Is Perception Reality? Improving Agricultural Messages by Discovering How Consumers Perceive Messages

This study assessed how consumers interpret agricultural messages typically found on commodity organizations’ websites in Florida. Four focus groups were held in the fall of 2010. Results indicate that the participants found most of the messages to be unfavorable, rather than favorable. Additionally, the conclusions made by the participants were explained as being influenced by previous experience, corporate influence, history, the creation of mental images, lack of supporting information, and media influence. Participants provided researchers with suggestions to improve the messages and create a more favorable response from consumers. Further research should be done in this area to continue to improve the effectiveness of agricultural messages. In addition, this research should be replicated in other geographic locations. The implications of this study provide valuable information for agricultural communicators, commodity organizations, industry professionals, and those wanting to tell the story of agriculture

A Picture is Worth a Thousand Words: Consumer Perceptions of Agricultural Images

Individuals interpret agricultural images differently according to the direct or cultural meanings they associate with the image, as well as the perspective through which they view the image. In addition, perceptions of agricultural images are commonly influenced by stereotypes. As agricultural communicators, it is important to understand the perceptions consumers have about agricultural images. Understanding these perceptions can allow communicators to use images in their communication that will promote favorable perceptions of the industry. To better understand consumers’ perceptions of agricultural images, this study asked consumers about their perceptions using focus group methodology. Four focus groups were completed with a total of 36 participants. The results indicated that elements of semiotics and perception theory were evident in the participants’ discussion. Thus, these theories combined with the results provide valuable information in regard to selecting images for communication that will create favorable responses among consumers

Minimum connected transversals in graphs: New hardness results and tractable cases using the price of connectivity

We perform a systematic study in the computational complexity of the connected variant of three related transversal problems: Vertex Cover, Feedback Vertex Set, and Odd Cycle Transversal. Just like their original counterparts, these variants are NP-complete for general graphs. A graph G is H-free for some graph H if G contains no induced subgraph isomorphic to H. It is known that Connected Vertex Cover is NP-complete even for H-free graphs if H contains a claw or a cycle. We show that the two other connected variants also remain NP-complete if H contains a cycle or claw. In the remaining case H is a linear forest. We show that Connected Vertex Cover, Connected Feedback Vertex Set, and Connected Odd Cycle Transversal are polynomial-time solvable for sP2-free graphs for every constant s≥1. For proving these results we use known results on the price of connectivity for vertex cover, feedback vertex set, and odd cycle transversal. This is the first application of the price of connectivity that results in polynomial-time algorithms

Looking back and beyond the 2017 diagnostic criteria for hypermobile Ehlers-Danlos syndrome: A retrospective cross-sectional study from an Italian reference center

The most common conditions with symptomatic joint hypermobility are hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD). Diagnosing these overlapping connective tissue disorders remains challenging due to the lack of established causes and reliable diagnostic tests. hEDS is diagnosed applying the 2017 diagnostic criteria, and patients with symptomatic joint hypermobility but not fulfilling these criteria are labeled as HSD, which is not officially recognized by all healthcare systems. The 2017 criteria were introduced to improve diagnostic specificity but have faced criticism for being too stringent and failing to adequately capture the multisystemic involvement of hEDS. Herein, we retrospectively evaluated 327 patients from 213 families with a prior diagnosis of hypermobility type EDS or joint hypermobility syndrome based on Villefranche and Brighton criteria, to assess the effectiveness of the 2017 criteria in distinguishing between hEDS and HSD and document the frequencies of extra-articular manifestations. Based on our findings, we propose that the 2017 criteria should be made less stringent to include a greater number of patients who are currently encompassed within the HSD category. This will lead to improved diagnostic accuracy and enhanced patient care by properly capturing the diverse range of symptoms and manifestations present within the hEDS/HSD spectrum

Deciphering disease signatures and molecular targets in vascular Ehlers-Danlos syndrome through transcriptome and miRNome sequencing of dermal fibroblasts

Vascular Ehlers-Danlos syndrome (vEDS) is a severe connective tissue disorder caused by dominant mutations in the COL3A1 gene encoding type III collagen (COLLIII). COLLIII is primarily found in blood vessels and hollow organs, and its deficiency leads to soft connective tissues fragility, resulting in life-threatening arterial and organ ruptures. There are no current targeted therapies available. Although the disease usually results from COLLIII misfolding due to triple helix structure disruption, the underlying pathomechanisms are largely unknown. To address this knowledge gap, we performed a comprehensive transcriptome analysis using RNA- and miRNA-seq on a large cohort of dermal fibroblasts from vEDS patients and healthy donors. Our investigation revealed an intricate interplay between proteostasis abnormalities, inefficient endoplasmic reticulum stress response, and compromised autophagy, which may significantly impact the molecular pathology. We also present the first detailed miRNAs expression profile in patient cells, demonstrating that several aberrantly expressed miRNAs can disrupt critical cellular functions involved in vEDS pathophysiology, such as autophagy, proteostasis, and mTOR signaling. Target prediction and regulatory networks analyses suggested potential interactions among miRNAs, lncRNAs, and candidate target genes linked to extracellular matrix organization and autophagy-lysosome pathway. Our results highlight the importance of understanding the functional role of ncRNAs in vEDS pathogenesis, shedding light on possible miRNAs and lncRNAs signatures and their functional implications for dysregulated pathways related to disease. Deciphering this complex molecular network of RNA interactions may yield additional evidence for potential disease biomolecules and targets, assisting in the design of effective patient treatment strategies

Clinical and molecular characterization of 40 patients with classic Ehlers--Danlos syndrome: identification of 18 COL5A1 and 2 COL5A2 novel mutations.

Classic Ehlers-Danlos syndrome (cEDS) is a rare autosomal dominant connective tissue disorder that is primarily characterized by skin hyperextensibility, abnormal wound healing/atrophic scars, and joint hypermobility. A recent study demonstrated that more than 90% of patients who satisfy all of these major criteria harbor a type V collagen (COLLV) defect. This cohort included 40 patients with cEDS who were clinically diagnosed according to the Villefranche nosology. The flowchart that was adopted for mutation detection consisted of sequencing the COL5A1 gene and, if no mutation was detected, COL5A2 analysis. In the negative patients the presence of large genomic rearrangements in COL5A1 was investigated using MLPA, and positive results were confirmed via SNP-array analysis. We report the clinical and molecular characterization of 40 patients from 28 families, consisting of 14 pediatric patients and 26 adults. A family history of cEDS was present in 9 patients. The majority of the patients fulfilled all the major diagnostic criteria for cEDS; atrophic scars were absent in 2 females, skin hyperextensibility was not detected in a male and joint hypermobility was negative in 8 patients (20% of the entire cohort). Wide inter- and intra-familial phenotypic heterogeneity was observed. We identified causal mutations with a detection rate of approximately 93%. In 25/28 probands, COL5A1 or COL5A2 mutations were detected. Twenty-one mutations were in the COL5A1 gene, 18 of which were novel (2 recurrent). Of these, 16 mutations led to nonsense-mediated mRNA decay (NMD) and to COLLV haploinsufficiency and 5 mutations were structural. Two novel COL5A2 splice mutations were detected in patients with the most severe phenotypes. The known p. (Arg312Cys) mutation in the COL1A1 gene was identified in one patient with vascular-like cEDS. Our findings highlight that the three major criteria for cEDS are useful and sufficient for cEDS clinical diagnosis in the large majority of the patients. The borderline patients for whom these criteria fail can be diagnosed when minor signs of connective tissue diseases and family history are present and when genetic testing reveals a defect in COLLV. Our data also confirm that COL5A1 and COL5A2 are the major, if not the only, genes involved in cEDS

Long term outcome in children affected by absence epilepsy with onset before the age of three years.

OBJECTIVE: The goal of this study was to define the long-term outcome of absence epilepsy presenting before the age of 3 years. METHODS: We retrospectively studied the medical records of 40 children from eight neuropediatric centers in Italy with respect to the personal and family histories of epilepsy or febrile seizures, time of follow-up, cognitive functions, treatment, and outcome. RESULTS: Forty patients were enrolled in this study. They all fulfilled the criteria for absence epilepsy with 3-Hz spike-wave complexes on the EEG, normal neurological examination, and no other seizures types. Seizure onset occurred between 24.1 and 36.0 months. There was a family history of epilepsy in 28%, and of febrile seizures in 13%. Thirty-three patients were treated with valproic acid (VPA), mostly used in monotherapy (26 patients) or in association with ethosuximide. At final follow-up, 33 patients were seizure free and 29 had normal EEGs. Thirty-four patients had a normal intelligence quotient (IQ), whereas 6 had a decreased IQ, mainly associated with poor control of seizures. CONCLUSION: In our series, absence seizures presenting before the age of 3 appeared to have quite a good long-term clinical prognosis; the neuropsychological outcome was comparable to that of childhood epilepsy presenting after 3 years of age

Asymmetric Dimethylarginine in Obese Youth: Relationship with 24-hour Ambulatory Blood Pressure

The incidence of amputation worldwide is 1.5 per 1000 habitants and the total number of amputees is about 10 million..

Short-term efficacy and safety of betamethasone valerate 2.25 mg medicated plaster in patients with chronic lateral epicondylitis: Results of a randomised, double blind, placebo-controlled study

Background. This placebo-controlled, double-blind study evaluated the short-term effects of betamethasone valerate (BMV) 2.25mg medicated plaster in patients with chronic lateral elbow tendinopathy (LET). Methods. Adult outpatients with LET and on-movement pain intensity ≥50 mm at a 0-100mm visual analogue scale (VAS) were randomised to receive BMV (N=101) or placebo (N=98), 12 hours/day for 4 weeks. Pain decrease from baseline to Day 28 was the primary endpoint. Other endpoints were: patient-rated tennis elbow evaluation (PRTEE), use of rescue paracetamol, tolerability at the application site. Results. Decrease in mean pain VAS from baseline to Day 28 was significantly higher with BMV vs. placebo: the difference between groups (intent-to-treat) was-8.57 mm (95% CI:-16.19 to-0.95 mm; p=0.028). Higher pain decreases in the BMV group over placebo were reported weekly during each control visit and daily in patients’ measurements on diaries. Treatment with BMV also led to higher decreases vs. placebo in PRTEE total, pain and functional disability score. Use of paracetamol was minimal. BMV plaster was well tolerated for general and local adverse events. Conclusions. BMV 2.25mg plaster was superior to placebo and well tolerated in patients with painful chronic LET

Arterial Tortuosity Syndrome: a vitamin C compartmentation disease?

Arterial tortuosity syndrome (ATS, MIM #208050) is a rare autosomal recessive connective tissue disorder characterized by tortuosity and elongation of the large and medium-sized arteries and a propensity towards aneurysm formation and vascular dissection. ATS is caused by mutations in SLC2A10 encoding the facilitative glucose transporter 10 (GLUT10), whose role in the ATS pathogenesis remains still controversial. We recently showed that GLUT10 deficiency causes the dysregulation of several genes/proteins involved in TGFβ signaling, extracellular matrix architecture and pathways that control oxidative stress response. GLUT10 should be located intracellularly; however, neither the exact localization, i.e., nuclear membrane, mitochondria, or endoplasmic reticulum (ER), nor the transported substances, i.e., glucose or dehydroascorbic acid (DAA), have been demonstrated. Here, we demonstrate that GLUT10 facilitates DAA uptake into the endomembranes and, in particular, into ER. GLUT10 produced by in vitro translation and incorporated into proteoliposomes efficiently transports DAA. Silencing of GLUT10 in hTERT immortalized human fibroblasts compromised DAA transport activity through the endomembranes. Similarly, in plasma membrane-permeabilized ATS fibroblasts a huge decrease in DAA transport was observed and the stable re-expression of GLUT10 restored the impaired DAA transport activity. Immunocytochemistry of human control fibroblasts showed a perinuclear abundance of GLUT10. Immunoblotting of subcellular fractions from human control fibroblasts revealed that GLUT10 was principally present in the microsomal fraction, containing ER-derived vesicles, as showed by the presence of the specific ER marker proteins GRP78 and GRP94, and by the almost complete absence of mitochondrial and cytoplasmic markers, VDAC1, cyclophilin D, and GAPDH, respectively. Transient expression of V5-tagged GLUT10 in ATS patients’ fibroblasts and co-localization experiments with the specific ER marker PDI definitely confirmed the ER localization of GLUT10. Overall, the present findings demonstrate that GLUT10 facilitates DAA uptake into the ER lumen and likely to the nucleoplasm through the nuclear envelope, which is a subdomain of the ER. Our findings support both “antioxidant-” and “enzyme cofactor-” models of a vitamin C-related pathology. Indeed, AA acts as an antioxidant/electron acceptor protecting against oxidative stress-induced cellular damage by scavenging free radicals also during the process of oxidative protein folding. Furthermore, AA is an essential cofactor for α-ketoglutarate-dependent dioxygenases, such as prolyl and lysyl hydroxylases inside the ER and for ten-eleven translocation demethylases and the Jumonji protein family present in the nucleus. Thus, shortage of AA in the lumenal compartments of the secretory pathway and in the nucleoplasm can depress the production of extracellular matrix proteins at both post-translational and epigenetic levels