Cognitive dysfunction and psychopathology: a cohort study of adults with intellectual developmental disorder.

BACKGROUND: Cognitive impairment of intellectual developmental disorders (IDD) is determined by several different combinations of specific cognitive alterations. People with IDD present a rate of mental health problems that is up to 4 times higher than that of the general population. Despite this, the relationship between specific cognitive dysfunctions and co-occurring mental disorders has not been adequately studied. The aim of the present paper is to investigate the association between specific cognitive dysfunctions and specific psychiatric symptoms and syndromes in people with IDD. METHODS: One hundred and twenty adults with mild to moderate IDD living in residential facilities underwent a clinical and instrumental assessment for specific cognitive and psychopathological features. RESULTS: Participants with IDD and ASD have significantly lower scores compared to those without respect to who has not the diagnosis on the Processing Speed Index (PSI) and Perceptual Reasoning Index (PRI) on the WAIS-IV and higher time scores on the TMT A. Moreover, there is a significant association between years of hospitalisation and TMT B and TMT B A time scores; the longer a participant with IDD was hospitalised, the worse their performance on the TMT. Although not statistically significant, many psychopathological clusters showed substantial cognitive profiles. CONCLUSIONS: Although further research is needed, neuropsychological and IQ tests scores seem to be differently associated to various psychopathological conditions co-occurring with IDD, and with ASD especially. Cognitive assessment seems to support diagnosis and treatment of psychopathological co-occurrences in persons with IDD, also in consideration of indirect implications including a better knowledge of the patient's characteristics beyond IQ deficit.

Retinal Degeneration Following Chronic Administration of the Parkinsonism-Inducing Neurotoxin MPTP.

During late stages, retinal degenerative disorders affecting photoreceptors progress independently from the specific disease trigger. In fact, a number of detrimental consequences occur downstream of photoreceptors, which are triggered by the loss of photoreceptors themselves. Such downstream anatomical alterations were originally thought to be compensatory events aimed to restore retinal function. At present, these phenomena are deciphered as detrimental effects and the term retinal degeneration is used to indicate the loss of cells and architecture within the inner retina as a consequence of damage to photoreceptors. In the process of testing a photoreceptor-dependent downstream spreading of neurodegeneration we applied a neurotoxin mimicking Parkinson's disease (PD), 1-methyl, 4-phenyl, 1,2,3,6-tetrahydropyridine (MPTP). Chronic MPTP administration produces degeneration within the mouse retina. This is evident by apoptosis quite circumscribed to photoreceptors, which is reminiscent of most phenotypes of retinal degeneration. Retinal pathology following plain HE histochemistry is more widespread with delamination and loss of neuronal packaging in the inner retina. The retinal damage is characterized by a marked synucleinopathy mostly within retinal ganglion cells. In contrast, dopamine-containing structures are intact while norepinephrine is significantly reduced. Despite the involvement of the retina in PD is documented, no study so far analyzed the onset of a synucleinopathy and a degenerative process mimicking what is now recognized in typical retinal degeneration. The present data provide a novel vista on the reciprocal role of the retina in neurodegenerative disorders.

Exosomes and alpha-synuclein within retina from autophagy to protein spreading in neurodegeneration.

In the course of age-related macular degeneration (AMD) as well as in multiple retinal disorders protein aggregates are described at various levels in the retina. In AMD this fills the space between retinal pigment epithelium (RPE) in the form of drusen, which contains amyloid and other protein aggregates along with lipids. Nonetheless, in very advanced stages of AMD, as well as in other retinal pathologies and early on in retinitis pigmentosa, a number of neuronal inclusions, which stain for α-synuclein spreads all over the retinal layers. Thus, an early or later defect in the clearance of α-synuclein may represent a final common pathway to these phenomena. The physiological clearance of α-synuclein is provided by the autophagy machinery starting at the level of the RPE and occurring throughout the retina. Such a process is also involved in the clearance of melanin-dependent toxic metabolites under the effects of different wavelengths and the stimulatory activity of the sympathetic nervous system. In search for the occurrence of these culprits, here we report the presence of α-synuclein in the retina combined with exosomal detection to document the presence of a α-synuclein spreading apparatus. This was correlated with the occurrence of autophagy markers throughout retinal layers, along with sympathetic innervation, which in turn was related to melanin content.

The neurobiology of nutraceuticals combined with light exposure, a case report in the course of retinal degeneration.

The present article presents a case report and discusses the neurobiology underlying the potential neuro-repair induced by combined administration of phytochemicals in a patient undergoing photo-bio-modulation (PBM), which improves anatomical and clinical abnormalities in the course of age-related macular degeneration (AMD). After combined treatments the patient with nutraceuticals and PBM had noticeable improvement of retinal tissue with excellent vision for her age and no worsening of corneal guttae, which was present at the time of diagnosis. The present treatment was tailored, based on translational evidence, to improve the autophagy pathway, which is a key determinant in the onset and progression of AMD. In fact, treatment with specific patterns of light exposure combined with specific phytochemicals, may synergize in improving the microanatomy of the retina by restoring its neurobiology. The combination of light exposure, at selective wavelengths, with the effects produced by the intake of specific phytochemicals to treat AMD is reported here as "Lugano Protocol". Such a clinical protocol represents an "in progress" development backed up by translational research. In fact, recent evidence indicates that, specific phytochemicals, when administered in combination may promote anatomical and functional integrity within the retina. These in turn synergize with analogous effects produced by specific wavelengths, when administered at specific time intervals. The synergism between specific light and combined phytochemicals is discussed at molecular level, where recent data indicate how these treatments, when delivered according to specific patterns, may enhance autophagy in the retina. The improvement of retinal morphology and visual acuity, observed in this case report is thoroughly discussed in the light of the key role of autophagy in regulating the integrity of the retinal epithelium. Despite exciting, and consistent with translational evidence, the clinical report of a disease modifying effect during AMD owns the inherent limit of a case report, which requires wide validation in large number of patients. The potential effectiveness of "Lugano protocol" may apply to other types of retinal degenerations, where common alterations in the autophagy pathway do occur. Thus, such a therapeutic approach may extend to a common late stage of retinal trans-synaptic degeneration, where maladaptive plasticity during several types of retinal degenerative disorders eventually converge.

Measurement of drusen and their correlation with visual symptoms in patients affected by age-related macular degeneration.

Age-related macular degeneration (AMD) is a common retinal disorder, which became more and more prevalent in the last decades. AMD is now the most prevalent cause of blindness in the western world. The disorder is classified into two phenotypes named dry and wet AMD. This is based on the recruitment of novel blood vessels and inflammatory exudates in wet AMD. In both phenotypes, the pathological hallmark is the presence of proteinaceous aggregates called drusen, which mostly accumulate between the choroid and the retinal pigment. Drusen in dry AMD represent the evident pathological finding although they are present, though less defined, in wet AMD. In AMD drusen are supposed to be a pathogenic trigger of the disorder. In fact, drusen may mechanically alter retinal function. A novel hypothesis exists, suggesting that a metabolic defect (systemic or focal within the retinal pigment epithelium) may be the real determinant of visual impairment, while causing the concomitant accumulation of proteinaceous debris and lipids forming the drusen. Here we face such an issue by analyzing the retinal anatomy to correlate visual impairment with the occurrence of drusen number, size and the extent of a drusenoid area in the foveal region. A comparison is made with wet AMD where new vessels and retinal exudates prevail. The study is carried out in 120 patients affected by dry or wet AMD and 21 patients where paradoxical findings are described. The main question consists in inferring whether the occurrence of visual impairment is due, in fact, to a drusen-dependent mechanical damage or drusen just occurs as an independent consequence of an upstream metabolic alteration, which concomitantly impairs the visual process. The present data indicate that, despite a significant difference in visual function between mild and severe AMD patients in the amount of drusen exists, a strong correlation between drusen and visual impairment does not occur. This suggests that drusen and visual deterioration develop as a consequence of similar upstream biochemical alterations but it is likely that drusen do not produce visual deterioration. This is strengthened here by extreme clinical conditions, where visual impairment is severe with a slight alteration in the planar pattern of the retina or, vice versa an extended drusenoid area occurs concomitantly with fair visual acuity, contrast sensitivity and lack of metamorphopsia. A biochemical analysis of key areas in the function of specific domains in the pigment epithelium as described in the accompanying manuscript should help to better disclose the real morpho-functional deficit, which takes place in AMD.

Nutraceuticals for dry age-related macular degeneration: a case report based on novel pathogenic and morphological insights.

Age-related macular degeneration represents the main retinal disorder leading to irreversible blindness in people over the age of 50 in the Western World. Here we describe a case report, which suggest that specific nutraceutical compounds may exert beneficial effects on the progression of dry age-related macular degeneration (AMD), an eye disease with no approved treatment or cure. Specific antioxidants, such as lutein, resveratrol and Vaccinium Myrtillus, which are known to reduce the risk of developing AMD, when co-administered alone, were supplemented to diet of an informed patient suffering from dry AMD. The case report indicates an improvement of visual acuity and a long lasting decrease in druse volume and number. The concomitant intake of lutein, resveratrol and Vaccinium Myrtillus when administered for six months produced a marked decrease in the drusen observed at OCT at the 6-month follow-up. At this time interval, the patient experienced a noticeable improvement in visual acuity, a decrease in eye strain, more color contrast, higher visual definition. The case report indicates the potential benefit for a non-invasive treatment with improved quality of vision in dry AMD. A larger population followed over a long-term period is warranted. The support of nutraceuticals could therefore offer a new non-invasive, adverse effect-free which may restore the pathology affecting the cross talk between choroid and retinal cells. The results of this case report are discussed within the frame of molecular mechanisms synergizing site-specifically at the anatomical border between the outer retina and inner choroid.

TNFR1 -383 A˃C polymorphism and ankylosing spondylitis in a Russian Caucasian population: a preliminary study.

The aim of this study was to assess the association between the TNFR1 rs2234649 polymorphism and ankylosing spondylitis susceptibility in a Russian Caucasian population. A total of 41 ankylosing spondylitis patients and 43 healthy controls, matched according to age and sex, were enrolled, and polymerase chain reaction-restriction fragment length polymorphism analysis was used to genotype the rs2234649 variant. We evaluated genotype distributions in the patient and control groups with the chi-square test, and assessed the relationship between genotypes and ankylosing spondylitis using the odds ratio. Our analysis showed that the rs2234649 polymorphism does not increase ankylosing spondylitis risk. In conclusion, the TNFR1 gene polymorphism tested does not appear to be useful for assessing predisposition to this disease or for its diagnosis or prognosis.

Genetic tests for low- and middle-income countries: a literature review.

The aim of this review is to describe a series of ten genetic diseases with Mendelian inheritance pattern in people of low- or middle-income countries, which can be easily identified with simple and affordable methods. Recent information shows that although genetic diseases account for more than 10% of infant mortality in such countries, testing, counseling, and treatment of genetic diseases is not a priority. The selection criteria for the genetic tests that are discussed in this review are: i) the frequency of the genetic disease in the general population, ii) the cost and ease of execution, and iii) the report of validated methods in the literature for the diagnosis of these diseases. The goal is to promote diagnosis of genetic diseases at low-cost and with relative ease, thereby enabling appropriate treatments, reducing mortality, and preventing genetic diseases in high-risk families.

Genetic evaluation of AMPD1, CPT2, and PGYM metabolic enzymes in patients with chronic fatigue syndrome.

Chronic fatigue syndrome (CFS) is a disease that can seriously impair one's quality of life; patients complain of excessive fatigue and myalgia following physical exertion. This disease may be associated with abnormalities in genes affecting exercise tolerance and physical performance. Adenosine monophosphate deaminase (AMPD1), carnitine palmitoyltransferase II (CPT2), and the muscle isoform of glycogen phosphorylase (PYGM) genes provide instructions for producing enzymes that play major roles in energy production during work. The aim of this study was to look for evidence of genotype-associated excessive muscle fatigue. Three metabolic genes (AMPD1, CPT2, and PYGM) were therefore fully sequenced in 17 Italian patients with CFS. We examined polymorphisms known to alter the function of these metabolic genes, and compared their genotypic distributions in CFS patients and 50 healthy controls using chi-square tests and odds ratios. One-way analysis of variance with F-ratio was carried out to determine the associations between genotypes and disease severity using CF scores. No major genetic variations between patients and controls were found in the three genes studied, and we did not find any association between these genes and CFS. In conclusion, variations in AMPD1, CPT2, and PGYM genes are not associated with the onset, susceptibility, or severity of CFS.

Prevalence of mutations in LEP, LEPR, and MC4R genes in individuals with severe obesity.

Obesity is a major public health concern; despite evidence of high heritability, the genetic causes of obesity remain unclear. In this study, we assessed the presence of mutations in three genes involved in the hypothalamic leptin-melanocortin regulation pathway (leptin, LEP; leptin receptor, LEPR; and melanocortin-4 receptor, MC4R), which is important for energy homeostasis in the body, in a group of patients with severe obesity. For this study, we selected 77 patients who had undergone bariatric surgery and had a pre-operative body mass index (BMI) >35 kg/m2, early onset and a family history of being overweight. Candidate genes were screened by direct sequence analysis to search for rare genetic variations. The common LEP -2548 G/A polymorphism was also evaluated for its influence on the BMI (in obesity patients) and for obesity risk, using a case-control study involving 117 healthy individuals. Two different non-synonymous alterations in MC4R were found in two patients: the p.(Thr112Met), previously described in the literature as a probable gene involved in the obesity phenotype, and the novel p.(Tyr302Asp) variant, predicted to be pathogenic by in silico evaluations and family segregation studies. The LEP -2548 G/A polymorphism was not associated with the BMI or obesity risk. In conclusion, we have reported a novel mutation in MC4R in a family of Italian patients with severe obesity. Screening for MC4R could be important for directing the carriers of mutations towards therapy including partial agonists of the MC4R that could normalize their appetite and inhibit compulsive eating. Next-generation sequencing could be used to clarify the genetic basis of obesity in the future.

A Rare Case of Emberger Syndrome Caused By a De Novo Mutation in the GATA2 Gene.

Emberger syndrome, or primary lymphedema with myelodysplasia, is a severe rare disease characterized by early primary lymphedema and blood anomalies including acute childhood leukemia. The syndrome is associated with heterozygous mutations in the GATA2 gene. We report on a 13-year-old boy who developed lymphedema of the right lower limb at age 6 years which was accompanied by severe panleukopenia and repeated episodes of erysipelas. The suspicion of Emberger syndrome was confirmed by detection of a new germinal line GATA2 mutation c.414_417del, p.Ser139Cysfs*78. Clinical treatment included a bone marrow transplant from the father.This case is one of a very limited number of Emberger syndrome cases documented in the literature, and genetic testing proved fundamental for definition of the condition and its association with a de novo mutation in the GATA2 which is reported here for the first time.

Genetic Screening in a Large Cohort of Italian Patients Affected by Primary Lymphedema Using a Next Generation Sequencing (NGS) Approach.

Primary lymphedema is a rare inherited condition characterized by swelling of body tissues caused by accumulation of fluid, especially in the lower limbs. In many patients, primary lymphedema has been associated with variations in a number of genes involved in the development and maintenance of the lymphatic system. In this study, we performed a genetic screening in patients affected by primary lymphedema using a next generation sequencing (NGS) approach. With this technology, based on a custom-made oligonucleotide probe library, we were able to analyze simultaneously in each patient all the coding exons of 10 genes (FLT4, FOXC2, CCBE1, GJC2, MET, HGF, GATA2, SOX18, VEGFC, KIF11) associated with primary lymphedema. In the study population, composed of 45 familial and 71 sporadic cases, we identified the presence of rare variants with a potential pathogenic effect in 33% of subjects. Overall, we found a total of 36 different rare nucleotidic alterations, 30 of which had not been previously described. Among these, we identified 23 mutations that we considered most likely to be disease causing. Patients with an FLT4 or FOXC2 alteration accounted for the largest percentage of the sample, followed by MET, HGF, KIK11, GJC2 and GATA2. No alterations were identified in SOX18, VEGFC, and CCBE1 genes. In conclusion, we showed that NGS technology can be successfully applied to perform molecular screening of lymphedema-associated genes in large cohort of patients with a reasonable effort in terms of cost, work, and time.

Genetic polymorphisms and retinal vein occlusion in an Italian population.

In this study, we assessed the prevalence of polymorphisms in genes involved in hyperhomocysteinemia or hemostasis to shed light on their role, if any, in retinal vein occlusion (RVO). We recruited 37 Italian patients (17 men and 20 women) with a diagnosis of central or branch RVO based on fundus examination and retinal fluorescein angiography, as well as 45 healthy controls. Risk factors and family history of RVO of all subjects were recorded. The distributions of polymorphisms in patients and controls were evaluated using the χ(2) test and OR. We confirmed an increased risk in subjects with dyslipidemia (high density lipoprotein <59 mg/dL: 17.8% of controls, 43.2% of patients, P = 0.0002; low density lipoprotein >130 mg/dL: 26.7% controls, 54.1% patients, P = 0.0002), arterial hypertension (60% controls, 75.7% patients, P = 0.023), and high body mass index (28.9% controls, 70.3% patients, P < 0.0001, and excluded involvement of the selected polymorphisms in RVO. Overall, the tested polymorphisms did not appear to be useful for assessing predisposition or for the diagnosis and prognosis of RVO.

Polymorphism of UGT1A1*28 (TA)7 and liver damage in hepatitis B virus-positive patients in Albania.

Hepatitis B virus (HBV) is the infectious agent of both acute and chronic hepatitis. HBV exists in multiple genotypic variants that differ in their capacity to become persistent chronic infections and in their clinical manifestations, including hepatocellular carcinoma. The 8 genotypes (A-H) of HBV show a specific worldwide geographic distribution and are correlated with different disease course, severity, and response to therapy. We isolated DNA from 75 HBV-positive blood donors, chosen randomly from the database of the National Blood Bank in Tirana, to specifically analyze the UGT1A1 polymorphism to determine its correlations with bilirubin levels and liver function. The large number of subjects who were HBV-positive carriers of heterozygosis or homozygosis for the UGT1A1*28 (TA)7 polymorphism suggests that these individuals may be more susceptible to cancer and should follow a strict regime of prevention.

Syndromic and non-syndromic forms of retinitis pigmentosa: a comprehensive Italian clinical and molecular study reveals new mutations.

Mutations in more than 60 different genes have been associated with non-syndromic and syndromic retinitis pigmentosa (RP), a heterogeneous group of inherited retinal dystrophies. To increase the understanding of the molecular epidemiology of the disease in Italy, we analyzed 56 patients with syndromic and non-syndromic forms of RP attending the Retinitis Pigmentosa Center of San Paolo Hospital (Milan, Italy). Patients underwent detailed clinical examination. Genomic DNA isolated from peripheral blood samples was screened for mutations in different genes according to RP form by direct sequencing analysis. The impact of novel missense mutations on protein functions was predicted by in silico analysis and protein sequence alignment. Cosegregation analysis was performed between available family members. Forty-one of the 56 probands analyzed had non-syndromic and 15 had syndromic RP forms. Putative disease-causing mutations were identified in 19 of 56 unrelated RP probands. Mutation screening identified a total of 22 different heterozygous variants. Notably, 12 of these putative pathogenic mutations have not been previously reported. New variants were found to be located on the USH2A, RPGR, EYS, and RHO genes. All 3 new variants detected in X-linked RP probands were confirmed in other affected family members. We found a positivity rate of 24.4% and 60% for probands with non-syndromic and syndromic RP, respectively. This is the first report of RPGR X-linked RP proband-ORF15 mutations in Italian patients with X-linked (XL)-RP. In addition, this is the first report of data regarding the association between EYS mutations and non-syndromic RP forms in the Italian population.

Retraction Note: Presence of viral spike protein and vaccinal spike protein in the blood serum of patients with long-COVID syndrome.

The article "Presence of viral spike protein and vaccinal spike protein in the blood serum of patients with long-COVID syndrome", by K. Dhuli, M.C. Medori, C. Micheletti, K. Donato, F. Fioretti, A. Calzoni, A. Praderio, M.G. De Angelis, G. Arabia, S. Cristoni, S. Nodari, M. Bertelli, published in Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 13-19-DOI: 10.26355/eurrev_202312_34685-PMID: 38112944 has been retracted by the Editor in Chief for the following reasons. Following some concerns raised on PubPeer, the Editor in Chief has started an investigation to assess the validity of the results. The outcome of the investigation revealed that the manuscript presented major flaws in the following: -       Unclear methodology and patient recruitment -       Discrepancies among data reported in the text and tables -       Unreliable results -       Undeclared conflict of interest Consequently, the Editor in Chief mistrusts the results presented and has decided to withdraw the article. The authors disagree with this retraction. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34685.

Author Correction: Aldo-keto reductase 1C2 (AKR1C2) as the second gene associated to non-syndromic primary lipedema: investigating activating mutation or overexpression as causative factors.

Correction to: Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 127-136-DOI: 10.26355/eurrev_202312_34697 After publication and following some post-publication concerns, the authors have applied the following corrections to the galley proof. -       The conflict of interest section has been amended as follows: J. Kaftalli and G. Marceddu are employees at MAGI EUREGIO. K. Donato is employee at MAGI EUREGIO and MAGISNAT. M. Bertelli is president of MAGI EUREGIO, MAGISNAT, and MAGI's LAB. G. Bonetti, K. Dhuli, A. Macchia, and P.E. Maltese are employees at MAGI's LAB. M. Bertelli, P.E. Maltese, K. Louise Herbst, Sa. Michelini, Se. Michelini, and P. Chiurazzi are patent inventors (US20220362260A1). M. Bertelli, P.E. Maltese, G. Marceddu are patent inventors (US20230173003A1). M. Bertelli, K. Dhuli and P.E. Maltese are patent inventors (WO2022079498A1). M. Bertelli, P.E. Maltese, Sa. Michelini, Se. Michelini, P. Chiurazzi, K. Louise Herbst, J. Kaftalli, K. Donato, and A. Bernini are patent applicants (Application Number 18/516,241). M. Bertelli, K. Donato, P. Chiurazzi, G. Marceddu, K. Dhuli, G. Bonetti and J. Kaftalli are patent applicants (Application Number: 18/466.879). M. Bertelli, G. Bonetti, G. Marceddu, K. Donato, K. Dhuli, J. Kaftalli, Sa. Michelini, and K. Louise Herbst are patent applicants (Application Number 63/495,155). The remaining authors have no conflict of interest to disclose. -       Figure 5 has been modified as follows to better distinguish outliers: -       The legend of Figure 5 has to be modified as follows: Relative expression of AKR1C1 and AKR1C3 in different groups (CTR = non affected controls, L = lipedema patients without overexpression of AKR1C2, L-over = Lipedema patients with overexpression of AKR1C2), showing that lipedema patients expressed AKR1C1 and AKR1C3 levels similar to the control group. Outliers are reported as black triangles. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34697.

Author Correction: Genetic variants identified in novel candidate genes for anorexia nervosa and analysis of molecular pathways for diagnostic applications.

Correction to: Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 77-88-DOI: 10.26355/eurrev_202312_34692 After publication and following some post-publication concerns, the authors have applied the following corrections to the galley proof. The conflict of interest section has been amended as follows: K. Donato is employee at MAGI EUREGIO and MAGISNAT. G. Marceddu is employee at MAGI EUREGIO. M. Bertelli is president of MAGI EUREGIO, MAGISNAT, and MAGI's LAB. M.C. Medori, A. Macchia, S. Cecchin, C. Micheletti, K. Dhuli, G. Madeo, G. Bonetti are employees at MAGI's LAB. M. Bertelli, M.R. Ceccarini, and P. Chiurazzi are patent inventors (US20220362260A11). M. Bertelli, P.E. Maltese, G. Marceddu, and S. Cecchin are patent inventors (US20230173003A1). M. Bertelli, K. Dhuli, and P.E. Maltese are patent inventors (WO2022079498A1). M. Bertelli, K. Donato, M.C. Medori, M.R. Ceccarini, T. Beccari, P. Chiurazzi, C. Micheletti, K. Dhuli, G. Bonetti, G. Marceddu are patent applicants (Application Number: 18/466.879). The remaining authors have no conflict of interest to disclose. Since the current study shares the same NGS panel for the genetic analysis as the study cited in Ref. 5 (Ceccarini MR, Precone V, Manara E, Paolacci S, Maltese PE, Benfatti V, Dhuli K, Donato K, Guerri G, Marceddu G, Chiurazzi P, Dalla Ragione L, Beccari T, Bertelli M. A next generation sequencing gene panel for use in the diagnosis of anorexia nervosa. Eat Weight Disord 2022; 27: 1869-1880), the authors amend the following sentence: "A subset comprising 163 genes from a dedicated Next-Generation Sequencing (NGS) panel was analyzed5" in "A subset comprising 163 genes from a dedicated Next-Generation Sequencing (NGS) panel, previously used in the study by Ceccarini et al5, was analyzed". The authors clarify that the analyzed patients of the two articles are completely independent. To clarify the data reported in Table II, the authors amend the following sentence: "Genetic variants identified in the AN population are reported in Table II." In "The genomic sequencing NGS was performed in all 135 patients recruited in the study. After obtaining the raw data, based on the ACMG guidelines (https://www.acmg.net/ACMG/Medical-Genetics-Practice-Resources/Practice-Guidelines.aspx), the results were filtered, and Table II reports the variants considered Pathogenic (P), likely pathogenic (LP), and Variable with Uncertain Significance (VUS), 61 patients in total". Consequently, to improve clarity, the legend of Table II has been amended as follows: Genetic variants identified in 61 patients out of the total 135 patients analyzed by NGS. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34692.

Author Correction: Achievement of sustainable development goals through the Mediterranean diet.

Correction to: Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 89-99-DOI: 10.26355/eurrev_202312_34693 After publication and following some post-publication concerns, the authors have applied the following corrections to the galley proof. -       The conflict of interest section has been amended as follows: M.C. Medori and D. Malacarne are employees at MAGI'S LAB. K. Donato is employee at MAGI EUREGIO and MAGISNAT. M. Bertelli is president of MAGI EUREGIO, MAGISNAT, and MAGI's LAB. E. Borghetti is president at AERSAFE srl. C. Zuccato is researcher at AERSAFE srl. E. Borghetti is patent inventor (IT202100021344A1, IT202100020330A1, WO2021260537A1, WO2022259165A1). M. Bertelli is patent inventor (US20220362260A1, US20230173003A1, WO2022079498A1). D. Malacarne is patent inventor (WO2022079498A1; US20230173003A1). S. Michelini is patent inventor (US20220362260A1). M. Bertelli, S. Michelini, and K. Donato are patent applicants (Application Number: 18/516,241). M. Bertelli and K. Donato are patent applicants (Application Number: 18/466.879). M. Bertelli, K. Donato, and S. Michelini are patent applicants (Application Number: 63/495,155). The remaining authors have no conflict of interest to disclose. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34693.

Retraction Note: Metabolomic profiling of amino acid alterations in anorexia nervosa: implications for appetite regulation and therapeutic strategies.

The article "Metabolomic profiling of amino acid alterations in anorexia nervosa: implications for appetite regulation and therapeutic strategies", by K. Donato, K. Dhuli, A. Macchia, M.C. Medori, C. Micheletti, G. Bonetti, M.R. Ceccarini, T. Beccari, P. Chiurazzi, S. Cristoni, V. Benfatti, L. Dalla Ragione, M. Bertelli, published in Eur Rev Med Pharmacol Sci 2023; 27 (6 Suppl): 64-76-DOI: 10.26355/eurrev_202312_34691-PMID: 38112949 has been retracted by the Editor in Chief for the following reasons. Following some concerns raised on PubPeer, the Editor in Chief has started an investigation to assess the validity of the results. The outcome of the investigation revealed that the manuscript presented major flaws in the following: -       Issues with ethical approval -       Undeclared conflict of interest Consequently, the Editor in Chief mistrusts the results presented and has decided to retract the article. The authors disagree with this retraction. This article has been retracted. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/34691.