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Elwakeel Eiman



  • Elwakeel Eiman
  • Eiman Elwakeel
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  • Targeting multiple cannabinoid anti-tumour pathways with a resorcinol derivative leads to inhibition of advanced stages of breast cancerBritish. Eiman Elwakeel's 2 research works with 18 citations and 94 reads, including: P Inflammation-induced cancer vs. cancer-induced inflammation is dependent. See what Eiman Elwakeel (eimanelwakeel) has discovered on Pinterest, the world's biggest collection of ideas.

    Elwakeel Eiman

    Because DCs are essential for T cell activation and since viral clearance in HCV infected patients is associated with a vigorous T cell response, this study proposed a new type of therapeutic HCV vaccine model of a strong antigenicity in humoral and cellular immunities, based on ex vivo stimulated HCV core protein-pulsed DCs and promoted by BCE treatment.

    This model might be used in a therapeutic setting to circumvent the diminished and down-regulated DCs function of HCV infected patients. As a therapeutic immunization approach this vaccine may present important new aspects since other vaccines are faced in HCV infected patients with the described down-regulated DCs function. The authors thank Prof. Salama El-darier for providing the plant material of this work in the powder form.

    Not applicable, because this data are part from unpublished project data. DG, participated by the idea, experimental design, practical work, and manuscript preparation. EE, participated in experimental design, and practical work. RK, participated in experimental design. MA, participated in experimental work, manuscript editing and drafting. AndIn addition, as the corresponding author. ME, participated by the idea, and tissue culture experimental work.

    All authors read and approved the final manuscript. National Center for Biotechnology Information , U. Published online Aug Ghareeb , 1 Eiman H. Elwakeel , 2 Rowaida Khalil , 3 Mina S. Aziz , 1 and Maha A. Author information Article notes Copyright and License information Disclaimer. Received Oct 21; Accepted Aug Associated Data Data Availability Statement Not applicable, because this data are part from unpublished project data. Abstract Background Virus-induced dendritic cells DCs functional deficiency leads to sub-optimal initiation of adaptive immune responses and consequently chronic infection establishment.

    Results There was no significant difference in surface phenotypic characterization of splenocytes from mice immunized with non-BCE-enriched-core-pulsed DCs iDcs-core compared to those from mice injected with RPMI medium.

    Background Approximately million people worldwide are chronically infected with HCV, but most are unaware of the infection based on the lack of symptoms at its first stages [ 1 ]. Methods BEC extraction and animal modeling Barberry dried roots were purchased and imported from Iran. Phenotypic characterization of splenocytes of immunized mice by flow cytometric analysis Splenocytes were washed and harvested in a well plate.

    Determination of the optimum effector cells: Open in a separate window. Mice group that received BCE-induced-core-pulsed DCs had a good T lymphocyte suppression capacity only when co-cultured with EL4-core cells A recent study reported that myeloid DCs have an up-regulated cytotoxic activity to kill T cells during HCV chronic infection, which represent a novel mechanism of HCV evasion [ 22 ].

    Potent and specific anti-core IgG antibodies only in the group that was immunized with BCE-induced-core-pulsed DCs Anti-HCV core IgG antibodies levels in the serum of each immunized mouse were monitored to assess the humoral immune response of mice to injection with DCs.

    Discussion Impaired cellular functions of immune system upon HCV Impairment of the maturation process in dendritic cells DCs is one of the mechanisms responsible for immune evasion of hepatitis C virus HCV [ 6 ]. Table 1 Phenotyping analysis of DCs.

    Anti-core cellular response The communication between DCs and T cells in this area of host—pathogen interaction seems to be a dialogue rather than a monologue in which mature DCs respond to T cells as well. Anti-core humoral response To determine if adequate levels of antibodies had been attained following vaccination, IgG antibodies recognizing HCV core protein were measured.

    Conclusion Because DCs are essential for T cell activation and since viral clearance in HCV infected patients is associated with a vigorous T cell response, this study proposed a new type of therapeutic HCV vaccine model of a strong antigenicity in humoral and cellular immunities, based on ex vivo stimulated HCV core protein-pulsed DCs and promoted by BCE treatment. Availability of data and materials Not applicable, because this data are part from unpublished project data.

    Competing interests The authors declare that they have no competing interests. Consent for publication Not applicable. Contributor Information Doaa A. American Association for the Study of Liver Diseases.

    Diagnosis, management, and treatment of hepatitis C: Global epidemiology of hepatitis C virus infection: Hepatology Baltimore, Md ; 57 4: Towards realistic estimates of HCV incidence in Egypt.

    The way forward in HCV treatment--finding the right path. Nat Rev Drug Discov. Coligan JE, Vogel S. Current Protocols in Immunology. Human dendritic cells expressing hepatitis C virus core protein display transcriptional and functional changes consistent with maturation.

    Immunopathogenesis of Hepatitis C Virus Infection. Gastroenterol Clin North Am. Ivanovska N, Philipov S. Study on the anti-inflammatory action of Berberis vulgaris root extract, alkaloid fractions, and pure alkaloids. Imanshahidi M, Hosseinzadeh H. Pharmacological and therapeutic effects of Berberis vulgaris and its active constituent, berberine.

    Immunomodulatory effect of Berberis vulgaris extracts on murine splenocytes and enrichment of dendritic cells in vitro. Antioxidants, cholinergic, anti-diabetic and anticancer effects. Biological assessment of Berberis vulgaris and its active constituent, berberine: Antibacterial, antifungal and anti-hepatitis C virus HCV effect.

    J Medicinal Plants Research. National Health and Medical Research Council. Guidelines to promote the wellbeing of animals used for scientific purposes: Vaccination by genetically modified dendritic cells expressing a truncated neu oncogene prevents. Chomczynski P, Sacchi N. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. NS3 primes Th1-like responses more effectively as a DNA-based immunogen than as a recombinant protein.

    Nimmerjahn F, Ravetch JV. Fc gamma receptors as regulators of immune responses. Immunobiology of dendritic cells. Zhao L, Tyrrell DL. Myeloid dendritic cells can kill T cells during chronic hepatitis C virus infection. Recent advances in the molecular biology of hepatitis C virus. The core of hepatitis C virus pathogenesis. Molecular virology of hepatitis C virus. Pavio N, Lai MM.

    The hepatitis C virus persistence: Hepatitis C virus-specific cytotoxic T cell response restoration after treatment-induced hepatitis C virus control. Life, activation and death of intrahepatic lymphocytes in chronic hepatitis C. Impaired allostimulatory function of dendritic cells in chronic hepatitis C infection. Impaired dendritic cell maturation in patients with chronic, but not resolved, hepatitis C virus infection.

    HCV viremia drives an increment of CD86 expression by myeloid dendritic cells. Specific anti-leukemic cell effect mediated by dendritic cells pulsed with chronic myelogenous leukemia lysate antigen in vitro. Professional and non-professional antigen-presenting cells in the porcine small intestine. On the dynamics of TCR: CD3 complex cell surface expression and down modulation. Hepatitis C virus core protein inhibits interferon production by a human plasmacytoid dendritic cell line and dysregulates interferon regulatory factor-7 and signal transducer and activator of transcription STAT 1 protein expression.

    Yamane H, Paul WE. Upregulation of endogenous intrahepatic interferon stimulated genes during chronic hepatitis C virus infection. Cytokine serum levels in patients with chronic HCV infection.

    J Clin Lab Anal. Serum interleukin 4 and interleukin 10 levels in patients with chronic hepatitis C virus infection. The regulation of IL production by immune cells. Akdis CA, Akdis M. Mechanisms of immune tolerance to allergens: Cytokine mRNA expression in hepatitis C virus infection: TH1 predominance in patients with chronic hepatitis C and TH1-TH2 cytokine profile in subjects with self-limited disease. Construction of a single-chain interleukinexpressing retroviral vector and its application in cytokine gene therapy against experimental coccidioidomycosis.

    Interleukin 12 a key immunoregulatory cytokine in infection applications. Int J Mol Sci. Support Center Support Center. Please review our privacy policy. This phenomenon might explain the anticancer effects observed in animal models upon blocking S1PR1. We therefore asked whether S1PR1 signaling in macrophages would be required for the protumor functions of TAMs in vivo.

    These mice express the PyMT oncoprotein in the mammary epithelium, which results in the formation of autochthonous mammary tumors in each gland, starting at 8 wk of age and progressing to metastatic disease after 15 wks. This became apparent when comparing the time until death Fig. At the end point, tumor size distribution Fig. Despite an unchanged tumor burden and size distribution at the end point, the number of pulmonary metastases was strongly reduced Fig.

    Thus, S1PR1 deletion had a minor impact on primary tumor development but a major impact on distant metastasis. Tumor burden and pulmonary metastasis in these animals was unchanged compared with WT animals.

    S1PR1 deletion in macrophages prevents pulmonary metastasis in breast cancer. Significant differences were not observed. Arrows indicate metastatic lung nodules. Polychromatic flow cytometry Fig. Metastasis-associated macrophages Qian et al. Their recruitment appears to be an essential component of the premetastatic niche Sceneay et al. To further test the involvement of macrophage S1PR1 in establishing the premetastatic niche, we adopted an experimental metastasis assay.

    We primed mice with hypoxic tumor cell supernatants to create a prometastatic environment in the lung, followed by i. Moreover, the number of epithelial cell adhesion molecule EpCAM —expressing tumor cells and the occurrence of macroscopic tumors was similar in both mouse strains Fig.

    Thus, loss of S1PR1 in macrophages did not affect immune cell accumulation at primary or secondary tumor sites and failed to support tumor cell growth in the lung. S1PR1 deletion in macrophages affects neither immune cell infiltration nor the premetastatic niche.

    Two separate experiments using two to three animals of each group were performed. Lungs were harvested after an additional 5 wks E. Schematic representation of experimental design. The circulatory system allows tumor cells to travel to distant sites. We asked whether the depletion of S1PR1 in macrophages would affect tumor angiogenesis. Lymphangiogenesis contributes to carcinoma metastasis in various ways. Lymph vessels may provide a route into the venous circulation, provide chemotactic factors for tumor cell mobilization, serve as a niche for cancer stem cells, or negatively modulate antitumor immunity Alitalo, ; Karaman and Detmar, Macrophages appear to be crucial for tumor lymphangiogenesis by providing growth factors that regulate lymphatic endothelial cell LEC proliferation Kubota et al.

    This prompted the question whether dysfunctional tumor lymphangiogenesis caused by S1PR1 deletion in macrophages also occurred in other tumors. To evaluate the robustness of the phenotype, we used the methylcholanthrene MCA -induced fibrosarcoma model. MCA tumors are strictly inflammation driven and barely metastasize. This observation may suggest that PyMT tumor cells were in a transitioning state rather than forming solid metastases in draining lymph nodes.

    S1PR1 deletion in macrophages prevents tumor lymphangiogenesis. Nuclei were stained with DAPI. P-values were calculated using log-rank test. Medium was replaced with fresh macrophage medium, and macrophage supernatants were harvested after another 21 h. After another 5 d for EBs, 7 d for aortic rings, and 8—10 d for lymphatic rings, EC and LEC content in EBs was analyzed by flow cytometry, and aortic ring and thoracic duct sprouting were analyzed microscopically. H Graphical representation of the experimental setup of the EB assay.

    J Graphical representation of the experimental setup of the aortic ring and lymphatic ring assays. Next, we asked whether macrophage-derived soluble factors provoked lymphangiogenesis downstream of S1PR1. We used an in vitro model in which we stimulated bone marrow—derived macrophages BMDMs with tumor cell supernatants. The resulting macrophage supernatants were added to 3D mouse embryoid bodies to monitor their differentiation to vascular cells Fig.

    These findings were confirmed in aortic ring and thoracic duct sprouting assays, in which sprouting angiogenesis of both lymph and blood vessels was increased upon stimulation with supernatants of WT BMDMs previously activated with tumor cells, but not when such supernatants were generated from macrophages with disrupted S1PR1 signaling Fig. Thus, S1PR1 signaling in macrophages in vitro promoted angiogenesis in addition to lymphangiogenesis via the production of soluble factors.

    We conclude that TAMs appear to be a redundant source of angiogenic, but a nonredundant source of lymphangiogenic, growth factors in vivo. Using multi-epitope ligand cartography Pierre et al. These cells constitute a minor subpopulation of TAMs in PyMT tumors that phenotypically resemble resident mammary gland macrophages Franklin et al. These data point to the minor subset of CD11b hi macrophages as being responsible for facilitating S1PR1-dependent lymphangiogenesis.

    Activation of the NLRP3 inflammasome is a two-step process that requires initial expression of its components by stimuli such as TLR ligands. Second, NLRP3 activators e. Representative images of five independent experiments are shown. B Representative contour plots show eGFP expression in tumor immune cell subpopulations. C Relative quantification of eGFP-expressing tumor immune cell subpopulations from tumors of four individual animals. P-values were calculated by two-sample t test after applying a variance filter to reduce microarray data complexity.

    The false discovery rate according to Benjamini and Hochberg was used to account for the multiple testing. Fold changes between the two groups of each supervised analysis were calculated for each gene. Matrigel plugs were maintained for 9 d and then analyzed by immunohistochemistry and flow cytometry for VEC and LEC content. These responses were completely blocked when IL-1R antagonist was added together with macrophage supernatants Fig.

    As observed in the mouse system, S1PR1 signaling in macrophages in vitro induced not only LEC tube formation; sprouting of blood endothelial cells upon incubation with macrophage supernatants largely followed the pattern of the LEC tube formation assay Fig.

    P-values were calculated using one-sample t test. Two individual experiments using two or three animals were performed. C Schematic representation of experimental design. To generate macrophage supernatants, macrophages were stimulated with supernatants of PyMT mammary carcinoma cells for 3 h, followed by medium replacement and harvesting of macrophage supernatants after another 21 h.

    Representative Western blot images M and quantification of three independent experiments N and O are displayed. D Representative phase-contrast images show tube formation after 6-h culture master junction indicated by arrow. G Representative phase-contrast images show human endothelial cell sprouting after h culture. We reasoned that the NLRP3 inflammasome might also be relevant in human cancer.

    To investigate this hypothesis, we first explored publicly available human breast cancer datasets. Because macrophages do not express the highest levels of S1PR1 among stromal cell populations e.

    Two gene expression datasets compared normal with breast tumor stroma Karnoub et al. Analysis of these datasets revealed increased NLRP3 expression in stroma of inflammatory ductal carcinoma Karnoub et al.

    The latter dataset further allowed the correlation of stromal NLRP3 expression with other tumor parameters. Finally, stromal cells of human epidermal growth factor receptor 2 HER2 -positive tumors, a marker of aggressiveness and nodal involvement Chikarmane et al.

    To be more specific in terms of stromal cell involvement, we analyzed tissue microarrays of human invasive breast cancer provided by the Cooperative Human Tissue Network and the Cancer Diagnosis Program for correlation of NLRP3 expression by macrophages with clinical parameters.

    Moreover, lymph node invasion Fig. These data support the notion that enhanced NLRP3 expression in human breast tumor stroma, containing macrophages as the major cell type expressing a functional inflammasome Kolb et al. NLRP3 expression in macrophages correlates with clinical parameters. Datasets of previous studies, Karnoub et al. H Survival rates of patients containing low or high numbers of NLRP3-expressing macrophages were compared.

    P-value was calculated using log-rank test. We previously noticed STAT3 signaling downstream of S1PR1 in human macrophages, which contributed to establishing an anti-inflammatory phenotype Weis et al. A number of germline mutations associated with lymphatic anomalies have been identified, albeit none of them in IL-1 signaling or production pathways Brouillard et al.

    We propose the NLRP3 inflammasome as a target to prevent metastatic disease. Inflammasomes have been implicated in the development of tumors that are inflammation driven, such as gastric and colorectal cancer Kolb et al. A number of other myeloid cells in the tumor microenvironment are known to produce proangiogenic factors Murdoch et al.

    Interestingly, not just protumor properties of inflammasomes and their products have been described Kolb et al. Therefore, it remains unclear whether interfering with S1PR1 may limit the success of immunogenic therapy. Expression of inflammasome components is likely triggered by damage-associated molecular patterns derived from necrotic tumor cells that are found in areas of hypoxia and nutrient deprivation Iyer et al.

    Thus, cell death in tumors might drive lymphangiogenesis and concomitant metastasis by inducing the NLRP3 inflammasome in bystander myeloid cells. Our data add to the emerging rationale to target S1P and its receptors in cancer. An S1P-neutralizing antibody Visentin et al.

    For instance, S1PR2 signaling apparently possesses antitumor potential mainly by inhibiting angiogenesis Du et al. Preventing metastasis remains a major challenge in cancer therapy. An attractive approach might be targeting lymphangiogenesis in carcinomas. Although the connection of tumor lymphangiogenesis with lymph node invasion is well established, the contribution of tumor lymphangiogenesis to metastasis at distant sites is still controversially discussed.

    It has been argued whether or not lymph vessels can serve as a direct or indirect through lymphovenous connections route of metastatic spread Ran et al. Besides this controversy, experimental studies indicate that lymphatic vessels in tumors can suppress antitumor immunity and provide a niche for cancer stem cells, thereby promoting disease development and metastasis, without serving as a highway for cancer cells to distant sites Alitalo, ; Card et al.

    Mouse care and experiments involving mice were approved by and followed the guidelines of the Hessian animal care and use committee. All treatments were initiated in animals at an age between 8 and 12 wks. All strains were crossed with mice expressing the PyMT oncoprotein under the mouse mammary tumor virus promoter Lin et al.

    To induce fibrosarcoma, mice received a single s. Experimental metastasis assays were performed essentially as described Sceneay et al. Animals were perfused, and tumors, lungs, and draining lymph nodes were harvested for further analyses.

    After 10 d, mice were killed, and Matrigel plugs were harvested. Animals were randomly assigned to the different treatment groups. Matrigel assays were performed in a blinded manner. All other animal experiments were performed nonblinded. Primary human monocytes and macrophages were cultured in RPMI supplemented with 2. The mouse embryonic stem cell line CGR8 provided by M. Investigators were blinded to group allocation during immunohistochemistry and immunofluorescence analyses.

    Primary tissue was Zn-fixed and paraffin-embedded or embedded in Tissue Tek Sakura Finetek for cryosections. Lung panorama pictures were produced using Autostitch v2.

    At least 10 independent sections of four different lung areas were analyzed. Fluorescent microscopy images were acquired using an automated confocal microscope LSM ; Zeiss. Vessel formation was analyzed by quantifying fluorescence positive area with Axiovision Zeiss in at least three independent sections. Multi-epitope ligand cartography was described before Pierre et al. Fluorescence images produced by each antibody were aligned pixel-wise.

    Nuclei were counterstained with DAPI. Breast cancer cores were evaluated based on tissue integrity after staining and macrophage content; only cores containing macrophages were considered. All antibodies and secondary reagents were titrated to determine optimal concentrations.

    CompBeads BD were used for single-color compensation to create multicolor compensation matrices. For gating, fluorescence minus one controls were used. Characterization of immune cell subsets in blood, spleen, liver, peritoneum, PyMT tumors, and lungs was performed essentially as described previously Weigert et al.

    The following antibodies were used: Statistical analysis was performed using the computing environment R.

    Eiman Elwakeel

    Semantic Scholar profile for Eiman Elwakeel, with fewer than 50 highly influential citations. Han, Yingying and Mora, Javier and Putyrski, Mateusz and Huard, Arnaud and da Silva, Priscila and Scholz, Anica and Elwakeel, Eiman and. Benjamin Weichand,1; Rüdiger Popp,2; Sarah Dziumbla,2; Javier Mora,1; Elisabeth Strack,1; Eiman Elwakeel,1; Ann-Christin Frank,1; Klaus.

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    Semantic Scholar profile for Eiman Elwakeel, with fewer than 50 highly influential citations.


    Han, Yingying and Mora, Javier and Putyrski, Mateusz and Huard, Arnaud and da Silva, Priscila and Scholz, Anica and Elwakeel, Eiman and.


    Benjamin Weichand,1; Rüdiger Popp,2; Sarah Dziumbla,2; Javier Mora,1; Elisabeth Strack,1; Eiman Elwakeel,1; Ann-Christin Frank,1; Klaus.


    Publications by authors named "Eiman Elwakeel". Are you Eiman Elwakeel? Register this Author. 4Publications. Reads. -Profile Views.


    See what Eiman Elwakeel (eimanelwakeel) has discovered on Pinterest, the world's biggest collection of everyone's favourite things.

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