Short range optical data links are experiencing bandwidth limitations making it very challenging to cope with the growing data transmission capacity demands. Parallel optics appears as a valid short-term solution. It is, however, not a viable solution in the long-term because of its complex optical packaging. Therefore, increasing effort is now put into the possibility of exploiting higher order modulation formats with increased spectral efficiency and reduced optical transceiver complexity. As these type of links are based on intensity modulation and direct detection, modulation formats relying on optical coherent detection can not be straight forwardly employed. As an alternative and more viable solution, this paper proposes the use of carrierless amplitude phase (CAP) in a novel multiband approach (MultiCAP) that achieves record spectral efficiency, increases tolerance towards dispersion and bandwidth limitations, and reduces the complexity of the transceiver. We report on numerical simulations and experimental demonstrations with capacity beyond 100 Gb/s transmission using a single externally modulated laser. In addition, an extensive comparison with conventional CAP is also provided. The reported experiment uses MultiCAP to achieve 102.4 Gb/s transmission, corresponding to a data payload of 95.2 Gb/s error free transmission by using a 7% forward error correction code. The signal is successfully recovered after 15 km of standard single mode fiber in a system limited by a 3 dB bandwidth of 14 GHz.

There is a clinical overlap between classic Ehlers-Danlos syndrome (cEDS) and benign joint hypermobility syndrome (BJHS), with hypermobility as the main symptom. The purpose of this study was to investigate the role of type V collagen mutations and tendon pathology in these 2 syndromes. In patients (cEDS, n‫;7؍‬ BJHS, n‫)8؍‬ and controls (Ctrl, n‫,)8؍‬ we measured patellar tendon ultrastructure (transmission electron microscopy), dimensions (magnetic resonance imaging), and biomechanical properties (force and ultrasonographic measurements during a ramped isometric knee extension). Mutation analyses (COL5A1 and COL5A2) were performed in the patients. COL5A1 mutations were found in 3 of 4 of the patients with cEDS. Patellar tendon dimensions were similar between the groups, but large, irregular collagen fibrils were in 4 of 5 patients with cEDS. In the cEDS group, tendon stiffness and Young's modulus were reduced to ϳ50% of that in BJHS and Ctrl groups (P<0.05). The nonhypermobile, healthy controls were matched with the patients in age, sex, body weight, and physical activity, to compare outcomes. COL5A1 mutations led to structural tendon pathology and low tendon stiffness in cEDS, explaining the patients' hypermobility, whereas no tendon pathology was found that explained the hypermobility in BJHS. Ehlers-Danlos syndrome (EDS) comprises a group of heritable connective tissue disorders characterized by joint hypermobility and tissue fragility (1, 2). The current diagnostic criteria, established in 1997 (1), subdivide EDS into 6 major types, with the 2 most common being the hypermobile (hEDS) and the classic (cEDS) types. The major diagnostic criteria for cEDS are joint hypermobility, skin hyperextensibility, and widened atrophic scarring (1). Mutations in the collagen type V-encoding genes COL5A1 and COL5A2 are the primary cause of cEDS; mutations in these genes have been demonstrated in Ͼ 90% of patients with cEDS who fulfilled the 3 major criteria (3). Joint hypermobility is also a major diagnostic criterion in hEDS, together with milder skin involvement and a positive family history. However, in contrast to cEDS, the causative gene is unknown and unmapped (4). Therefore, hEDS is a clinical diagnosis that can be difficult to distinguish from benign joint hypermobility syndrome (BJHS) because of the considerable overlap of clinical signs in the criteria sets (1, 5). In fact, some researchers argue that hEDS and BJHS are the same disease (4, 6). In the current study, we wanted to investigate patients with cEDS and compare them with those with BJHS with hypermobility and no skin involvement.

Background: The mechanism behind the cardiovascular protection observed with human GLP-1 RA (glucagon-like peptide-1 receptor agonists) in type 2 diabetes is unknown. We hypothesized that treatment with the GLP-1 RA liraglutide had a positive effect on vascular inflammation. Methods: LIRAFLAME (Effect of liraglutide on vascular inflammation in type-2 diabetes: A randomized, placebocontrolled, double-blind, parallel clinical PET/CT trial) was a double-blind, randomized controlled trial performed at a single university hospital clinic in Denmark. Patients with type 2 diabetes were via computer-generated randomization list assigned (1:1) liraglutide up to 1.8 mg or placebo once daily for 26 weeks. The primary end point was change in vascular inflammation over 26 weeks assessed by [ 18 F]-fluorodeoxyglucose positron emission tomography/computed tomography. Analyses were based on intention-to-treat. Key secondary outcomes included change in other indices of atherosclerosis. Results: Between October 26, 2017, and August 16, 2019, 147 patients were screened and 102 were randomly assigned to liraglutide (n=51) or placebo (n=51) and 99 (97%) completed the trial. Change in the [ 18 F]-fluorodeoxyglucose positron emission tomography measure of vascular inflammation (active-segment target-to-background ratio) did not differ between treatment groups: change from baseline to 26 weeks was −0.04 (95% CI, −0.17 to 0.08) in the liraglutide group compared with −0.09 (−0.19 to 0.01) in the placebo group (mean difference, 0.05 [95% CI, −0.11 to 0.21], P =0.53). Secondary analyses restricted to [ 18 F]-fluorodeoxyglucose positron emission tomography of the carotid arteries as well as other indices of atherosclerosis confirmed the primary result. We performed an explorative analysis of interaction between treatment group and history of cardiovascular disease ( P =0.052). Conclusions: In this low to moderate risk population with type 2 diabetes, liraglutide did not change vascular inflammation assessed as [ 18 F]-fluorodeoxyglucose uptake compared with placebo. An explorative analysis indicated a possible effect in persons with history of cardiovascular disease, in line with current guidelines where liraglutide is recommended to patients with history of cardiovascular disease. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03449654.

Background: Tesofensine (TE) is a new drug producing twice the weight loss in obese individuals as seen with currently marketed drugs. It inhibits the presynaptic reuptake of the neurotransmitters noradrenaline, dopamine and serotonin, and is thought to enhance the neurotransmission of all three monoamines. The mechanisms by which it produces weight loss in humans are unresolved. Objective: The aim of this study is to investigate the mechanism(s) behind weight reduction by measuring energy expenditure and appetite sensations in overweight and obese individuals. Design: Thirty-two healthy, overweight or moderately obese men were treated with 2.0 mg TE daily for 7 days followed by an additional 7 days with 1.0 mg TE daily or corresponding placebo (PL) in a randomized, controlled trial. They were instructed to maintain habitual food intake and physical activity throughout. Twenty-four-hour energy expenditure (24-h EE), fat oxidation and spontaneous physical activity were measured in a respiration chamber before and after treatment. Body composition was assessed by dual-energy X-ray absorption and appetite was evaluated by visual analogue scales in conjunction with a standardized dinner. Results: Despite efforts to keep body weight and composition constant, TE induced a 1.8 kg weight loss above PL after 2 weeks' treatment (Po0.0001). TE also induced higher ratings of satiety and fullness and concomitantly lower prospective food intake than placebo. No significant effect of TE on total 24-h EE could be demonstrated compared with PL, but higher energy expenditure was observed during the night period (4.6%; Po0.05) when adjusted for changes in body composition. Furthermore, TE increased 24-h fat oxidation as compared with PL (18 g; Po0.001). Conclusion: TE has a pronounced effect on appetite sensations and a slight effect on energy expenditure at nightFboth effects can contribute to the strong weight-reducing effect of TE.