Education is essential to improve nurses' ability to give patients the holistic care they deserve. Studies are needed to understand fully what mechanisms underlie the barriers that clearly prevent nurses from addressing patients' sexuality.

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This study shows that single-injection NASHA was well tolerated and non-inferior to MPA at 12 weeks. The benefit of NASHA was maintained to 26 weeks while that of MPA declined. An injection of NASHA at 26 weeks conferred long-term improvements without increased sensitivity or risk of complications. STUDY IDENTIFIER: NCT01209364 (www.clinicaltrials.gov).

In type 1 diabetes (T1D), there is a specific destruction of the insulin secreting pancreatic ␤ cell. Although the exact molecular mechanisms underlying ␤ cell destruction are not known, sera from T1D patients have been shown to promote Ca 2؉ -induced apoptosis. We now demonstrate that apolipoprotein CIII (apoCIII) is increased in serum from T1D patients and that this serum factor both induces increased cytoplasmic free intracellular Ca 2؉ R esearch over the last 30 years has established that type 1 diabetes (T1D) is an autoimmune disease, but the mechanisms͞events that trigger the initiation and progression of the disease are still not identified. Genetic, immunological, and environmental factors are involved in the pathogenesis of T1D and most likely the events involved differ between different patients. Voltage-gated L-type Ca 2ϩ channels have an important physiological role in pancreatic ␤ cell signal transduction (1). These channels constitute an essential link between transient changes in membrane potential and insulin release. Changes in cytoplasmic free intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) in the ␤ cell are associated with the activation of a spectrum of intracellular signals and are strictly regulated because prolonged high [Ca 2ϩ ] i is harmful to the cells. Sera from newly diagnosed T1D patients have been shown to increase the activity of voltage-gated L-type Ca 2ϩ channels in ␤ cells, resulting in increased [Ca 2ϩ ] i upon depolarization and ␤ cell apoptosis, effects that can be prevented by Ca 2ϩ channel blockers (2). The key question has been what factor in T1D serum that is responsible for the changes in [Ca 2ϩ ] i . In the present study, we have revealed the identity of a key factor in T1D sera that increases [Ca 2ϩ ] i as well as promotes apoptosis and found it to correspond to apolipoprotein CIII (apoCIII). The fact that not all sera from T1D patients affected [Ca 2ϩ ] i indicates that T1D is not caused by a single factor like apoCIII, which is in agreement with clinical observations, suggesting that different factors can act in concert with the autoimmune abnormalities resulting in ␤ cell destruction. MethodsMedia. The basal medium used both for isolation of cells and for experiments was a Hepes buffer (pH 7.4), containing: 125 mM NaCl, 5.9 mM KCl, 1.3 mM CaCl 2 , 1.2 mM MgCl 2 , and 25 mM Hepes. BSA was added to the medium at a concentration of 1 mg͞ml. For cell culture, RPMI medium 1640 was supplemented with 100 g͞ml streptomycin, 100 units of penicillin, and 10% FCS, normal human, or diabetic serum.Preparation of Cells. Adult mice from a local colony (3) were starved overnight. Pancreatic islets were isolated by a collagenase technique, and cell suspensions were prepared as described (4, 5). Cells were seeded onto glass coverslips and cultured at 37°C in a humidified atmosphere of 5% CO 2 in air.Preparation and Purification of Sera. Sera from T1D patients and control subjects were collected, identically sterile-processed, and stored frozen at Ϫ20°C until used. The sera we...