27, no. 7 (May 29, 2019): 804–11. http://dx.doi.org/10.1177/1066896919849679.

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Eosinophilic solid and cystic renal cell carcinoma (ESCRCC) is a recently described distinct renal neoplasm known to occur almost exclusively in female patients with or without tuberous sclerosis complex (TSC). We report a case of ESCRCC with 2 synchronous angiomyolipomas, including 1 angiomyolipoma with epithelial cysts (AMLEC), a rare cystic variant of AML that typically arises sporadically in the absence of TSC, in a 46-year-old woman with TSC. Besides additional copy number alterations identified in ESCRCC via molecular karyotyping, we also report a unique histologic feature of TSC-associated ESCRCC previously not described in detail, with formation of semicircular multinucleated neoplastic giant cells engulfing an additional intact neoplastic cell, simulating emperipolesis. To the best of our knowledge, this is the first reported case of ESCRCC with concurrent AMLEC in a patient with TSC, confirmed through additional genetic testing showing a germline heterozygous mutation in TSC1. Awareness of ESCRCC helps avoid the pitfall of a diagnosis of unclassified renal cell carcinoma, a typically much more aggressive tumor.

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Diffee, Gary M., Eric A. Seversen, Thor D. Stein, and Jeffrey A. Johnson. "Microarray expression analysis of effects of exercise training: increase in atrial MLC-1 in rat ventricles." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (March 1, 2003): H830—H837. http://dx.doi.org/10.1152/ajpheart.00761.2002.

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Previous studies have shown that endurance exercise training increases myocardial contractility. We have previously described training-induced alterations in myocardial contractile function at the cellular level, including an increase in the Ca2+ sensitivity of tension. To determine the molecular mechanism(s) of these changes, oligonucleotide microarrays were used to analyze the gene expression profile in ventricles from endurance-trained rats. We used an 11-wk treadmill training protocol that we have previously shown results in increased contractility in cardiac myocytes. After the training, the hearts were removed and RNA was isolated from the ventricles of nine trained and nine control rats. With the use of an Affymetrix Rat Genome U34A Array, we detected altered expression of 27 genes. Several genes previously found to have increased expression in hypertrophied myocardium, such as atrial natriuretic factor and skeletal α-actin, were decreased with training in this study. From the standpoint of altered contractile performance, the most significant finding was an increase in the expression of atrial myosin light chain 1 (aMLC-1) in the trained ventricular tissue. We confirmed microarray results for aMLC-1 using RT-PCR and also confirmed a training-induced increase in aMLC-1 protein using two-dimensional gel electrophoresis. aMLC-1 content has been previously shown to be increased in human cardiac hypertrophy and has been associated with increased Ca2+sensitivity of tension and increased power output. These results suggest that increased expression of aMLC-1 in response to training may be responsible, at least in part, for previously observed training-induced enhancement of contractile function.

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35

Yiu, Chun Lai, and Philip K. T. Mok. "Process-independent analogue data driver for polysilicon TFT AMLCD." International Journal of Electronics 91, no. 4 (April 2004): 199–210. http://dx.doi.org/10.1080/00207210410001687335.

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36

Abileah, Adi, Willem den Boer, Terrance Larsson, Tom Baker, Scott Robinson, Roy Siegel, Noah Fickenscher, Brent Leback, Terry Griffin, and Pat Green. "59.3: Integrated Optical Touch Panel in a 14.1ʺ AMLCD." SID Symposium Digest of Technical Papers 35, no. 1 (2004): 1544. http://dx.doi.org/10.1889/1.1821371.

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37

Senda, M., Y. Tsutsui, R. Yokoyama, K. Yoneda, S. Matsumoto, and A. Sasaki. "22.1: Ultra-Low-Power Polysilicon AMLCD with Full Integration." SID Symposium Digest of Technical Papers 33, no. 1 (2002): 790. http://dx.doi.org/10.1889/1.1830901.

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38

Murata, T., S. Miwa, H. Yamazaki, and S. Yamamoto. "P-46: Suitable Scribing Conditions for AMLCD Glass Substrates." SID Symposium Digest of Technical Papers 34, no. 1 (2003): 374. http://dx.doi.org/10.1889/1.1832289.

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39

Westbrook, Jamie T., John F. Bayne, Stephen H. Carley, K. Hemanth Vepakomma, Jum S. Kim, and Suresh T. Gulati. "73.3:Invited Paper: Four Point Bending of AMLCD Panel." SID Symposium Digest of Technical Papers 43, no. 1 (June 2012): 996–97. http://dx.doi.org/10.1002/j.2168-0159.2012.tb05959.x.

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40

Hintermann, Markus, Eckart Rzittka, and Marko Radovic. "Implementation aspects of a low-power AMLCD single chip." Journal of the Society for Information Display 12, no. 4 (2004): 443. http://dx.doi.org/10.1889/1.1847745.

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41

Lebrun, H., F. Maurice, J. Magarino, and N. Szydlo. "AMLCD with integrated drivers made with amorphous-silicon TFTs." Journal of the Society for Information Display 3, no. 4 (1995): 177. http://dx.doi.org/10.1889/1.1984963.

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42

Martin, Russel A., T. Chuang, Hugo Steemers, R. Fulks, Susan Stuber, David D. Lee, Michael Y. T. Young, et al. "The electronic document display: A 6.3-million-pixel AMLCD." Journal of the Society for Information Display 4, no. 2 (1996): 65. http://dx.doi.org/10.1889/1.1984992.

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43

Abileah, A., and Z. Yaniv. "A full color AMLCD with NVG class B compatibility." IEEE Aerospace and Electronic Systems Magazine 7, no. 7 (July 1992): 20–23. http://dx.doi.org/10.1109/62.149788.

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44

Im, James S., and Robert S. Sposili. "Crystalline Si Films for Integrated Active-Matrix Liquid-Crystal Displays." MRS Bulletin 21, no. 3 (March 1996): 39–48. http://dx.doi.org/10.1557/s0883769400036125.

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Abstract:

The fabrication of thin-film-transistor (TFT) devices on a transparent substrate lies at the heart of active-matrix-liquid-crystal-display (AMLCD) technology. This is both good and bad. On one hand it is a difficult task to manufacture millions of intricate semiconductor devices reliably over such large display substrates. On the positive side, AMLCD technology can aspire to become much more than a “display” technology. The idea is as follows: It is possible for one to readily fabricate additional transistors to execute various electronic functions—those that would otherwise be handled by separate large-scale-integration (LSI) and very large-scale-integration (VLSI) circuits—on the periphery of the display. Since this can be done, in principle, with no—or a minimal number of—additional processing steps, substantial cost reduction is possible and significant value can be added to the final product.Doing so and doing it well can ultimately lead to “system-on-glass” products in which the entire electronic circuitry needed for a product is incorporated directly onto a glass substrate. This means that integrated active-matrix liquid-crystal displays (IAMLCDs) have the potential to bypass conventional Si-wafer-based products and may lead TFT technology to compete directly against Si-wafer-based monolithic integrated circuits.

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45

Santoni, Giorgio, Massimo Nabissi, Consuelo Amantini, Matteo Santoni, Lucia Ricci-Vitiani, Roberto Pallini, Federica Maggi, and Maria Beatrice Morelli. "ERK Phosphorylation Regulates the Aml1/Runx1 Splice Variants and the TRP Channels Expression during the Differentiation of Glioma Stem Cell Lines." Cells 10, no. 8 (August 10, 2021): 2052. http://dx.doi.org/10.3390/cells10082052.

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The identification of cancer stem cells in brain tumors paved the way for new therapeutic approaches. Recently, a role for the transcriptional factor Runx1/Aml1 and the downstream ion channel genes in brain cancer development and progression has been suggested. This study aimed to explore the expression and the role of Runx1/Aml1, its Aml1b and Aml1c splice variants and the downstream TRPA1 and TRPV1 ion channels in undifferentiated and day-14 differentiated neural stem cells (NSCs and D-NSCs) and glioblastoma stem cells (GSCs and D-GSCs) lines with different proneural (PN) or mesenchymal (MES) phenotype. Gene and protein expression were evaluated by qRT-PCR, cytofluorimetric, western blot and confocal microscopy analyses. Moreover, by western blot, we observed that ERK phosphorylation enhances the Aml1b and Aml1c protein expression during glioma differentiation. Furthermore, the agonists of TRPA1 and TRPV1 channels stimulated apoptosis/necrosis in GSCs and D-GSCs as evaluated by Annexin V and PI staining and cytofluorimetric analysis. Finally, by qRT-PCR, the modulation of Wnt/β catenin, FGF, and TGFβ/SMAD signaling pathways in PN- and MES-GSCs was reported. Overall, our results provide new evidence regarding Runx1/Aml1 isoform overexpression and modulation in TRP channel expression during gliomagenesis, thus offering new directions for glioblastoma therapy.

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Akinwande, A. I., B. R. Johnson, B. G. Heil, J. O. Holmen, and D. P. Murphy. "Paper 42.1: Invited Paper: Field-Emission Lamp for Avionics AMLCD." SID Symposium Digest of Technical Papers 30, no. 1 (1999): 904. http://dx.doi.org/10.1889/1.1834170.

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Chang, Young-Jin, Young-ll Kim, Seung-Hwan Shim, Sun Park, Ki-Wan Ahn, Seock-Cheon Song, Jae-Beom Choi, Hoon-Kee Min, and Chi-Woo Kim. "28.3: World's Largest (21.3 in.) UXGA Non-Laser LTPS AMLCD." SID Symposium Digest of Technical Papers 37, no. 1 (2006): 1276. http://dx.doi.org/10.1889/1.2433212.

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Soh, Hoe Sup, Cheolse Kim, Hyung Beom Shin, Eung Do Kim, Hong Sik Kim, and Byung Chul Ahn. "P-14: New Pixel Structure with Kickback Voltage Free AMLCD." SID Symposium Digest of Technical Papers 37, no. 1 (2006): 241. http://dx.doi.org/10.1889/1.2433465.

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den Boer, W., G. S. Smith, W. C. Wang, L. Lin, H. Kang, S. J. Chen, and C. M. Huang. "4.4: Invited Paper: Low Cost Dual-Select-Diode AMLCD Technology." SID Symposium Digest of Technical Papers 37, no. 1 (2006): 29. http://dx.doi.org/10.1889/1.2433484.

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Fruehauf, Norbert, Holger Baur, Steffen Hergert, Rene Hlawatsch, Sven Jelting, Efstathios Persidis, Fabio Pieralisi, and Patrick Schalberger. "7.1:Invited Paper: LTPS Processes for AMLCD and AMOLED Applications." SID Symposium Digest of Technical Papers 38, no. 1 (May 2007): 69–72. http://dx.doi.org/10.1889/1.2785228.

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