Miracle-dz/UniFAR-FTUs huggingface dataset:
Genetic Background of Taste Perception, Taste Preferences, and Its Nutritional Implications: A Systematic Review

Background: The rise in nutrition-related morbidity and mortality requires public health intervention programs targeting nutritional behavior. In addition to socio-economical, socio-cultural, psychological determinants, taste is one of the main factors that influence food choices. Differences in taste perception and sensitivity may be explained by genetic variations, therefore the knowledge of the extent to which genetic factors influence the development of individual taste preferences and eating patterns is important for public policy actions addressing nutritional behaviors. Our aim was to review genetic polymorphisms accounting for variability in taste and food preferences to contribute to an improved understanding of development of taste and food preferences. Methods: The electronic databases PubMed, Scopus, and Web of Science were searched using MeSH in PubMed and free text terms for articles published between January 1, 2000 and April 13, 2018. The search strategy was conducted following the PRISMA statement. The quality of the included studies was assessed by the validated Q-Genie tool. Results: Following the PRISMA flowchart, finally 103 articles were included in the review. Among the reviewed studies, 43 were rated to have good quality, 47 were rated to have moderate quality, and 13 were rated to have low quality. The majority of the studies assessed the association of genetic variants with the bitter taste modality, followed by articles analyzing the impact of polymorphisms on sweet and fat preferences. The number of studies investigating the association between umami, salty, and sour taste qualities and genetic polymorphisms was limited. Conclusions: Our findings suggest that a significant association exists between TAS2R38 variants (rs713598, rs1726866, rs10246939) and bitter and sweet taste preference. Other confirmed results are related to rs1761667 (CD36) and fat taste responsiveness. Otherwise further research is essential to confirm results of studies related to genetic variants and individual taste sensitivity. This knowledge may enhance our understanding of the development of individual taste and related food preferences and food choices that will aid the development of tailored public health strategy to reduce nutrition-related disease and morbidity.
Gaming Green: The Educational Potential of Eco – A Digital Simulated Ecosystem

Research into the use of videogames in education is on the rise, and they are cementing their position as part of the modernized, digital classroom. Sustainability education has also become a subject of interest among environmentally minded game developers and understanding the educational impact of such games is rapidly becoming an important field. This study examined the educational potential of the digital simulated ecosystem known as Eco, in order to reveal how playing Eco might promote environmental consciousness surrounding ecosystems. Qualitative data from seven respondents were subjected to a thematic analysis, revealing two main themes that highlight both game-based learning outcomes as well as barriers against learning. The findings indicate that Eco is a viable tool for promoting some aspects of environmental consciousness about ecosystems, and suggestions for future implementation of Eco are provided.
MRI Evaluation of Axonal Remodeling After Combination Treatment With Xiaoshuan Enteric-Coated Capsule and Enriched Environment in Rats After Ischemic Stroke

Xiaoshuan enteric-coated capsule (XSEC) is a compound Chinese medicine widely used for the treatment of ischemic stroke. Enriched environment (EE) is a rehabilitative intervention designed to facilitate physical, cognitive, and social activity after brain injury. This study aimed to assess whether the XSEC and EE combination could provide synergistic efficacy in axonal remodeling compared to that with a single treatment after ischemic stroke using magnetic resonance imaging (MRI) followed by histological analysis. Rats were subjected to permanent middle cerebral artery occlusion and treated with XSEC and EE alone or in combination for 30 days. T2-weighted imaging and diffusion tensor imaging (DTI) were performed to examine the infarct volume and axonal remodeling, respectively. The co-localization of Ki67 with NG2 or CNPase was examined by immunofluorescence staining to assess oligodendrogenesis. The expressions of growth associated protein-43 (GAP-43) and growth inhibitors NogoA/Nogo receptor (NgR)/RhoA/Rho-associated kinase2 (ROCK2) were measured using western blot and qRT-PCR. The Morris water maze (MWM) was performed to evaluate the cognitive function. MRI and histological measurements indicated XSEC and EE individually benefited axonal reorganization after stroke. Notably, XSEC + EE decreased infarct volume compared with XSEC or EE monotherapy and increased ipsilateral residual volume compared with vehicle group. DTI showed XSEC + EE robustly increased fractional anisotropy while decreased axial diffusivity and radial diffusivity in the injured cortex, striatum, and external capsule. Meanwhile, diffusion tensor tractography revealed XSEC + EE elevated fiber density in the cortex and external capsule and increased fiber length in the striatum and external capsule compared with the monotherapies. These MRI measurements, confirmed by histology, showed that XSEC + EE promoted axonal restoration. Additionally, XSEC + EE amplified oligodendrogenesis, decreased the expressions of NogoA/NgR/RhoA/ROCK2, and increased the expression of GAP-43 in the peri-infarct tissues. In parallel to these findings, rats treated with XSEC + EE exhibited higher cognitive recovery than those treated with XSEC or EE monotherapy, as evidenced by MWM test. Taken together, our data implicated that XSEC + EE exerted synergistic effects on alleviating atrophy and encouraging axonal reorganization partially by promoting oligodendrogenesis and overcoming intrinsic growth-inhibitory signaling, thereby facilitating higher cognitive recovery.
Limited Associations Between 5-HT Receptor Gene Polymorphisms and Treatment Response in Antidepressant Treatment-Free Patients With Depression

Major depressive disorder has become a prominent cause of disability, as lifetime prevalence has increased to ~15% in the Western world. Pharmacological effects of serotonin (5-hydroxytryptamine, 5-HT) are mediated through 5-hydroxytryptamine receptor (5-HTR) binding. Serotonin regulation of amygdala activity is attained through activation of three 5-HT2 family receptor subtypes, 5-HT2A, 5-HT2B, and 5-HT2C. Specifically, HT2A and the HT2C receptors have similar gross cerebral distribution and function, with higher constitutive activity found in HT2C than in HT2A. We investigated the possible association of 5-HTR gene polymorphisms to specific and non-specific antidepressant treatment responses in treatment-free patients in Siberia. 156 patients, aged between 18–70 years and clinically diagnosed with depressive disorders, were treated with antidepressants for 4 weeks. Patients were genotyped for a subset of 29 SNPs from the following 5-HT Receptor genes: HTR1A, HTR1B, HTR2A, HTR2C, HTR3A, HTR3B and HTR6. Primary outcome was measured by differences in Hamilton Depression Rating Scale (ΔHAM‐D 17) scores between baseline/week two, week two/week four and baseline/week four. Univariate linear regression was initially conducted to determine the 5-HTR SNPs to be studied within the multiple linear regression. Multiple linear regression analyses over the three time periods were conducted for ΔHAM‐D 17 with independent factors including: age, gender, depression diagnosis, antidepressant treatment and selected 5-HTR SNPs. We found improved ∆HAM-D 17 in patients taking tricyclic antidepressants (0–4 weeks: B = 4.85, p = 0.0002; 0–2 weeks: B = 3.58, p = 0.002) compared to patients taking SSRIs. Over the course of study, significant associations between 5-HT receptors SNPs and antidepressant response were not identified.
Complex trauma, PTSD and complex PTSD in African refugees

ABSTRACT Background: The introduction of the diagnosis of complex posttraumatic stress disorder (CPTSD) by ICD-11 is a turning point in the field of traumatic stress studies. It’s therefore important to examine the validity of CPTSD in refugee groups exposed to complex trauma (CT) defined as a repeated, prolonged, interpersonal traumatic event. Objective: The objective of this study was to compare DSM-5 and ICD-11 post-traumatic stress disorder diagnoses and to evaluate the discriminant validity of ICD-11 PTSD and CPTSD constructs in a sample of treatment-seeking refugees living in Italy. Method: The study sample included 120 treatment-seeking African refugees living in Italy. All participants were survivors of at least one CT. PTSD and CPTSD diagnoses were assessed according to both DSM-5 and ICD-11 criteria. Results: Findings revealed that 79% of the participants met the DSM-5 criteria for PTSD, 38% for ICD-11 PTSD and 30% for ICD-11 CPTSD. Generally, ICD-11 CPTSD items evidenced strong sensitivity and negative predictive power, low specificity and positive predictive power. Latent class analysis results identified two distinct groups: (1) a PTSD class, (2) a CPTSD class. None of the demographic and trauma-related variables analysed was significantly associated with diagnostic group. On the other hand, the months spent in Italy were significantly associated with PCL-5 score. Conclusions: Findings extend the current evidence base to support the discriminant validity of PTSD and CPTSD amongst refugees exposed to torture and other gross violations of human rights. The results suggest also that, in the post-traumatic phase, the time spent in a ‘safe place’ condition contributes to improve the severity of post-traumatic symptomatology, but neither this variable nor other socio-demographic factors seem to contribute to the emergence of complex PTSD. Further investigations are needed to clarify which specific vulnerability factors influence the development of PTSD or CPTSD in refugees exposed to complex trauma. HIGHLIGHTS • Complex PTSD (CPTSD) diagnosis newly introduced 80 by ICD-11 has been scarcely evaluated with treatmentseeking refugees exposed to complex trauma (CT). • This study evaluated the 85 validity of ICD-11 PTSD and CPTSD in a sample of African refugees exposed to CT and recently arrived in Italy. • Findings indicated that 90 complex trauma leads to CPTSD in a minority of refugees only, approximately in one third of cases. • Latent class analysis results identified two distinct groups PTSD and CPTSD supporting the ICD-11 classification.
Occurrence of Transmembrane Protein 119 in the Retina is Not Restricted to the Microglia: An Immunohistochemical Study

Purpose Recently, a new marker protein for microglial cells in the brain was postulated, transmembrane protein 119 (TMEM119), raising the hope for a new opportunity to reliably and unambiguously detect microglial cells in histologic sections. It was of interest whether TMEM119 also was a reliable microglial marker in the retina. Methods Anti-TMEM119 antibodies of two providers were used to label microglia in the murine retina, and labeling properties were compared to those of antibodies against Iba1 and CD11b. As an example of a pathologic situation, labeling for TMEM119 was also performed in eyes treated by an argon laser as an experimental model for choroidal neovascularization. Results TMEM119 immunoreactivity (IR) was found on microglial cells in the naïve retina. However, specificity and sensitivity of TMEM119 IR varied clearly depending on the source of the antibody, age of the mouse, and location of retinal microglia. After laser treatment, however, microglial cells lost their IR for TMEM119 at the site of the laser spot. Moreover, other cells became positive for TMEM119; for example, Müller cells. Conclusions TMEM119 is a useful marker for the microglia in the brain. However, retinal microglia shows variable IR for TMEM119, and the microglia is not the only cell showing TMEM IR. Therefore, TMEM119 appears not to be applicable as a general marker for the retinal microglia in pathologic situations. Translational Relevance Reliable detection and quantification of microglial cells is of high importance to study disease mechanisms and effects of therapeutic approaches in the retina.
Association Between Sodium Density and Grip Strength Among Older Korean Adults: A Nationwide Cross-Sectional Study Clinical Interventions in Aging

Purpose: Handgrip strength is a key diagnostic criterion for sarcopenia, and sodium is an essential mineral for muscle contraction. We investigated the association between grip strength and sodium intake using sodium density. Patients and methods: A total of 2982 older adults (aged ≥ 65 years) from the 2014 – 2016 Korea National Health and Nutrition Examination Survey were included. Dietary intake was assessed by a 24 hr dietary recall, and grip strength was measured using a digital grip strength dynamometer. Based on the recommendation of the Asian Working Group for Sarcopenia, low grip strength (dynapenia) was de ﬁ ned as <26 kg for men and <18 kg for women. Multivariable logistic regression was performed to estimate the adjusted odds ratio (OR) and 95% con ﬁ dence interval (CI) and to investigate the association between the quartiles of sodium per calorie (mg/1000 kcal; sodium density) and dynapenia. Results: A total of 577 subjects (19.3%) had dynapenia. Subjects in the second quartile of sodium density had the lowest prevalence of dynapenia and were de ﬁ ned as the reference group. Among women, those in the highest quartile of sodium density showed a signi ﬁ cantly higher risk for dynapenia (OR 1.51, 95% CI 1.10 – 2.07). ORs in the ﬁ rst and third quartiles of sodium density were 1.01 (95% CI 0.74 – 1.38) and 1.18 (95% CI 0.89 – 1.58), respectively. However, there was no association between sodium density and dynapenia in men. Conclusion: High sodium density was associated with dynapenia in older women. A balanced diet of minerals is important to preserve muscle strength among older adults.
Title Page

This work or any part thereof has not previously been submitted in any form to the University or to any other body whether for the purpose of assessment, publication or for any other purpose (unless otherwise indicated). Save for any express acknowledgements, references and/or bibliographies cited in the work, I confirm that the intellectual content of the work is the result of my own efforts and no other person. The right of Patrick Ackom Manu to be identified as author of this work is asserted in accordance with ss. 77 and 78 of Copyright, Designs and Patents Act 1988. At this date copyright is owned by the author.
Surveillance of mosquito vectors in Southern Sweden for Flaviviruses and Sindbis virus

ABSTRACT There are three human pathogenic bird-viruses transmitted by Culex mosquitoes in Europe: the alphavirus Sindbis and the flaviviruses West Nile virus and Usutu virus. Cases of Sindbis fever occur in the north while the flaviviruses are reported from southern Europe. In this study, 7933 Culex pipiens/torrentium mosquitoes from southern Sweden were screened by RTqPCR for these viruses. None of the mosquitoes were positive for viral RNA. The importance of mosquito species composition is discussed as a potential explanation to the lack of detection of mosquito-borne viruses in southern Sweden. However, continued surveillance of mosquitoes for Flaviviruses would be valuable as an early warning for public health awareness.
Comparison of Serum Trace Nutrient Concentrations in Epileptics Compared to Healthy Dogs

Idiopathic epilepsy (IE) is a common cause of seizures in dogs. There are several investigations regarding serum concentrations of trace nutrients, including copper, selenium, zinc, manganese, and iron in human epileptics and animal models. However, research of this nature in dogs with epilepsy is lacking. The purpose of this prospective study was to compare serum concentrations of several trace nutrients in healthy dogs to dogs with idiopathic epilepsy. Healthy client-owned dogs (n = 50) and dogs with IE (n = 92) were enrolled and blood samples were collected for trace nutrient analysis. Epileptics were subdivided into three groups: controlled: n = 27, uncontrolled: n = 42, and untreated: n = 23. Serum was evaluated for concentrations of copper, selenium, zinc, cobalt, manganese, molybdenum, and iron using inductively coupled plasma mass spectroscopy. Uncontrolled epileptics had significantly higher manganese concentrations compared to normal dogs (p = 0.007). Untreated epileptics had higher iron levels than the other three groups (p = 0.04). Significantly higher levels of copper (p < 0.0001) were found in controlled and uncontrolled epileptics compared to normal or untreated dogs. Significantly higher levels of molybdenum (p = 0.01) were found in controlled epileptics compared to normal or untreated epileptics. Uncontrolled and controlled epileptics had significantly higher levels of selenium (p = 0.0003) vs. normal dogs, and uncontrolled epileptics had higher levels of zinc (p = 0.0002) than normal and untreated dogs. The significant difference in serum concentrations of several trace nutrients (manganese, selenium, and zinc) may suggest a role for these nutrients in the pathophysiology and/or treatment of epilepsy. Additionally, these results suggest that anti-convulsant therapy may affect copper and molybdenum metabolism.
Folic acid supplementation reduces multigenerational sperm miRNA perturbation induced by in utero environmental contaminant exposure

Abstract Persistent organic pollutants (POPs) can induce epigenetic changes in the paternal germline. Here, we report that folic acid (FA) supplementation mitigates sperm miRNA profiles transgenerationally following in utero paternal exposure to POPs in a rat model. Pregnant founder dams were exposed to an environmentally relevant POPs mixture (or corn oil) ± FA supplementation and subsequent F1–F4 male descendants were not exposed to POPs and were fed the FA control diet. Sperm miRNA profiles of intergenerational (F1, F2) and transgenerational (F3, F4) lineages were investigated using miRNA deep sequencing. Across the F1–F4 generations, sperm miRNA profiles were less perturbed with POPs+FA compared to sperm from descendants of dams treated with POPs alone. POPs exposure consistently led to alteration of three sperm miRNAs across two generations, and similarly one sperm miRNA due to POPs+FA; which was in common with one POPs intergenerationally altered sperm miRNA. The sperm miRNAs that were affected by POPs alone are known to target genes involved in mammary gland and embryonic organ development in F1, sex differentiation and reproductive system development in F2 and cognition and brain development in F3. When the POPs treatment was combined with FA supplementation, however, these same miRNA-targeted gene pathways were perturbed to a lesser extend and only in F1 sperm. These findings suggest that FA partially mitigates the effect of POPs on paternally derived miRNA in a intergenerational manner.
Observational study of inflammatory arthritis treatment by etanercept originator switched to an etanercept biosimilar

Objectives The aim of the study was to assess the safety and efficacy of switching an etanercept originator to an etanercept biosimilar in rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, and ankylosing spondylitis patients. Material and methods In 162 patients etanercept originator treatment had been replaced with the biosimilar (Group 1), and in six patients the biosimilar was initiated as the first biological agent (Group 2). The efficacy and safety of the treatment were monitored at 3–6 months. Results In the majority of patients in Group 1 (n = 138) the etanercept biosimilar was well tolerated, whereas in 24 patients a switch back to the originator was required. The loss of efficacy was confirmed in nine patients using clinical scoring system, and nine patients reported subjective loss of efficacy; 13 patients reported adverse events, most often headache (n = 3) and skin lesions (n = 3). In four patients injection site reactions were present. The adverse events (AE) and/or the loss of the biosimilar efficacy were more commonly observed in women, patients with rheumatoid arthritis (especially in those who did not receive methotrexate), and in patients with a previous history of any other biological treatment. In patients in Group 2 the therapy was effective and no adverse events were observed. Conclusions The etanercept biosimilar seems to be effective and well-tolerated in the majority of patients. Nevertheless, in some cases, switching from the originator to the biosimilar was associated with AEs or loss of efficacy.
Dexmedetomidine ameliorates memory impairment in sleep-deprived mice

ABSTRACT The selective α2-adrenergic receptor agonist dexmedetomidine acts as an analgesic, sedative, and anesthetic adjuvant. The most common consequence of sleep deprivation is memory impairment. We investigated whether dexmedetomidine can counteract memory impairment caused by sleep deprivation and suppress the production of inflammatory factors. For inducing sleep deprivation, adult male mice were placed inside a water cage containing 15 platforms immersed in water up to 1 cm for 7 days. One day after sleep deprivation, dexmedetomidine at the respective dosage (5, 10, and 20 μg/kg) and α2-adrenoceptor antagonist atipamezole (250 μg/kg) were intraperitoneally injected into the mice, once per day for six days. The step-down avoidance task and the Morris water maze test were performed. Western blot analysis was performed to determine the levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), tyrosine kinase B (TrkB), nuclear transcription factor-κB (NF-κB), inhibitor of κBα (IκBα), and ionized calcium binding adapter molecule I (Iba-1) in the hippocampus. Immunohistochemistry was performed for the determination of Ki-67 and glial fibrillary acidic protein (GFAP) expression in the hippocampal dentate gyrus. Dexmedetomidine ameliorated sleep deprivation-induced deterioration of short-term memory and spatial learning ability. Dexmedetomidine inhibited production of inflammatory mediators caused by sleep deprivation. Dexmedetomidine also prevented the decrease in BDNF, TrkB expression, and cell proliferation induced by sleep deprivation. Dexmedetomidine could be used to counteract the neuropathological effects of sleep deprivation.