Bespoke is a relatively old school word we have started to adopt into our new school designs . . . but what does it mean exactly?
On a trip to London last year, Celina returned inspired, invigorated and with this word she wanted to bring home . . . bespoke. Loving the idea that like a tailored suit; our made-to-order, one-off, custom-made furniture could adopt a more mature description, fitting for the products we produce.
Bespoke is an adjective for anything commissioned to a particular specification. It may be altered or tailored to the customs, tastes or usage of an individual purchaser. Although the term is more prevalent in British English, American English has begun to adopt the term replacing “custom” in many made to suit companies.
Recently we created a bespoke sofa for the Address design show curated by the talented Kate Duncan who’s vision was to bring together local creators and furniture builders under one roof. This sofa coined the “Bossalina”, is a great example of what a piece of bespoke furniture can be. Celina used her keen understanding of furniture design to keep in mind proportion and comfort, using the golden ratio as a guide. This sofa can be adjusted, altered and tailored to suit any space. Modular sections can be added to create large sectionals and mirrored seating arrangements. We happily adopt this term and look forward to sharing with you some of the exceptional and unique bespoke designs we have been working on this year, for you and for our amazing and talented designers.
Here are (albeit a late post) some photos from the Address show!
Exposed walnut shelf, natural latex foam and feather cushions. Soft and durable upholstery.
Never one for a dull moment, Celina quickly stuffs the last cushion on site!
Gorgeous wares featuring: Propellor lighting, table by Nicholas Purcell, and hand crafted rug by Zoe Luyendijk
Perfectly crafted goods; ceramics by Heyday, votives by Woodlot
Lighting by Propellor, credenza by Nicholas Purcell
Slipped in like a glove; local natural driftwood featured inset
Can we sleep here please?! Lighting by Propellor, art work by Christine Breakell-Lee
The stuff dreams are made of: credenza by the talented Nicholas Purcell
The post Bespoke Furniture; what does it mean? appeared first on Fabulous Furnishings Upholstery & Blinds.
Kapche, who lives with type 1 diabetes, argued he could not be denied a job simply because he has diabetes. In 2002, a federal circuit court ruled in Kapche’s favor.
A door was opened.
The need for education about the legal requirements of the ADA was not limited to employers. Around the same time, some large national day care chains denied enrollment to young children with diabetes, believing they couldn’t accommodate their daily diabetes care needs.
At the time, multiple daily injections of insulin was not the standard of care for children with diabetes, so the required care was limited to checking blood glucose levels and treating hypoglycemia with juice. Still, there was great resistance to accommodating children with diabetes, and eventually the Department of Justice stepped in to enforce the law. Another door was opened.
When Kapche and the young children attending these day care programs won their cases, it was because the ADA gave them a way to enforce their rights if they were treated unfairly because of their diabetes. Between 1990 and 1999, many doors that had for years been closed to people with diabetes were pushed open. No longer was it acceptable to keep a worker with diabetes out of a job because of fears about safety. No more could schools and other programs refuse to let people with diabetes participate.
Soon, though, this progress was halted by a series of court decisions. Over time the Supreme Court narrowed the scope of what was considered a disability under the law. Then, the lower courts followed suit.
Starting in 1999 and continuing for the next 10 years, the discrimination cases of people with diabetes were routinely tossed out of court. They were told their diabetes was not a disability under the law—with the maddening result that they could be fired for diabetes and could not challenge it.
Doors started closing once again for people with diabetes. Told their use of insulin or other medications “mitigated,” or lessened, their diabetes, they were deemed not sick enough to be covered by the law that provided the protections against the very treatment they were in court to protest.
In 2008, after years of work by advocates including the American Diabetes Association, Congress recognized the problem with the law and unanimously voted to amend it to restore its original intent. People with diabetes benefitted greatly from the ADA Amendments Act. The new law made clear that diabetes is a disability and people with diabetes are afforded its full protections and remedies.
In recent years the Americans with Disabilities Act has helped childcare providers learn how to accommodate children with diabetes. It has opened up public places such as amusement parks and courthouses and concert venues to people with diabetes. The law has also helped people make inroads in careers as firefighters, law enforcement officers, bus and truck drivers and boat captains, just to name a few. These jobs were once thought off-limits to people with chronic diseases such as diabetes.
So how do people with diabetes feel about the law turning 25? Just ask Jeff Kapche, who now lives in Katy, Texas. He faced discrimination a second time when he fought for the right to be hired as an FBI special agent based on his qualifications, not his diabetes: “Every one of us should be able to follow their dreams, not find doors slammed shut because of a disability. As we celebrate 25 years of the ADA, let’s commit to working even harder to break down barriers for people with diabetes. Our children deserve it.”
Or take it from Mike Greene, a lawyer in Portland, Ore., who also lives with type 1 diabetes. As chair of the Association’s national Board of Directors in the early 1990s, he had a vision for ending discrimination. “Today people with diabetes have many more opportunities because of the Americans with Disabilities Act and its amendments. People with diabetes are finally beginning to achieve what we have dreamed about for decades: an equal opportunity to fully participate in employment and education.”
Kathy Butler, JD, Chair, Legal Advocacy Subcommittee, American Diabetes Association
Katie Hathaway, JD, Managing Director, Legal Advocacy, American Diabetes Association
Administration of lipids into the upper intestine of rats has been shown to acutely decrease endogenous glucose production (EGP) in the preabsorptive state, postulated to act through a gut-brain-liver axis involving accumulation of long-chain fatty acyl-CoA, release of cholecystokinin, and subsequent neuronal signaling. It remains unknown, however, whether a similar gut-brain-liver axis is operative in humans. Here, we infused 20% Intralipid (a synthetic lipid emulsion) or saline intraduodenally for 90 min at 30 mL/h, 4 to 6 weeks apart, in random order, in nine healthy men. EGP was assessed under pancreatic clamp conditions with stable isotope enrichment techniques. Under these experimental conditions, intraduodenal infusion of Intralipid, compared with saline, did not affect plasma glucose concentration or EGP throughout the study period. We conclude that Intralipid infusion into the duodenum at this rate does not elicit detectable effects on glucose homeostasis or EGP in healthy men, which may reflect important interspecies differences between rodents and humans with respect to the putative gut-brain-liver axis.
Elevated sympathetic nerve activity (SNA) coupled with dysregulated β-adrenoceptor (β-AR) signaling is postulated as a major driving force for cardiac dysfunction in patients with type 2 diabetes; however, cardiac SNA has never been assessed directly in diabetes. Our aim was to measure the sympathetic input to and the β-AR responsiveness of the heart in the type 2 diabetic heart. In vivo recording of SNA of the left efferent cardiac sympathetic branch of the stellate ganglion in Zucker diabetic fatty rats revealed an elevated resting cardiac SNA and doubled firing rate compared with nondiabetic rats. Ex vivo, in isolated denervated hearts, the intrinsic heart rate was markedly reduced. Contractile and relaxation responses to β-AR stimulation with dobutamine were compromised in externally paced diabetic hearts, but not in diabetic hearts allowed to regulate their own heart rate. Protein levels of left ventricular β1-AR and Gs (guanine nucleotide binding protein stimulatory) were reduced, whereas left ventricular and right atrial β2-AR and Gi (guanine nucleotide binding protein inhibitory regulatory) levels were increased. The elevated resting cardiac SNA in type 2 diabetes, combined with the reduced cardiac β-AR responsiveness, suggests that the maintenance of normal cardiovascular function requires elevated cardiac sympathetic input to compensate for changes in the intrinsic properties of the diabetic heart.
Diabetes affects bone marrow (BM) structure and impairs mobilization of stem cells (SCs) into peripheral blood (PB). This amplifies multiorgan complications because BMSCs promote vascular repair. Because diabetes skews macrophage phenotypes and BM macrophages (BMM) prevent SC mobilization, we hypothesized that excess BMM contribute to diabetic SC mobilopathy. We show that patients with diabetes have increased M1 macrophages, whereas diabetic mice have increased CD169+ BMM with SC-retaining activity. Depletion of BMM restored SC mobilization in diabetic mice. We found that CD169 labels M1 macrophages and that conditioned medium (CM) from M1 macrophages, but not from M0 and M2 macrophages, induced chemokine (C-X-C motif) ligand 12 (CXCL12) expression by mesenchymal stem/stromal cells. In silico data mining and in vitro validation identified oncostatin M (OSM) as the soluble mediator contained in M1 CM that induces CXCL12 expression via a mitogen-activated protein kinase kinase-p38-signal transducer and activator of a transcription 3–dependent pathway. In diabetic mice, OSM neutralization prevented CXCL12 induction and improved granulocyte-colony stimulating factor and ischemia-induced mobilization, SC homing to ischemic muscles, and vascular recovery. In patients with diabetes, BM plasma OSM levels were higher and correlated with the BM-to-PB SC ratio. In conclusion, BMM prevent SC mobilization by OSM secretion, and OSM antagonism is a strategy to restore BM function in diabetes, which can translate into protection mediated by BMSCs.
