Dynamics of bacterial and fungal communities of mango: From the tree to ready-to-Eat products.

Processing, such as fresh cutting and drying, is essential to enhance profitability; therefore, to limit waste and reduce losses in fruit production such as mangoes. Metabarcoding and microbial enumeration methods were utilized to explore the structure of mango microbiota, as well as their evolution after processing. Two mango ripening stages of cv. Cogshall were selected and processed into fresh-cut pieces or dried slices. Microbiological and physicochemical parameters were monitored during product storage, in order to assess the dynamics of quantitative and qualitative variations of the microbial flora. Proteobacteria was the dominant bacterial phylum of the mango surface and accounted for 73.16%, followed by Actinobacteria (10.16%), Bacteroidetes (7.82%) and Firmicutes (6.68%). Aureobasidium and Cladosporium were the only two genera shared between all types of samples (peel surface, dried slices and mango fresh-cut). However, the bacterial genera Lactobacillus and Pantoea were the most abundant in fresh-cut mango after 14 days of storage. Ascomycota was the dominant fungal phylum in the mango surface and accounted for 90.76% of the total number of detected sequences, followed by Basidiomycota (9.21%). In total, 866 microbial genera were associated with mango surface (562 bacterial and 304 fungal). Among detected yeast genera, Saccharomyces, Candida and Malassezia prevailed in mango flesh and were replaced by Wickerhamomyces after 14 days of storage. Alpha and beta diversity analyzes revealed differences in fungal and bacterial communities on fruit peel, in fresh-cut, dried slices, and during conservation (fresh-cut and dried slices). Mango processing (washing, peeling, cutting and drying) reduced the richness and the microbial diversity (bacterial and fungal) associated to the fruit, and drying limits the development of cultivable microorganisms during storage in comparison to fresh-cuts mangoes.

Drug-resistant epilepsy: From multiple hypotheses to an integral explanation using preclinical resources.

Drug-resistant epilepsy affects approximately one-third of the patients with epilepsy. The pharmacoresistant condition in epilepsy is mainly explained by six hypotheses. In addition, several experimental models have been used to understand the mechanisms involved in pharmacoresistant epilepsy and to identify novel therapies to control this condition. However, the global prevalence of this disease persists without changes. Several factors can explain this situation. First of all, the pharmacoresistant epilepsy is explained by different and independent hypotheses. Each hypothesis indicates specific mechanisms to explain the drug-resistant condition in epilepsy. However, there are different findings suggesting common mechanisms between the different hypotheses. Other important situation is that the experimental models designed for the screening of drugs with potential anticonvulsant effect do not consider factors such as age, gender, type of epilepsy, and comorbid disorders. The present review focuses on indicating the limitations for each hypothesis and the relationships among them. The relevance to consider central and peripheral phenomena associated with the drug-resistant condition in different types of epilepsy is also indicated. The necessity to establish a global hypothesis that integrates all the phenomena associated with the pharmacoresistant epilepsy is proposed. This article is part of the Special Issue "NEWroscience 2018".

Castleman disease. Histopathological and immunohistochemical analysis of 39 cases. / Enfermedad de Castleman. Análisis histopatológico e inmunohistoquímico de treinta y nueve casos.

Introduction: Castleman disease (CD) is a rare lymphoproliferative that comprises two distinct clinical subtypes (unicentric and multicentric) and has two basic histopathology patterns that are hyaline-vascular (HV) and plasma-cell (PC) type. Some cases of multicentric PC disease are associated with HHV-8 infection. Objective: To present the histopathologic and immunohistochemical characteristics of 39 cases of CD. Methods: A review of cases with the diagnosis CD from the files of the Department of Pathology of the ABC Medical Centre in Mexico City was performed. Thirty-nine cases of CD were identified, and a detailed paraffin immunophenotypic study of 9 of them was completed using desmin, cytokeratin OSCAR (CO) and Epidermal growth factor receptor (EGFR), to evaluate the dendritic cell population. Results and Conclusions: Of the 39 cases of CD, 24 were HV and 15 CP. All HV cases were unicentric and only one case of CP was multicentric. The most frequent localization in both subtypes was in lymph nodes; 21/24 cases in HV and 15 cases of CP. All cases were immunostained with CD20 that was expressed in the germinal centers (CGs), CD3 in the paracortical zone, and CD21 in follicular dendritic cells (CDF) within CGs, with expansion towards the area of the hyperplastic mantle zone (only in the HV variant). One case of CD CP was positive for HHV-8. Of the nine cases (6 HV and 3 PC cases) that were detailed with IHC, we found EGFR expression in FDC in all but one of the 9 cases studied and desmin was positive in fibroblastic reticulum cells (FRC) in all, but one of the cases of CD. CO was positive FRC in 3 of 6 cases of HV type and all (3) of the PC type. Clinical, histopathological and HIV and HHV-8 status markers, allow for the classification of CD into groups with markedly different outcomes and disease associations.

Dysgerminoma Probably Due to a Novel SOHLH1-pathogenic Variant Causing Familial Ovarian Dysgenesis.

Pathogenic variants of the SOHLH1 gene are responsible for an autosomal recessive form of ovarian dysgenesis; this gene encodes a transcription factor expressed early in spermatogonia and oocytes and contributes to folliculogenesis. Previously, four affected women from two unrelated families reported homozygous variants in the SOHLH1 gene, but none had a history of gonadal malignancy or a histologic description. We present two sisters and their paternal great-aunt with a history of primary amenorrhea, pubertal delay, and hypergonadotrophism who came from an inbred Mexican family. The proband was the younger sister who was referred for bilateral dysgerminoma. She had a normal blood karyotype, and whole-exome sequencing analysis revealed a novel homozygous missense variant, c.275C>T, in SOHLH1; several family members were also analyzed. In addition to pure dysgerminoma, histopathological analysis revealed an ovarian cortex with fibrosis and almost total absence of follicles. This work confirms the inheritance of ovarian dysgenesis 5, supports the occurrence of cell loss in mouse models, and suggests that affected women should undergo periodic imaging surveillance due to the likely risk of tumor development.

Dopamine abnormalities in the neocortex of patients with temporal lobe epilepsy.

Experiments were designed to evaluate different variables of the dopaminergic system in the temporal cortex of surgically treated patients with temporal lobe epilepsy (TLE) associated with mesial sclerosis (MTLE, n=12) or with cerebral tumor or lesion (n=8). In addition, we sought to identify dopaminergic abnormalities in those patients with epilepsy that had comorbid anxiety and depression. Specifically, we investigated changes in dopamine and its metabolites, D1 and D2 receptors, tyrosine hydroxylase (TH) and dopamine transporter. Results obtained from patients with epilepsy were compared with those found in experiments using autopsy material. The neocortex of patients with MTLE demonstrated high D1 expression (1680%, p<0.05) and binding (layers I-II, 31%, p<0.05; layers V-VI, 28%, p<0.05), and decreased D2 expression (77%, p<0.05). The neocortex of patients with TLE secondary to cerebral tumor or lesion showed high expression of D1 receptors (1100%, p<0.05), and D2-like induced activation of G proteins (layers I-II, 503%; layers III-IV, 557%; layers V-VI, 964%, p<0.05). Both epileptic groups presented elevated binding to the dopamine transporter and low tissue content of dopamine and its metabolites. Analysis revealed the following correlations: a) D1 receptor binding correlated negatively with seizure onset age and seizure frequency, and positively with duration of epilepsy; b) D2 receptor binding correlated positively with age of seizure onset and negatively with duration of epilepsy; c) dopamine transporter binding correlated positively with duration of epilepsy and frequency of seizures; d) D2-like induced activation of G proteins correlated positively with the age of patients. When compared with autopsies and patients with anxiety and depression, patients without neuropsychiatric disorders showed high D2-like induced activation of G proteins, an effect that correlated positively with age of patient and seizure onset age, and negatively with duration of epilepsy. The present study suggests that alterations of the dopaminergic system result from epileptic activity and could be involved in the physiopathology of TLE and the comorbid anxiety and depression.

Drug-resistant epilepsy: Drug target hypothesis and beyond the receptors.

Epilepsy is a chronic neurological disorder that affects more than 50 million people worldwide. Despite a recent introduction of antiseizure drugs for the treatment of epileptic seizures, one-third of these patients suffer from drug-resistant epilepsy (DRE). The therapeutic target hypothesis is a cited theory to explain DRE. According to the target hypothesis, the failure to achieve seizure freedom leads to alteration of the structure and/or function of the antiseizure medication (ASM) target. However, this hypothesis fails to explain why patients with DRE do not respond to antiseizure medications of different targets. This review presents different conditions, such as epigenetic mechanisms and protein-protein interactions that may result in alterations of diverse drug targets using different mechanisms. These novel conditions represent new targets to control DRE.

Pineapple Mycobiome Related to Fruitlet Core Rot Occurrence and the Influence of Fungal Species Dispersion Patterns.

Fruitlet Core Rot (FCR) is a fungal disease that negatively impacts the quality of pineapple, in particular the 'Queen Victoria' cultivar. The main FCR causal agent has been identified as Fusariumananatum. This study focused on the correlation between FCR disease occurrence, fungal diversity, and environmental factors. FCR incidence and fungal species repartition patterns were spatially contextualized with specific surrounding parameters of the experimental plots. The mycobiome composition of healthy and diseased fruitlets was compared in order to search for potential fungal markers. A total of 240 pineapple fruits were sampled, and 344 fungal isolates were identified as belonging to 49 species among 17 genera. FCR symptom distribution revealed a significant gradient that correlated to that of the most abundant fungal species. The association of wind direction and the position of proximal cultivated crops sharing pathogens constituted an elevated risk of FCR incidence. Five highly represented species were assayed by Koch's postulates, and their pathogenicity was confirmed. These novel pathogens belonging to Fusariumfujikuroi and Talaromycespurpureogenus species complexes were identified, unravelling the complexity of the FCR pathosystem and the difficulty of apprehending the pathogenesis over the last several decades. This study revealed that FCR is an airborne disease characterized by a multi-partite pathosystem.

Cannabidiol modifies the seizure expression and effects of antiseizure drugs in a rat model of recurrent severe seizures.

PURPOSE: To evaluate the effects of cannabidiol alone or in combination with antiseizure drugs in the expression of recurrent generalized seizures in a rat model. METHODS: Group A: Male Wistar rats received 3-mercaptopropionic acid (MP) every 12 h for 5 days to induce recurrent generalized seizures. Thereafter, the animals were submitted to a crossover protocol to receive different treatments with cannabidiol, phenytoin and phenobarbital, alone and in combination. Group B: Rats were manipulated as group A, but they received cannabidiol during the induction of recurrent seizures. RESULTS: Minor and major seizures were induced after each MP administration. Status epilepticus (SE) detected during the last MP administrations was considered a sign of high seizure severity. Cannabidiol did not modify the expression of the MP induced seizures but reduced the prevalence of SE in both experimental groups. Phenytoin decreased the expression of major seizures but did not modify the prevalence of SE (groups A and B). Cannabidiol combined with phenytoin did not modify these effects. Phenobarbital diminished the expression of major seizures, an effect more evident when combined with cannabidiol (groups A and B). The combination of phenobarbital and cannabidiol reduced the expression of SE of group B. The mortality rate of groups A and B at the end of the crossover protocol was 30% and 9%, respectively (p=0.2). CONCLUSION: CBD associated with appropriate antiseizure drugs reduces the severity and prevalence of generalized seizures. In contrast, CBD alone reduces the seizure severity, but does not avoid the expression of generalized seizures.

Is cannabidiol a drug acting on unconventional targets to control drug-resistant epilepsy?

Cannabis has been considered as a therapeutic strategy to control intractable epilepsy. Several cannabis components, especially cannabidiol (CBD), induce antiseizure effects. However, additional information is necessary to identify the types of epilepsies that can be controlled by these components and the mechanisms involved in these effects. This review presents a summary of the discussion carried out during the 2nd Latin American Workshop on Neurobiology of Epilepsy entitled "Cannabinoid and epilepsy: myths and realities." This event was carried out during the 10th Latin American Epilepsy Congress in San José de Costa Rica (September 28, 2018). The review focuses to discuss the use of CBD as a new therapeutic strategy to control drug-resistant epilepsy. It also indicates the necessity to consider the evaluation of unconventional targets such as P-glycoprotein, to explain the effects of CBD in drug-resistant epilepsy.

[The histopathology and immunohistochemistry of granular cell tumour. A study of 12 cases with a brief historical note]. / Análisis histopatológico e inmunohistoquímico del tumor de células granulares. Estudios de 12 casos con una breve nota histórica.

INTRODUCTION AND OBJECTIVE: Granular cell tumour (GCT) is a benign neoplasm of neural/schwannian origin, usually presenting as a single asymptomatic lesion, mainly located in the dermis and subcutaneous tissue or submucosa, although multiple tumours may occur. Microscopically, GCTs are composed of large cells with abundant eosinophilic, granular cytoplasm arranged in sheets, nests, cords or trabeculae. Based on the cytological characteristics and the presence of necrosis, three types are recognized: benign, atypical and malignant. We aim to present the cytological and immunohistochemical characteristics of 12 granular cell tumours. MATERIALS AND METHODS: 12 cases of GCT were selected from the consultation files of one of the authors (COH) The paraffin embedded tissue was processed for immunostaining with S-100 protein, calretinin, CD68, α-inhibin, PGP9.5, CD57 (Leu7), CD63 (NKI / C3), Gap43 (growth-associated protein-43), SOX10, TFE-3 and Ki-67. RESULTS AND CONCLUSIONS: 6 male and 6 female patients, with an average age of 40, made up the study group. The most frequent location for the tumours was in the subcutaneous soft tissues of the arms. There were no malignant cases. All tumours were positive for S-100, CD57, SOX10, calretinin, CD68, PGP9.5, α-inhibin and TFE-3, with a low Ki-67 (1-5%). Additionally, we reported, for the first time, the positive immunoreaction to Gap43 (growth-associated protein-43) in GCT.