Biomedical subjects

L Chen

Publications and source records attributed to L Chen.

At least 55 records · Page 3Linked to original sources

PubMed2005

Kinetics and mechanism of (CF3)2CHOCH3 reaction with OH radicals in an environmental reaction chamber.

The atmospheric chemistry of (CF3)2CHOCH3, a possible HCFC/HFC alternative, was studied using a smog chamber/FT-IR technique. OH radicals were prepared by the photolysis of ozone in a 200-Torr H2O/O3/O2 gas mixture held in an 11.5-dm3 temperature-controlled chamber. The rate constant, k1, for the reaction of (CF3)2CHOCH3 with OH radicals was determined to be (1.40 +/- 0.28) x 10(-12) exp[(-550 +/- 60)/T] cm3 molecule(-1) s(-1) by means of a relative rate method at 253-328 K. The value of k1 at 298 K was (2.25 +/- 0.04) x 10(-13) cm3 molecule(-1) s(-1). The random errors are reported with +/-2 standard deviations, and potential systematic errors of 15% could increase k(1). In considering OH-radical reactions, we estimated the tropospheric lifetime of (CF3)2CHOCH3 to be 2.0 months using the rate constant at 288 K. The degradation mechanism of (CF3)2CHOCH3 initiated by OH radicals was also investigated using FT-IR spectroscopy at 298 K. Products (CF3)2CHOC(O)H, CF3C(OH)2CF3, CF3C(O)OCH3, and COF(2) were identified and quantified. The branching ratio, k1a/k1b, was estimated to be 2.1:1 for reactions (CF3)2CHOCH3 + OH --> (CF3)2CHOCH2*+ H2O (k1a) and (CF3)2CHOCH3 + OH --> (CF3)2C*OCH3 + H2O (k1b).

Journal Article↗

PubMed2005

Expression and spatial distribution of secretin and secretin receptor in human cerebellum.

The expression and spatial distribution of secretin and its receptor in human cerebellum were investigated by in situ hybridization and immunohistochemical techniques. Secretin mRNAs are found in Purkinje cells whereas secretin receptor transcripts are present in Purkinje cells and basket cells in the molecular cell layer. In addition, secretin-immunoreactivities are localized in both the soma and dendrites of Purkinje cells. These data are the first demonstration of the spatial distribution of secretin and its receptor in distinct neurons within the human cerebellum. The cellular localizations of this ligand-receptor pair are consistent with the proposed actions of secretin in the cerebellum of rodents and hence suggest that secretin also serves specific neural functions in the human cerebellum.

Cerebellum↗

PubMed2005

Dosimetric verification of IMRT treatment planning using Monte Carlo simulations for prostate cancer.

The purpose of this work is to investigate the accuracy of dose calculation of a commercial treatment planning system (Corvus, Normos Corp., Sewickley, PA). In this study, 30 prostate intensity-modulated radiotherapy (IMRT) treatment plans from the commercial treatment planning system were recalculated using the Monte Carlo method. Dose-volume histograms and isodose distributions were compared. Other quantities such as minimum dose to the target (D(min)), the dose received by 98% of the target volume (D98), dose at the isocentre (D(iso)), mean target dose (D(mean)) and the maximum critical structure dose (D(max)) were also evaluated based on our clinical criteria. For coplanar plans, the dose differences between Monte Carlo and the commercial treatment planning system with and without heterogeneity correction were not significant. The differences in the isocentre dose between the commercial treatment planning system and Monte Carlo simulations were less than 3% for all coplanar cases. The differences on D98 were less than 2% on average. The differences in the mean dose to the target between the commercial system and Monte Carlo results were within 3%. The differences in the maximum bladder dose were within 3% for most cases. The maximum dose differences for the rectum were less than 4% for all the cases. For non-coplanar plans, the difference in the minimum target dose between the treatment planning system and Monte Carlo calculations was up to 9% if the heterogeneity correction was not applied in Corvus. This was caused by the excessive attenuation of the non-coplanar beams by the femurs. When the heterogeneity correction was applied in Corvus, the differences were reduced significantly. These results suggest that heterogeneity correction should be used in dose calculation for prostate cancer with non-coplanar beam arrangements.

Computer Simulation↗

PubMed2005

Humanin delays apoptosis in K562 cells by downregulation of P38 MAP kinase.

Humanin (HN) is a newly identified neuroprotective peptide. In this study, we investigated its antiapoptotic effect and the potential mechanisms in K562 cells. Upon serum deprivation, expression of HN in K562 cells decreased and its intracellular distribution changed from cytoplasm to cell membrane. In HN stably transfected K562 cells, apoptosis was delayed compared with control vector transfected cells as measured by flow cytometry. Furthermore, analysis of different mitogen-activated protein (MAP) kinases activity revealed that extracellular signal-regulated kinase (ERK) pathway was inhibited while p38 signaling was activated following serum deprivation in K562 cells. And in HN transfected K562 cells, ERK downregulation was not affected, but p38 activation was suppressed, which may responsible for the delayed apoptosis in these cells. Activation of the ERK signaling pathway by phorbol myristate 13-acetate (PMA) and sorbitol protected K562 cells from serum deprivation induced apoptosis. Additionally, overexpression of HN reduced megakaryocytic differentiation of K562 cells. The present data outline the role of ERK and p38 MAP kinases in serum deprivation induced apoptosis in K562 cells and figure out p38 signaling pathway as molecular target for HN delaying apoptosis in K562 cells.

Apoptosis↗

PubMed2005

Enhanced striatal opioid receptor-mediated G-protein activation in L-DOPA-treated dyskinetic monkeys.

Long-term l-3,4-dihydroxyphenylalanine (L-DOPA) treatment in Parkinson's disease leads to dyskinesias in the majority of patients. The underlying molecular mechanisms for L-DOPA-induced dyskinesias (LIDs) are currently unclear. However, the findings that there are alterations in opioid peptide mRNA and protein expression and that opioid ligands modulate dyskinesias suggest that the opioid system may be involved. To further understand its role in dyskinesias, we mapped opioid receptor-stimulated G-protein activation using [35S]guanylyl-5'-O-(gamma-thio)-triphosphate ([35S]GTPgammaS) autoradiography in the basal ganglia of normal and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned squirrel monkeys administered water or L-DOPA. Subtype-selective opioid receptor G-protein coupling was investigated using the mu-opioid agonist [D-Ala, N-Me-Phe, Gly-ol]-enkephalin, delta-agonist SNC80 and kappa-agonist U50488H. Our data show that mu-opioid receptor-mediated G-protein activation is significantly enhanced in the basal ganglia and cortex of L-DOPA-treated dyskinetic monkeys, whereas delta- and kappa-receptor-induced increases were limited to only a few regions. A similar pattern of enhancement was observed in both MPTP-lesioned and unlesioned animals with LIDs suggesting the effect was not simply due to a compromised nigrostriatal system. Opioid receptor G-protein coupling was not enhanced in non-dyskinetic L-DOPA-treated animals, or lesioned monkeys not given L-DOPA. The increases in opioid-stimulated [35S]GTPgammaS binding are directly correlated with dyskinesias. The present data demonstrate an enhanced subtype-selective opioid-receptor G-protein coupling in the basal ganglia of monkeys with LIDs. The positive correlation with LIDs suggests this may represent an intracellular signaling mechanism underlying these movement abnormalities.

Animals↗

PubMed2005

Endogenous release and multiple actions of secretin in the rat cerebellum.

Previous studies demonstrated that secretin could modulate synaptic transmission in the rat cerebellum. In the present report, we provide evidence for the endogenous release of secretin in the cerebellum and further characterize the actions of secretin in this brain area. First, to show that secretin is released endogenously, blocks of freshly dissected cerebella were challenged with a high concentration of KCl. Incubation with KCl almost doubled the rate of secretin release. This KCl-induced release was sensitive to tetrodotoxin and cadmium suggesting the involvement of voltage-gated sodium and calcium channels. The use of specific channel blockers further revealed that L-type and P/Q-type calcium channels underlie both basal and KCl-evoked secretin release. In support of this, depolarization of Purkinje neurons in the presence of NMDA, group II mGluR and cannabinoid CB1 receptor blockers resulted in increased inhibitory postsynaptic current frequency. Second, we found that the previously reported facilitatory action of secretin on GABAergic inputs to Purkinje neurons is partly dependent on the release of endogenous glutamate. In the presence of CNQX, an AMPA/kainate receptor antagonist, the facilitatory effect of secretin on GABA release was significantly reduced. In support of this idea, application of AMPA, but not kainate receptor agonist, facilitated GABA release from inhibitory terminals, an action that was sensitive to AMPA receptor antagonists. These data indicate that a direct and an indirect pathway mediate the action of secretin in the basket cell-Purkinje neuron synapse. The results provide further and more solid evidence for the role of secretin as a neuropeptide in the mammalian CNS.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2005

DNA fragment encoding human IL-1beta 163-171 peptide enhances the immune responses elicited in mice by DNA vaccine against foot-and-mouth disease.

DNA vaccine has been tested for protection against foot-and-mouth disease. However, the relatively low efficacy of DNA vaccine in inducing immune responses in large animals has restricted its practical use. Interleukin-1 plays an essential role in amplifying both the cellular and humoral immune responses to foreign antigens, and may therefore represent a good candidate as an adjuvant of DNA vaccines. Since the inflammatory activity of IL-I may restrict its application in DNA vaccine treatment, we explored the possibilities of augmenting immune responses without unwanted inflammatory effects using the IL-1beta fragment (amino acids (aa) 163-171), which is essential for IL-1 receptor-1 binding. The DNA fragment encoding the human IL-1beta fragment (aa 163-171) was fused to foot-and-mouth disease virus (FMDV) DNA vaccine, and injected into mice to analyse its immune response. Compared with control mice receiving FMDV DNA vaccine alone, significant increases in the FMDV-specific antibody response and also in T cell proliferation were observed in mice receiving IL-1beta (163-171)-FMDV. These results suggested that DNA fragment encoding IL-1beta 163-171 peptide might represent a good candidate for an adjuvant of FMDV DNA vaccine.

Adjuvants, Immunologic↗

PubMed2005

Cytokine expression during acute graft-versus-host disease after allogeneic peripheral stem cell transplantation.

Acute graft-versus-host disease (aGVHD) is one of the major problems following allogeneic peripheral blood stem cell transplantation (allo-PBSCT). In order to investigate the pathogenesis of human aGVHD, we analyzed cytokine gene expression and cytokine secretion by peripheral blood mononuclear cells (PBMC) in 30 patients who underwent allo-PBSCT. In this study, reverse transcription-polymerase chain reaction (RT-PCR) was used to explore the mRNA expression of interleukin (IL)-2, interferon (IFN)-gamma, IL-4, IL-10 and IL-12 in the PBMC of allo-PBSCT patients with aGVHD and in controls. The concentrations of these cytokines and of IL-18 were also measured by means of ELISA in medium obtained from cultured leukocytes after stimulation with PHA or LPS. Compared with the normal allo-PBSCT group (n=14), IL-2 and IFN-gamma were detected more frequently in aGVHD group (n=16). IL-12 and IL-18 were elevated, while IL-10 level decreased in the same group. There is no difference in IL-4 gene expression between patients with or without aGVHD, but the concentration of IL-4 for patients with grade II-IV aGVHD decreased. These data suggest that IL-2, IFN-gamma, IL-12 and IL-18 play important roles in the development of aGVHD in humans.

Acute Disease↗

PubMed2005

Relationship between the regulatory region polymorphism of human tissue kallikrein gene and essential hypertension.

Ten alleles with length and nucleotide sequence variations were identified in the regulatory region of human tissue kallikrein gene. This present study aimed to study the polymorphisms of the regulatory region of human tissue kallikrein gene of the Chinese and investigate the relationship of the polymorphisms with essential hypertension. A case-control study was conducted in 200 hypertensive and 200 normotensive subjects of unrelated Chinese Han origin. All subjects were aged from 30 to 70 years and had no history of diabetes mellitus, kidney failure, or thyroid gland disease. The alleles were detected by polymerase chain reaction (PCR) and genotyping was performed with allele-specific oligonucleotide analysis (ASO). Data from the essential hypertensive and control subjects were statistically analysed by the Student's t-test and chi2-test. The age- and gender-matching of the groups were accurate. The case group and the control group were in Hardy-Weinberg equilibrium at this locus (cases, P=0.313; control subjects, P=0.457). There were nine alleles among the case and control groups, and the allele frequencies were found to be significantly different between cases and controls (chi2=25.701, P<0.001). The genotype frequencies were also significantly different (chi2=70.100, P<0.001) between these two groups. In conclusion, there are polymorphisms in the regulatory region of human tissue kallikrein gene in the Chinese Han people. Differences in both allele frequencies and genotype frequencies between these two groups have provided evidence towards the association of hypertension with the polymorphisms in this studied site.

Asian People↗

PubMed2005

VEGF-induced phosphorylation of Bcl-2 influences B lineage leukemic cell response to apoptotic stimuli.

Post-translational modification of Bcl-2 protein has been described in a variety of cell models with effects varying from enhanced to abrogated function. In this study, we demonstrated that Bcl-2 was constitutively phosphorylated in several hematopoietic tumor cell lines and in primary ALL cells. Increased phosphorylation of Bcl-2 protein in the JM1 ALL cell line, achieved by expression of the phosphomimetic Bcl-2 construct S70E, enhanced JM1 cell chemoresistance. In contrast, initiation of JM1 cell apoptosis was coincident with dephosphorylation of Bcl-2 and elevated protein phosphatase 2A activity. S70E expression also diminished tBid-mediated cytochrome c release and blunted chemotherapy-induced activation of caspases-9 and -3 in JM1 cells. To determine whether soluble factors produced by stromal cells in the bone marrow influence phosphorylation of Bcl-2 protein, a panel of recombinant cytokines was evaluated. Of those tested, vascular endothelial growth factor (VEGF) induced phosphorylation of Bcl-2 protein and blunted cytochrome c release during chemotherapy or tBid treatment of ALL cells. In contrast, JM1 cells transfected with S70A, resulting in expression of Bcl-2 protein that cannot be phosphorylated, were not efficiently rescued from apoptosis by VEGF. These observations suggest that optimal protection of leukemic cells by VEGF may require activation of a pathway that includes Bcl-2 phosphorylation.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2005

Genetic analysis of microsomal epoxide hydrolase gene and its association with lung cancer risk.

The human microsomal epoxide hydrolase (EH) gene contains polymorphic alleles, which may be linked to increased risk for tobacco-related lung cancer. The purpose of this study is to screen new polymorphisms and determine whether these polymorphisms can be used to predict individual susceptibility to lung cancer. The polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis was used to screen for polymorphisms in the coding region of the EH gene. Eleven polymorphisms, including previously reported polymorphisms, were identified and the prevalence of these variants was assessed in at least 50 healthy Caucasians and African-Americans. Among the 11 polymorphisms, the prevalence of the amino acid-changing EH polymorphisms in codons 43, 113 and 139 was examined in 182 Caucasian incident cases with primary lung cancer, as well as in 365 frequency-matched controls to examine the role of EH polymorphisms in lung cancer risk. A significant increase in lung cancer risk was observed for predicted high EH activity genotypes (odds ratio (OR) 2.3, 95% confidence interval (CI) 1.2-4.3) as compared with low EH activity genotypes. This association was more pronounced among patients with lung adenocarcinoma (OR 4.7, 95% CI 1.7-13.1). These results suggest that the EH polymorphism plays an important role in lung cancer risk and is linked to tobacco smoke exposure.

Adenocarcinoma↗

PubMed2005

Subversion of the Bcl-2 life/death switch in cancer development and therapy.

The Bcl-2 protein family, which largely determines commitment to apoptosis, has central roles in tumorigenesis and chemoresistance. Its three factions of interacting proteins include the BH3-only proteins (e.g., Bim, Puma, Bad, Noxa), which transduce diverse cytotoxic signals to the mammalian pro-survival proteins (Bcl-2, Bcl-x(L), Bcl-w, Mcl-1, A-1), whereas Bax and Bak, when freed from pro-survival constraint, provoke the mitochondrial permeabilization that triggers apoptosis. We have discovered unexpected specificity in their interactions. Only Bim and Puma, which mediate multiple cytotoxic signals, engage all the pro-survival proteins. Noxa and Bad instead bind subsets and cooperate in killing, indicating that apoptosis requires neutralization of different pro-survival subsets. Furthermore, Mcl-1 and Bcl-x(L), but not Bcl-2, directly sequester Bak in healthy cells, and Bak is freed only when BH3-only proteins neutralize both its guards. BH3-only proteins such as Bim are tumor suppressors and mediate many of the cytotoxic signals from anticancer agents. Hence, compounds mimicking them may prove valuable for therapy. Indeed, the recently described ABT-737 is a promising "BH3 mimetic" of Bad. We find that, like Bad, ABT-737 kills cells efficiently only if Mcl-1 is absent or down-regulated. Thus, manipulation of apoptosis by targeting the Bcl-2 family has exciting potential for cancer treatment.

Animals↗

PubMed2005

The disease progression in the keratin 14 IL-4-transgenic mouse model of atopic dermatitis parallels the up-regulation of B cell activation molecules, proliferation and surface and serum IgE.

We have previously characterized the keratin 14 interleukin-4-transgenic (IL-4-Tg) mouse model of atopic dermatitis as a chronic pruritic inflammatory skin disease typified by skin infiltration of inflammatory cells and early up-regulation of Th2 cytokines and late surge of Th1 cytokines. In the present study, we examined the involvement of B cells. Systematic examinations of the following immunological parameters on B cells were carried out in non-Tg control mice and in IL-4-Tg mice at before disease onset and early and late disease stages so that we could determine the immunological sequence of events leading to the disease development: surface expressions of IA/IE, activation and costimulatory molecules, proliferation under LPS or IgM stimulation, quantification of cell surface and serum IgE, IgG1, and IgG2a. Our results showed that as the disease progresses from before onset to early disease and to late disease, there is a parallel increase in surface markers of B cell activation (IA/IE, CD44, CD69, CD80 and CD86), in B cell proliferation, and in cell surface and serum IgE. Significant increases of Th2-driven serum IgG1 and IgE in early disease was followed by significant increase of Th1-driven IgG2a in late disease. Importantly the significant increases of activation molecule (IA/IE), proliferation (to LPS), and surface IgE on B cells of the IL-4-Tg mice precedes the up-regulation of serum IgE and disease onset. These data suggest that activated B cells may play a role in atopic dermatitis disease development by up-regulating serum IgE concentration, which serves as a marker of disease onset.

Animals↗

PubMed2005

Effect of IL-2 on hepatitis C virus RNA levels in patients co-infected with human immunodeficiency virus receiving HAART.

The effect of interleukin-2 (IL-2) on the plasma levels of hepatitis C RNA (HCV-RNA) has varied in published reports. We measured the impact of IL-2 on plasma HCV RNA levels in 54 human immunodeficiency virus (HIV)/HCV coinfected patients enrolled in a randomized trial of 512 participants designed to compare the virologic and immunologic effects of cycled IL-2 plus antiretroviral therapy (ART) vs ART alone in the treatment of HIV in patients with CD4 cell counts > or =300 cells/mm(3). The mean decreases in average HCV RNA levels (copies/mL, log (10)) were 0.28 log in the IL-2 group (n = 26) and 0.04 log in the ART alone group (n = 28) at 12 months (P = 0.18). The changes in HCV RNA level were not associated with baseline or nadir CD4 cell counts, baseline aspartate aminotransferanse, CD4 cell response to IL-2, or changes in plasma HIV RNA values. Compared with those participants who only had HIV, the HIV/HCV co-infected patients did not have a significantly different CD4 cell response to IL-2 therapy. Intermittent IL-2 therapy does not produce a significant sustained decrease in plasma HCV RNA levels among patients co-infected with HIV/HCV who are on highly active ART.

Adult↗

PubMed2005

Systolic and diastolic heart failure are associated with different plasma levels of B-type natriuretic peptide.

Previous studies have found that plasma B-type natriuretic peptide (BNP) is elevated during left ventricular systolic or diastolic dysfunction. It is unclear whether the ventricular systolic and diastolic function is associated with different levels of plasma BNP. Plasma BNP was measured in 149 heart failure patients by a rapid point-of-care assay. The patients were divided into left ventricular diastolic dysfunction (n = 48), left ventricular systolic dysfunction (n = 62) and right ventricular systolic dysfunction group (n = 39). The mean BNP level in the left ventricular diastolic dysfunction, left ventricular systolic dysfunction and right ventricular systolic dysfunction was 115 +/- 80 pg/ml, 516 +/- 445 pg/ml and 345 +/- 184 pg/ml, respectively (p < 0.05). We concluded that ventricular systolic and diastolic dysfunction increases plasma BNP levels to a different extent. Left and right ventricular systolic dysfunction is associated with a higher level of plasma BNP than left ventricular diastolic dysfunction.

Adult↗

PubMed2005

Growth mechanism and ultraviolet-light emission of the self-assembled complex of MgO nanostructures.

Bulk-quantity net-like nanodendrites and four-fold hierarchical nanostructures were synthesized by direct thermal evaporation and oxidation of metallic Mg powder. Their formation mechanism is explained using the self-catalytic vapor-liquid-solid mechanism together with dendritic-crystal epitaxial growth mechanism. Four-branch and eight-branch nanodendrites were also detected. The photoluminescence spectrum reveals that the peak with the maximum intensity is centered at about 3.16 eV (392 nm). Through Gaussian fitting, a strong and narrow ultraviolet-light emission peak centered at 3.16 eV (392 nm) and a relatively weak but broad blue-light emission band centered at 2.74 eV (453 nm) were observed in the photoluminescence emission spectrum, which are respectively attributed to the recombination luminescence of the F+ and F centers (belonging to oxygen-vacancy related defect levels) in the MgO nanostructures. In addition, another very weak and broad red-infrared emission band can also be detected, which is probably due to the relaxation luminescence of impurity levels in the MgO nanostructures.

Crystallization↗

PubMed2005

Latent membrane protein-1 of Epstein - Barr virus increases sensitivity to arsenic trioxide-induced apoptosis in nasopharyngeal carcinoma cell.

BACKGROUND AND AIM: Epstein - Barr virus (EBV)-encoded LMP1 is suggested to have an important role in the pathogenesis and development of nasopharyngeal carcinoma (NPC). Our previous study showed that As2O3 exhibited growth inhibition of NPC in animal model. Here, we further explore whether LMP1 is involved in As2O3 anticancer effects in NPC cell line. METHODS: Both the stable expressing LMP1 cell line HNE1-LMP1 and its parental cell line HNE1 without LMP1 expression were used as in vitro models to assess arsenic trioxide effect. Both cell lines were treated with As2O3 for 72 h. The median inhibition concentration (IC50) was assessed by the MTT assay. Apoptosis was observed by phase-contrast microscopy and TUNEL staining. The alteration of telomere lengths was detected by Southern blotting. RESULTS: IC50 for As2O3 in HNE1-LMP1 cells and HNE1 cells was 2.22 and 5.09 micromol/L, respectively. After exposure to 2 and 4 micromol/L As2O3 for 72 h, the apoptotic index in HNE1-LMP1 was 26.27 -/+ 1.3 and 49.13 -/+ 1.4%, respectively. On the contrary, in HNE1 cells the apoptotic index was 12.6 -/+ 0.9 and 33.20 -/+ 1.3%, respectively. As compared with parental cell line HNE1, HNE1-LMP1 cells were more sensitive to growth inhibition and apoptosis (p < 0.001). The elongation of telomere length was also found in HNE1-LMP1 cells. Meanwhile, longer telomeres in HNE1-LMP1 cells failed to maintain telomere stabilization, instead, it prone to be shortened when exposure to As2O3, as comparing with HNE1 cells. CONCLUSION: LMP1 plays important role in enhancing NPC cell response to As2O3. The elongation of telomere length induced by LMP1 may contribute to the mechanisms of As2O3 sensitivity.

Animals↗

PubMed2004

Steady-state fluorescence study on release of camptothecin from agar hydrogel.

The slow drug release processes from agar hydrogel were studied by steady-state fluorescence (SSF) measurement. An anticancer drug, camptothecin (CPT), was used as the release drug and the fluorescence probe for the real-time monitoring of the release processes by measuring the fluorescence intensity of the probe. The release kinetics of CPT at different temperatures was investigated. The Fickian diffusion model was adopted to fit the results and a good linear relationship could be observed between the logarithmic release fraction and the releasing time. The diffusion coefficients (D) at these conditions were thus obtained from the slopes of the fitting curves. By plotting D against temperature, the diffusion coefficient of CPT was found to obey the Arrhenius relation and the activation energy was then obtained to be 70.6 kJ mol(-1).

Agar↗