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Abstractβ-Glucanase has received great attention in recent years regarding their potential biotechnological applications and antifungal activities. Herein, the specific objectives of the present study were to purify, characterize and immobilize β-glucanase from Aspergillus niger using covalent binding and cross linking techniques. The evaluation of β-glucanase in hydrolysis of different lignocellulosic wastes with subsequent bioethanol production and its capability in biocontrol of pathogenic fungi was investigated. Upon nutritional bioprocessing, β-glucanase production from A. niger EG-RE (MW390925.1) preferred ammonium nitrate and CMC as the best nitrogen and carbon sources, respectively. The soluble enzyme was purified by (NH4)2SO4, DEAE-Cellulose and Sephadex G200 with 10.33-fold and specific activity of 379.1 U/mg protein. Tyrosyl, sulfhydryl, tryptophanyl and arginyl were essential residues for enzyme catalysis. The purified β-glucanase was immobilized on carrageenan and chitosan with appreciable yield. However, the cross-linked enzyme exhibited superior activity along with remarkable improved thermostability and operational stability. Remarkably, the application of the above biocatalyst proved to be a promising candidate in liberating the associate lignocellulosic reducing sugars, which was utilized for ethanol production by Saccharomyces cerevisiae. The purified β-glucanase revealed an inhibitory effect on the growth of two tested phytopathogens Fusarium oxysporum and Penicillium digitatum.

AbstractThe present paper experimentally explores the influence of the fiber hybridization and layering sequence on crashworthiness behavior and deformation history of polymer/metal thin-walled pipes. Jute (J)/glass (G) reinforced epoxy over wrapped aluminum (Al) pipes were prepared via hand wet wrapping then subjected to axial quasi-static compressive loads. The load versus displacement plots and crashing indicators, i.e. peak crushing load ($${\mathrm{F}}_{\mathrm{ip}}$$ F ip ), mean crushing load ($${\mathrm{F}}_{\mathrm{m}}$$ F m ), total energy absorption ($$\mathrm{U})$$ U ) , specific energy absorption $$\left(\mathrm{SEA}\right)$$ SEA , and crush force efficiency $$\left(\mathrm{CFE}\right)$$ CFE were determined. Experimental results revealed that the maximum $$\left(\mathrm{SEA}\right)$$ SEA was recorded for Al/2J/4G/2J pipe with a value of about 42.92 kJ/g, with an enhancement of 20.56% in $$\left(\mathrm{SEA}\right)$$ SEA compared with pure Al-pipes. Al/2J/4G/2J specimens display the maximum ($$\mathrm{U})$$ U ) , $$\left(\mathrm{SEA}\right)$$ SEA , and $$\left(\mathrm{CFE}\right)$$ CFE and could be employed as energy absorbing members in automobiles.

AbstractThe Fram Strait is the only deep gateway between the Arctic Ocean and the Nordic Seas and thus is a key area to study past changes in ocean circulation and the marine carbon cycle. Here, we study deep ocean temperature, δ18O, carbonate chemistry (i.e., carbonate ion concentration [CO32−]), and nutrient content in the Fram Strait during the late glacial (35,000–19,000 years BP) and the Holocene based on benthic foraminiferal geochemistry and carbon cycle modeling. Our results indicate a thickening of Atlantic water penetrating into the northern Nordic Seas, forming a subsurface Atlantic intermediate water layer reaching to at least ∼2,600 m water depth during most of the late glacial period. The recirculating Atlantic layer was characterized by relatively high [CO32−] and low δ13C during the late glacial, and provides evidence for a Nordic Seas source to the glacial North Atlantic intermediate water flowing at 2,000–3,000 m water depth, most likely via the Denmark Strait. In addition, we discuss evidence for enhanced terrestrial carbon input to the Nordic Seas at ∼23.5 ka. Comparing our δ13C and qualitative [CO32−] records with results of carbon cycle box modeling suggests that the total terrestrial CO2 release during this carbon input event was low, slow, or directly to the atmosphere.

Cyclophosphamide (CP) is an anticancer drug that causes infertility disorders. This study was designed to evaluate a nanoformulation of chitosan with an ethanolic extract from Spirulina platensis in terms of its protection against cyclophosphamide-induced ovarian toxicity. Nine groups of female Wistar rats were randomly assigned as follows: 1: control vehicle, 2: chitosan polymer, 3: telmisartan, 4: Spirulina platensis extract, 5: nanoformulation of the Spirulina platensis, and 6: single injection of CP; groups 7, 8, and 9 received the same treatments as those used in groups 3, 4, and 5, respectively, with a single dose of CP (200 mg/kg, I.P). The results displayed that the CP treatment decreased estradiol, progesterone, anti-mullerian hormone, and GSH content, and it downregulated PPAR-γ, Nrf-2, and HO-1 gene expression. In addition, the CP treatment caused an increase in the FSH, LH, and MDA levels. In the same manner, the protein expression of caspase-3, NF-kB, and TNF-α was upregulated in response to the CP treatment, while PPAR-γ was downregulated in comparison with the control. The rats treated with SPNPs exhibited a substantial reduction in the detrimental effects of oxidative stress and inflammation of the ovarian tissue. This study’s conclusions showed that SPNPs counteracted the effects of CP, preventing the death of ovarian follicles and restoring the gonadotropin hormone balance and normal ovarian histological appearance.

L'étude a été réalisée pour déterminer l'effet cytotoxique, antioxydant et gastro-protecteur de l'éthyl-4-[(3,5-di-tert-butyl-2-hydroxybenzylid ene)amino] benzoate (ETHAB) chez le rat. L'effet cytotoxique de l'ETHAB a été évalué à l'aide d'un test de clivage MTT sur une lignée cellulaire WRL68, tandis que son activité antioxydante a été évaluée in vitro. Dans l'étude anti-ulcéreuse, les rats ont été divisés en six groupes. Le groupe 1 et le groupe 2 ont reçu 10 % de Tween 20 (véhicule). Le groupe 3 a reçu 20 mg/kg d'oméprazole. Les groupes 4, 5 et 6 ont reçu ETHAB à des doses de 5, 10 et 20 mg/kg, respectivement. Après une heure, le groupe 1 a reçu le véhicule. Les groupes 2 à 6 ont reçu de l'éthanol absolu pour induire des lésions de la muqueuse gastrique. Dans la lignée cellulaire WRL68, une CI50 supérieure à 100 µg/mL a été observée. Les résultats de l'ETHAB ont montré une activité antioxydante dans les dosages DPPH, FRAP, oxyde nitrique et chélatant des métaux. Il n'y avait pas de toxicité aiguë même à la dose la plus élevée (1000 mg/kg). La microscopie a montré que les rats prétraités avec ETHAB ont révélé une protection de la muqueuse gastrique telle que déterminée par des augmentations significatives de la superoxyde dismutase (SOD), du niveau de pH, de la sécrétion de mucus, des lésions gastriques réduites, du niveau de malondialdéhyde (MDA) et de la muqueuse gastrique aplatie remarquable. Histologiquement, le prétraitement avec ETHAB a entraîné une protection gastrique comparativement meilleure, en raison de la réduction de l'œdème sous-muqueux avec infiltration leucocytaire. La coloration PAS a montré une intensité accrue dans l'absorption du bleu d'Alcian. En termes d'immunohistochimie, l'ETHAB a montré une diminution de l'expression des protéines Bax et une surexpression des protéines Hsp70. L'effet gastroprotecteur de l'ETHAB peut être attribué à l'activité antioxydante, à l'augmentation du mucus de la paroi gastrique, au niveau de pH du contenu gastrique, à l'activité de la SOD, à la diminution du niveau de MDA, à la zone d'ulcère, à l'aplatissement de la muqueuse gastrique, à la réduction de l'œdème et de l'infiltration leucocytaire de la couche sous-muqueuse, à l'augmentation de la coloration PAS, à la régulation positive de la protéine Hsp70 et à la suppression de l'expression de Bax. El estudio se llevó a cabo para determinar el efecto citotóxico, antioxidante y gastroprotector del etil-4-[(3,5-di-terc-butil-2-hidroxibencilid eno)amino] benzoato (ETHAB) en ratas. El efecto citotóxico de ETHAB se evaluó mediante un ensayo de escisión MTT en una línea celular WRL68, mientras que su actividad antioxidante se evaluó in vitro. En el estudio antiulceroso, las ratas se dividieron en seis grupos. El grupo 1 y el grupo 2 recibieron un 10% de Tween 20 (vehículo). El grupo 3 recibió 20 mg/kg de omeprazol. Los grupos 4, 5 y 6 recibieron ETHAB a dosis de 5, 10 y 20 mg/kg, respectivamente. Después de una hora, el grupo 1 recibió el vehículo. Los grupos 2-6 recibieron etanol absoluto para inducir lesiones de la mucosa gástrica. En la línea celular WRL68, se observó una IC50 de más de 100 µg/mL. Los resultados de ETHAB mostraron actividad antioxidante en los ensayos de DPPH, FRAP, óxido nítrico y quelantes de metales. No hubo toxicidad aguda incluso a la dosis más alta (1000 mg/kg). La microscopía mostró que las ratas pretratadas con ETHAB revelaron protección de la mucosa gástrica según lo determinado por aumentos significativos en la superóxido dismutasa (SOD), el nivel de pH, la secreción de moco, la reducción de las lesiones gástricas, el nivel de malondialdehído (MDA) y la notable mucosa gástrica aplanada. Histológicamente, el pretratamiento con ETHAB resultó en una protección gástrica comparativamente mejor, debido a la reducción del edema submucoso con infiltración de leucocitos. La tinción con PAS mostró una mayor intensidad en la absorción de azul alcián. En términos de inmunohistoquímica, ETHAB mostró expresión negativa de proteínas Bax y sobreexpresión de proteínas Hsp70. El efecto gastroprotector de ETHAB puede atribuirse a la actividad antioxidante, aumento del moco de la pared gástrica, nivel de pH del contenido gástrico, actividad SOD, disminución del nivel de MDA, área de la úlcera, aplanamiento de la mucosa gástrica, reducción del edema y la infiltración de leucocitos de la capa submucosa, aumento de la tinción de PAS, regulación positiva de la proteína Hsp70 y supresión de la expresión de Bax. The study was carried out to determine the cytotoxic, antioxidant and gastro-protective effect of ethyl-4-[(3,5-di-tert-butyl-2-hydroxybenzylid ene)amino] benzoate (ETHAB) in rats.The cytotoxic effect of ETHAB was assessed using a MTT cleavage assay on a WRL68 cell line, while its antioxidant activity was evaluated in vitro. In the anti-ulcer study, rats were divided into six groups. Group 1 and group 2 received 10% Tween 20 (vehicle). Group 3 received 20 mg/kg Omeprazole. Groups 4, 5 and 6 received ETHAB at doses of 5, 10, and 20 mg/kg, respectively. After an hour, group 1 received the vehicle. Groups 2-6 received absolute ethanol to induce gastric mucosal lesions. In the WRL68 cell line, an IC50 of more than 100 µg/mL was observed. ETHAB results showed antioxidant activity in the DPPH, FRAP, nitric oxide and metal chelating assays. There was no acute toxicity even at the highest dosage (1000 mg/kg). Microscopy showed that rats pretreated with ETHAB revealed protection of gastric mucosa as ascertained by significant increases in superoxide dismutase (SOD), pH level, mucus secretion, reduced gastric lesions, malondialdehyde (MDA) level and remarkable flattened gastric mucosa. Histologically, pretreatment with ETHAB resulted in comparatively better gastric protection, due to reduction of submucosal edema with leucocyte infiltration. PAS staining showed increased intensity in uptake of Alcian blue. In terms of immunohistochemistry, ETHAB showed down-expression of Bax proteins and over-expression of Hsp70 proteins.The gastroprotective effect of ETHAB may be attributed to antioxidant activity, increased gastric wall mucus, pH level of gastric contents, SOD activity, decrease in MDA level, ulcer area, flattening of gastric mucosa, reduction of edema and leucocyte infiltration of the submucosal layer, increased PAS staining, up-regulation of Hsp70 protein and suppressed expression of Bax. تم إجراء الدراسة لتحديد التأثير السام للخلايا ومضادات الأكسدة والحماية المعدية للإيثيل-4 - [(3,5 - di - tert - butyl -2 - hydroxybenzylid ene)amino] بنزوات (ETHAB) في الفئران. تم تقييم التأثير السام للخلايا لـ ETHAB باستخدام اختبار الانقسام MTT على خط خلية WRL68، بينما تم تقييم نشاطه المضاد للأكسدة في المختبر. في دراسة مكافحة القرحة، تم تقسيم الفئران إلى ست مجموعات. تلقت المجموعة 1 والمجموعة 2 10 ٪ توين 20 (مركبة). تلقت المجموعة 3 20 ملغم/كغم من أوميبرازول. تلقت المجموعات 4 و 5 و 6 ETHAB بجرعات 5 و 10 و 20 مجم/كجم على التوالي. بعد ساعة، استلمت المجموعة 1 السيارة. تلقت المجموعات 2-6 إيثانول مطلق للحث على حدوث آفات مخاطية في المعدة. في خط خلية WRL68، لوحظ أن التركيز النصفي المثبط يزيد عن 100 ميكروغرام/مل. أظهرت نتائج ETHAB نشاطًا مضادًا للأكسدة في فحوصات DPPH و FRAP وأكسيد النيتريك وخلاب المعادن. لم تكن هناك سمية حادة حتى في أعلى جرعة (1000 ملغم/كغم). أظهر الفحص المجهري أن الفئران المعالجة مسبقًا بـ ETHAB كشفت عن حماية الغشاء المخاطي في المعدة كما يتضح من الزيادات الكبيرة في ديسموتاز الأكسيد الفائق (SOD)، ومستوى الأس الهيدروجيني، وإفراز المخاط، وانخفاض الآفات المعدية، ومستوى المالونديالديهايد (MDA)، والغشاء المخاطي المسطح الرائع في المعدة. من الناحية النسيجية، أدى العلاج المسبق باستخدام ETHAB إلى حماية أفضل نسبيًا للمعدة، بسبب تقليل الوذمة تحت المخاطية مع ارتشاح الكريات البيض. أظهر تلطيخ PAS كثافة متزايدة في امتصاص أزرق ألسيان. من حيث الكيمياء النسيجية المناعية، أظهر ETHAB انخفاضًا في التعبير عن بروتينات Bax والإفراط في التعبير عن بروتينات Hsp70. يمكن أن يعزى التأثير الواقي للمعدة لـ ETHAB إلى النشاط المضاد للأكسدة، وزيادة مخاط جدار المعدة، ومستوى الأس الهيدروجيني لمحتويات المعدة، ونشاط السد، وانخفاض مستوى MDA، ومنطقة القرحة، وتسطيح الغشاء المخاطي للمعدة، وتقليل الوذمة وتسلل الكريات البيض في الطبقة تحت المخاطية، وزيادة تلطيخ PAS، وزيادة تنظيم بروتين Hsp70 والتعبير المكبوت عن Bax.

2,3-Butanediol (2,3-BDO) has gained much attention due to its bulk chemical uses in numerous applications such as the production of pharmaceuticals, cosmetics, synthetic rubber, inks, resins, perfumes, foodstuffs, fuel additives, and aviation fuel.

We have investigated in the current study the possible protective effects of two carnitine esters known to have powerful anti-oxidant potential namely, propionyl L-carnitine (PLC) and acetyl L-carnitine (AC) against alcohol-induced gastric lesions in rats. Both drugs were administered as a single oral dose of 200 mg kg(-1) body weight 1h before alcohol intake. Both carnitine esters could protect the gastric mucosa against the injurious effect of absolute alcohol and promote ulcer healing as evidenced from the ulcer index (UI) values. Propionyl L-carnitine prevented alcohol-induced increase in thiobarbituric acid-reactive substances (TBARS), an index of lipid peroxidation. The propionyl carnitine ester also increased the gastric content of reduced glutathione (GSH), besides it increased the enzymatic activities of gastric superoxide dismutase (SOD) and glutathione-S-transferase (GST). Likewise, AC did protect against the ulcerating effect of alcohol and mitigate most of the biochemical adverse effects induced by alcohol in gastric mucosa, but to a lesser extent than PLC. Neither PLC nor AC did affect catalase activity in gastric tissue. Based on these observations, one could conclude that carnitine esters, particularly PLC could partly protect gastric mucosa from alcohol-induced acute mucosal injury, and these gastroprotective effects might be probably induced, at least partly, through anti-oxidant mechanisms.