Impact of different sesame intercropping dates with cotton on agronomic performance and insect pests infestation

Climate change has a negative impact on cotton and sesame yields. Intercropping can promote climate resilience through higher plant resources efficiency and natural suppression of insect pests, pathogens and weeds. A the two-year field trial was conducted to determine the best dates for intercropping sesame and cotton with respect to cotton and sesame agronomic performance and infestation by major pests. Sesame was planted two weeks before cotton, simultaneously with cotton, and two weeks after cotton into cotton planted on April 1, April 15 and May 1. Delayed intercropping of sesame increased cotton yield and yield-related traits at all cotton seeding dates and reduced infestations of insect pests, especially bollworms. Conversely, intercropping sesame two weeks before cotton was sown on May 1 produced the highest sesame agronomic trait values and decreased infestations of insect pests, including the sesame capsule borer. The highest land equivalent ratio (1.21) was obtained by intercropping sesame after two weeks with cotton planted on April 1. However, the lowest land equivalent ratio (1.0) was obtained by intercropping sesame two weeks before cotton in the cotton planted on April 15. On April 1, the relative crowding coefficient for intercropping treatments exhibited greater values than one, while April 15 displayed the lowest value. All of the intercropping treatments of sesame after cotton produced the best total return compared to the sole culture of cotton on the three dates. In summary, intercropping sesame after two weeks with cotton planted on April 1 was the best option for better cotton and sesame productivity, reduced pest pressure and higher economic returns. Keywords: Cotton, Insect pests, Land equivalent ratio, Sesame, Total retur

Molecular characterization of full fusion protein (F) of Newcastle disease virus genotype VIId isolated from Egypt during 2012-2016

Aim: The aim of this work was to study the sequence F gene of Newcastle disease virus (NDV) in regard to pathotyping and genotyping and to study the evolution of this NDV in Egypt. Materials and Methods: The present study was conducted using samples from seven suspected NDV flocks of vaccinated chickens during 2012-2016 from six governorates in Egypt. The NDV was successfully isolated from pathological specimens through inoculation in specific pathogen-free embryonated chicken eggs. Results: Pathogenicity of the NDV isolates has been estimated through intracerebral pathogenicity index and ranged from 1.66 to 1.73 which indicates the velogenic type of NDV isolates. Pathotyping and genotyping of these isolates were done through sequencing of full-length F gene. Results indicated that the seven NDV isolates showed characteristic cleavage site motif (112RRQKRF117) for the velogenic strains of NDV. Phylogenetic analysis of the F gene clustered these isolates within Group I of genotype VIId within Israeli strains NDV/IS/2015, NDV-Ch/SD883, and most of the Middle East strains. Six of seven sequenced isolates have six potential N-linked glycosylation sites. The neutralization epitope on the five antigenic sites of fusion is conserved in all Egyptian strains of this study except NDV-KFR-B7-2012 which has a substitution at D 170 N in epitope A4. In all our strains, 10 cysteine residues are recorded, except one loss of cysteine at residue 370 in both NDV-EG-35-2014 and NDV-GHB-328F-2016. Conclusion: All viruses in this study have 52 amino acid substitutions within fusion gene in compared with Lasota strain that reveals importance for its antigenic and structural function. The present work highlights the important need to sequence F gene of NDV genotype VIId to investigate the evolution of this NDV in Egypt

Characterization and Genotyping of Avian Infectious Bronchitis Virus in Egypt from 2019 to 2022

Avian infectious bronchitis virus (IBV) causes a major problem in broiler chickens due to increasing mortality and lowering body weight. This group of gammacorona viruses has the ability to emerge frequent new variants. In the present study, 18 broiler chicken farms from 7 Egyptian governorates that showed respiratory signs were sampled from 2019 to 2022. There were 11 farms positive for detection of IBV with real time RT-PCR. The samples were inoculated in specific pathogen free (SPF) embryos for three successive blind passages and the obtained viruses were sequenced for hypervariable region of spike protein (S1) to study their genetic diversity. The results showed that the S1 gene was clustered into two major groups, the first group has only one virus belong to classical vaccine strain of GI-1 lineage and the second group contain nine viruses belong to genotype GI-23 (variant II). They are further separated in two subgroups, first subgroup GI-23.2.1, contains 8 viruses, second subgroup contain one virus belong to genotype GI-23.2.2. The selection pressure analysis revealed episodic diversifying selection on multiple sites, with positive selection observed at five amino acid residues of the S1 protein, as demonstrated by FEL models. The recombination analysis of the S1 gene reveled two viruses with recombination events. The F1282-7-IB-2022 exhibited a slight recombination from IS/1494/2006 and a larger recombination from M41-2004. Meanwhile, the F1282-8-IB-2022 had a minor recombination of strain 4/91-1998 and a larger recombination from the Egyptian strain IBV-D1344/2/4/10-EG. The 3D structural models of hypervariable region HVR of S1 protein also showed that the recent viruses in this study from subgroup GI-23.2.1 (F1282-6-IB-2022) have high structural similarity with vaccine strain D274 and local vaccine seed virus IBV-EG/1212B-2012 than classic or variant GI-23.2.2 subgroup. These results can support efforts to compare the efficacy of local and imported vaccines both in-vivo and in-vitro and to help in controlling the disease

Characterization and Genotyping of Avian Infectious Bronchitis Virus in Egypt from 2019 to 2022

Avian infectious bronchitis virus (IBV) causes a major problem in broiler chickens due to increasing mortality and lowering body weight. This group of gammacorona viruses has the ability to emerge frequent new variants. In the present study, 18 broiler chicken farms from 7 Egyptian governorates that showed respiratory signs were sampled from 2019 to 2022. There were 11 farms positive for detection of IBV with real time RT-PCR. The samples were inoculated in specific pathogen free (SPF) embryos for three successive blind passages and the obtained viruses were sequenced for hypervariable region of spike protein (S1) to study their genetic diversity. The results showed that the S1 gene was clustered into two major groups, the first group has only one virus belong to classical vaccine strain of GI-1 lineage and the second group contain nine viruses belong to genotype GI-23 (variant II). They are further separated in two subgroups, first subgroup GI-23.2.1, contains 8 viruses, second subgroup contain one virus belong to genotype GI-23.2.2. The selection pressure analysis revealed episodic diversifying selection on multiple sites, with positive selection observed at five amino acid residues of the S1 protein, as demonstrated by FEL models. The recombination analysis of the S1 gene reveled two viruses with recombination events. The F1282-7-IB-2022 exhibited a slight recombination from IS/1494/2006 and a larger recombination from M41-2004. Meanwhile, the F1282-8-IB-2022 had a minor recombination of strain 4/91-1998 and a larger recombination from the Egyptian strain IBV-D1344/2/4/10-EG. The 3D structural models of hypervariable region HVR of S1 protein also showed that the recent viruses in this study from subgroup GI-23.2.1 (F1282-6-IB-2022) have high structural similarity with vaccine strain D274 and local vaccine seed virus IBV-EG/1212B-2012 than classic or variant GI-23.2.2 subgroup. These results can support efforts to compare the efficacy of local and imported vaccines both in-vivo and in-vitro and to help in controlling the disease

Table1_Synergistic cardioprotective effects of melatonin and deferoxamine through the improvement of ferritinophagy in doxorubicin-induced acute cardiotoxicity.DOCX

Ferritinophagy is one of the most recent molecular mechanisms affecting cardiac function. In addition, it is one of the pathways by which doxorubicin, one of the anticancer drugs commonly used, negatively impacts the cardiac muscle, leading to cardiac function impairment. This side effect limits the use of doxorubicin. Iron chelators play an important role in hindering ferritinophagy. Antioxidants can also impact ferritinophagy by improving oxidative stress. In this study, it was assumed that the antioxidant function of melatonin could promote the action of deferoxamine, an iron chelator, at the level of ferritinophagy. A total of 42 male Wistar rats (150–200 g) were divided into seven groups (n = 6) which consisted of group I: control normal, group II: doxorubicin (Dox), group III: melatonin (Mel), group IV: deferoxamine (Des), group V: Mel + Dox, group VI: Des + Dox, and group VII: Mel + Des + Dox. Groups III, V and VII were orally pretreated with melatonin 20 mg/kg/day for 7 days. Groups IV, VI and VII were treated with deferoxamine at a 250 mg/kg/dose once on D4 before Dox was given. Doxorubicin was given at a 20 mg/kg ip single dose. On the 8th day, the rats were lightly anaesthetized for electrocardiography analysis and echocardiography. Serum samples were collected and then sacrificed for tissue sampling. The following biochemical assessments were carried out: PCR of NCOA4, IREB2, FTH1, SLC7A11, and GPX4; and ELISA for serum cTnI, serum transferrin, tissue GSH, and malondialdehyde. In addition, histopathological assessment of heart injury; immunostaining of caspase-3, Bax, and Bcl2; and physiological function assessment by ECG and ECHO were carried out. Doxorubicin-induced acute significant cardiac injury with increased ferritinophagy and apoptosis responded to single and combined prophylactic treatment, in which the combined treatment showed mostly the best results. In conclusion, using melatonin as an antioxidant with an iron chelator, deferoxamine, could hinder the hazardous cardiotoxic effect of doxorubicin. However, further studies are needed to detect the impact of higher doses of melatonin and deferoxamine with a prolonged treatment period.</p

Image6_Synergistic cardioprotective effects of melatonin and deferoxamine through the improvement of ferritinophagy in doxorubicin-induced acute cardiotoxicity.TIF

Ferritinophagy is one of the most recent molecular mechanisms affecting cardiac function. In addition, it is one of the pathways by which doxorubicin, one of the anticancer drugs commonly used, negatively impacts the cardiac muscle, leading to cardiac function impairment. This side effect limits the use of doxorubicin. Iron chelators play an important role in hindering ferritinophagy. Antioxidants can also impact ferritinophagy by improving oxidative stress. In this study, it was assumed that the antioxidant function of melatonin could promote the action of deferoxamine, an iron chelator, at the level of ferritinophagy. A total of 42 male Wistar rats (150–200 g) were divided into seven groups (n = 6) which consisted of group I: control normal, group II: doxorubicin (Dox), group III: melatonin (Mel), group IV: deferoxamine (Des), group V: Mel + Dox, group VI: Des + Dox, and group VII: Mel + Des + Dox. Groups III, V and VII were orally pretreated with melatonin 20 mg/kg/day for 7 days. Groups IV, VI and VII were treated with deferoxamine at a 250 mg/kg/dose once on D4 before Dox was given. Doxorubicin was given at a 20 mg/kg ip single dose. On the 8th day, the rats were lightly anaesthetized for electrocardiography analysis and echocardiography. Serum samples were collected and then sacrificed for tissue sampling. The following biochemical assessments were carried out: PCR of NCOA4, IREB2, FTH1, SLC7A11, and GPX4; and ELISA for serum cTnI, serum transferrin, tissue GSH, and malondialdehyde. In addition, histopathological assessment of heart injury; immunostaining of caspase-3, Bax, and Bcl2; and physiological function assessment by ECG and ECHO were carried out. Doxorubicin-induced acute significant cardiac injury with increased ferritinophagy and apoptosis responded to single and combined prophylactic treatment, in which the combined treatment showed mostly the best results. In conclusion, using melatonin as an antioxidant with an iron chelator, deferoxamine, could hinder the hazardous cardiotoxic effect of doxorubicin. However, further studies are needed to detect the impact of higher doses of melatonin and deferoxamine with a prolonged treatment period.</p

Image3_Synergistic cardioprotective effects of melatonin and deferoxamine through the improvement of ferritinophagy in doxorubicin-induced acute cardiotoxicity.TIF

Ferritinophagy is one of the most recent molecular mechanisms affecting cardiac function. In addition, it is one of the pathways by which doxorubicin, one of the anticancer drugs commonly used, negatively impacts the cardiac muscle, leading to cardiac function impairment. This side effect limits the use of doxorubicin. Iron chelators play an important role in hindering ferritinophagy. Antioxidants can also impact ferritinophagy by improving oxidative stress. In this study, it was assumed that the antioxidant function of melatonin could promote the action of deferoxamine, an iron chelator, at the level of ferritinophagy. A total of 42 male Wistar rats (150–200 g) were divided into seven groups (n = 6) which consisted of group I: control normal, group II: doxorubicin (Dox), group III: melatonin (Mel), group IV: deferoxamine (Des), group V: Mel + Dox, group VI: Des + Dox, and group VII: Mel + Des + Dox. Groups III, V and VII were orally pretreated with melatonin 20 mg/kg/day for 7 days. Groups IV, VI and VII were treated with deferoxamine at a 250 mg/kg/dose once on D4 before Dox was given. Doxorubicin was given at a 20 mg/kg ip single dose. On the 8th day, the rats were lightly anaesthetized for electrocardiography analysis and echocardiography. Serum samples were collected and then sacrificed for tissue sampling. The following biochemical assessments were carried out: PCR of NCOA4, IREB2, FTH1, SLC7A11, and GPX4; and ELISA for serum cTnI, serum transferrin, tissue GSH, and malondialdehyde. In addition, histopathological assessment of heart injury; immunostaining of caspase-3, Bax, and Bcl2; and physiological function assessment by ECG and ECHO were carried out. Doxorubicin-induced acute significant cardiac injury with increased ferritinophagy and apoptosis responded to single and combined prophylactic treatment, in which the combined treatment showed mostly the best results. In conclusion, using melatonin as an antioxidant with an iron chelator, deferoxamine, could hinder the hazardous cardiotoxic effect of doxorubicin. However, further studies are needed to detect the impact of higher doses of melatonin and deferoxamine with a prolonged treatment period.</p

Image2_Synergistic cardioprotective effects of melatonin and deferoxamine through the improvement of ferritinophagy in doxorubicin-induced acute cardiotoxicity.PNG

Ferritinophagy is one of the most recent molecular mechanisms affecting cardiac function. In addition, it is one of the pathways by which doxorubicin, one of the anticancer drugs commonly used, negatively impacts the cardiac muscle, leading to cardiac function impairment. This side effect limits the use of doxorubicin. Iron chelators play an important role in hindering ferritinophagy. Antioxidants can also impact ferritinophagy by improving oxidative stress. In this study, it was assumed that the antioxidant function of melatonin could promote the action of deferoxamine, an iron chelator, at the level of ferritinophagy. A total of 42 male Wistar rats (150–200 g) were divided into seven groups (n = 6) which consisted of group I: control normal, group II: doxorubicin (Dox), group III: melatonin (Mel), group IV: deferoxamine (Des), group V: Mel + Dox, group VI: Des + Dox, and group VII: Mel + Des + Dox. Groups III, V and VII were orally pretreated with melatonin 20 mg/kg/day for 7 days. Groups IV, VI and VII were treated with deferoxamine at a 250 mg/kg/dose once on D4 before Dox was given. Doxorubicin was given at a 20 mg/kg ip single dose. On the 8th day, the rats were lightly anaesthetized for electrocardiography analysis and echocardiography. Serum samples were collected and then sacrificed for tissue sampling. The following biochemical assessments were carried out: PCR of NCOA4, IREB2, FTH1, SLC7A11, and GPX4; and ELISA for serum cTnI, serum transferrin, tissue GSH, and malondialdehyde. In addition, histopathological assessment of heart injury; immunostaining of caspase-3, Bax, and Bcl2; and physiological function assessment by ECG and ECHO were carried out. Doxorubicin-induced acute significant cardiac injury with increased ferritinophagy and apoptosis responded to single and combined prophylactic treatment, in which the combined treatment showed mostly the best results. In conclusion, using melatonin as an antioxidant with an iron chelator, deferoxamine, could hinder the hazardous cardiotoxic effect of doxorubicin. However, further studies are needed to detect the impact of higher doses of melatonin and deferoxamine with a prolonged treatment period.</p

Image1_Synergistic cardioprotective effects of melatonin and deferoxamine through the improvement of ferritinophagy in doxorubicin-induced acute cardiotoxicity.TIF

Ferritinophagy is one of the most recent molecular mechanisms affecting cardiac function. In addition, it is one of the pathways by which doxorubicin, one of the anticancer drugs commonly used, negatively impacts the cardiac muscle, leading to cardiac function impairment. This side effect limits the use of doxorubicin. Iron chelators play an important role in hindering ferritinophagy. Antioxidants can also impact ferritinophagy by improving oxidative stress. In this study, it was assumed that the antioxidant function of melatonin could promote the action of deferoxamine, an iron chelator, at the level of ferritinophagy. A total of 42 male Wistar rats (150–200 g) were divided into seven groups (n = 6) which consisted of group I: control normal, group II: doxorubicin (Dox), group III: melatonin (Mel), group IV: deferoxamine (Des), group V: Mel + Dox, group VI: Des + Dox, and group VII: Mel + Des + Dox. Groups III, V and VII were orally pretreated with melatonin 20 mg/kg/day for 7 days. Groups IV, VI and VII were treated with deferoxamine at a 250 mg/kg/dose once on D4 before Dox was given. Doxorubicin was given at a 20 mg/kg ip single dose. On the 8th day, the rats were lightly anaesthetized for electrocardiography analysis and echocardiography. Serum samples were collected and then sacrificed for tissue sampling. The following biochemical assessments were carried out: PCR of NCOA4, IREB2, FTH1, SLC7A11, and GPX4; and ELISA for serum cTnI, serum transferrin, tissue GSH, and malondialdehyde. In addition, histopathological assessment of heart injury; immunostaining of caspase-3, Bax, and Bcl2; and physiological function assessment by ECG and ECHO were carried out. Doxorubicin-induced acute significant cardiac injury with increased ferritinophagy and apoptosis responded to single and combined prophylactic treatment, in which the combined treatment showed mostly the best results. In conclusion, using melatonin as an antioxidant with an iron chelator, deferoxamine, could hinder the hazardous cardiotoxic effect of doxorubicin. However, further studies are needed to detect the impact of higher doses of melatonin and deferoxamine with a prolonged treatment period.</p