Morphological identification of scorpion species from Jazan and Al-Medina Al-Munawara regions, Saudi Arabia

The present work is a complementary contribution to the comprehensive study of the scorpion sting syndrome in Saudi Arabia. It deals with the identification and determination of medically important scorpions and the other ones, which were collected from two regions (Jazan and Al-Medina Al-Munawara), based on their morphology (the molecular phylogeny and venom characteristics will appear in subsequent publications). The specimens collected from those two regions were brought to the Research Center laboratories in several batches. Morphological identification of the collected specimens was done employing identification keys. There were 646 specimens collected from Jazan Region. A single species, Nebo hierichonticus (Family Diplocentridae), and five genera with four identified species, Parabuthus liosoma, Hottentotta jayakari (salei?), Compsobuthus werneri, Leiurus quinquestriatus (Vachoniolus globimanus?), Vachoniolus spp. (other species) and Orthochirus innesi (Family Buthidae), were classified as extant scorpions in the region. Three hundred and ninety-six specimens from Al-Medina Al-Munawara Region were categorized into eight groups; four of them were identified. Three buthids, Leiurus quinquestriatus, Androctonus crassicauda, Orthochirus innesi and one scorpion specimen, Scorpio maurus, were identified and classified as extant scorpions in this region. The other four species are still not completely identified. They are Vachoniolus (Buthacus minipectinibus?) globimanus? (Unidentified-1), Compsobuthus spp (arabicus?) (Unidentified-2), Compsobuthus spp (werneri?) (Unidentified-3) and a single specimen of Androctonus spp (australis?) (Unidentified-4), all of which belong to the family Buthidae

Prevalence and Determinants of Epilepsy among School Children in Aseer Region- KSA

Epilepsy is a heterogeneous collection of neurological conditions and syndromes characterized by recurrent, unprovoked, paroxysmal seizure activity. It is estimated that 10.5 million children under 15 years have active epilepsy, representing about 25% of the global epilepsy population.2  Of the 3.5 million people who develop epilepsy annually, 40% are younger than 15 years, and more than 80% live in developing countries.  Epilepsy is an important cause of neurological morbidity in .children. Family history of epilepsy, neonatal complications, perinatal brain damage, congenital cerebral malformations, intracranial infection, neonatal seizures, febrile seizure were found as predictors of childhood seizure disorder in many of the studies. In early onset epilepsy perinatal asphyxia, neonatal meningitis and neonatal seizure was found to be the important predictors little research has been done on childhood epilepsy in Aseer region. Greater knowledge on risk factors of epilepsy in the early years of life could help to improve understanding of epilepsy, can tell us about its prognosis and allow early intervention. Objectives: This research aimed to determine the prevalence of epilepsy among the school children and determine the risk factors associated with epilepsy Methodology: A case control study was conducted among school students aged 6 up to 18 years. Primary , preparatory and secondary schools was randomly selected in Abha and Khamis Mushait.  Results: 20 cases of epilepsy was detected among the studied group. The identified major etiologic factors of the epilepsies were cerebral trauma , febrile convulsions, A family history of epilepsy was a risk factor of the cases, and the consanguinity rate among the parents was high. Conclusion :The most important risk factors for epilepsy in this study only head trauma, febrile convulsions, consanguinity and family history of epilepsy were significant Keywords: Prevalence, Determinants, Epilepsy, children, schoo

Viridiflorol Induces Anti-Neoplastic Effects on Breast, Lung, and Brain Cancer Cells Through Apoptosis

All active natural molecules are not fully exploited as therapeutic agents, causing delays in the advancement of anticancer drug discovery. Viridiflorol is a natural volatile element that may work as anti-cancer compound. We tested the anticancer properties of viridiflorol at different concentrations ranging from 0.03 to 300 μM in vitro on three cancer cells including breast (MCF-7), lung (A549) and brain (Daoy). The cancer cells responses were documented after treatment using MTT and Annexin V assays. Viridiflorol showed cytotoxic effects against all tested cell lines, reducing cell viability in a concentration-dependent manner with variable IC50 values. Daoy and A549 cell lines were more sensitive to viridiflorol when compared with temozolomide and doxorubicin, respectively. Viridiflorol demonstrated the highest anticancer activity against the Daoy cells with an estimated IC50 of 0.1 µM followed by MCF-7 at 10 µM, and A549 at 30 µM. In addition, upon exposure to concentrations ranging from 30 µM to 300 µM of viridiflorol, early and late apoptotic cell death was induced in a concentration dependent manner in Daoy (55.8%-72.1%), MCF-7 (36.2%-72.7%) and A459 (35%-98.9%) cell lines, respectively. In conclusion, viridiflorol demonstrates cytotoxic and apoptotic ability in three different cancer cell lines (brain, breast and lung)

Effect of fat contents of buttermilk on fatty acid composition, lipolysis, vitamins and sensory properties of cheddar-type cheese

Cheddar-type cheese produced from buttermilk had softer texture than standard cheddar cheese due to lower fat content of buttermilk. Fat is extremely important for the functional characteristics and optimum textural attributes of cheese. The effect of different fat contents of buttermilk on chemical characteristics of cheddar-type cheese is not previously investigated. This investigation was conducted to know the effect of different fat contents of buttermilk on fatty acids composition, organic acids, vitamins, lipolysis and sensory characteristics of cheddar-type cheese. Cheddar-type cheese was produced from buttermilk having 1, 1.75, 2.50 and 3.25% fat contents (control, T1, T2 and T3). Fat content of control, T1, T2 and T3 were 9.81, 16.34, 25.17 and 31.19%. Fatty acids profile was determined on GC–MS, organic acids and vitamin A and E were determined on HPLC. Free fatty acids, peroxide value and cholesterol were determined. Cheddar-style cheese produced from buttermilk (1% fat) showed that it had softer texture and lacking typical cheese flavor. Gas chromatography–mass spectrometry (GC–MS) analysis showed that long-chain unsaturated fatty acids in control, T1, T2 and T3 samples were 45.88, 45.78, 45.90 and 46.19 mg/100 g. High Performance Liquid Chromatography (HPLC) analysis showed that lactic acid, propionic acid, citric acid and acetic acid gradually and steadily increased during the storage interval of 90 days. At the age of 90 days, lactic acid in control, T1, T2 and T3 was 4,789, 5,487, 6,571 and 8,049 ppm, respectively. At the end of ripening duration of 90 days, free fatty acids in control, T1, T2 and T3 were 0.29, 0.31, 0.35 and 0.42% with no difference in peroxide value. Stability of vitamin A after 90 days storage control, T1, T2 and T3 was 87.0, 80.0, 94.0 and 91.0%. Flavor score of cheddar-type cheese produced from butter milk having 1.0, 2.5 and 3.25% fat content was 81, 89 and 91% of total score (9). Hence, it is concluded that cheddar-type cheese can be produced from buttermilk having 2.5 and 3.25% fat contents with acceptable sensory attributes. Application of buttermilk for the production of other cheese varieties should be studied

Effect of fat contents of buttermilk on fatty acid composition, lipolysis, vitamins and sensory properties of cheddar-type cheese

Cheddar-type cheese produced from buttermilk had softer texture than standard cheddar cheese due to lower fat content of buttermilk. Fat is extremely important for the functional characteristics and optimum textural attributes of cheese. The effect of different fat contents of buttermilk on chemical characteristics of cheddar-type cheese is not previously investigated. This investigation was conducted to know the effect of different fat contents of buttermilk on fatty acids composition, organic acids, vitamins, lipolysis and sensory characteristics of cheddar-type cheese. Cheddar-type cheese was produced from buttermilk having 1, 1.75, 2.50 and 3.25% fat contents (control, T1, T2 and T3). Fat content of control, T1, T2 and T3 were 9.81, 16.34, 25.17 and 31.19%. Fatty acids profile was determined on GC–MS, organic acids and vitamin A and E were determined on HPLC. Free fatty acids, peroxide value and cholesterol were determined. Cheddar-style cheese produced from buttermilk (1% fat) showed that it had softer texture and lacking typical cheese flavor. Gas chromatography–mass spectrometry (GC–MS) analysis showed that long-chain unsaturated fatty acids in control, T1, T2 and T3 samples were 45.88, 45.78, 45.90 and 46.19 mg/100 g. High Performance Liquid Chromatography (HPLC) analysis showed that lactic acid, propionic acid, citric acid and acetic acid gradually and steadily increased during the storage interval of 90 days. At the age of 90 days, lactic acid in control, T1, T2 and T3 was 4,789, 5,487, 6,571 and 8,049 ppm, respectively. At the end of ripening duration of 90 days, free fatty acids in control, T1, T2 and T3 were 0.29, 0.31, 0.35 and 0.42% with no difference in peroxide value. Stability of vitamin A after 90 days storage control, T1, T2 and T3 was 87.0, 80.0, 94.0 and 91.0%. Flavor score of cheddar-type cheese produced from butter milk having 1.0, 2.5 and 3.25% fat content was 81, 89 and 91% of total score (9). Hence, it is concluded that cheddar-type cheese can be produced from buttermilk having 2.5 and 3.25% fat contents with acceptable sensory attributes. Application of buttermilk for the production of other cheese varieties should be studied.info:eu-repo/semantics/publishedVersio

Metabolomics analysis as a tool to measure cobalt neurotoxicity : an in vitro validation

In this study, cobalt neurotoxicity was investigated in human astrocytoma and neuroblastoma (SH-SY5Y) cells using proliferation assays coupled with LC–MS-based metabolomics and transcriptomics techniques. Cells were treated with a range of cobalt concentrations between 0 and 200 µM. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay revealed cobalt cytotoxicity and decreased cell metabolism in a dose and time-dependent manner was observed by metabolomics analysis, in both cell lines. Metabolomic analysis also revealed several altered metabolites particularly those related to DNA deamination and methylation pathways. One of the increased metabolites was uracil which can be generated from DNA deamination or fragmentation of RNA. To investigate the origin of uracil, genomic DNA was isolated and analyzed by LC–MS. Interestingly, the source of uracil, which is uridine, increased significantly in the DNA of both cell lines. Additionally, the results of the qRT-PCR showed an increase in the expression of five genes Mlh1, Sirt2, MeCP2, UNG, and TDG in both cell lines. These genes are related to DNA strand breakage, hypoxia, methylation, and base excision repair. Overall, metabolomic analysis helped reveal the changes induced by cobalt in human neuronal-derived cell lines. These findings could unravel the effect of cobalt on the human brain

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy

AbstractDevelopmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients’ primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy.</jats:p

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy

Developmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients’ primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy