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iMedia program celebrates Class of 2020 in virtual degree conferral ceremony
By Patrick Wright, staff
The iMedia Class of 2020 poses for a class photo at the beginning of the 10-month program.
The 30 members of Elon's Master of Arts in Interactive Media program were honored for their dedication even during uncertain times globally during the program's virtual degree conferral ceremony on Wednesday, May 20.
The Master of Arts in Interactive Media graduate program celebrated its newest class of graduates during a virtual degree conferral ceremony on Wednesday. It was a chance to recognize the Class of 2020 for its dedication to the intense, 10-month program despite navigating it during a global pandemic.
Watch the entire iMedia program degree conferral ceremony here.
Rochelle Ford, dean of the School of Communications, which houses the iMedia program, said during Wednesday's virtual ceremony that she compares the 10-month journey to "the process of becoming a fine teacup." She explained students are like balls of clay molded by faculty and then placed into a fiery furnace where they hone their skills before graduating with unique abilities and knowledge that they will carry with them into their careers. The furnace was a bit hotter for the Class of 2020, Ford said, because of COVID-19's impact on in-person learning.
"You demonstrated to us through virtual capstone presentations that you've got this, you're prepared," Ford told graduates during the virtual degree conferral ceremony. "And here you are – formed into beautiful, unique and strong teacups that can be used to refresh the world."
The iMedia graduate program, in its 11th year, offers students the opportunity to learn from award-winning professors and build media projects in state-of-the art facilities using the latest coding, graphic design and production techniques. Through hands-on experiences in classes and with real-world clients, students discover the creation, strategies and application of interactivity through content development and marketing, UX design, responsive web design, prototyping, usability testing, analytics, social media, app development and human computer interaction.
During Wednesday's ceremony David Copeland, A.J. Fletcher Professor and director of the iMedia program, congratulated graduates for completing two years' worth of work in 10 months, despite unforeseeable obstacles.
"A lesser group of students would have, no doubt, given up, but not this cohort," Copeland said. "The Class of 2020 found a way to succeed. We know that 'necessity is the mother of invention,' and this group of students, out of necessity and out of their creativity, figured out how to complete their capstone projects, their work in elective courses, and how to put on a virtual exhibition of what they've produced."
Melissa Dale G'20, who was selected as the ceremony's student speaker, thanked classmates for their support and encouragement throughout the past 10 months.
"This program was tough, but I always felt relief knowing there were 29 other students who could empathize with what I was feeling," Dale said during the virtual ceremony. "And although we didn't get to spend the latter part of the program together, I still felt that same sense of connectedness with my iMedia comrades."
Provost and Vice President for Academic Affairs Aswani Volety presented the 30 members of the Class of 2020 during the virtual ceremony, and President Connie Ledoux Book conferred the degrees and issued a charge to graduates, encouraging them to be resilient and steadfast in the face of all future challenges.
iMedia graduates will be invited back to campus in the fall for an in-person hooding ceremony and celebration where they will receive their official, printed diplomas.
Master of Arts in Interactive Media
Kwame Amponsah
B.A., Kwame Nkrumah University
Rakhia Ardasia Bass
B.S., North Carolina Agricultural and Technical State University
Hyllary Tiana Bell
Tabari Jamaal Boykin
B.A., North Carolina Agricultural and Technical State University
William Arthur Brown
B.A., Millsaps College
Elizabeth Mae Bunce
B.S., North Carolina State University
Tirza Nicole Aubrey Chase
Melissa Enid Dale
B.S., Norfolk State University
Makeda Shanygne Dawson
Rachel Alexandra Eggleston
B.A., The University of North Carolina at Greensboro
John Edward Fennell
A.B., Elon University
Colton Townsend Flick
B.A., Kenyon College
Juliet Diana Goodman
Arlette Danielle Hawkins
Michael David Hemstreet
Tehya Rashan Jackson
Ashleigh Marie Kimble
B.A., The University of North Carolina at Wilmington
Cassidy Dawn Kolczun
B.A., Loyola University
Brianna Tayla Lawrence
Ethan Wallace McElvaney
B.A., William Peace University
Amonie Jennifer Moore
B.A., North Carolina Central University
Victoria Elise Murrell
Anna Jane Sizemore
Shama Adin Stephenson
Warren Gregory Stewart Jr.
Laticia Danae Taylor
London Nicole Thompson
Gaurav Kalpesh Vyas
Felecia Lashay Wilkins
Mela Matrice Williams
B.A., The University of North Carolina at Chapel Hill
Posted in: Academics & Research Alumni Awards & Recognitions Events Student Experience
Tagged: Graduate Admissions iMedia School of Communications
Rochelle Ford
Dean of the School of Communications and Professor of Strategic Communications
A.J. Fletcher Professor, Professor of Journalism and Distinguished University Professor
Aswani Volety
Provost and Vice President for Academic Affairs and Professor of Biology
Connie Book
Elon, American Red Cross partner for January Blood Drive
The American Red Cross and Elon's Kernodle Center for Civic Life hosted the January Blood Drive on Wednesday, Jan. 20, to collect blood donations in a time when the Red Cross desperately needs them.
Deena Hayes-Greene urges organizing and action in MLK Commemorative Address
The Jan. 19 event was a discussion with Hayes-Greene, co-founder of The Racial Equity Institute, by Vice President and Associate Provost Randy Williams and Assistant Professor Stephanie Baker.
Alex Lewis '16 reflects on Adweek's Hottest Content Marketer award
The Elon alumnus is a social media specialist for Jeni's Splendid Ice Creams, a fast-growing ice cream company based in Columbus, Ohio.
January 20 update from Vice President for Student Life Jon Dooley
Throughout Winter Term and Spring Semester, Vice President for Student Life Jon Dooley is providing regular email update messages to keep students and parents informed about the efforts related to COVID-19.
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My 3 Year Old Won't Leave Her 18 Mo Brother Alone. Any Ideas Besides Time Out?
Top Communities Stories How To Stop Breastfeeding To A 2 Yrs Old Baby #3...? First Time Mom Husband That Travels Every Week.
My 3 (almost 4) year old won't leave her 18 mo old brother alone. She is constantly tugging, hugging, smushing him. She loves him dearly and isn't trying to hurt him, totally mothering him though. I know a lot of the time she is just bored or seeking my attention, which I give quit a bit. I just need to get the dishes done sometimes without having to turn around and intervene. Time out is getting old. Any creative ideas?
Is it ok to buy my son a baby doll?


Disclaimer: This guide provides general information only and is not intended to be legal advice. Organisations should confirm the legal requirements that apply to them and seek legal advice about their specific situation as required.
If interacting with children, Victorian organisations are required by legislation to meet 7 Child Safety Standards.
1. Ensure you have policies that address each of the 7 Child Safety Standards.
2. Ensure that you place a Policy Statement or Commitment to Child Safety Statement on the wall to alert parents to your policies/procedures and how they can gain access to them.
Please explore the Live Performance Australia website for excellent resources and directions.


Airlie Forest is a small, upscale, gated community located between Wrightsville Avenue and Airlie Road. The neighborhood is a single street and includes 15 homes of various styles built after 2001; some with big wrap around porches perfect for sitting outside on this quiet street. There are also a few lots still available for construction.
The community is close to beautiful Airlie Gardens and the shopping and restaurants of Mayfaire Town Center, the Forum and Lumina Station. It is located two and half miles from Wrightsville Beach and less than eight miles from Downtown Wilmington.


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Deep fried cauliflower cooked in Indo-Chinese style.
Deep fried cauliflower marinated with ginger and garlic.
Spring chicken marinated with ginger and garlic.
Chicken wings marinated in spices coated in zesty batter and deep fried.
Shrimp spiced with green chili sauce and curry leaves.
Yellow lentils sauteed with onions, tomatoes and spices. Served with rice.
Garbanzo beans cooked with tomatoes. Served with rice.
Boiled eggs cooked in freshly ground spices with onions served with tomato gravy. Served with rice.
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Salvador Sulce (born 30 July 1992) is an Albanian footballer, who currently plays in the Portuguese lower leagues.

Club career

Partizani Tirana
Sulce began his professional career with Partizani Tirana at the age of 16, making his debut under the coach Shpëtim Duro.

CDR Penelense
After spending the first half of the 2010–11 season with NK Adriatic Split, he was transferred to Portugal and played with the third-tier team of CDR Penelense, making 13 appearances and scoring 5 goals. He later played once more for Partizani, having joined them in February 2012 from CDR Penelense.

References

1992 births
Living people
Sportspeople from Lushnjë
Albanian footballers
Association football forwards
FK Partizani Tirana players
FK Dinamo Tirana players
Kategoria e Parë players
Albanian expatriate footballers
Expatriate footballers in Croatia
Expatriate footballers in Portugal
Albanian expatriate sportspeople in Croatia
Albanian expatriate sportspeople in Portugal

redpajama_set_name: RedPajamaWikipedia


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The Best American Essays 2003
By Anne Fadiman Robert Atwan Jan 15, 2021 Jan 15, 2021
The Best American Essays Since The Best American Essays has gathered the most interesting and provocative writing of the year establishing a firm place as the leading annual of its kind The volume is edited each year b
Title: The Best American Essays 2003
Author: Anne Fadiman Robert Atwan
Since 1986, The Best American Essays has gathered the most interesting and provocative writing of the year, establishing a firm place as the leading annual of its kind The volume is edited each year by an esteemed writer who brings a fresh eye to the selections Previous editors have included Elizabeth Hardwick, Susan Sontag, Geoffrey C Ward, Cynthia Ozick, and Stephen JSince 1986, The Best American Essays has gathered the most interesting and provocative writing of the year, establishing a firm place as the leading annual of its kind The volume is edited each year by an esteemed writer who brings a fresh eye to the selections Previous editors have included Elizabeth Hardwick, Susan Sontag, Geoffrey C Ward, Cynthia Ozick, and Stephen Jay Gould This year s volume is terrifically diverse, with subjects ranging from driving lessons to animal rights to citizenship in times of emergency.
↠ The Best American Essays 2003 ↠ Anne Fadiman Robert Atwan
Anne Fadiman Robert Atwan 102 Anne Fadiman Robert Atwan
Anne Fadiman Robert Atwan says:
Anne Fadiman, the daughter of Annalee Whit Jacoby Fadiman, a screenwriter and foreign correspondent, and Clifton Fadiman, an essayist and critic, was born in New York City in 1953 She graduated in 1975 from Harvard College, where she began her writing career as the undergraduate columnist at Harvard Magazine For many years, she was a writer and columnist for Life, and later an Editor at Large at Civilization She has won National Magazine Awards for both Reporting 1987 and Essays 2003 , as well as a National Book Critics Circle Award for The Spirit Catches You and You Fall Down Ex Libris Confessions of a Common Reader, a collection of first person essays on books and reading, was published by Farrar, Straus and Giroux in 1998 Fadiman was the editor of the intellectual and cultural quarterly The American Scholar from 1997 to 2004 She now holds the Francis chair in nonfiction writing at Yale Fadiman lives in western Massachusetts with her husband, the writer George Howe Colt, and their two childrencmillan author annefa
Comment 217 on "The Best American Essays 2003"
I took me almost one year to just finish this book, because this was not easy reading and I needed time to digest each essay I have to say this is an excellent book almost all essays were excellent and offered me some kind of knowledge Some of them were filled with emotions and autobiographical notes that tasted like some intense short films The following essays are my favorite from the collection Lavender Andre Aciman this could be due to primacy effects, but this is the BEST essay of the book [...]
It s really funny looking at the change in essay styles from the mid 80 s to the early 21st century Basically people dropped a lot of the word dropping and pretentious bullshit, and started writing funnier, accessible stuff I really the like the 2003 edition, both for the Anne Fadiman s selection of essays and her excellent introduction, where she talks about how she wanted to bust the series out of it s heavy use of essays from the New Yorker and Granta, then found that when it came down to he [...]
Kyle Minor says:
I like this edition of Best American Essays because Anne Fadiman used her editorship to champion the expansive, muscular personal essay Best American Essays is one of the only places generally interested readers of the personal essay can reliably discover new essays and new writers each year, but in recent years, guest editors David Foster Wallace, David Brooks, Mary Oliver, Christopher Hitchens, etc have chased other preoccupations at the expense of the personal essay.Meantime, check out some o [...]
There are times when writing seems like magic you re lifted out of yourself into somewhere that shows you the world in a new way So many of the essays in this book leave me breathless The three I have in mind so far are The Reporter s Kitchen, by Jane Kramer, Learning to Drive, by Katha Pollett, and Citizenship in Emergency, by Elaine Scarry The first two show how much can be explored through a single image okay, experience over time Scarry s essay got me thinking about national defense in a way [...]
This BAE is quite good Among its strengths 10 of the 24 essays are read agains 11 of the 24 are by women Cheryl Strayed s 2013 BAE also has a respectable showing of women, suggesting yet again that, shockingly, female editors tend to give less of an edge to male writers than do male editors My two favorite essays from this collection are Atul Gawande s The Learning Curve, which I might use when I teach my next research writing class, and Francis Spufford s The Habit, a standout piece about readi [...]
I ve never read essays before, but it was recommended I read Atul Gawande s The Learning Curve, which is all about the practice of medicine I found it uncomfortably true to life, but very interesting Now I m plowing through the rest of the essays, which so far have covered buying a bed, the search for the perfect lavender, and Martha Stewart.
Hamuel Sunter says:
This was the only result of a search for Susan Sontag in the Sapporo library database.The highlights were Anne Fadiman s introductory essay, Adam Gopnik s Bumping Into Mr Ravioli, Cheryl Strayed s The Love of My Life, Donald Antrim s I Bought A Bed, and Rachel Cohen s Lost Cities.
Anne Fadiman is a brilliant editor This volume is one of best in this series that is to say, the best of the best.
Avis Black says:
Fadiman s taste in essays is very dull.
I love reading essays, but hadn t done so for years until I picked up this book at a book sale Some of the essays were phenomenal It makes me want to subscribe to The New Yorker.
I feel like a failure saying this, but these essays other than Anne Fadiman s introductory essay about choosing essays didn t work for me at all.Maybe I will try again another time.
Anne Fadiman is a goddess All these intro essays are so fascinating to read from the point of view of how to write an essay about writing an essay Fadiman takes a not obvious approach.
One of my favorite collections of essays.
Andria alefhi says:
There are some gems in here, especially looking for mr ravioli , a must read.
Jeff Lacy says:
An inconsistent dynamic of essays for which I was searching to teach a college freshman English composition course I had a wide scope.
El Método HYDRA: LA FORMA MÁS FÁCIL DE MANTENER...
Maquinaria de Propaganda: El Nacional Socialismo
Recetas Americanas: 25 Recetas de Tartas Caseras: ...
Hitler triunfante (Tempus)
Guderian. General Panzer (Tempus)
Roma (Novela Historica(la Esfera))
Héroes, aventureros y cobardes (NARRATIVAS)
La ciudad autosuficiente (ACTUALIDAD)
Roma e Imperio (Novela histórica)
Ein verhängnisvolles Versprechen - Myron Bolitar ...
Unter die Haut: Roman
Vom selben Blut
Wenn die Wahrheit stirbt. Roman (Die Kincaid-James...
Mordgier: Ein Alex-Delaware-Roman 22
Der König der Lügen: Roman
Kolyma (Leo Demidow, Band 2)
Die Lieferung: Roman
Todesgier: Thriller
Blutschande: Thriller

redpajama_set_name: RedPajamaCommonCrawl


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Innovations and Challenges in Renal Cancer
Implications of B7-H1 Expression in Clear Cell Carcinoma of the Kidney for Prognostication and Therapy
R. Houston Thompson, Haidong Dong and Eugene D. Kwon
R. Houston Thompson
Haidong Dong
Eugene D. Kwon
DOI: 10.1158/1078-0432.CCR-06-1868 Published January 2007
B7-H1 encompasses a recently discovered cell surface glycoprotein within the B7 family of T-cell coregulatory molecules. B7-H1 expression can be induced on activated T lymphocytes and is normally expressed by macrophage lineage cells. In addition, some human tumors acquire the ability to aberrantly express B7-H1. Tumor-associated B7-H1, as well as B7-H1 on activated lymphocytes, has been shown to impair antigen-specific T-cell function and survival in vitro. In contrast, in vivo monoclonal antibody–mediated blockade of B7-H1 has been shown to potentiate antitumoral responses in several murine cancer models. Consequently, tumor-associated B7-H1 has garnered much attention in the recent literature as a potential inhibitor of host antitumoral immunity. Our group has recently reported that B7-H1 is aberrantly expressed in both primary and metastatic renal cell carcinoma (RCC) as revealed via immunohistochemical staining of both fresh-frozen and paraffin-embedded nephrectomy specimens. In addition, we have shown that B7-H1 expression by clear cell RCC tumors (or infiltrating mononuclear cells) correlates with aggressive pathologic features, including advanced tumor-node-metastasis stage, tumor size, higher nuclear grade, and coagulative necrosis. In one study of 306 patients, with a median clinical follow-up of 11 years, we reported that RCC B7-H1 expression correlates with increased risk of disease progression, cancer-specific death, and overall mortality even after multivariate adjustment. Five-year cancer-specific survival rates in this study were 42% and 83% for patients harboring B7-H1+ versus B7-H1− RCC tumors, respectively. Such associations may relate to the recognized ability of B7-H1 to inhibit T-cell–mediated antitumoral immunity. In summary, B7-H1 encompasses a potent independent predictor of prognosis for patients with RCC and an extremely promising target to facilitate immunotherapeutic responses during the management of this treatment-refractory tumor.
carcinoma, renal cell
T lymphocytes
antigen, CD
Despite the fact that the incidence of renal cell carcinoma (RCC) continues to increase, stage migration and advances in the surgical management of this form of cancer have culminated in notable improvements in RCC patient survival (1). A sobering reality, however, is that the number of patients who present with regional or systemic dissemination has also increased within the contemporary era (1). At present, it is estimated that ∼60% of RCC patients will ultimately experience metastatic progression during the course of their disease (1, 2). Median survival for patients with metastatic dissemination remains only 6 to 10 months (3). Based on this, it is alarmingly clear that more effective systemic therapies for treatment of advanced RCC are desperately needed.
As is the case with melanoma and other immunogenic tumors, subsets of advanced RCC patients exhibit objective responses to cytokine-based immunotherapy (3–5). It has been reported that allogeneic stem cell transplantation may also induce sustained regression in patients with disseminated RCC (6). Spontaneous and complete regression of RCC metastases has been reported to occur, albeit on very rare occasions, (7) and a few studies have reported profuse infiltration of RCC tumors by infiltrating lymphocytes and other mononuclear cells (8, 9). It is these observations that have collectively implicated RCC as an immunogenic tumor. Unfortunately, it is also apparent that mononuclear infiltrates within RCC are frequently composed of dysfunctional lymphocytes that have been rendered incapable of effectively mediating tumor regression (10–14). Thus, an exhaustive effort has been pursued to understand the mechanism whereby RCC tumors acquire the ability to undermine or impair host antitumoral immunity. To date, this mechanism has remained frustratingly elusive.
Recent basic science observations have suggested that the fate and activity of T cells (i.e., activation, proliferation, acquisition of memory, and cytolytic function versus induction of anergy, ignorance, and programmed death) are ultimately governed by the balance between positive and negative signaling within T cells conferred through interactions between various T-cell coregulatory receptors and ligands (15). Related to this, we have recently reported strong associations between tumor expression of a particular T-cell coregulatory molecule and cancer progression in RCC patients. Specifically, B7-H1 (also known as PD-L1) has recently been introduced as a novel T-cell coregulatory molecule that is capable of inhibiting generalized and antitumoral T-cell–mediated immunity (16, 17). Cell surface expression of B7-H1 has been reported to be primarily restricted to macrophage lineage cells (16). Aberrant B7-H1 expression, however, has also been reported to be exhibited by several human malignancies, including RCC (17–23). Perhaps, most interesting is the observation that blockade of tumor-associated B7-H1 has been shown to promote in vivo tumor regression in several murine cancer models (17, 24, 25). Thus, we surmise that B7-H1, along with other negative regulators of T-cell activation, may act in concert to thwart host antitumoral immunity in patients with RCC and other forms of malignancy as well. In this report, we provide a comprehensive review of the literature and describe important clinical observations that suggest that B7-H1 overexpression by RCC tumors may encompass a mechanism whereby RCC tumors impair host T-cell–mediated antitumoral immunity before and during immunotherapeutic treatment.
A Medline search was done using the keywords "B7-H1," "PD-L1," and "carcinoma, renal cell." Mapping the keywords "B7-H1" or "PD-L1" produced 130 articles, which were reviewed for background information on mechanism and function of this molecule. Combining these 130 articles with the keyword "carcinoma, renal cell" produced four peer-reviewed articles that specifically addressed the clinical role of B7-H1 in RCC (23, 26–28). These articles are reviewed herein.
B7-H1 is a coregulatory inhibitor of antitumoral T-cell responses. Recently, it has become clear that T-cell responses are ultimately governed by a balance between positive and negative coregulatory signals that are generated within the T cell (15). It has been shown that highly orchestrated T-cell coregulatory receptor-ligand interactions act to direct, modulate, and fine tune T-cell receptor signaling to either promote or suppress T-cell activation; depending on timing and location, costimulatory molecules can control T-cell priming, growth, differentiation, and functional maturation (15). More simply stated, T-cell coregulatory receptor-ligand interactions can provide either positive "go" signals to amplify antigen-specific T-cell activation or "stop" signals that can inactivate or kill T cells (Fig. 1 ). For example, OX-40 (CD134; ref. 29) and 4-1BB (CD137; ref. 30) represent positive coregulators (also referred to as "accessory costimulators") that generally function to bolster antigen-specific T-cell stimulation, thereby intensifying immune assaults against specific antigens that are formally presented to the T cell. In contrast, CTLA-4 and B7-H1 represent negative coregulators (also referred to as "coinhibitors") that can down-regulate T-cell function and truncate T-cell survival presumably to preempt self-antigen recognition and, thus, the genesis and evolution of autoimmune disease (15, 31).
Various T-cell–associated receptors, ligands, cytokines, conditions, and cell types that have been implicated in the coregulatory inhibition or further activation of antigen-specific T-cell function.
Hence, beginning in late 2003, our group initiated an exhaustive survey of T-cell phenotypes, coregulatory receptors and ligands, and markers of T-cell activation expressed within human RCC tumors. This survey included immunohistochemical analyses of RCC tumors for levels of CD3+, CD4+, CD8+ T cells, T-cell accessory costimulators, including OX-40 and 4-1BB, activation markers, such as high-affinity interleukin-2 receptor (CD25), cytolytic T-cell perforins, and granzymes, and, finally, T-cell coinhibitors, such as B7-H1. Of all of the T-cell phenotypes, markers, receptors, and ligands studied, only B7-H1 immediately showed a robust association with RCC disease progression and patient outcome even despite the preliminary nature of our earliest studies.
B7-H1 was first discovered by Dong et al. (16) in 1999. B7-H1 is a cell surface glycoprotein within the B7 family of T-cell coregulatory molecules. B7-H1 mRNA is expressed in nearly all human tissues, but cell membrane protein expression is largely restricted to a fraction of macrophage lineage cells and subsets of activated T lymphocytes (16, 17). Several human malignancies, including cancers of the breast, colon, and lung, can also exhibit cell surface B7-H1 expression (17–22). Thus, these and other molecular studies indicate that B7-H1 protein expression is posttranscriptionally regulated perhaps in response to proinflammatory cytokines, such as IFN-γ, which have been shown to up-regulate B7-H1 expression (15, 17). Various studies have also reported that B7-H1 can both positively and negatively coregulate T-cell responses depending on the location and context of expression (15–17, 32). Although the significance of this apparent duality in B7-H1 function is not well understood, some evidence exists that B7-H1 may facilitate naive T-cell activation in lymphoid tissues and within areas of acute inflammation, whereas in peripheral tissues, including solid tumors, B7-H1 may primarily function to inhibit activated or memory T-cell phenotypes to down-regulate and, thereby, stem immune responses (15).
Cancer cell expression of B7-H1 inhibits antitumor immunity. Experimental studies to date uniformly suggest that B7-H1 acts to down-regulate antitumoral T-cell–mediated immunity. Tumor-associated B7-H1 has been shown to inhibit antitumoral T-cell–mediated immunity by interacting with T-cell PD-1 (or a not-yet-identified non-PD-1 receptor), resulting in tumor-specific T-cell apoptosis or impairments in cytokine production and cytotoxicity of activated antitumoral T cells (17, 20, 24, 33). B7-H1 expressed by murine tumors has been reported to abrogate immune-mediated tumor regression after both adoptive transfer of tumor antigen-specific CD8+ T-cell clones and treatment with agonistic costimulatory antibodies (i.e., 4-1BB) that typically promote T-cell activation (25). On the other hand, in vivo monoclonal antibody–mediated blockade of B7-H1 has been shown to potentiate antitumoral T-cell responses against immunogenic murine cancers that express B7-H1 either endogenously or after gene transduction (17, 24, 25). Thus, preclinical studies support that B7-H1 blockade can be immunotherapeutically exploited to facilitate antitumor immunity in murine cancer models (22, 25). Because several human cancers have now been reported to aberrantly express B7-H1 (Table 1 ), it is hypothesized that B7-H1 may facilitate human cancer progression by impairing host antitumoral immunity.
Human tumors reported to express the costimulatory molecule B7-H1
B7-H1 is expressed in clear cell RCC. In December 2004, we reported the first investigation of B7-H1 expression in RCC (23). Specifically, we immunohistochemically stained 196 clear cell RCC nephrectomy specimens for B7-H1 expression levels using an anti-B7-H1 monoclonal antibody (clone 5H1). All tissue slides in this study were centrally reviewed by a single urologic pathologist (Dr. John C. Cheville, Division of Anatomic Pathology, Mayo Clinic, Rochester, MN), who was blinded to patient outcome. At the time of these studies, the immunohistochemical staining method for B7-H1 was only applicable to fresh-frozen tissue specimens. Consequently, the duration of follow-up in our initial study was somewhat limited (median, 2 years) because all patients with available fresh-frozen tissue specimens had undergone nephrectomy beginning in 2000 and beyond. Despite the somewhat limited interval of follow-up, several important findings were revealed by this study. First, we observed that B7-H1 protein is expressed by both clear cell RCC tumor cells (present in 66% of specimens) and tumor-infiltrating mononuclear cells (present in 59% of specimens; Fig. 2 ; ref. 23). This finding in itself was deemed novel because B7-H1 was not observed to be expressed in normal human kidney tissues (16, 17). The observation that malignant cells of the kidney acquire the ability to express surface B7-H1 protein and that RCC tumors are infiltrated by B7-H1+ mononuclear cells suggested the possibility that, perhaps, B7-H1 might modulate the immunogenicity of this tumor. Second, we noted that patients with high levels of B7-H1, present on either their tumor cells or tumor-infiltrating mononuclear cells, were significantly more likely to exhibit adverse pathologic features within their tumors, including (a) higher nuclear grade (P < 0.001), (b) positive lymph node metastatic involvement (P < 0.001), (c) distant metastases (P = 0.022), and (d) increased levels of histologic tumor necrosis (P < 0.001; ref. 23). For this study, we defined high levels of B7-H1 as specimens containing ≥10% of B7-H1+ tumor cells or specimens with an adjusted lymphocyte count of >100 (moderate to marked lymphocytic infiltration with ≥50% of the lymphocytes staining positive for B7-H1; ref. 23). These observations were generally consistent with our overall hypothesis that B7-H1+ RCC tumors are associated with a more aggressive tumor phenotype. Third, we observed that RCC patients with high tumor-associated or lymphocyte-associated B7-H1 were at significantly increased risk of cancer-specific death in a univariate statistical model [risk ratio, 4.53; 95% confidence interval (95% CI), 1.94-10.56; P < 0.001; ref. 23]. However, risk of death for B7-H1+ patients did not achieve statistical significance in multivariate analysis (risk ratio, 2.19; P = 0.079). Based on this, we speculated that the statistical power of our study was somewhat constrained by limited follow-up and low number of events (cancer-specific deaths) and that statistical significance would eventually be achieved with additional follow-up. Based on the notion that RCC is an immunogenic tumor that commonly harbors high levels of dysfunctional lymphocytes, we proposed that B7-H1 may function at the clinical level to impair host T-cell–mediated immunity, thereby promoting cancer progression. Hence, additional studies with longer intervals of patient follow-up seemed warranted.
Photomicrographs at ×400 magnification. A, RCC specimen with high tumor B7-H1 expression. B, RCC specimen with high lymphocyte B7-H1 expression. C, RCC specimen with no B7-H1 staining in either the tumor cells or lymphocytes. D, normal kidney specimen with no B7-H1 staining in the proximal tubules. Reprinted with permission from Thompson et al. (23).
B7-H1 is expressed in metastatic RCC. With 1 additional year of follow-up, we reported a second clinical investigation of B7-H1 in RCC (26). Using the same cohort of patients mentioned above, we confirmed that patients with high tumor- or lymphocyte-associated B7-H1 remained at a significantly increased risk of death (risk ratio, 2.63; 95% CI, 1.23-5.64; P = 0.013) even after multivariate adjustment for prognostic indices encompassed in the Mayo Clinic tumor-node-metastasis stage, tumor size, grade, and necrosis score, a prognostic algorithm specifically developed for patients with the clear cell subtype of RCC and one that has been externally validated (34, 35). Additionally, in this second study, we examined metastatic clear cell RCC specimens for B7-H1 expression and observed that both disseminated tumor cells and infiltrating lymphocytes express B7-H1 at rates similar to what was observed in primary clear cell RCC tumor specimens (Fig. 3 ; ref. 26). This finding is important because immunotherapy is often rendered after cytoreductive nephrectomy. Prompted by the observation that clear cell RCC metastases also express B7-H1, we surmised that advanced RCC patients may still derive a benefit from B7-H1 targeted therapy even after surgical primary tumor extirpation (26). One critique of these translational studies, however, was the definition of high B7-H1 levels. The cut-point levels that we used to define high B7-H1 levels in our earliest studies (which were somewhat underpowered because of limited patient follow-up) were elucidated using statistical analyses of scatter plots and survival differences in the Cox proportional hazards regression model. However, we observed that a significant number of patients harbored RCC tumors that contained 5% tumor-associated B7-H1 (29%), and these patients were thus excluded from the 10% or more high tumor B7-H1 group. Moreover, the reproducibility of discerning 5% versus 10% B7-H1+ tumor staining remained unknown. We speculated that if B7-H1 functions to protect cancer cells from T-cell–mediated immune destruction, then patients with any level of B7-H1 protein, including 5%, should be at risk of poor outcome.
Photomicrograph at ×400 magnification. Metastatic RCC specimen to lung with high B7-H1 expression on both tumor cells (circled, red arrow) and infiltrating lymphocytes (black arrow). Reprinted with permission from Thompson et al. (26).
To address this concern, we conducted another clinical investigation using the same cohort of patients mentioned above (27). Now, with a median follow-up of 2.7 years, the clinical effect of B7-H1+ RCC tumors (≥5% of tumor cells) was simply compared against negative RCC tumors that essentially lacked B7-H1 expression (<5% of tumor cells); that is, RCC patients with 5% to 100% of tumor cells expressing B7-H1 (positive tumor) were compared against RCC patients with <5% of tumor cells expressing B7-H1 expression (negative tumors). The results of this study confirmed that patients with B7-H1+ tumors remained at a significantly increased risk of cancer-specific death relative to patients with B7-H1− tumors even after a multivariate adjustment (risk ratio, 3.52; P = 0.010; ref. 27). Thus, this study was congruent with our previous thoughts that B7-H1+ RCC tumors are more aggressive tumors and likely to disseminate and kill the patient. These associations were also consistent with the recognized ability of tumor-associated B7-H1 to inhibit T-cell–mediated immunity as was reported in the basic science literature. However, as we noted, confirmatory reports with longer follow-up were needed to more rigorously validate these conclusions.
Long-term clinical follow-up of B7-H1 expression in RCC patients. Until 2006, B7-H1 immunohistochemical staining was only feasible using fresh-frozen RCC nephrectomy specimens that we began collecting in 2000. Other mRNA-based methods, such as in situ hybridization, to assess B7-H1 levels in formalin-fixed, paraffin-embedded specimens were ruled out to extend our studies because expression of mRNA does not necessarily correlate with the presence or absence or absolute levels of encoded protein (15). Hence, after roughly 6 months of arduous and systematic testing, Susan Kuntz in our laboratory was able to generate a reproducible antigen retrieval method that permitted B7-H1 to be immunohistochemically stained in paraffin-embedded specimens (28). Shortly thereafter, we immunohistochemically stained 306 paraffin-embedded clear cell RCC tumor specimens recovered from patients who underwent nephrectomy during the years 1990 to 1994 (28). Our results obtained using paraffin-embedded tissues were consistent with our earlier observations made using fresh-frozen specimens. That is, RCC tumors expressing B7-H1 (24%) were significantly more likely to exhibit a higher nuclear grade, larger tumor size, higher tumor-node-metastasis stage, and coagulative tumor necrosis (P < 0.001 for all) than tumors lacking B7-H1 expression (28). Similarly, RCC patients with B7-H1+ tumors remained at significantly higher risk of cancer-specific death (risk ratio, 3.92; 95% CI, 2.61-5.88; P < 0.001) and overall mortality (risk ratio, 2.37; 95% CI, 1.72-3.28; P < 0.001) compared against patients whose tumors scored negative for B7-H1 expression. This increased risk of death from RCC persisted in multivariate models that adjusted for tumor-node-metastasis stage, grade, and performance status and even after adjusting for the Mayo Clinic tumor-node-metastasis stage, tumor size, grade, and necrosis score (28). In this study, 5-year cancer-specific survival rate was 42% for patients with B7-H1+ tumors versus 83% for patients with B7-H1− tumors (Fig. 4 ). Moreover, for the subset of RCC patients with completely localized forms of disease (pTxN0M0), patients with B7-H1+ tumors were at significantly increased risk of experiencing metastatic disease progression (risk ratio, 3.46; 95% CI, 2.11-5.69; P < 0.001; Fig. 5 ) and death from RCC (risk ratio, 4.13; 95% CI, 2.49-6.86; P < 0.001) relative to patients with B7-H1− tumors. Thus, these data support the finding that B7-H1 independently portends a poorer prognosis for RCC patients (even for patients with seemingly localized disease) and encompass some of the most compelling evidence to date that B7-H1 may be clinically operational in RCC patients impairing host immunity and fostering tumor progression.
Association of tumor B7-H1 expression with death from RCC for 306 patients with clear cell RCC (risk ratio, 3.92; 95% CI, 2.61-5.88; P < 0.001). Cancer-specific survival rates at 5 and 10 yrs after nephrectomy were 42% and 37%, respectively, for patients with positive tumor B7-H1 expression compared with 83% and 77%, respectively, for patients with negative tumor B7-H1 expression. Reprinted with permission from Thompson et al. (28).
Association of tumor B7-H1 expression with progression to distant metastases for 268 patients with localized clear cell RCC (risk ratio, 3.46; 95% CI, 2.11-5.69; P < 0.001). Progression-free survival rates at 5 and 10 yrs after nephrectomy were 57% and 51%, respectively, for patients with positive tumor B7-H1 expression compared with 86% and 79%, respectively, for patients with negative tumor B7-H1 expression. Reprinted with permission from Thompson et al. (28).
Our understanding of the fundamental regulatory mechanisms that govern host immune cell activation, with a particular emphasis on T-cell coregulation, has expanded exponentially within the last decade. B7-H1 encompasses the first T-cell coregulatory molecule reported to be significantly and independently associated with disease progression and patient survival for any solid human malignancy. Our studies show that B7-H1+ clear cell RCC tumors typically exhibit more severe pathologic features. In addition, patients who harbor B7-H1+ tumors are at significantly increased risk of experiencing cancer progression, cancer-specific death, and overall mortality. Although the precise role of B7-H1 in the regulation of T-cell responses in inflammation and autoimmunity remains a topic for further investigation, B7-H1 has consistently been reported as an immunoinhibitory molecule in the context of tumor immunity (15, 25). In fact, we are now aware of two additional recent studies that suggest that tumor B7-H1 expression is associated with a poorer outcome for patients with malignancies of the breast and colon (36, 37). Hence, it seems that B7-H1 may well represent a general promoter of tumor progression. However, further studies will need to be conducted to establish this notion.
The basic science and translational investigations of B7-H1 in RCC now strongly support the development of a fully humanized monoclonal antibody for use in phase 1 clinical trials. At present, it is anticipated that clinical grade antibody for B7-H1 blockade in humans may be available within 18 to 24 months. Until then, B7-H1 still encompasses a potent independent predictor of outcome for clear cell RCC patients and may ultimately help determine which patients will benefit from adjuvant therapy.
A compelling precedent for abrogating inhibitory T-cell signaling to potentiate antitumor immunity has been established by the experience with CTLA-4 blockade immunotherapy (31). Similar to B7-H1, CTLA-4 is an inducible cell surface glycoprotein that participates in T-cell coregulation, functioning as a potent inhibitor of T-cell–mediated immunity (31). In fact, CTLA-4 knockout mice have been shown to survive for <1 month, secondary to aggressive polyclonal multiorgan lymphocytic infiltration (38). CTLA-4 blockade is currently being tested in clinical trials for patients with advanced melanoma, prostate cancer, and several other forms of malignancy (39). There is, however, one distinct difference between CTLA-4 and B7-H1; B7-H1 is aberrantly expressed on human cancer cells, whereas CTLA-4 is present on all forms of activated T cells irrespective of the source of antigenic stimulation. Thus, B7-H1 blockade may, by definition, potentiate T-cell–mediated responses in a more tumor-specific fashion, thereby limiting autoimmune side effects.
Current applications of immunotherapy and vaccination for human malignancies are often capable of eliciting strong and functionally intact T-cell responses; however, these responses against tumor-associated antigens do not often culminate in tumor regression in clinical trials (25, 40). These findings suggest a tumor escape mechanism whereby cancer cells are capable of evading antitumor immunity in a microenvironment of immune resistance. For patients with clear cell RCC, B7-H1 may contribute to the profile of immunosuppression by forming a "molecular shield" to prevent tumor destruction (25). Analogous to this, it has been recently shown that B7-H1 seems to facilitate states of chronic viral infection and, conversely, that B7-H1 blockade is capable of reviving "exhausted" memory CD8+ cytotoxic T cells that subsequently may participate in clearing viral burden (41). That B7-H1 is present on numerous other human malignancies suggests that it may facilitate tumor evasion of host immunity. Although it is tempting to attribute immune dysfunction in RCC and other tumors to aberrant B7-H1 expression, it is likely that multiple other host factors also contribute. Nevertheless, further investigation of B7-H1 and other T-cell coregulatory molecules is clearly warranted. Such investigations should include (a) evaluation of PD-1, a known receptor of B7-H1, in relationship to RCC outcome; (b) investigation of B7-H1 in non–clear cell RCC histologic subtypes; and (c) investigations of other T-cell coregulatory molecules that may potentially collaborate with B7-H1 to help RCC militate against host immunity. Obviously, a fully humanized antibody to block B7-H1 needs to be developed and tested for toxicity and efficacy. RCC has garnered much attention in modern oncology due to major recent advances in molecular genetics and targeted therapies (42). We believe that B7-H1 is a potent prognostic marker and one of the most promising and targetable RCC molecules reported to date. We are confident that further investigations of B7-H1 will not only improve our understanding of tumor-induced immune dysfunction but also broaden the availability of useful therapeutic options for patients afflicted with advanced RCC.
B7-H1 is aberrantly expressed in clear cell RCC and is associated with increased aggressive pathologic features and risk of cancer progression, cancer-specific death, and overall mortality. The basis for these associations may relate to the recognized ability of tumor-associated B7-H1 to inhibit T-cell–mediated immunity. Therefore, blockade of B7-H1 represents a realistic potential immunotherapeutic treatment approach for patients with RCC. Finally, it is clear that B7-H1, alone or in combination with other cancer biomarkers, may prove extremely useful to identify high-risk patients who may require and respond to standard-of-care adjunctive therapy or newly emerging treatments that are to be tested in the context of clinical trials.
Dr. Atkins: One would think that if B7-H1 expression correlated with poor prognosis that you would see an enrichment of B7-H1 expression in metastatic disease compared with primary rather than the expression being essentially equivalent.
Dr. Kwon: One possibility is that there is another molecule like B7-H1 that also does the same thing and it is on the metastases. Another possibility is that B7-H1 does not necessarily stick to the cells and is actually shed into the serum. Yet, another possibility is that B7-H1 is not relevant at all to renal cell carcinoma or its ability to metastasize.
Dr. Ochoa: Why would B7-H1 be present in T cells that infiltrate those tumors?
Dr. Kwon: The observation thus far has been that, when a T cell gets activated, a subset of T cells will express B7-H1 on the surface. The reason the B7-H1 appears on those activated T cells is not yet elucidated.
Dr. Sosman: Would you predict that the B7-H1-expressing tumors might respond better to anti-CTLA-4?
Dr. Kwon: There are at least 10 different ways that these tumors are impairing immune responses. Anti-CTLA-4 monoclonal antibody is a good strategy to use in combination with B7-H1 blockade. B7-H1 blockade has an advantage in that it is intrinsically specific to the tumor in this case, unlike anti-CTLA-4, which is a generalized way of preventing down-regulation of T-cell responses where autoimmunity might easily prevail. I like the B7-H1 approach, but it can be used in combination with anti-CTLA-4.
Dr. Vieweg: With your B7-H1 studies, you have an opportunity to look at knockdown or down-regulation of your target molecule, which was not the case in the trials using the CTLA-4 antibody. What frustrated me the most with the CTLA-4 studies is that there was no proof that you have actually impacted CTLA-4 signaling. Therefore, I presume B7-H1 is a better target.
Dr. Atkins: Data were presented at ASCO last year showing that, in melanoma patients receiving CTLA-4 antibody, the patients who developed autoimmunity but did not have tumor response were reportedly patients who had PD-1 expression on their lymphocytes. The hypothesis is that the melanoma cells that express B7-H1 are able to evade the immune system, suggesting that a combination of CTLA-4 antibody and B7-H1 antibody might be able to overcome the resistance in this group of patients and produce responses in all the patients who are predisposed to develop autoimmunity with CTLA-4 antibody administration.
Dr. Kwon: We are naive if we think that one bullet will bring down these cancers. It is going to have to be multiple agents, and then multiple agents may be used in combination with certain kinds of drugs or a surgical approach.
Grant support: The Richard M. Schulze Family Foundation, The Commonwealth Foundation for Cancer Research, and Helen and Martin Kimmel Foundation.
Presented at the Second Cambridge Conference on Innovations and Challenges in Renal Cancer, March 24-25, 2006, Cambridge, Massachusetts.
Accepted October 12, 2006.
Received July 27, 2006.
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KISS' Farewell Tour Will Conclude in Late 2022
Graham Hartmann Published: September 23, 2021
Kevin Winter, Getty Images
KISS' farewell tour (seriously, they mean it this time) will apparently conclude in late 2022. According to longtime manager Doc McGhee, the "End of the Road" tour will not stretch into 2023.
The "End of the Road" tour was originally meant to wrap up in New York City on July 17, 2021, but the COVID pandemic pushed those plans back. Like many acts, KISS are finally back on the road, and assuming no cancellations take place, they'll only be on the road for another year.
"So it looks like the last show of KISS as you know it, with Gene [Simmons] and Paul [Stanley], will be some time at the end of next year," McGhee tells Talking Metal. "We don't have a locked in date yet. Because of what's going on, it's very difficult for people to hold dates because we don't even know if we're gonna be able to play. So we're trying to hold dates. But it will be next year."
"We wanna get through what we said," Doc continues. "The guys wanted to play to everybody. It meant we'll go to your town, big or small. We're not the red-carpet band that you have to come out. We've always been the people's band in the sense that the KISS Army that supported us for all these years, we go to all the little towns to play."
Doc McGhee on Talking Metal
Former KISS guitarist Ace Frehley recently told Eddie Trunk that he's open to joining the reunion tour "if the money's right." "I'm on good terms with Paul and Gene," Frehley affirmed, "which is nice, because we created something really special in the early '70s that has outlasted so many other bands. And God bless 'em. They're still doing it; I'm still doing it. Peter [Criss] is still around. I'm not quite sure why Peter hadn't toured over the years as much as I have, but it is what it is."
For the full list of KISS' End of the Road tour dates, click here.
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As more research continues to unfold about migraine, including increased knowledge about the pathogenesis, genetic and environmental influences, the economic burden to the individual and society, the toll on jobs and careers, and the affect of migraine on family relationships, the way we speak about migraine is beginning to change. For me, after living with migraine for so many years, I am beyond grateful to see the reference to migraine as a "bad headache" be replaced with migraine is a "neurological disease".
Raise awareness and brand migraine as a severe neurological disease.
Empower and mobilize patients to advocate for themselves and live healthy and fulfilling lives.
Inspire, motivate, and drive more funding for research into the causes and treatment of migraine so we can eventually and hopefully bring safer and more effective treatments to patients.
In an interview with the American Migraine foundation, in a discussion of "It's simply not a headache", Dr. Dodick mentions that the word "headache" is used flippantly and thus migraine isn't seen as a serious debilitating disease. He adds, "the stigma is that migraine patients can't withstand the stressors in life so they develop headaches".
In my case, throughout my life, as I was told to pace myself and if I just learned to manage stress my headaches would disappear, I bought into this idea that somehow, because I couldn't cope with pressure, these "headaches" were my fault. Even, with the hours I spent at a migraine clinic and my visits with a psychologist and a biofeedback therapist, as well as lengthy discussions with my neurologist, I did not gain appreciation for migraine as a disease until my attacks became chronic and I was diagnosed with medication overuse headache. At that time, when my doctor told me I had to do something besides take medication for my headache and other symptoms, I began to educate myself. As I waded through the most recent evidence and research available about migraine, it was then I learned migraine was a severe neurological disease and headache was only one of many debilitating symptoms of a migraine attack...something, with the branding of migraine as a "severe neurological disease", I am much quicker to point out now to everyone, including my family, friends, doctors, and other members of my health care team.
As I gain more knowledge about the pathogenesis (cause), genetics, and environmental influences (triggers) associated with migraine disease, I am increasingly empowered to take control of everything I can to help manage my attacks. For example, as I discover more about the hypothalamus and homeostasis and how a change in homeostasis like too much or too little sleep, dehydration, or skipped meals (hypoglycemia) may activate a migraine attack, I work harder to stick to routines like regular sleep, exercise and eating habits to manage these and other triggers for my attacks. In addition, where I had previously bought into stress as being the cause of my "headaches", I am firm on the realization that, although stress is a trigger for my attacks and makes me more susceptible to other triggers such as poor sleep, it is not the cause. However, that said, because stress is a factor in the frequency of my attacks, I am committed to managing my stress response through therapies like biofeedback and meditation. As I continue to approach migraine as a disease and focus on preventing attacks, not just treating symptoms like headache during attacks, I have been able to maintain the remittance to infrequent episodic migraine I achieved a number of years ago, and with many more migraine-free days, live a healthy and fulfilling life with migraine.
Excited about the Move Against Migraine campaign, I became a member of the American Migraine Foundaton Move Against Migraine Facebook Group, an effort to mobilize a community of migraine patients to become self-advocates and help us learn from one another. As well, along with resources available from the American Migraine Foundation, Facebook Live events provide access to experts who speak on a variety of topics. For me, being a part of this group, both as a member and a moderator, is a rich and rewarding experience.
Inspire, motivate and drive more funding for research into the causes and treatments of migraine so we can eventually and hopefully bring safer and more effective treatments to patients.
We all want safer and more effective treatments for migraine. By taking an active role in our care, educating the uniformed, raising our voices, and changing the conversation about migraine from "headache" to "migraine...a life-changing, debilitating disease that affects all aspects of our lives", we can inspire, motivate, and drive more funding into the causes and treatments of migraine and achieve our goal..."Plunge into it, move with it, and join the dance..."
WE'RE NOW A PROUD PARTNER OF THE AMERICAN MIGRAINE FOUNDATION!
As part of our ongoing commitment to providing meaningful information, resources and support for those living with migraine, Sharron Murray is thrilled to announce our new partnership with the American Migraine Foundation.The American Migraine Foundation is the official resource for millions of Americans living with migraine seeking reliable information about diagnosis, treatment and advancements in research. Launched in 2010 as a patient support and advocacy effort of the American Headache Society, AMF's mission is to mobilize a community for people living with migraine and their support networks, and to drive impactful research into the third most common and sixth most disabling disease around the globe.
Like Sharron Murray, the American Migraine Foundation is dedicated to helping people with migraine live meaningful and pain-free lives. We're so excited to join forces with AMF to provide support, advocacy and treatment innovations to people living with this disabling disease.
Although research about cold therapy (cryotherapy) in patients with migraine is limited, one thing is known, as the pain begins, many of us reach for the cold pack. In an article by Sprouse-Blum, et al., (2013), the authors report, "of all self-administered pain-relieving maneuvers, cold therapy is the most common maneuver applied in migraine without aura and the second most common maneuver applied in migraine with aura second only to compression" (p. 237). Before we take a look at the possible physiological effects of cold therapy, and some of our respective methods of application, let's have a quick review of helpful things to know about headache and neck pain in migraine.
We need to be aware that migraine is a genetic neurological disease and headache is a phase of a migraine attack (a person may have an attack without headache). Headache is commonly unilateral, pulsating, moderate to severe intensity, and may be aggravated by movement. However, pain may be felt all over the head (on one or both sides and in the middle of the head), including the eyes, frontal, occipital and neck areas (Kelman, 2005; ICHD-3 beta, 2013; Burstein et al., 2015). The headache phase is thought to begin with activation of meningeal receptors at the origin of the trigeminovascular system. As the headache progresses, in activation and sensitization of the trigeminovascular pathway, a number of complicated electrical and chemical events take place, including the involvement of neurotransmitters, neuropeptides and inflammatory mediators. In the process, we may experience a wide variety of autonomic, affective, cognitive, and sensory symptoms, including allodynia. The clinical manifestations of cephalic allodynia may include scalp and muscle tenderness and sensitivity to touch (Burstein et al., (2015).
Neck pain has the highest prevalence in coexistant migraine and tension-type headache.
Now, keeping these things in mind, let's take a look at the possible physiological effects of cold therapy for symptomatic relief in migraine. In general, local cold therapy is thought to cool skin, decrease temperature, decrease blood flow (vasoconstriction), reduce inflammation in adjacent tissues, relieve pressure on affected nerves, decrease muscle spasm and muscle tension, and numb pain. That said, let's review some of the proposed pathophysiological mechanisms of action in migraine.
there may be a minimal contribution of decreased metabolic activity in locally cooled areas (page 239).
Little is written about the contraindications of cold therapy in migraine. In the study by Ucler et al., (2006), the authors report one patient could not use cold therapy because of cold intolerance and another patient due to vertigo. Robbins, (1989), reports contraindications may include Raynaud's phenomenon and cold sensitivity. As well, Robbins, (1989), notes ice may cause some problems in rheumatoid conditions and in patients with paroxysmal cold hemoglobinuria. Taking these factors into consideration, in addition, if you have circulatory problems, are diabetic, are pregnant or are nursing, you should discuss individual concerns about cold therapy with your doctor.
Today, there are a number of products on the market designed to meet our individual cold therapy needs and comfort levels, including gel packs, pillows, caps, hats, and collars. For example, a hat that covers the entire head may be appropriate for one person, while another person may like something that covers the eyes.
In my case, since my migraines escalated to chronic migraine and then remitted to infrequent episodic migraine, I have become increasingly sensitive to hats or anything tight around my head, or neck, because of allodynia. As well, when I do have an attack, neck pain has become a troublesome symptom for me in the premonitory phase, throughout the headache phase, and into the postdrome.
with the the seam side of the cloth cover down and Velcro closure to the front of my neck, where I can easily access it for adjustments, I turn the two top corners down and fasten the lower portion just at, or slightly below, the level of my clavicle .
This way the contact of the Cryo-gel ice pack is at the back of my neck and base of my skull, not the sides and front of my neck. If the pain moves to my head, I can remove the hat from my neck, readjust the Cryo-gel pack to its original size, and place it where it hurts, including around my head, top of my head, or over my eyes.
In addition to the flexibility of the Migraine Hat, I am impressed with the versatility of the well designed cooler, which comes as a gift. Because I don't eat fast food and avoid foods with MSG, preservatives and artificial ingredients, I often take a healthy snack or sandwich with me when I am away from home. Along with two Cryo-gel ice packs, I am able to tuck in my food choice and keep it cool for the day.
Robbins, L., D., (1989). "Cryotherapy for Headache." Headache: The Journal of Head and Face Pain. Oct;29(9).
Sprouse-Blum, A., S., Gabriel, A., K., Brown, J. P., et al., (2013). "Randomized controlled trial: targeted neck cooling in the treatment of the migraine patient." Hawaii JMed Public Health. Jul;72(7):237-41.
Ulcer, S., Coskun, O., Inan, L., E., et al., (2006). "Cold Therapy in Migraine Patients: Open-label, Non-controlled, Pilot Study." Evid Based Compliment Alternat Med. Dec;3(4):489-493.
This article is not intended as a substitute for medical advice. If you have any specific concerns about your health or nutrition, please consult a qualified healthcare professional.


Standard 1: refers to achieving familiarity with motor skills and movement patterns used in a variety of physical activities (note that the wording of this standard does not restrict the uses to sports, athletics, activities, or games).
Standard 2: refers to the theoretical understanding of physical activities embodied in principles, concepts, strategies, and tactics. These sorts of understandings help one to know how, when, and in what way to apply the motor skills and patterns one has learned.
Standard 4: refers to the achievement and maintenance of a level of physical fitness that is healthy for the person in question; this may, of course, vary from person to person.
Standard 5: refers to exhibiting and maintaining responsible and respectful behavior in physical activity settings.
Standard 6: refers to finding value in physical activity for the variety of benefits it can bring to one's life, including in the areas of health, enjoyment, socialization, etc.
One kind of reference that is useful for homeschool physical education include instructions for physical games and activities. If you have instructions for capture the flag, flashlight tag, or any other game you want to play right there along with you on your family camping trip, it's more likely that you can get a game going and avoid arguments as well. You can also look to official rulebooks for sports (some of which can be found online for free), which can help you determine court size, net height, and other parameters, depending on the sport in question. Keep in mind that you can play with official regulations and equipment or adapt as desired and appropriate for your situation. Knowing the official rules can also add to the fun and understanding of being a spectator, for example, if you choose to watch the Olympics.
you will be able to find a large number of games, and likely learn some you don't know. If you want a specific game, search by name. Be aware that many games are like folk songs: there are many variations, and you may find something that is not quite what you know. Unless there's a good reason not to adapt, you should feel free.
Physical education field trips do not have to be focused only on the student, and they can have several purposes: to exercise, to inspire interest, to make physical education enjoyable, and to present opportunities for analyzing and learning more about various physical activities.
Go sledding or sliding (depending on where you live).
Jump in a neighboring swimming pool or lake.
Play bocce, croquet, catch, other lawn games like volleyball or tether ball, miniature golf, or Frisbee™.
Try bicycles for transportation, maybe even a bicycle built for two.
Watch local high school or college students, semi-professionals, or professionals engage in the sport that your student most enjoys being active in, either in person or on television.
Teach the student to keep score at, say, a professional baseball game.
Go to watch a practice of the sport that your student most enjoys.


text:
Paula Deen Talks 'Dancing With The Stars' Debut
Sarah Field
Paula Deen may be best known for cooking rich recipes with a whole lot of butter, but the former Food Network chef is going to give it her all on the new season of Dancing With the Stars. Deen told Entertainment Tonight she has her eyes on bringing home the show's ultimate prize, the Mirror Ball trophy.
"I have gotten so many thousands upon thousands of well-wishers contacting me. It's so important that I not let them down. I want to dance to the moon and make them proud and just bring hope."
At age 68, Deen is the show's oldest female contestant. She wants to inspire other women in her age group.
"I just want to bring hope, especially to older women in the middle part of their life. You can have a lot of obstacles come your way that are unexpected. I just want to help women realize that they can overcome."
Deen is part of a cast of many lesser-known stars, leading TV Line to question ABC's choices.
"Is this the best the show's casting department can do?"
The website notes DWTS is a ratings draw, with last season's finale bringing in 13.3 million viewers.
In addition to Deen, the cast includes recognizable stars such as Gary Busey, Chaka Khan, Nick Carter, and Tamar Braxton. Fans might not know jockey Victor Espinoza, but probably know his horse, American Pharoah.
Deen is paired with pro Louis van Amstel, over whom she gushed to ET.
"I feed people's bellies, and he has fed me with movements and words — words of wisdom. He's fed me — just not the way I've fed him!"
Van Amstel's past partners include Priscilla Presley and Kelly Osbourne.
The Daily Mail reported that van Amstel was spotted eating some of Deen's deep-fried food during a promotional event for DWTS. Deen chose to change some of her eating and cooking habits after a diabetes diagnosis in 2009.
Deen denied to TMZ that her turn on Dancing With the Stars is an attempt to restore her reputation, which was damaged in 2013 when she was sued by an employee who accused her of making racially derogatory remarks. The lawsuit was dismissed.
Paula Deen and Louis van Amstel will dance one of five styles — the cha cha, foxtrot, salsa, quickstep, or jive — to "Hey Good Lookin'," by Carol Welsman. No one will be eliminated the first week.
Dancing With the Stars Season 21 debuts Monday, September 14, on ABC.
[Photo by Aaron Davidson / Getty Images Entertainment]


text:
Home Top 30 Janet Jackson Singles
SoulBounce's Top 30 Janet Jackson Singles: #10 'Got 'Til It's Gone'
August 21, 2015 | 12:00 pm
When Janet Jackson first released her sixth studio album, The Velvet Rope, she utilized a filter of introspection and reflection as the concept project's underlying theme. Nowhere was that introspection felt moreso than on the album's lead single, "Got 'Til It's Gone," as we find her lamenting the loss of something after taking it for granted. Produced by Jackson, alongside her frequent collaborators Jimmy Jam and Terry Lewis, and co-written by the trio, in addition to Jackson's then-husband Rene Elizondo Jr., Joni Mitchell and Q-Tip, the 1997 single found her trading in her mainstream pop sound for a grittier, hip hop-influenced sound. Jackson's feathery vocals buoyantly floated atop the thumping mid-tempo groove of the track.
Despite the fact that "Got 'Til It's Gone" had an official video directed by Mark Romanek, the song received little promotion and was not released as a commercial single, thus making it ineligible for the Billboard Hot 100 chart. This rather inexplicable detail did little to hinder the song's popularity, quickly becoming a hit on urban radio and internationally and appearing on music charts in over 15 countries. It also went on to garner acclaim for its pre-Apartheid South African-influenced visuals, nabbing a GRAMMY Award for Best Short Form Music Video in the process.
If I could turn back the hands of time / Make you, fall in love, in love with me again / So would you give me another chance to love / To love you, love you the right way, no games
Eighteen years after its release, "Got 'Til It's Gone' remains a major turning point on Jackson's road to self-discovery. As the precursor for other Velvet Rope singles such as "Together Again" and "Go Deep," the song introduced audiences to both a sexually adventurous and emotionally vulnerable Janet who admitted to battling depression, body dysmorphia and eating disorders. Her decision to funnel her traumatic personal struggles into the project paid off, with The Velvet Rope quickly being certified triple platinum, proving that when it comes to Janet Jackson, taking risks can pay off.
TAGS: #31DaysOfJanet, 31 Days Of Janet, 31 Days Of Janet Jackson, janet jackson, jimmy jam, joni mitchell, mark romanek, q-tip, Rene Elizondo Jr., terry lewis
Previous: The Weeknd Will Bring His 'Madness' To A City Near You This Fall Next: Track Record: Behind Janet Jackson's Groove
Janet Jackson Gets Even More Real In 'JANET' Extended Trailer
Janet Jackson Gives Us The Inside Scoop On Her Most Iconic Videos For 'Allure'
DJ Premier Digs In The R&B Crates 'Again' For A Vintage Janet Jackson Remix
Janet Jackson Is Ready To Reveal All In 'JANET' Documentary Teaser
Yebba Gets Into Her 'Louie Bag' With Help From Smino


This race was incredibly fun: the weather was perfect, the crowd exuded great energy, and I absolutely loved the course, but it did have an incline. The incline was not to steep, but it was long.
Now, on the way to the race, I was telling my teammate, Tina, that I was not going to road race anymore, I prefer CX racing...blah, blah, blah!
At the start of the race, I was leading the pack. My people, it felt sooo good to be in the front. I felt like my very own hero. However, we got to a turn, and I slowed down, and I was not longer leading the pack, but I was still in a good position.
We got to that incline, I did ok, but I lost steam quickly. I made it to the top exhausted, but the other girls kept on moving at race pace, and I just couldn't hold the speed.
Several times I wanted to give up, but this awesome crowd would not let me; they were yelling for me to keep pedaling, and I did.
Being that this is my second season racing, and I cycle a lot in the community, the love that I felt after the race was completely liberating. I just love the sense of community of cycling.
So, I asked myself "If I had a daughter and she loved racing, but needed to put in a lot of work to see the results that she wanted, would I encourage her to quit, or would I encourage her to keep racing and training knowing that she will get better?"
My people, I LOVE ROAD RACING!!!
Find a hobby that you love and become its slave.


It may surprise some of us that there are people who think that worship is for us instead of for God. Many also see or treat worship as entertainment (worship-tainment as some call it). Worship does benefit us, but it is something that we do for God. I was incredibly surprised myself to find that some seem to view worship as being for us. Worship isn't about us, but is truly for God to show our gratitude toward God for all He has done for us and to glorify Him.
When worship involves singing or speaking, the words we are expressing to God must be felt and understood in our hearts and minds (often in our own personal way). Our words must be genuinely expressed to Him. If we don't mean what we're singing about, then we may not be worshiping God in truth or with the whole of our hearts and minds.
Worship is about so much more than the music of a Sunday church service. The way we live our lives as Christians is worship! Worshiping–living our lives in order to please God, delight in Him and glorify Him in all we do, be it via corporate worship in church, working at your 9-5 job, singing His praises in the car, or just by loving your family selflessly!
We don't worship for our own gain, though it can benefit us. It is for our Almighty Creator! Worship is our way of life in living for God and in a relationship with Him.
This entry was posted in Christian Living, Worship & Worship Leading and tagged Music on 07/30/2007 by Amanda.
Amen! Great post. It reminds me of the song "its all about You Jesus-Getting back to the heart of worship." Whenever we sing that corporately I always am wondering if the people are really understanding what it means-it always breaks me. I know my heart is not always in the right place. It is ALL about HIM.
Hi there….I had to smile when I read your answer to my question today….I'm in the very same place with the very same dream which inspired the question in the first place…Isn't our God just awesome!!! I'll be praying for those doors to open to you!!!


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Proximity Effect is a boost in the upper bass frequencies that increases with the closeness (proximity) of the sound source. Microphones with cardioid and bi-directional polar patterns exhibit this effect much more than omnidirectional microphones. Proximity effect can be used to add fullness to a track, such as vocals, where a few inches on or off the microphone can make a big difference. Proximity effect can also cause unwanted boominess, for example, on acoustic guitar, so proper mic positioning is important. Placing the microphone too close to the instrument, especially the sound hole, will result in an overly bassy sound. Many engineers find the sweet spot to be 9-12″ off the twelfth fret or where the neck meets the body. Much of today's modern rock takes advantage of proximity effect when miking guitar amplifiers by putting a dynamic mic and/or a ribbon mic right up on the cone of the speaker, creating a 'larger than life' sound.
Why do I need a Shock Mount?
Do I need a Pop Filter or Windscreen?


to reveal why spirits roam this hamlet.
They only see you when a camera flashes.
spirits, please secure welding glasses.
alert our staff with careful gestures.
JEFFREY H. MACHLACHLAN has recent or forthcoming work in New Ohio Review, the minnesota review, Eleven Eleven, and Clay Bird Review, among others. He is a PhD candidate in the Center for Writers at The University of Southern Mississippi. You can read his jokes about sports and music on Twitter @jeffmack.


text:
Les Asterodiscididae sont une famille d'étoiles de mer de l'ordre des Valvatida.

Systématique
La famille des Asterodiscididae a été créée en 1977 par  avec comme genre type Asterodiscides. Sa création répondait à la nécessité d'inclure des taxons intermédiaires entre Goniasteridae et Oreasteridae, et la famille a été revue plusieurs fois et pourrait l'être encore à l'avenir, incluant notamment le genre Goniaster.

Caractéristiques

Cette famille assez restreinte porte des tubercules plus ou moins coniques sur la face aborale et le plus souvent des papules sur les plaques intermarginales. Elle a également pour particularité que la paire de plaques terminales supéromarginales est très apparente sur les bras, alors que les autres plaques marginales sont dissimulées sous l'épiderme granuleux ; cependant ce caractère n'est plus systématique depuis la révision de 2021.

Les jeunes spécimens sont aplatis et pentagonaux comme de nombreuses Goniasteridae, mais avec des épines ou tubercules déjà bien manifestes au moins sur les plaques supéromarginales.

Liste des espèces
Selon  :
 genre Amphiaster Verrill, 1868
 Amphiaster insignis Verrill, 1868 -- Pacifique est
 genre Asterodiscides A. M. Clark, 1974
 Asterodiscides belli Rowe, 1977 -- Somalie
 Asterodiscides bicornutus Lane & Rowe, 2009 -- Philippines
 Asterodiscides cherbonnieri Rowe, 1985 -- Madagascar (sud)
 Asterodiscides crosnieri Rowe, 1985 -- Madagascar (nord)
 Asterodiscides culcitulus Rowe, 1977 -- Australie occidentale
 Asterodiscides elegans (Gray, 1847) -- Indo-Pacifique tropical
 Asterodiscides fourmanoiri Rowe, 1985 -- Madagascar (sud)
 Asterodiscides grayi Rowe, 1977 -- Australie orientale et peut-être Arabie
 Asterodiscides helonotus (Fisher, 1913) -- Philippines
 Asterodiscides japonicus Imaoka, Irimura, Okutani, Oguro, Oji & Kanazawa, 1991 -- Japon
 Asterodiscides lacrimulus Rowe, 1977 -- Somalie
 Asterodiscides macroplax Rowe, 1985 -- Australie occidentale et peut-être orientale
 Asterodiscides multispinus Rowe, 1985 -- Nord-Est de l'Australie
 Asterodiscides pinguiculus Rowe, 1977 -- Australie occidentale
 Asterodiscides soleae Rowe, 1985 -- Australie occidentale et peut-être mer Jaune
 Asterodiscides tessellatus Rowe, 1977 -- Australie occidentale
 Asterodiscides truncatus (Coleman, 1911) -- Sud-Est de l'Australie et Nouvelle-Zélande
 Asterodiscides tuberculosus (Fisher, 1906) -- Hawaï
 genre  Kionaster Blake & Portell, 2011
  Kionaster petersonae Blake & Portell, 2011
 genre Paulia Gray, 1840
 Paulia horrida Gray, 1840 -- Pacifique est (Galapagos)
 genre Pauliastra Mah, 2021
 Pauliastra aenigma (Ludwig, 1905) -- Costa Rica
 genre Uokeaster Mah, 2021
 Uokeaster ahi Mah, 2021 -- Île de Pâques

Blake & Portell (2011) ajoutent également le genre fossile du Miocène Kionaster (trouvé en Floride).

Publication originale

Référence taxonomique

Bibliographie
 .

Notes et références

Famille d'échinodermes (nom scientifique)
Asteroidea


TORONTO — Canadian Tire Corporation Ltd.'s $985 million purchase of Helly Hansen gives the retailer access to a lucrative global marketplace without the overhead risk of a large new bricks and mortar store network, executives said Thursday.
The most significant acquisition for Canadian Tire since it bought sporting goods retailer Forzani Group in 2011 and casual apparel chain Marks in 2001, the purchase of the premium sportswear brand comes at a time of investor trepidation about the future of store-based retail amid the rise of online shopping.
Founded in 1877 and based in Oslo, Norway, Helly Hansen has annual revenue of $500 million and is sold in over 40 countries around the world including the U.S. at stores such as Nordstrom and REI, as well as the U.K., Sweden, Germany, Spain, Russia and Australia. In Canada, the brand sells workwear, outerwear, ski and sailing apparel and footwear at retailers including Hudson's Bay and Sporting Life, though Canadian Tire is its biggest customer through Sport Chek and Marks.
Currently owned by the Ontario Teachers' Pension Plan, Helly Hansen has a global e-commerce platform and 57 small stores, including nine in Canada, though its primary business is wholesale. The brand had compound annual revenue growth of 12 per cent in last three years and compound annual operating earnings growth of 36 per cent, executives said.
This is not Canadian Tire's first international business foray. The retailer of housewares and auto parts bought Texas-based automotive chain White Stores in 1982 before selling it at a loss four years later. It later opened an auto parts chain in the early 1990s in Indiana and expanded to surrounding states, but closed it in 1995 after disappointing sales at its ten stores.
Since those bruising experiences, Canadian Tire has been very cautious about making international moves, said Alex Arifuzzaman, partner in Toronto-based retail real estate specialist InterStratics Consultants.
Canadian Tire has been accelerating the acquisitions of national brands and its development of its own in-house brands since 2016 in order to drive more brand-loyal consumers to its stores and increase profitability. Prior to this acquisition, private-label goods accounted for 30 per cent of sales at Canadian Tire stores, up from 20 per cent in 2012, and 70 per cent of sales at Marks.
The retailer's executives had said in the past that they were mulling the international potential of some of their house brands, which include Motomaster, Noma, and Paderno, but they did not reveal what sales channels they were considering.
The acquisition could see the retailer introduce new products to Helly Hansen and bring Canadian Tire's proprietary brands to other parts of the world through Helly Hansen's existing global distribution network.
"Traditionally if we launched a product in Canada we would have registered a trademark in Canada," said Wetmore, who returned to helm the company two years ago after previously serving as CEO from 2009 to 2014.
BMO Capital Markets analyst Peter Sklar believes the brand aligns well with Canadian Tire's three main banners, including Sport Chek and Mark's, but deemed the transaction "expensive," given its ratio of 18 to 20 times enterprise value to operating earnings on a trailing basis, compared with Canadian Tire's own valuation of ten times within the same measure.
"While the growth may justify the valuation, we believe that managing a high-end, high-growth, international brand represents a shift in strategy for Canadian Tire, and introduces all the associated uncertainties," Sklar wrote in a note to clients on Thursday, noting that it will likely be several years before Canadian Tire begins wholesale international distribution of its existing house brands.
Wetmore noted that the company's acquisition of Forzani made good strategic sense at the time and the investment has paid off, but the company was required to winnow down 17 separate store banners and remodel stores under its top banners, a lengthy and capital intensive effort.
Canadian Tire also reported Thursday that net income fell 8 per cent to $99.1 million, or $1.18 per share, as expenses rose 7.8 per cent in the three month period ended March 31. Excluding one-time items, the company earned $1.37 per share, a penny below analysts' average estimate, according to Thomson Reuters. Same-store sales were robust, rising 5.2 per cent, and overall revenue climbed 3.4 per cent to $2.81 billion.


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Finding Favour to Release First Full Album "Reborn" June 23
Early Pre-orders for New Project Begins April 7 on iTunes
NEWS SOURCE: Bozeman Media
Nashville, Tenn. (April 07, 2015) ---- Gotee Record's Finding Favour, is scheduled to release their first full album, Reborn, June 23, 2015. Produced by Casey Brown (Love & the Outcome, All Things New), the new project shows the maturity and growth of Finding Favour since they first signed with Gotee Records in 2012. Reborn features 10 new songs that were co-written by the group, along with a reprise of their Top 25 National Christian Audience chart hit, "Say Amen." The first radio single from the album is the anthem ballad, "Cast My Cares," that is currently going for adds at AC and Hot AC/CHR radio, but receiving early airplay at KLJY-JoyFM/St. Louis, WVFJ- JoyFM/Atlanta, WCIE-JoyFM/Tampa, FL and PulseFM/South Bend, IN.
For those fans who can't wait to hear the new record, pre-orders for Reborn will also begin today on iTunes (http://itun.es/us/t75v6). Every person who makes an early purchase of the album will receive three songs instantly from the project, "Refuge," the title track "Reborn," and "Cast My Cares." Those songs are also available today at all other digital outlets. Lyric videos for the songs "Refuge," and the title track can be viewed at www.findingfavour.com.
Finding Favour fans are being treated to early performances of the new music as the band is featured on the current 42-city Newsboys We Believe God's Not Dead Tour that started in February and ends May 9, 2015. The band will unveil some of the new songs on an upcoming appearance for LeSea Broadcasting's Live From Studio B.
For additional updates on Finding Favour please visit online, www.findingfavour.com, www.facebook.com/findingfavour, www.twitter.com/findingfavour, www.instagram.com/findingfavour.
About Finding Favour
Finding Favour was formed in 2005 in Lyons, GA and consists of band members, Blake NeeSmith (vocals), Allen Dukes (guitar), Dustin Daniels (bass guitar) and Josh Duckworth (drums). The band signed with Gotee Records in 2012 and released their first studio EP, Finding Favour EP, in March 2013. The first two singles, "Slip On By" and "Shake The World" reached the Top 30 on Billboard's Christian Singles chart. "Slip On By" also became a Top 40 Country radio hit for country artist, Austin Webb. Finding Favour's single, "Say Amen," released in 2014 and reached Top 25 on Billboard's NCA chart. The group is poised to release their first full album, Reborn, June 23, 2015. The first single is "Cast My Cares" that has a radio add date of April 10.
ABOUT GOTEE RECORDS
In 1992, a production team of three talented guys with diverse tastes shared a love for music. Producers Joey Elwood and Todd Collins, along with Grammy-winning artist TobyMac, launched Gotee Records in 1994 after unsuccessfully finding a label deal for the R&B trio, Out of Eden. With a steady focus on artistry, the new label expanded to reflect the diverse interests of its founders. Within 12 months, Christafari, GRITS, and Johnny Q. Public were signed, easily representing four different music categories; R&B, reggae, rap and rock. In the 20 years since Gotee's founding as a record label, it has launched the careers of Relient K, Jennifer Knapp, Sonicflood and more recently, Jamie Grace, Capital Kings, Finding Favour, Ryan Stevenson and Morgan Harper Nichols. The present day in the Gotee story is much like the label's early days. Through all the changes in a tumultuous music industry, the boutique label's independent spirit is maintained through a steady focus on artist development and diversity.
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For more info on Finding Favour visit the JFH Artists Database.


Members of the Quantum Photonics Lab including its director Professor Dirk Englund and EECS graduate student Hannah Clevenson have developed a new, ultrasensitive magnetic-field detector that is 1,000 times more energy-efficient than its predecessors. This work, which could lead to miniaturized, battery-powered devices for medical and materials imaging, contraband detection, and geological exploration, is reported in the latest issue of Nature Physics.
Read more in the April 6, 2015 MIT News Office article by Larry Hardesty titled "Better sensors for medical imaging, contraband detection - Magnetic-field detector is 1,000 times more efficient than its predecessors," also posted below.