Displaying publications 1 - 20 of 26 in total

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  1. Roy RN
    Med J Malaya, 1968 Mar;22(3):204-16.
    PMID: 4234357
  2. Ahmad M, Roy RA
    Endod Dent Traumatol, 1994 Apr;10(2):71-6.
    PMID: 8062810
    The incidence of breakage of Piezon-Master ultrasonic K files were evaluated. Three groups of unused files were subjected to three treatments, namely; free vibration in air without irrigation, free vibration in root canal while minimizing contact with the wall of canal in the presence of irrigation and light filing in root canal with free flow of irrigation. Cavitation produced by files in contact and free of contact with a glass surface was examined in order to observe the relationship between cavitation defects and breakage. In addition, the fractured and unfractured files were examined under a scanning electron microscope for the presence of cavitation pits. The results indicated that more files broke in air. In water, a higher incidence of breakage occurred when files were allowed to freely vibrate while no breakage occurred when the files were used in filing. All files generated cavitation which resulted in pitting of their surfaces. However, it was considered unlikely that the pits contributed to fracture. Fatigue cracks which could be the result of the manufacturing process were observed at some of the corners of the cross sections of the fractured files and could be the main contributory factor to fracture.
  3. Ahmad M, Roy RA, Kamarudin AG
    Int Endod J, 1994 Jan;27(1):26-31.
    PMID: 7806408
    The present study was undertaken to see if there was any variability in the power output of Piezon-Master 400 ultrasonic files when driven using different generators, tranducers and file holders. The displacement amplitude of the oscillating tip of the file in air was used as a measure of the power output. The results showed that there was considerable variability in the power output of Piezon-Master 400 ultrasonic files of similar size and length when driven using different generators, transducers and file holders. In consideration of this, it is recommended that a calibration device be incorporated in the ultrasonic unit so that the operator will have some knowledge of when the unit is working at its maximum efficiency.
  4. Ahmad M, Roy RA, Kamarudin AG, Safar M
    Int Endod J, 1993 Mar;26(2):120-4.
    PMID: 8330934
    The pattern of oscillation of a Piezon-Master 400 ultrasonic file driven by a piezoelectric transducer was studied in air and on water. In addition, the displacement amplitudes of the files were measured. The findings were compared with those observed with the Cavi-Endo unit reported in another study (Ahmad 1969). It was observed that the file vibrated such that a standing wave was formed on the file and it exhibited points of maximum deflection (antinode) and points of minimum deflection (node) with the largest deflection occurring at the apical end. This pattern of oscillation was similar to that exhibited by the Cavi-Endo file which employed a magnetostrictive transducer. However, the displacement amplitudes were very much higher than those exhibited by the Cavi-Endo. It is considered that the 120 degrees angle of the file holder inherent in the Piezon-Master 400 unit and the more effective power transmission with the piezoelectric transducer may have contributed to the large amplitudes.
  5. Ahmad M, Roy RA, Kamarudin AG
    Endod Dent Traumatol, 1992 Oct;8(5):189-94.
    PMID: 1302678
    The steady acoustic streaming generated around straight and precurved oscillating ultrasonic files driven by the Piezon-Master 400 unit was examined in the free field and in small channels using a stereomicroscope. In addition, the effect of file-wall contact on streaming production was also investigated. The results indicated that the ultrasonic files can generate acoustic streaming both in the free field and in the small channel. Higher velocity streaming was observed when smaller size files were employed and when the file was precurved. Light file-wall contact did not totally inhibit streaming while severe file-wall contact inhibited movement of the file and, as a result, no streaming was observed. The positions and length scales of the streaming vortices appeared to be influenced by the presence of boundaries. In the free field, two rows of vortices were situated along the sides of the file while in the small channel, the vortices were positioned above the surface of the file. These results indicated that it is possible for acoustic streaming to occur in a confined space as in a root canal provided that severe file-wall contact is avoided. It is therefore recommended that light filing or allowing the file to freely vibrate during some stage of treatment should be carried out in order to generate streaming in the root canal.
  6. Brackstone K, Marzo RR, Bahari R, Head MG, Patalinghug ME, Su TT
    PLOS Glob Public Health, 2022;2(10):e0000742.
    PMID: 36962550 DOI: 10.1371/journal.pgph.0000742
    With the emergence of the highly transmissible Omicron variant, large-scale vaccination coverage is crucial to the national and global pandemic response, especially in populous Southeast Asian countries such as the Philippines and Malaysia where new information is often received digitally. The main aims of this research were to determine levels of hesitancy and confidence in COVID-19 vaccines among general adults in the Philippines and Malaysia, and to identify individual, behavioural, or environmental predictors significantly associated with these outcomes. Data from an internet-based cross-sectional survey of 2558 participants from the Philippines (N = 1002) and Malaysia (N = 1556) were analysed. Results showed that Filipino (56.6%) participants exhibited higher COVID-19 hesitancy than Malaysians (22.9%; p < 0.001). However, there were no significant differences in ratings of confidence between Filipino (45.9%) and Malaysian (49.2%) participants (p = 0.105). Predictors associated with vaccine hesitancy among Filipino participants included women (OR, 1.50, 95% CI, 1.03-1.83; p = 0.030) and rural dwellers (OR, 1.44, 95% CI, 1.07-1.94; p = 0.016). Among Malaysian participants, vaccine hesitancy was associated with women (OR, 1.50, 95% CI, 1.14-1.99; p = 0.004), social media use (OR, 11.76, 95% CI, 5.71-24.19; p < 0.001), and online information-seeking behaviours (OR, 2.48, 95% CI, 1.72-3.58; p < 0.001). Predictors associated with vaccine confidence among Filipino participants included subjective social status (OR, 1.13, 95% CI, 1.54-1.22; p < 0.001), whereas vaccine confidence among Malaysian participants was associated with higher education (OR, 1.30, 95% CI, 1.03-1.66; p < 0.028) and negatively associated with rural dwellers (OR, 0.64, 95% CI, 0.47-0.87; p = 0.005) and online information-seeking behaviours (OR, 0.42, 95% CI, 0.31-0.57; p < 0.001). Efforts should focus on creating effective interventions to decrease vaccination hesitancy, increase confidence, and bolster the uptake of COVID-19 vaccination, particularly in light of the Dengvaxia crisis in the Philippines.
  7. Marzo RR, El-Fass KA, Osman NA, Kyaw TM, Arivanandan PKA, Morgan LM, et al.
    Tob Induc Dis, 2022;20:109.
    PMID: 36530212 DOI: 10.18332/tid/154964
    INTRODUCTION: Proper understanding of the prevalence and determinants of nicotine dependence is crucial for developing and implementing effective tobacco control interventions. The aim of the study was to identify the intrinsic and extrinsic barriers to smoking cessation, and to assess the association between nicotine dependence with demographic variables in Malaysia.

    METHODS: A cross-sectional survey based on the Challenges to Stopping Smoking Scale (CSS-21) and Fagerström test for nicotine dependence (FTND) was performed on smoking Malaysian citizens aged ≥18 years, from February to June 2021.

    RESULTS: A total of 1026 parents responded to the survey. As for the smoking dependence based on FTND, 39.1% suffered low-moderate dependence, while about 33.6% suffered moderate dependence. Only 1.8% suffered high dependence. Considering the barriers of quitting smoking based on CSS-21, the mean score of the intrinsic barriers domain was 5.7 ± 2.9, and for the extrinsic domain was 7.4 ± 4.0. The most common barrier reported in the intrinsic domain was the easy availability of cigarettes (69.8%), followed by experiencing withdrawal symptoms (68.5%). On the other hand, the most common barrier reported in the extrinsic domain was the belief in the capability of stopping smoking in the future (72.8%), followed by the fear of having side effects after stopping smoking (63.2%). Gender, race, education level, occupation, marital status, place of residence, and monthly income were also significantly associated with the FTND nicotine dependence category (all p<0.05). Pearson correlation analysis reported a positive association between intrinsic score (r=0.38), extrinsic score (r=0.43) and FTND score (all p<0.001).

    CONCLUSIONS: Barriers to stopping smoking should be taken into consideration in initiatives to decrease smoking-related mortality. Vulnerable populations that are susceptible to high nicotine dependence should be given particular attention.

  8. Kravchenko J, Corsini E, Williams MA, Decker W, Manjili MH, Otsuki T, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S111-27.
    PMID: 26002081 DOI: 10.1093/carcin/bgv033
    An increasing number of studies suggest an important role of host immunity as a barrier to tumor formation and progression. Complex mechanisms and multiple pathways are involved in evading innate and adaptive immune responses, with a broad spectrum of chemicals displaying the potential to adversely influence immunosurveillance. The evaluation of the cumulative effects of low-dose exposures from the occupational and natural environment, especially if multiple chemicals target the same gene(s) or pathway(s), is a challenge. We reviewed common environmental chemicals and discussed their potential effects on immunosurveillance. Our overarching objective was to review related signaling pathways influencing immune surveillance such as the pathways involving PI3K/Akt, chemokines, TGF-β, FAK, IGF-1, HIF-1α, IL-6, IL-1α, CTLA-4 and PD-1/PDL-1 could individually or collectively impact immunosurveillance. A number of chemicals that are common in the anthropogenic environment such as fungicides (maneb, fluoxastrobin and pyroclostrobin), herbicides (atrazine), insecticides (pyridaben and azamethiphos), the components of personal care products (triclosan and bisphenol A) and diethylhexylphthalate with pathways critical to tumor immunosurveillance. At this time, these chemicals are not recognized as human carcinogens; however, it is known that they these chemicalscan simultaneously persist in the environment and appear to have some potential interfere with the host immune response, therefore potentially contributing to promotion interacting with of immune evasion mechanisms, and promoting subsequent tumor growth and progression.
  9. Thompson PA, Khatami M, Baglole CJ, Sun J, Harris SA, Moon EY, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S232-53.
    PMID: 26106141 DOI: 10.1093/carcin/bgv038
    An emerging area in environmental toxicology is the role that chemicals and chemical mixtures have on the cells of the human immune system. This is an important area of research that has been most widely pursued in relation to autoimmune diseases and allergy/asthma as opposed to cancer causation. This is despite the well-recognized role that innate and adaptive immunity play as essential factors in tumorigenesis. Here, we review the role that the innate immune cells of inflammatory responses play in tumorigenesis. Focus is placed on the molecules and pathways that have been mechanistically linked with tumor-associated inflammation. Within the context of chemically induced disturbances in immune function as co-factors in carcinogenesis, the evidence linking environmental toxicant exposures with perturbation in the balance between pro- and anti-inflammatory responses is reviewed. Reported effects of bisphenol A, atrazine, phthalates and other common toxicants on molecular and cellular targets involved in tumor-associated inflammation (e.g. cyclooxygenase/prostaglandin E2, nuclear factor kappa B, nitric oxide synthesis, cytokines and chemokines) are presented as example chemically mediated target molecule perturbations relevant to cancer. Commentary on areas of additional research including the need for innovation and integration of systems biology approaches to the study of environmental exposures and cancer causation are presented.
  10. Hu Z, Brooks SA, Dormoy V, Hsu CW, Hsu HY, Lin LT, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S184-202.
    PMID: 26106137 DOI: 10.1093/carcin/bgv036
    One of the important 'hallmarks' of cancer is angiogenesis, which is the process of formation of new blood vessels that are necessary for tumor expansion, invasion and metastasis. Under normal physiological conditions, angiogenesis is well balanced and controlled by endogenous proangiogenic factors and antiangiogenic factors. However, factors produced by cancer cells, cancer stem cells and other cell types in the tumor stroma can disrupt the balance so that the tumor microenvironment favors tumor angiogenesis. These factors include vascular endothelial growth factor, endothelial tissue factor and other membrane bound receptors that mediate multiple intracellular signaling pathways that contribute to tumor angiogenesis. Though environmental exposures to certain chemicals have been found to initiate and promote tumor development, the role of these exposures (particularly to low doses of multiple substances), is largely unknown in relation to tumor angiogenesis. This review summarizes the evidence of the role of environmental chemical bioactivity and exposure in tumor angiogenesis and carcinogenesis. We identify a number of ubiquitous (prototypical) chemicals with disruptive potential that may warrant further investigation given their selectivity for high-throughput screening assay targets associated with proangiogenic pathways. We also consider the cross-hallmark relationships of a number of important angiogenic pathway targets with other cancer hallmarks and we make recommendations for future research. Understanding of the role of low-dose exposure of chemicals with disruptive potential could help us refine our approach to cancer risk assessment, and may ultimately aid in preventing cancer by reducing or eliminating exposures to synergistic mixtures of chemicals with carcinogenic potential.
  11. Engström W, Darbre P, Eriksson S, Gulliver L, Hultman T, Karamouzis MV, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S38-60.
    PMID: 26106143 DOI: 10.1093/carcin/bgv030
    The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.
  12. Robey RB, Weisz J, Kuemmerle NB, Salzberg AC, Berg A, Brown DG, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1(Suppl 1):S203-31.
    PMID: 26106140 DOI: 10.1093/carcin/bgv037
    Environmental contributions to cancer development are widely accepted, but only a fraction of all pertinent exposures have probably been identified. Traditional toxicological approaches to the problem have largely focused on the effects of individual agents at singular endpoints. As such, they have incompletely addressed both the pro-carcinogenic contributions of environmentally relevant low-dose chemical mixtures and the fact that exposures can influence multiple cancer-associated endpoints over varying timescales. Of these endpoints, dysregulated metabolism is one of the most common and recognizable features of cancer, but its specific roles in exposure-associated cancer development remain poorly understood. Most studies have focused on discrete aspects of cancer metabolism and have incompletely considered both its dynamic integrated nature and the complex controlling influences of substrate availability, external trophic signals and environmental conditions. Emerging high throughput approaches to environmental risk assessment also do not directly address the metabolic causes or consequences of changes in gene expression. As such, there is a compelling need to establish common or complementary frameworks for further exploration that experimentally and conceptually consider the gestalt of cancer metabolism and its causal relationships to both carcinogenesis and the development of other cancer hallmarks. A literature review to identify environmentally relevant exposures unambiguously linked to both cancer development and dysregulated metabolism suggests major gaps in our understanding of exposure-associated carcinogenesis and metabolic reprogramming. Although limited evidence exists to support primary causal roles for metabolism in carcinogenesis, the universality of altered cancer metabolism underscores its fundamental biological importance, and multiple pleiomorphic, even dichotomous, roles for metabolism in promoting, antagonizing or otherwise enabling the development and selection of cancer are suggested.
  13. Carnero A, Blanco-Aparicio C, Kondoh H, Lleonart ME, Martinez-Leal JF, Mondello C, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1(Suppl 1):S19-37.
    PMID: 26106138 DOI: 10.1093/carcin/bgv029
    Carcinogenesis is thought to be a multistep process, with clonal evolution playing a central role in the process. Clonal evolution involves the repeated 'selection and succession' of rare variant cells that acquire a growth advantage over the remaining cell population through the acquisition of 'driver mutations' enabling a selective advantage in a particular micro-environment. Clonal selection is the driving force behind tumorigenesis and possesses three basic requirements: (i) effective competitive proliferation of the variant clone when compared with its neighboring cells, (ii) acquisition of an indefinite capacity for self-renewal, and (iii) establishment of sufficiently high levels of genetic and epigenetic variability to permit the emergence of rare variants. However, several questions regarding the process of clonal evolution remain. Which cellular processes initiate carcinogenesis in the first place? To what extent are environmental carcinogens responsible for the initiation of clonal evolution? What are the roles of genotoxic and non-genotoxic carcinogens in carcinogenesis? What are the underlying mechanisms responsible for chemical carcinogen-induced cellular immortality? Here, we explore the possible mechanisms of cellular immortalization, the contribution of immortalization to tumorigenesis and the mechanisms by which chemical carcinogens may contribute to these processes.
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