A two year experiment was carried out in newly reclaimed soils (sandy soils) to investigate the effect of cutting and phosphorus and potassium fertilization on the growth, yield, seed mucilage content and seed protein content of guar plant. The results revealed that different cutting treatments significantly decreased the plant weight, seed yield, seed mucilage content and seed protein content. Phosphorus fertilization up to 350 kg super-phosphate (15% P2O5)/feddan* significantly increased plant weight, seed yield, seed mucilage content and seed protein content. Fertilization with 150 kg potassium sulfate (48% K2O)/feddan was quite capable to meet guar plant potassium demands in this kind of soil. Without cutting plants, fertilization with 350 kg super-phosphate and 150 kg potassium sulfate/feddan resulted in the highest seed yield, seed muculage content and seed protein content.
In this study, we investigated the immunomodulatory effects of a supplemented killed influenza virus (V) by Echinacea purpurea (E) and Nigella sativa (N) extracts and effect of changing the route of immunization from intramuscular (IM) to intraperitoneal (IP). At the 2-, 3- and 4-week post-IM immunizations (WPIMI), the supplemented V with N (VN) induced the most significant IgM response unlike N alone. At the 2 WPIMI, V or VN induced the highest significant IgG levels. At the 2-week post-IP immunization (WPIPI), E and VN induced the most significant IgG levels. Both at the 3 and 4 WPIMI or WPIPI, various treatments induced significant increases in IgG. At the 4 WPIMI, E, V, and V with E (VE) induced significant increases in the CD4+ thymocytes while all IP treatments caused significant increase in their counts. V and VN induced the most significant IM induction of CD8+ thymocytes while their best IP stimulation was induced by N, VE, and VN. At the 4 WPIMI, various treatments caused significant increases in the mesenteric lymph node (MLN) CD4+, CD8+ counts. WPIPI with V or VE caused significant increases in both the CD4+- and CD8+ MLN cells, whereas VN significantly induced CD8+ MLN cells only. WPIPI with various treatments caused significant increases in the B-cell counts and the peak was obtained by VN.
Introduction -Egypt has the highest prevalence of hepatitis C virus (HCV) infection which is reported to be associated with autoimmune manifestations. Aim -There is a need for markers that enable differentiation between viral and non-infected-autoimmune patients. Material and Methods -Levels of the B-cell activation factor (BAFF), IL6, IL10 and TNF-α were quantified by ELISA in sera from HCVinfected-autoimmune patients (HCV-AI), HCV-infected patients with no autoimmune diseases (HCV-NAI), non-infected autoimmune patients (NIAI) and healthy control humans (C). Results -HCV-infected patients were 12.96, 8.33, 69.44 and 36.11% positive for the auto-antibodies ANA, AMA, ASMA and AGPCA respectively. The BAFF level was significantly (P<0.05) higher among the NI-AI patients compared to the HCV-NAI, HCV-AI patients and healthy control humans (C). For the IL6, no significant differences were seen between various patients' groups. In case of the IL10, its , levels were significantly higher (P<0.05) in the HCV-AI, NI-AI and HCV-NAI patients in comparison to the C humans. Levels of TNF-α were significantly (P<0.001 and 0.0001) higher amongst the HCV-NAI and HCV-AI than in the NI-AI patients respectively. Also, levels of the TNF-α were significantly (P<0.0001) higher amongst the C compared to the NI-AI. Levels of TNF-α were not significant amongst the HCV-NAI and HCV-AI patients than in C subjects. Conclusion -The obtained results showed that both IL6 and BAFF can serve as markers for autoimmunity and/or autoimmunity resulting from severe HCV infection, whereas, IL10 and TNF-α can be considered as markers for HCV infection in Egypt (genotype is mostly 4a).
Toll-like receptors (TLRs) represent the immune link between the innate and the adaptive immune signals against various pathogens. This study aimed to evaluate the TLRs3 and 7 as immune-markers in differentiating between hepatitis C virus (HCV)-infected and -uninfected patients. Also, the use of the TLR3 and TLR7 as immune markers was compared with the prevalent bio and immune markers for autoimmune diseases in HCVinfected or -uninfected patients. The levels of GPT, GOT, B cell activated factors, tumor necrosis factor-alpha (TNF-a), and interleukin (IL)-10 were measured in plasma, while the levels of TLR3 and TLR7 were quantified in lysates of peripheral blood mononuclear cells from healthy donors, HCV-infected patients, nonalcoholic fatty liver (NAFL) patients without autoimmune diseases and with autoimmune diseases (HCV-infected patients with autoimmune diseases [HCV+auto], nonalcoholic fatty liver patients with autoimmune diseases [NAFL+auto]), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE) patients. The relative expression of TLR3, TLR7, TNF, and IL-10 in cell lysates was assessed against glyceraldehyde 3-phosphate dehydrogenase (GAPDH) by quantitative real time-polymerase chain reaction (qRT-PCR). Results showed that TLRs 3 and 7 levels were significantly higher in SLE, RA, HCV, HCV+auto, and the NAFL patients compared to the normal control. The cell lysates from SLE patients expressed TLR3 at relatively significantly higher mRNA levels compared to normal subjects or other patient groups. The NAFL+auto patients expressed TLR7 at relatively significantly high mRNA levels compared to normal subjects or other patients. The RA patients expressed TLR7 at relatively significantly higher mRNA levels when compared to HCV, HCV+auto, and NAFL+auto patients. Conclusions: At the protein level, TLR7 can differentiate between HCV and NAFL patients. In addition, both TLRs3 and 7 can serve as potent markers in differentiating between NAFL and NAFL+auto.
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