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Media Law In Singapore By Teo Yi Ling Pdf 16
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In 2018, Ngerng took part in an Al Jazeera documentary, Singapore: The House that Lee Built.[16] The documentary was Ngerng's first media appearance since his participation in the 2015 Singapore general election and showed snippets of Ngerng's life in Taiwan.
On 18 May, Lee's lawyer, Senior counsel Davinder Singh of Drew & Napier, stated that the blog post alleged that Lee \"is guilty of criminal misappropriation of the monies paid by Singaporeans to the CPF\" and that the allegations were \"false and baseless\".[19] It was demanded that Ngerng issue an apology and take down the blog post within three days, as well as pay damages and legal fees, failing which Ngerng could be sued for defamation.[5][20]
On 27 May, Ngerng offered S$5,000 in damages \"with each party to bear their own costs\",[26] which was rejected by Singh as \"derisory\".[27] Meanwhile, Singh said that Ngerng had once again \"misled\" Lee and the public by not removing his YouTube video as agreed upon, claimed that the video was merely made private, and alleged that Ngerng had sent two emails with links to the posts and video to \"a far wider audience\" including local and international media.[26] In response, Ngerng's lawyer, M Ravi, claimed no knowledge of the emails.[27]
On 29 May, Lee filed a defamation lawsuit against Ngerng.[28] In response, Ngerng made an online plea for help in settling his legal fees through crowdfunding, leaving instructions on how to transfer money to his bank account.[29] Within a week, Ngerng said that he had raised more than his targeted S$70,000.[30] It was later reported that Ngerng had managed to raise more than S$110,000 from over a thousand contributions.[4] While Lee did not address the case directly, he wrote on Facebook that \"freedom of speech does not come free from the need to be responsible for what one says, either online or offline\".[9] Singaporean writer Catherine Lim has criticised the lawsuit against Ngerng.[31][32]
On 7 November, the High Court found Ngerng liable of defamation with damages to be assessed, which was the first such ruling in Singapore over a purely online article.[6] The court ruled that there was \"no triable defence\" and \"no doubt that it is defamatory to suggest that the plaintiff is guilty of criminal misappropriation\".[6] An injunction against Ngerng was granted, barring him from publishing future similar accusations regarding Lee and the CPF.[37] Ngerng expressed disappointment at the verdict, but maintained that he would \"still continue to speak up on the CPF and other issues that concern Singaporeans\".[6]
The hearing prompted much comment from international press freedom advocacy groups and a legal opinion in favour of minimal damages against defendant from the International Commission of Jurists: \"It is humbly submitted that a decision awarding a disproportionately high amount of damages to the plaintiff in this case would cast a chilling effect on freedom of expression in Singapore\".[43] The High Court requested both parties to make written submissions on their respective cases by 31 August 2015. No date was given for the court's decision.[44]
On 17 December, the court handed down a judgement ordering Ngerng to pay S$100,000 in general damages and S$50,000 in aggravated damages. Ngerng, through his lawyer Eugene Thuraisingam, proposed to pay the S$150,000 in instalments. Lee granted Ngerng his request on the condition that Ngerng paid the S$30,000 in hearing costs immediately, i.e., by 16 March 2016. Ngerng is expected to repay S$100 a month from 1 April 2016 onwards over five years until 1 April 2021 when instalments are increased to S$1,000 until the full sum has been paid by the year 2033.[45] Lee also rejected Ngerng's request to reimburse part of the damages, i.e., S$36,000.[46]By 16 April 2021, a crowdfunding campaign had raised the S$144,389.14 required to pay the outstanding damages in full.[47]
A controversial incident occurred on 27 September 2014 when another Return Our CPF protest, again organised by Han Hui Hui,[54] took place at Hong Lim Park at the same time as the YMCA Proms @ the Park event, a charity carnival attended by the elderly and disabled, featuring performances by children.[55] Agence France-Presse described Ngerng and Han as having \"led a march ... despite having only a permit to stage a rally at a fixed spot\".[56] The Straits Times described that Han had led the protesting group in \"marching around the park\" together with Ngerng, with the group \"heckling special needs children and confronting\" Minister of State Trade and Industry Teo Ser Luck, who attended the YMCA event.[57] A few days later, Teo confirmed that Ngerng had issued an apology for the disruption; Teo himself apologised due to his \"presence\" causing the protesters to \"go after\" him.[58]
Current recommended first-line treatment in the management of GPP and EP are retinoids (such as etretinate and acitretin) and cyclosporine [3, 9]. However, these treatments are associated with safety concerns (including teratogenicity and renal toxicity, and long-term AEs) [2, 3, 8]. In severe cases of GPP and EP, where rapid and effective treatments are essential to prevent complications and mortality, the response observed with conventional agents is often inadequate [2, 3, 7, 8]. As such, there is a need for new treatment options for patients with these severe forms of psoriasis. Although current treatment options for GPP are based on therapies indicated for PSO due to the similarities in pathophysiology, recent evidence has identified the role of IL-36 as a key contributor in the pathophysiology of GPP, compared with PSO, which is predominantly driven by the TNF-α/IL-23/IL-17 axis [8, 18, 19]. As such, anti-IL-36 therapies are currently being studied for the treatment of GPP. Clinical trials for these anti-IL-36 therapies are still ongoing, although phase 1 results have been promising [20]. However, given that these anti-IL-36 therapies are still in very early stages of development and clinical trials, it is still uncertain if they will demonstrate efficacy with a good safety profile. On the other hand, anti-TNFs are available now and are well established in other chronic inflammatory diseases. For patients with GPP and EP, anti-TNFs will provide more immediate and certain treatment options.
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Cancer drug resistance is a complex phenomenon that is influenced by various mechanisms. Drug resistance may arise intrinsically from host factors or may be acquired by genetic or epigenetic alterations in the cancer cells1. Cancers are known to exhibit micro-clonality with a high degree of genetic heterogeneity making it possible for resistant cells to continue proliferating even in the presence of therapeutic treatments2. This genetic heterogeneity may confer upon cancer cells the ability to regulate rates of drug efflux, DNA damage repair processes, and signaling pathways affecting cell survival and death3.
Drugs including platinum-based drugs and others such as 5-fluorouracil (5-FU) and epirubicin remain the major chemotherapeutic agents used in the treatment of a wide variety of solid malignancies, including colorectal, ovarian, lung, and head and neck cancer4,5. There are three platinum-based drugs, cisplatin, carboplatin, and oxaliplatin, which are used throughout the world, with four additional drugs, heptaplatin, lobaplatin, miriplatin, and nedaplatin, having regulatory approval in individual countries such as Korea, China, and Japan6. Cisplatin is currently one of the most potent chemotherapeutic drugs and is widely used either alone or in combination with other drugs in cancer treatment. For instance, it is the most frequently used therapeutic agent in treating metastatic nasopharyngeal carcinoma (NPC)7, a malignancy particularly endemic to Southeast Asia and Southern China8,9. In the treatment and management of colorectal carcinoma, platinum compound-based chemotherapeutic agents, including cisplatin, are used in combination with other drugs10,11. Studies have also supported the use of platinum-based chemotherapy in breast cancer, showing cytostatic effects of cisplatin in clinical trials12, and as part of neoadjuvant chemotherapy leading to remission13. The cytotoxicity of cisplatin and other platinum-based drugs is mediated by their interaction with DNA to form DNA adducts, leading to DNA damages that activate signal transduction pathways and consequently cell apoptosis14. 5-FU, on the other hand, is an apyrimidine analog that inhibits thymidylate synthase and can also misincorporate into DNA during polynucleotide biosynthesis, which leads to DNA damage and apoptosis15. Epirubicin, an anthracycline drug widely employed to treat solid tumors, acts through intercalating between nucleic acid base pairs to inhibit both DNA and RNA biosynthesis and also triggering DNA cleavage and promoting the production of reactive oxygen species, eventually leading to cell death16.
The mitogen-activated protein kinase (MAPK) pathways, including the extracellular signal-regulated kinase (ERK), the c-Jun N-terminal kinase (JNK), and the p38 kinase, are evolutionarily conserved signaling pathways that regulate cell proliferation, survival, and apoptosis in cancer19,20,21,22,23. Previous studies have implicated the MAPK signaling pathways in responses to chemotherapeutic agents. For instance, ERK1/2 activation has been shown to promote cancer cell survival in ovarian cancer24,25, melanoma26, cervical cancer27, myeloid leukemia28, and gastric cancer29 cells in response to cisplatin treatment. However, there is also evidence showing that ERK1/2 activation is necessary for cisplatin-mediated apoptosis of cells of cervical cancer30,31, osteosarcoma and neuroblastoma32, glioma33, NPC34, and human small cell lung cancer35. Activation of the p38 pathway by cisplatin has been observed in different types of cancer cells36. Inhibition of p38 suppressed cisplatin-induced apoptosis while prolonged p38 activation has been associated with increased sensitivity to cisplatin-induced apoptosis in cervical37, ovarian38, and breast cancers39. Similarly, activation of the JNK pathway plays a major role in mediating apoptosis by cisplatin treatment40,41. Interestingly, the oncogenic EBV gene, LMP-1, has been found to activate the JNK pathway and promote cisplatin-induced caspase activation and apoptosis42,43,44. Moreover, inhibition of cytokeratin 8 in NPC cell lines increased cancer cell sensitivity to cisplatin by activating the JNK pathway45,46,47. In addition, the MAPKs have been shown to mediate sensitivity of a variety of cancer cells such as colorectal cancer, pancreatic cancer, and breast cancer to other therapeutic drugs including 5-FU and epirubicin15,48,49,50. 153554b96e