Personality disorders in individuals with functional seizures: a systematic review.

Functional seizures (FS) are classified as conversion disorders in the DSM-5 and dissociative disorders in the ICD-11, showing a multifactorial psychopathology with various psychiatric comorbidities, such as depression and anxiety. Several studies have found a correlation between FS and personality disorders, mainly those in cluster B. Within this cluster, borderline personality disorder (BPD) or borderline personality traits are the most prevalent in FS. Emotion dysregulation is a hallmark of BPD and is commonly reported in individuals with FS. Cluster C personality disorders, such as avoidant or obsessive-compulsive disorders, have also been reported in FS. In this review, we aim to evaluate the relationship between FS and personality disorders. Assessing personality disorders in the context of FS is relevant for determining the most appropriate intervention. Cognitive-behavioral therapy (CBT) is considered the first-line approach to treating FS. Among various CBT strategies, dialectical behavior therapy, which specifically targets emotion dysregulation, may be helpful for individuals with BPD. Future research should assess the advantages of systematically evaluating personality disorders in FS to address specific treatment planning and evaluate its effectiveness on seizure recurrence, psychological comorbidities, and quality of life. Systematic review registration: https://www.crd.york.ac.uk/PROSPEROFILES/509286_STRATEGY_20240203.pdf, identifier CRD42024509286.

An overview on glycation: molecular mechanisms, impact on proteins, pathogenesis, and inhibition.

The formation of a heterogeneous set of advanced glycation end products (AGEs) is the final outcome of a non-enzymatic process that occurs in vivo on long-life biomolecules. This process, known as glycation, starts with the reaction between reducing sugars, or their autoxidation products, with the amino groups of proteins, DNA, or lipids, thus gaining relevance under hyperglycemic conditions. Once AGEs are formed, they might affect the biological function of the biomacromolecule and, therefore, induce the development of pathophysiological events. In fact, the accumulation of AGEs has been pointed as a triggering factor of obesity, diabetes-related diseases, coronary artery disease, neurological disorders, or chronic renal failure, among others. Given the deleterious consequences of glycation, evolution has designed endogenous mechanisms to undo glycation or to prevent it. In addition, many exogenous molecules have also emerged as powerful glycation inhibitors. This review aims to provide an overview on what glycation is. It starts by explaining the similarities and differences between glycation and glycosylation. Then, it describes in detail the molecular mechanism underlying glycation reactions, and the bio-molecular targets with higher propensity to be glycated. Next, it discusses the precise effects of glycation on protein structure, function, and aggregation, and how computational chemistry has provided insights on these aspects. Finally, it reports the most prevalent diseases induced by glycation, and the endogenous mechanisms and the current therapeutic interventions against it.

Insight into the Effect of Methylglyoxal on the Conformation, Function, and Aggregation Propensity of α-Synuclein.

It is well-known that people suffering from hyperglycemia have a higher propensity to develop Parkinson's disease (PD). One of the most plausible mechanisms linking these two pathologies is the glycation of neuronal proteins and the pathological consequences of it. α-Synuclein, a key component in PD, can be glycated at its fifteen lysine. In fact, the end products of this process have been detected on aggregated α-synuclein isolated from in vivo. However, the consequences of glycation are not entirely clear, which are of crucial importance to understand the mechanism underlying the connection between diabetes and PD. To better clarify this, we have here examined how methylglyoxal (the most important carbonyl compound found in the cytoplasm) affects the conformation and aggregation propensity of α-synuclein, as well as its ability to cluster and fuse synaptic-like vesicles. The obtained data prove that methylglyoxal induces the Lys-Lys crosslinking through the formation of MOLD. However, this does not have a remarkable effect on the averaged conformational ensemble of α-synuclein, although it completely depletes its native propensity to form soluble oligomers and insoluble amyloid fibrils. Moreover, methylglyoxal has a disrupting effect on the ability of α-synuclein to bind, cluster and fusion synaptic-like vesicles.

Jejunal gastrointestinal stromal tumor: a diagnostic challenge.

Gastrointestinal stromal tumors (GIST) are rare mesenchymal tumors of the gastrointestinal tract and a rare cause of gastrointestinal bleeding. These tumors usually affect people over 50 years of age and they exhibit a wide range of clinical manifestations, including asymptomatic patients, nonspecific symptoms, obstruction or bleeding, which may delay diagnosis. Early diagnosis and treatment are crucial because GISTs can be aggressive and metastasize. This case highlights the importance of considering GISTs in the differential diagnosis of obscure gastrointestinal bleeding.

Simultaneous determination of abamectin homologs H 2 B 1a and H 2 B 1b in gel formulation by high performance liquid chromatography

ABSTRACT Abamectin is a drug with antiparasitic properties used in several pharmaceutical formulations. The objective of this research was to develop and validate a high performance liquid chromatographic (HPLC) method for quantification of the two abamectin homologs (H2B1a and H2B1b) in gel formulation. This HPLC method was validated using a LichroCart(r) 100 RP-18 (125 x 4 mm, 5 µm) column. The mobile phase contained of acetonitrile and water (95:5 v/v) with 1% acetic acid. The flow rate was 1.0 mL min-1 and UV detection was performed at 245 nm. Mobile phase solutions were prepared containing a nominal concentration 185.2 µg mL-1 H2B1a and 9.6 µg mL-1 H2B1b. The method displayed good linearity in the concentration range of 148.1 - 222.3 µg mL-1 and 7.7 - 11.5 µg mL-1, for H2B1a and H2B1b, respectively, with a correlation coefficient of (r)> 0.99 for both compounds, calculated by the least mean squares method. Detection limits (DLs) were 2.8 µg mL-1 and 1.2 µg mL-1 and quantitation limits (QLs) were 8.6 µg mL-1 and 3.8 µg mL-1, for H2B1a and H2B1b, respectively. The method is simple, economical and efficient for the quantitative determination of abamectin H2B1a and H2B1b homologs in pharmaceutical preparations.

Persistencia del conducto onfalomesentérico / Patent omphalomesenteric duct

La persistencia del conducto onfalomesentérico es una de las formas de presentación más raras de los restos embrionarios derivados de este conducto. Se presenta el caso de un recién nacido en el que se constata salida de contenido intestinal através del ombligo. Se confirma el diagnóstico de persistencia del conducto onfalomesentérico mediante fistulografía umbilical, procediéndose a su corrección quirúrgica (resección de conducto onfalomesentérico). Se describe la metodología diagnóstica, su tratamiento y se revisa la bibliografía sobre esta patología.