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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Cannabidiol CBD is a non-intoxicating phytocannabinoid from cannabis sativa that has demonstrated anti-inflammatory effects in several inflammatory conditions including arthritis. However, CBD binds to several receptors and enzymes and, therefore, its mode of action remains elusive. These effects were pronounced under inflammatory conditions by activating transient receptor potential ankyrin TRPA1 , and by opening of the mitochondrial permeability transition pore. In addition, an inhibitor of the mitochondrial permeability transition pore, cyclosporin A, also blocked the effects of CBD on cell viability and IL-8 production. PoPo3 uptake was inhibited by the voltage-dependent anion-selective channel inhibitor DIDS and Decynium, an inhibitor for all organic cation transporter isoforms. Thus, CBD possesses anti-arthritic activity and might ameliorate arthritis via targeting synovial fibroblasts under inflammatory conditions. Cannabidiol CBD is a non-intoxicating cannabinoid found in cannabis sativa 1. In contrast to the psychoactive constituent tetrahydrocannabinol THC , CBD demonstrates no direct effect at cannabinoid receptors 1 and 2 CB 1 and CB 2 but modulates the effect of agonists suggesting an allosteric function 2. Despite its promiscuous pharmacology, CBD is well tolerated even when given in high concentrations 12 , Side effects of CBD in humans include diarrhea and fatigue and, more importantly, CBD interacts with other drugs since it is metabolized by CYP enzymes in the liver thereby inhibiting the degradation of other therapeutic compounds 14 , While the therapeutic benefits of CBD in childhood epilepsy are well documented, its effects on inflammation have only been investigated in animal models 13 , Studies in rodents with osteoarthritis or collagen-induced arthritis demonstrated anti-inflammatory and analgesic effects of CBD, but these studies did not identify the mechanism of action 17 , 18 , Here, we investigate the effect of CBD on intracellular calcium, cell viability, and cytokine production in rheumatoid arthritis synovial fibroblasts RASF. RASF are one major contributor of joint destruction in RA as they secrete pro-inflammatory cytokines and matrix degrading enzymes In fact, subsets of RASF selectively mediate joint destruction or the inflammatory response, emphasizing their important role in the pathogenesis of RA CBD also binds TRPA1 7 , 23 , and therefore we hypothesized that CBD has detrimental effects on cell viability, which might explain in part its mechanism of action at sites of inflammation. Therefore, we investigated the effect of fetal calf serum content with CBD on proliferation. DMSO vehicle control alone had a stimulatory effect on proliferation Fig. These findings underline the need for relatively high concentrations of CBD when used in in vivo settings Two-tailed t -test was used for comparisons in f. The error bars in c — f represent the standard error of mean sem. Under these conditions, intracellular calcium levels were significantly increased compared to untreated RASF Fig. PoPo3 uptake increases when membrane integrity is compromised during apoptosis or necrosis. RR, a general inhibitor for several TRP channels 26 , 27 , 28 , reduced intracellular calcium levels Fig. A increased PoPo3 uptake under basal conditions Fig. Mean intracellular calcium mobilization a , b , e , f , i , j , m , n , q , r , u , v and mean PoPo3 uptake c , d , g , h , k , l , o , p , s , t , w , x of RASF after CBD challenge and concomitant inhibition with the antagonists given in the figure. CBD stabilizes a closed conformation of VDAC, which excludes the exchange of metabolites from the cytosol into mitochondria, but enhances its calcium transport function 8 , Cationic and uncharged compounds are taken up by organic cation transporters OCT 39 , 40 and therefore we assessed the effects of Decynium D22 , an inhibitor of all OCT isoforms on intracellular calcium and the uptake of PoPo3. Mean intracellular calcium mobilization a , b , e , f , i , j , m , n and mean PoPo3 uptake c , d , g , h , k , l , o , p of RASF after CBD challenge and concomitant inhibition with the antagonists given in the figure. The error bars represent the standard error of mean. In this study, we demonstrated that CBD decreases cell viability, proliferation, and cytokine production but increases intracellular calcium and PoPo3 levels of RASF and all effects were enhanced by TNF pre-stimulation. We demonstrated that CBD reduces cell viability, but RealTime-Glo assays were conducted in serum-free medium without carrier protein. Consequently, for in vivo applications, CBD needs to be administered in high concentrations to elicit beneficial effects as shown in the treatment of Dravet syndrome Moreover, we found that CsA reversed the detrimental effects of CBD on cell viability, which confirms results from Olivas-Aguirre et al. This confirms own previous results demonstrating calcium mobilization in response to TRPA1 ligation In fact, in dorsal root ganglia neurons it has been shown that TRPA1 is located in lysosomes, where its activation fosters neurotransmitter release Although we do not provide direct evidence regarding the localization of TRPA1, the use of the cell-impermeable pan-TRP inhibitor RR 43 , which was only able to slightly attenuate the effects of CBD suggests an intracellular target protein. In line with this, the lipophilic antagonist A decreased calcium mobilization and PoPo3 uptake after CBD challenge. Moreover, we used Thapsigargin to deplete ER calcium stores and GPN to disrupt lysosomes and both compounds reduced the elevation of intracellular calcium after CBD exposure. This shows that ER calcium stores are involved and it has been shown that even if calcium originates from lysosomes, the signal is amplified by depletion of ER stores This is important, because although GPN has been reported to mobilize lysosomal calcium, a recent study claimed that GPN increases calcium through an ER-dependent mechanism CPZ is also an agonist at TRPA1 48 , and we did detect a small increase in basal intracellular calcium in response to this ligand alone. Besides binding to TRPs, it has been demonstrated that CBD ligates several proteins 11 , 49 with mitochondrial targets being the most prominent 8 , 9 , 10 , 25 , Although protective effects of CBD against mitochondrial toxins have been shown 10 , 50 , the majority of studies demonstrated that CBD induces cell death by disturbing calcium homeostasis 8 , 9 , This confirms our results, since CBD augmented calcium levels with a concomitant increase in cell death. Excess cytosolic calcium is taken up by mitochondria which are depolarized in this process If mitochondrial calcium levels exceed a certain threshold, mPTP is assembled leading to cell death In line with this, CsA reduced intracellular calcium, which is another indicator that mitochondria provide a significant contribution to the increase in calcium by CBD. Calcium is increased by mPTP formation as mitochondria are permeabilized releasing stored calcium into the cytosol Thus, inhibiting mPTP formation by CsA decreases calcium leakage from mitochondria and subsequent cell death. CGP blocks calcium transport from the mitochondrial matrix into the intermembrane space, thus increasing mitochondrial and reducing cytosolic calcium levels In the latter it can act as forward or reverse mode antagonist dependent on cell type, NCLX isoform, and concentration 55 , This might depend on the initial calcium signal generated by CBD, because DIDS can permeabilize the inner mitochondrial membrane depending on calcium concentration leading to formation of mPTP Besides calcium, PoPo3 uptake served as readout for changes in cell viability as it is supposed to enter cells with a compromised plasma membrane only. In addition, it has been demonstrated that the family of organic cation transporters OCT mediates the uptake of many charged but also electroneutral compounds into the cell Therefore, it is quite possible that PoPo3 is also taken up by OCT and indeed we show that decynium, which inhibits all OCT isoforms 39 strongly reduced PoPo3 uptake and it also blunted the increase of intracellular calcium, which might be due to the electrogenic properties of D22 D22 did not influence basal uptake of PoPo3, but reduced the CBD-induced uptake and this might be related to changes in intracellular calcium since the activity of OCT is regulated by calcium-dependent proteins CsA was able to rescue RASF from cell death and increased Il-6 and IL-8 production confirming that cell death is the influencing factor on cytokine production. Eventually, mitochondrial calcium overload occurs and mPTP is assembled leading to cell death. CBD has been used in animal model of RA, demonstrating anti-inflammatory and analgesic effects but the mechanism of action has not been identified 17 , CBD might decrease chronic inflammation since RA is characterized by a hypoxic environment in the joint with concomitant mitochondrial dysfunction In addition, CBD might also synergize with anti-rheumatic drugs like methotrexate or JAK inhibitors, since it has been reported in tumor cell lines that CBD works in synergy with e. In conclusion, CBD might be beneficial as an adjuvant treatment in rheumatoid arthritis that might support the action of currently used disease-modifying anti-rheumatic drugs. In total, 40 patients with long-standing RA fulfilling the American College of Rheumatology revised criteria for RA 24 were included in this study. The RA group comprised of 32 females and 8 males with a mean age of C-reactive protein was IN all, 11 out of 40 patients received glucocorticoids, 7 out of 40 methotrexate, 3 out of 40 biologicals, and 1 out of 40 a JAK inhibitor. All patients underwent elective knee joint replacement surgery, and they were informed about the purpose of the study and gave written consent. We confirm that all experiments were performed in accordance with relevant guidelines and regulations Table 1. Samples from RA synovial tissue were isolated and prepared as described previously 22 for details see also Supplementary methods. Cells were permeabilized with 0. Then, 0. The statistic tests used are given in the figure legends. When data are presented as box plots, the boxes represent the 25th to 75th percentiles, the lines within the boxes represent the median, and the lines outside the boxes represent the 10th and 90th percentiles. When data are presented as line plots, the line represents the mean. When data are presented as bar charts, the top of the bar represents the mean and error bars depict the standard error of the mean sem. ElSohly, M. Phytochemistry of Cannabis sativa L. Navarro, G. Sonego, A. Cannabidiol prevents haloperidol-induced vacuos chewing movements and inflammatory changes in mice via PPARgamma receptors. Brain Behav. Miller, S. Delta9-tetrahydrocannabinol and cannabidiol differentially regulate intraocular pressure. Lin, X. Laun, A. Acta Pharmacol. Iannotti, F. Nonpsychotropic plant cannabinoids, cannabidivarin CBDV and cannabidiol CBD , activate and desensitize transient receptor potential vanilloid 1 TRPV1 channels in vitro: potential for the treatment of neuronal hyperexcitability. ACS Chem. Rimmerman, N. Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 VDAC1 by cannabidiol: a novel mechanism for cannabinoid-induced cell death. Cell Death Dis. Wu, H. Cannabidiol induced apoptosis in human monocytes through mitochondrial permeability transition pore-mediated ROS production. Free Radic. Ryan, D. De Gregorio, D. Cannabidiol modulates serotonergic transmission and reverses both allodynia and anxiety-like behavior in a model of neuropathic pain. Pain , — PubMed Google Scholar. Millar, S. A systematic review of cannabidiol dosing in clinical populations. Laux, L. Long-term safety and efficacy of cannabidiol in children and adults with treatment resistant Lennox-Gastaut syndrome or Dravet syndrome: expanded access program results. Epilepsy Res. Jiang, R. Identification of cytochrome P enzymes responsible for metabolism of cannabidiol by human liver microsomes. Life Sci. Huestis, M. Cannabidiol adverse effects and toxicity. Burstein, S. Cannabidiol CBD and its analogs: a review of their effects on inflammation. Hammell, D. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Pain 20 , — Philpott, H. Attenuation of early phase inflammation by cannabidiol prevents pain and nerve damage in rat osteoarthritis. Malfait, A. The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. USA 97 , — Bustamante, M. Fibroblast-like synoviocyte metabolism in the pathogenesis of rheumatoid arthritis. Arthritis Res. Croft, A. Distinct fibroblast subsets drive inflammation and damage in arthritis. Nature , — Lowin, T. Selective killing of proinflammatory synovial fibroblasts via activation of transient receptor potential ankyrin TRPA1. De, P. Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes. Elmes, M. Olivas-Aguirre, M. Cannabidiol directly targets mitochondria and disturbs calcium homeostasis in acute lymphoblastic leukemia. Caterina, M. A capsaicin-receptor homologue with a high threshold for noxious heat. Ambrus, L. Human podocytes express functional thermosensitive TRPV channels. Hamilton, N. Weller, K. Neuropeptides 45 , — Brenneman, D. Knockdown siRNA targeting the mitochondrial sodium-calcium exchanger-1 inhibits the protective effects of two cannabinoids against acute paclitaxel toxicity. Kim, J. Mitochondrial permeability transition: a common pathway to necrosis and apoptosis. Ben-Hail, D. Acta , — Benitez-Rangel, E. Cell Death Discov. Shoshan-Barmatz, V. VDAC, a multi-functional mitochondrial protein as a pharmacological target. Mitochondrion 12 , 24—34 Papp, B. Demonstration of two forms of calcium pumps by thapsigargin inhibition and radioimmunoblotting in platelet membrane vesicles. Thastrup, O. The calcium mobilizing tumor promoting agent, thapsigargin elevates the platelet cytoplasmic free calcium concentration to a higher steady state level. A possible mechanism of action for the tumor promotion. Morgan, A. McGuinness, L. Neuropharmacology 52 , — Hayer-Zillgen, M. Inyushin, M. Papa, V. The effects of pH and temperature on the in vitro bindings of deltatetrahydrocannabinol and other cannabinoids to bovine serum albumin. CAS Google Scholar. Shang, S. Cell Biol. Buch, T. Functional expression of the transient receptor potential channel TRPA1, a sensor for toxic lung inhalants, in pulmonary epithelial cells. Kilpatrick, B. Cell Sci. Atakpa, P. Luo, H. Cannabidiol increases proliferation, migration, tubulogenesis, and integrity of human brain endothelial cells through TRPV2 activation. Nabissi, M. Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Carcinogenesis 34 , 48—57 Kistner, K. Systemic desensitization through TRPA1 channels by capsazepine and mustard oil - a novel strategy against inflammation and pain. Ferro, R. GPR55 signalling promotes proliferation of pancreatic cancer cells and tumour growth in mice, and its inhibition increases effects of gemcitabine. Oncogene 37 , — Cannabidiol normalizes caspase 3, synaptophysin, and mitochondrial fission protein DNM1L expression levels in rats with brain iron overload: implications for neuroprotection. Duchen, M. Mitochondria and calcium: from cell signalling to cell death. Giorgi, C. The machineries, regulation and cellular functions of mitochondrial calcium. Kinnally, K. Is mPTP the gatekeeper for necrosis, apoptosis, or both? Ruiz, A. Amran, M. Drug Rev. Santo-Domingo, J. Bernardes, C. Acta , 93— Stueber, T. Anesthesiology , — Schilling, W. Sodin-Semrl, S. Lipoxin A4 inhibits IL-1 beta-induced IL-6, IL-8, and matrix metalloproteinase-3 production in human synovial fibroblasts and enhances synthesis of tissue inhibitors of metalloproteinases. Fearon, U. Hypoxia, mitochondrial dysfunction and synovial invasiveness in rheumatoid arthritis. Fraguas-Sanchez, A. CBD loaded microparticles as a potential formulation to improve paclitaxel and doxorubicin-based chemotherapy in breast cancer. Laragione, T. The cation channel Trpv2 is a new suppressor of arthritis severity, joint damage, and synovial fibroblast invasion. Skonieczna, M. Cox, D. Sahoo, S. Transient receptor potential ankyrin1 channel is endogenously expressed in T cells and is involved in immune functions. Sandor, Z. Effects of cinnamaldehyde on smooth muscle preparations. Pharmacology , — Mayer, F. Liver Physiol. Maher, M. Activation of TRPA1 by farnesyl thiosalicylic acid. Engler, A. Expression of transient receptor potential vanilloid 1 TRPV1 in synovial fibroblasts from patients with osteoarthritis and rheumatoid arthritis. Radulovic, M. ESCRT-mediated lysosome repair precedes lysophagy and promotes cell survival. EMBO J. Perez, M. Redox Biol. Download references. We thank Birgit Opgenoorth for excellent technical assistance. This work was supported by an unlimited grant of the Hiller Foundation. You can also search for this author in PubMed Google Scholar. Correspondence to Torsten Lowin. Reprints and permissions. Cannabidiol CBD : a killer for inflammatory rheumatoid arthritis synovial fibroblasts. Cell Death Dis 11 , Download citation. Received : 26 February Revised : 06 August Accepted : 06 August Published : 01 September Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Clinical and Translational Oncology Skip to main content Thank you for visiting nature. Download PDF. Subjects Immune cell death Rheumatoid arthritis. Abstract Cannabidiol CBD is a non-intoxicating phytocannabinoid from cannabis sativa that has demonstrated anti-inflammatory effects in several inflammatory conditions including arthritis. Differential inflammation-mediated function of prokineticin 2 in the synovial fibroblasts of patients with rheumatoid arthritis compared with osteoarthritis Article Open access 15 September Introduction Cannabidiol CBD is a non-intoxicating cannabinoid found in cannabis sativa 1. Full size image. Materials and methods Biochemicals Patients In total, 40 patients with long-standing RA fulfilling the American College of Rheumatology revised criteria for RA 24 were included in this study. Table 1 Biochemicals used in this study. Full size table. References ElSohly, M. Acknowledgements We thank Birgit Opgenoorth for excellent technical assistance. View author publications. Ethics declarations Conflict of interest The authors declare that they have no conflict of interest. Edited by H. Supplementary information. About this article. Cite this article Lowin, T. Copy to clipboard. This article is cited by A narrative review of the therapeutic and remedial prospects of cannabidiol with emphasis on neurological and neuropsychiatric disorders Oluwadara Pelumi Omotayo Yolandy Lemmer Shayne Mason Journal of Cannabis Research Association between cannabis use and physical activity in the United States based on legalization and health status Ray M. Search Search articles by subject, keyword or author. Show results from All journals This journal. Advanced search.

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This judgment text has undergone conversion so that it is mobile and web-friendly. This may have created formatting or alignment issues. Please refer to the PDF copy for a print-friendly version. Amran Bin Eusuff 2. Rabu Bin Rahmat Public Prosecutor Criminal Law — Entrapment — Whether entrapment is a valid defence to a criminal charge. The next day, he managed to get in contact with Daud and his partner who was called 'Abu'. CPL Fazuri posed as a buyer named 'Boy' and negotiated with both of them to purchase 3 kg of cannabis to be delivered on 3 May These officers met with Amran and Rabu, who introduced themselves as 'Daud' and 'Abu' respectively. Both Amran and Rabu got into a car that the undercover officers were in. The car was driven to Bukit Merah View where Rabu alighted to collect the drugs. He returned to the car and handed the drugs to one of the undercover officer. The CNB officer then signalled to his colleagues to move in to arrest the two suspects whereupon the undercover car was intercepted. Amran and Rabu tried to flee but were eventually arrested. Amran made two long statements to the Investigating Officer. He admitted that he did so for the commission he was promised. As for Rabu, he also made two long statements to the Investigating Officer. In the first one, he denied flatly that he was involved in drug trafficking. However, in the second statement, he admitted that he procured the drugs to sell to Boy. During the trial, Amran claimed that he did not own the drugs and that he was entrapped to commit the offence. Rabu argued that he made the statements to the CNB involuntarily and that he was actually not involved in the trafficking at all. The trial judge rejected all the defences raised by both accused, convicted them of drug trafficking and sentenced them to death. Both accused appealed against his decision. Misuse of Drugs Act Cap , Ed. The judge sentenced both appellants to suffer death. On 1 May , at about p. When contacted, Daud asked the agent to relay the message to CPL Fazuri to call him at telephone number '' the next night to discuss the deal. This number belonged to a public telephone at a coffeeshop along Sixth Avenue. Daud said he had to check the stuff and the price first. He called back about ten minutes later and informed CPL Fazuri that the price would be cheaper if he were to buy 3 kg of cannabis instead. CPL Fazuri said that he would check with his partner and call Daud back. About 15 minutes later, CPL Fazuri called and told Daud that he would take 3 kg if the price was right. Daud then handed the phone over to a person called 'Abu'. He told CPL Fazuri that either he or Daud would contact him the next day to confirm the time and place of delivery of the drugs. Daud agreed to the arrangement and told CPL Fazuri that either he or Abu would call again in the evening for a final confirmation. CPL Fazuri agreed to buy the drugs at that price. He also informed Abu that the registration number of the car that his men would be driving was 'SZA M'. They would drive the car bearing the registration plate of 'SZA M' to meet Daud and Abu and be led by the pair to another place to collect the drugs. Three other teams would follow the undercover car in three separate cars. The telephone line would be kept on so that CPL Fazuri could monitor the conversation in the car. Once the cannabis was handed over, CPL Nabil would give a pre-arranged signal by saying the words 'barang bagus'. Upon receiving this signal, CPL Fazuri would notify the rest of the teams to move in and arrest the suspects. They parked the car near the 7-eleven store at Sixth Avenue as arranged. At about p. Amran then introduced himself as 'Daud' and Rabu said he was 'Abu'. Both men entered the car. When the car stopped, Rabu alighted on his own accord and crossed the road. He headed towards Block , Bukit Merah View and was out of sight of the people in the car. While Rabu was collecting the drugs, Daud told CPL Nabil that the stuff was still wet which meant that the drugs were good. SGT Aldi made a U-turn to pick him up. Rabu handed the bag over to CPL Nabil and when he saw that the bag contained some bundles, he said 'barang bagus'. When the undercover car stopped, both men ran out and tried to escape. They put up a violent struggle to evade arrest and suffered minor injuries in the course of their struggle. However, both were eventually subdued and arrested by the CNB officers. Amran admitted that he knew that the yellow paper bag contained 2. However, he said that the drugs belonged to Rabu and that they were for 'Boy'. He admitted that he arranged for Rabu to sell the drugs to 'Boy'. He claimed that he did not know what was inside the bag. Subsequently, the suspects were brought to the Jurong Police Regional Headquarters for their urine tests. CPL Nabil also handed the yellow paper bag over to ASP Tan who weighed the drugs in the presence of the suspects and locked them in his metal cabinet. ASP Tan instructed the arresting officers to bring the suspects for a pre-statement medical examination. Between about 4 a. Rabu denied that he knew what was in the yellow paper bag while Amran stated that it was Rabu who owned the drugs. Then, he instructed his men to bring the two suspects for their post statement medical examination and left for home. He testified that he found recent abrasions on the forehead, nose, right cheek and lip of Amran. As for Rabu, he found a bruise on his forehead and his right hand and back as well as an abrasion on his left shoulder. Tan Sing Huang, also a doctor at the Alexandra Hospital, conducted the post statement medical examination. She found seven injuries on Amran instead of the four found by Dr. However, she found approximately the same injuries noted by Dr. Chiam on Rabu. She also testified that both Amran and Rabu did not complain to her that any CNB officer has assaulted them. She found that Rabu, but not Amran, tested positive for cannabis consumption. Amran made a long statement on 8 May and a further one on 15 May In the statement recorded on 8 May , he described the events of 2 and 3 May as the following: On 2 May , he spoke with Boy and told him that he could obtain some cannabis for him. On 3 May , he and Rabu contact Boy to negotiate the sale of the cannabis. When Rabu reached an agreement with Boy, Rabu passed the phone to him. At this point, Boy informed him that his men would pick him and Rabu up at about p. When the car arrived, Rabu and him got in. The car drove to Bukit Merah View where Rabu left to collect the drugs. Shortly after that, the car was intercepted and he was arrested. In his statement recorded on 15 May , he admitted that he promised Boy to get the drugs for him because he wanted the commission that Boy promised him badly. He denied that he was involved in the negotiations for the sale of the cannabis. He admitted that, on 3 May , he followed Amran into the undercover car. Furthermore, he admitted that when the car reached Bukit Merah View, he left the car to collect a yellow paper bag from another person waiting at Block , Bukit Merah View. However, Rabu denied that he knew what was in the bag. He admitted that he was involved in procuring and selling the cannabis to CPL Fazuri. His version of what happened on 3 May was the following: that day, Amran asked him whether he could obtain some cannabis for him and he replied that he would try. Rabu said that he would try to get the drugs and subsequently, he contacted a person called 'Daud' not Amran , whom he met in Batam previously. Daud told him that he could supply him with 2. Rabu then informed Amran who in turn told Boy that only 2. Boy agreed to both the quantity and price. Rabu also knew that Amran had been promised a commission for setting up the sale. In his defence, he testified that he did not own the drugs and that he was entrapped into committing the offence. However, in his closing submissions, Mr. Luke Lee, counsel for Amran, conceded that entrapment was not a defence to the charge. Furthermore, Mr. Lee conceded that Amran had admitted to all the essential facts constituting the charge even though he denied ownership of the drugs. Ownership was not an essential element of drug trafficking. Amran pleaded for leniency in court but Mr. Lee also conceded that no leniency was possible since Amran was charged with an offence that was punishable with a mandatory death penalty. He had his dinner at the hawker centre near the World Trade Centre and returned home after that. He did not go to the coffeeshop at Sixth Avenue or speak to Boy that day. He pointed out that Boy spoke to a person called 'Abu' and testified that he was not 'Abu' since he was never known by that name. Amran arrived at the coffeeshop at about p. Amran told him that his friends would be coming to the coffeeshop in a car and that they were proceeding to Bukit Merah View. He was invited to come along with Amran and he did so because he thought that Amran wanted to give him some tips about racing horses. He did not ask Amran any other questions about the purpose of the trip. During the journey, there was no mention about drugs. He did not talk to the CNB officers. It was Amran who instructed the officers to proceed to Bukit Merah View. He decided to collect the bag as a favour to Amran. Thus, he went to the void deck of Block where he met a man, called 'Ahmad', whom he had never seen before. Ahmad refused to tell him what he promised to give Amran and Rabu did not press the issue. He followed Ahmad to the landing between the second and third floor. Ahmad then took a paper bag that was tied up from a heap of rubbish and handed it to him. He took the bag without opening it and gave it to Amran in the car. Rabu testified that he did not know the contents of the bag. In the car, Amran handed the paper bag to the front seat passenger. Rabu gave evidence that he only realised that the bag contained cannabis when the front seat passenger opened up the bag and he smelt the drugs. He heard the front seat passenger say 'barang bagus'. Soon after that, the car was intercepted. Rabu suspected that CNB officers were conducting arrests and he attempted to flee because he thought he might be implicated for drug trafficking or at the very least for drug consumption. He had consumed cannabis while he was in Batam. However, he was eventually arrested. In court, Rabu claimed that the contents of that long statement, together with his statement that was recorded on 9 May , were inaccurate because he had made them involuntarily. Rabu alleged that he was suffering from a toothache and was not feeling well. He testified that he suffered from a lack of sleep and missed his family. In addition, when he made the statement on 15 May , ASP Tan read the statement made on 9 May and he felt that this was a signal that he must give a different answer when he recorded the later statement. Furthermore, he alleged that ASP Tan told him that if he co-operated, his sentence for the offence may be reduced. For these reasons, he contended that his statement was involuntary as they were made as a result of a threat or inducement. He alleged that ASP Tan did not record the full facts and contended that the accurate version of the facts was that he did not know anything about the drug deal or the contents of the paper bag that he collected. It was immaterial that Amran did not own the drugs. In any case, he found that Amran participated voluntarily in the drug deal. He relied on the statement made on 15 May as evidence that Rabu knew about and became involved in selling Boy 2. Sofia, the Malay interpreter who was present during the recording of both statements in question. Both emphatically denied that any threat, inducement or promise were offered to Rabu during the recording of his statements. He also contended that he was entrapped to commit the offence. We agreed. Amran had already admitted to all the essential elements of the charge against him by his own evidence, in court as well as in his statements to the CNB. He also took part in the delivery of the drugs by going with Rabu and the undercover CNB officers to Bukit Merah View to collect the drugs. Amran did not dispute all these facts in this appeal. It is trite law that entrapment is not a valid defence to a charge. The observation of the Law Lords that the defences of agent provocateur and entrapment do not exist in English law would also reflect the position in Singapore. It is not the province of the court to consider whether the CNB should have proceeded about its work in one way or the other. The court can only be concerned with the evidence before it. The fact that he was induced to act by a law enforcement officer could not exonerate him from his guilt. The appeal on this matter was purely factual. It reads:. A confession made by an accused person is irrelevant in a criminal proceeding if the making of the confession appears to the court to have been caused by any inducement, threat or promise having reference to the charge against the accused person, proceeding from a person in authority and sufficient in the opinion of the court to give the accused person grounds which would appear to him reasonable for supposing that by making it he would gain any advantage or avoid any evil of a temporal nature in reference to the proceeding against him. The court held that the prosecution had the burden to prove beyond reasonable doubt that the confession was made voluntarily although it need not remove 'every lurking shadow of influence or remnants of fear'. The court described the test of voluntariness as a partly objective and partly subjective one. The prosecution must prove objectively that there was no threat, inducement or promise, i. If the prosecution failed to prove this, it must then show beyond reasonable doubt that although there was objectively a threat, inducement or promise, it did not actually operate on the mind of the accused in question. Sofia to read his earlier statement back to him at the beginning of the recording of the later statement. First, he argued that this itself constituted a threat which Rabu had actually succumbed to. He also urged the Court to consider that he was particularly susceptible to any inducements or threats because he was unwell and was deprived of food, sleep and family visits. We agreed that such a situation could not amount to a threat objectively. It is not reasonable for an accused person to believe that he will avoid some evil of a temporal nature to himself by making an incriminating statement merely because the investigating officer reads back his previous statement. An accused who views the reading back of his own statement as a threat must clearly be labouring under his own delusions. It is trite law that such self-induced threats will not cause a statement made pursuant to it to be inadmissible. Sofia to threaten him by reading his previous statement back to him, it was probable that ASP Tan also offered him an inducement and the judge should have found in his favour. This argument clearly involved a leap of logic and we rejected it. Even if ASP Tan did threaten Rabu once which clearly had not been shown on the facts , it did not necessarily imply that he offered another separate inducement as well. No other reasons were raised to show that the judge was clearly wrong in finding that ASP Tan had not offered a lighter sentence to Rabu if he co-operated. Rabu claimed that he was unwell and complained that he was deprived of food, sleep and family visits. In his written submissions, Counsel for Rabu argued that these circumstances made Rabu more susceptible to any form of threat or inducement held out to him. He urged the Court to find that the statement were made involuntarily because he actually felt that he was threatened and offered inducements to make them. First, it was unnecessary to consider whether the circumstance actually operated on Rabu when he made the statement the subjective limb. Rabu did not raise a reasonable doubt that an inducement or a threat that would reasonably affect an accused and cause such a person to make statements involuntarily did not exist the objective limb. Under Gulam bin Notan v PP , it was unnecessary to consider the subjective limb of the test of voluntariness when the objective limb of the test had not been met. He noted particularly, that Ms. Sofia had no interest in ensuring that Rabu made an incriminating statement. Sofia that Rabu did not appear unwell and that he said nothing about feeling unwell or being unable to carry on with the statements at anytime. He was also satisfied that Rabu had not been deprived of food or sleep to such an extent that he could not comprehend what was going on during the recording of the statement. Consequently, we affirmed the trial judge findings of fact on this issue. Furthermore, although Rabu had been denied family visits, this would not make him more susceptible to inducements compared to any other accused person since the deprivation of family visits is necessary during the period of interrogation. Rabu had no basis to argue that he was more susceptible to an inducement or threat because he felt unwell and was deprived of food, sleep and family visits. We agreed that the trial judge rightly admitted and gave due weight to these statements. The law on confessions of a co-accused is clear. Section 30 of the Evidence Act Cap 97 reads:. When more persons than one are being tried jointly for the same offence and a confession made by one such persons affecting himself and some other of such person is proved, the court may take into consideration the confession as against the other person as well as against the person who makes the confession. However, this went to the weight of the evidence, not its admissibility. Pursuant to s 30 of the Evidence Act, these confessions were admissible and could be taken into consideration against Rabu. Rabu argued that this evidence should be rejected because it was unreliable. Amran had an incentive to lie and shift the blame on Rabu since he believed that he could obtain leniency from the Court. In his confessions, Amran implicated himself fully for a serious offence that carried the mandatory death penalty. He accepted his own role in the matter fully. Although Amran did dispute the fact that he gave directions to the CNB officers to go to Bukit Merah View, this was merely a minor discrepancy. In the rest of his testimony, Amran did not seek to push the blame onto Rabu to lessen his role in the offence. Rabu contended that the judge made two main errors of fact. The first error was finding that he took part in the negotiations with CPL Fazuri to sell the drugs. Secondly, he argued that the judge wrongly found that he knew the true purpose of the journey in the undercover car and the contents of the yellow paper bag. Rabu argued that he could not have taken part in the negotiations with CPL Fazuri on 2 May at about 8 p. This was because he had just arrived in Singapore from Batam. However, the prosecution produced documentary proof in the form of the records kept by the Singapore Immigration and Registration to show that Rabu had disembarked from the ferry at the World Trade Centre Terminal at p. It was possible for him to be at Sixth Avenue at about 8 p. Rabu claimed that he did not know that the people in the undercover car intended to obtain drugs at Bukit Merah View. He testified that he was simply accompanying Amran on a journey with unknown men so that Amran could talk to him about horses. The judge found this explanation incredulous. It was illogical for a fully-grown up man to go along with Amran to Bukit Merah View with strangers without even first enquiring about the purpose or the length of time that they would stay there. In any case, there was no talk about horses and it was inconceivable that a person expecting to talk about horses would later just sit in the car silently while Amran and the front seat passenger continued talking. In light of the evidence, this inference was perfectly justifiable. The judge chose to believe these witnesses over Rabu. The Notes of Evidence did not show that the judge was clearly wrong to accept the testimonies of the CNB officers that Rabu acted on his own accord to collect the yellow paper bag. He explained that he bolted because he feared being caught for drug consumption. On appeal, he added that he tried to escape to avoid the beatings by the CNB officers who were trying to effect his arrest. He negotiated with CPL Fazuri for the sale of the drugs and he contacted the supplier in Batam to provide the drugs. On the 3 May , he and Amran entered the undercover car to go to Bukit Merah View to collect the drugs. Upon reaching the destination, he got down on his own accord and went to pick up the drugs from the supplier, brought it back to the car and passed them to Amran who in turn delivered it to CPL Nabil. We found that his appeal against conviction was devoid of merits and we upheld his conviction. He submitted that the Court should consider the fact that Rabu was entrapped into committing the offence as a mitigating factor in sentencing him. Section 33 1 read with the Second Schedule of the Act prescribes a mandatory death sentence for persons convicted under s 5 1 a of the Act for trafficking more than grams of cannabis. There was no room for judicial discretion in sentencing in the face of the clear wording of the section. Criminal Appeal No 23 of Court of Appeal.

Amran buy ganja