Co-orthologs of KATANIN1 Impact Plant Morphology and Show Differential Evolution in Maize

Understanding how the size and shape of crop plants and their specific organs are genetically controlled may allow for the development of cultivars with improved plant architecture. A microtubule-severing enzyme called katanin p60 is encoded by KATANIN1 (KTN1) in Arabidopsis or by an ortholog, dwarf and gladius leaf1 (dgl1), in rice. Katanin p60 has been implicated in the control of anisotropic cell growth, which is cell growth directed in a specific direction instead of equally in all directions. Anisotropic cell growth is crucial for proper plant shape and its disruption in ktn1/dgl1 mutants leads to morphological changes such as stunted plant height, shorter leaves and reduced inflorescence size

Gaseous Pollutants Emission from Diesel Vehicles in Hong Kong

The current study presents the detailed investigation of diesel vehicles emissions utilizing chassis dynamometer test in Hong Kong. Gaseous pollutants from diesel vehicle exhaust, including nitrogen oxides (NOx), total hydrocarbon (THC) and carbon monoxide (CO), are chosen to be the targets of this study. These pollutants were monitored real-time during different testing cycles and the data collected were used to calculate the fuel-based emission factor of each pollutant. Results showed that emission standard and driving conditions are the two main factors governing the trend of emission of these pollutants. Outliers observed in these trends are probably caused by the difference in level of maintenance of the vehicles, which is another important factor affecting the emission of pollutants

Overexpression of cytochrome P450 1A1 and its novel spliced variant in ovarian cancer cells: alternative subcellular enzyme compartmentation may contribute to carcinogenesis

Epithelial ovarian cancer derived from the human ovarian surface epithelium (HOSE) is the leading cause of death from gynecologic malignancies among American women. Metabolic activation of endogenous and exogenous chemicals by cytochrome P450 (CYP) class I enzymes has been implicated in its etiology. In this study, we showed overexpression of CYP1A1 mRNA, but not CYP1B1 transcripts, in ovarian cancer cell lines when compared with primary cultures or immortalized HOSE cell lines. Importantly, we identified a novel, enzymatically active, spliced variant of CYP1A1 (CYP1A1v) formed by excision of an 84-bp cryptic intron in exon 2. CYP1A1v is overexpressed in ovarian cancer cell lines and exhibits a unique subcellular distribution restricted to the nucleus and mitochondria, contrary to the endoplasmic reticulum localization of the wild-type enzyme. In concordance, total CYP1A1 activity, as measured by the ethoxyresorufin O-deethylase assay, was detected in mitochondrial, nuclear, and microsomal fractions of ovarian cancer cells but was notably absent in all subcellular fractions of HOSE cells. Immunocytochemistry studies in 30 clinical specimens revealed overexpression of CYP1A1 in various types of ovarian cancers compared with benign epithelia and frequent localization of the enzyme to cancer cell nuclei. Forced expression of CYP1A1wt or CYP1A1v in HOSE cells resulted in nuclear localization of the enzyme and acquisition of anchorage-independent growth, which was further exacerbated following exposure to benzo(a)pyrene or 17beta-estradiol. Collectively, these data provided the first evidence that CYP1A1 overexpression and alternative splicing could contribute to ovarian cancer initiation and progression

Characteristics of a silk fibre reinforced biodegradable plastic

Silk fibre is one kind of well recognized animal fibres for bio-medical engineering and surgical operation applications because of its biocompatible and bio-resorbable properties. Recently, the use of silk fibre as reinforcement for some bio-polymers to enhance the stiffnesses of scaffolds and bone fixators has been a hot research topic. However, their mechanical and biodegradable properties have not yet been fully understood by many researchers, scientists and bio-medical engineers although these properties would govern the usefulness of resultant products. In this paper, a study on the mechanical properties and bio-degradability of silk fibre reinforced Poly (lactic-acid) (PLA) composites is conducted. It has been found that the Young’s modulus and flexural modulus of the composites increased with the use of silk fibre reinforcement while their tensile and flexural strengths decreased. This phenomenon is attributed to the disruption of inter- and intra-molecular bonding on the silk fibre with PLA during the mixing process, and consequent reduction of the silk fibre strength. Moreover, bio-degradability tests showed that the hydrophilic properties of the silk may alter the biodegradation properties of the composites compared to that of a pristine PLA sample

Expression of estrogen receptor (ER)-alpha and ER-beta in normal and malignant prostatic epithelial cells: regulation by methylation and involvement in growth regulation

The aim of the current study is to demonstrate normal and malignant prostatic epithelial cells (PrECs) as targets for receptor-mediated estrogenic and antiestrogenic action. Using an improved protocol, we have successfully isolated and maintained highly enriched populations of normal PrECs from ultrasound-guided peripheral zone biopsies, individually determined to be morphologically normal. Semiquantitative reverse transcription-PCR analyses were used to determine whether transcripts of estrogen receptor (ER)-alpha and those of ER-beta were expressed in our normal PrEC primary cultures, in a commercially available PrEC preparation (PrEC; Clontech), in an immortalized PrEC line established from a benign prostatic hyperplasia specimen (BPH-1), and in three prostatic cancer cell lines (LNCaP, PC-3, and DU145). Expression levels of ER-alpha and ER-beta transcripts were related to those of two estrogen-responsive genes [progesterone receptor (PR) and pS2], at the message levels, to gain insights into the functionality of the ER subtypes in PrECs. Interestingly, only transcripts of ER-beta, but not those of ER-alpha, were found in our primary cultures of normal PrECs, along with both PR and pS2 mRNA. These data strongly suggest that estrogen action was signaled exclusively via ER-beta in normal human PrECs. In contrast, PrEC (Clontech) and BPH-1 cells expressed both ER-alpha and ER-beta transcripts and no PR nor pS2 mRNA in PrEC and only a minimal level of PR mRNA in BPH-1. Among the three prostate cancer cell lines, LNCaP expressed ER-beta mRNA along with transcripts of PR and pS2, DU145 expressed messages of ER-beta and PR, and PC-3 cells exhibited ER-alpha, ER-beta, and pS2 mRNA. Thus, unlike normal PrECs, expression patterns of these genes in malignant PrECs are more variable. Treatment of prostate cancer cells with demethylation agents effectively reactivated the expression of ER-alpha mRNA in LNCaP and DU145 and that of pS2 message in DU145. These findings provide experimental evidence that ER-alpha gene silencing in prostate cancer cells, and perhaps also in normal PrECs, are caused by DNA hypermethylation. To evaluate the potential of using antiestrogens as prostate cancer therapies, we have assessed the growth-inhibitory action of estrogens (estradiol and diethylstilbestrol) and antiestrogens (4-hydroxy-tamoxifen and ICI-182,780) on PC-3 and DU-145 cells. In PC-3 cells, which express both ER subtypes, estrogens as well as antiestrogens are effective inhibitors. In contrast, in DU145 cells, which express only ER-beta, antiestrogens, but not estrogens, are growth inhibitors. By comparison, ICI 182,780 is the more effective cell growth inhibitor. Importantly, the ICI 182,780-induced antiproliferative effects were reversed by cotreatment of DU145 cells with an ER-beta antisense oligonucleotide, hence lending additional support to a central role played by ER-beta in mediating growth-inhibitory action of antiestrogens

Cigarette Smoke-Induced Cerebral Cortical Interleukin-6 Elevation is not Mediated Through Oxidative Stress

The author group has previously established an in vivo subchronic cigarette smoke (CS) exposure rat model, in which the systemic oxidative burden as well as the modulation of local anti-oxidative enzymes in the lung has been demonstrated. Oxidative stress has been shown to induce pro-inflammatory cytokine release, including interleukin (IL)-6 in the airways. In this study, we aimed to investigate the changes in IL-6 production, as well as the oxidative/anti-oxidative responses in the cerebral cortex using the same in vivo model. IL-6 was determined by RT-PCR and western-blot analysis. Local oxidative and anti-oxidative responses were determined by measuring cerebral cortical malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels, superoxide dismutase (SOD) and catalase activities, and the reduced to oxidized glutathione (GSH/GSSG) ratio. Nitrite level was measured by fluorescent spectrophotometry. Our results demonstrated a significant increase in both IL-6 mRNA and protein levels. Reductions of SOD activity and manganese (Mn)SOD protein level were observed together with the increased level of superoxide measured by chemiluminescent signal, after 56 days of CS exposure. There were no significant changes in the cerebral cortical levels of MDA, AOPP, catalase activity, and the GSH/GSSG ratio. Nitrite level was significantly reduced, together with the decreased protein level of nNOS in the cerebral cortex, after 56 days of CS exposure. Our results suggest that exposure to CS induces IL-6 expression in the cerebral cortex, which is not mediated by the oxidative/anti-oxidative imbalance

Evaluation of a peer counselling programme to sustain breastfeeding practice in Hong Kong

<p>Abstract</p> <p>Background</p> <p>Peer counselling is reported to increase breastfeeding rates. We evaluated an intervention consisting of mainly telephone contact peer counselling programme on breastfeeding duration and exclusivity.</p> <p>Methods</p> <p>Peer counsellors (PCs) were mothers who had successfully breastfed and had received formal training. Following a postnatal visit, they provided scheduled telephone consultations (Days 1, 4, 7, Weeks 2, 4, 8, and Month 4) to PC group mothers (n = 100) who continued breastfeeding their infants after discharge. Control group mothers (n = 100) received routine care.</p> <p>Results</p> <p>After adjusting for mothers' previous breastfeeding experiences, mothers' working status and breastfeeding problems, no statistical differences in mothers' feeding methods (exclusive, almost exclusive or predominant breastfeeding) were noted at the three follow-up times for intervention and control mothers respectively (Day 5: 37%/38%, 46%/53%, 57%/63%; Month 3: 10%/9%, 17%/23%, 20%/26%; Month 6: 2%/1%, 18%/18%, 18%/19%). All differences between the groups were not significant. Also, there was no evidence to suggest that PC intervention prolonged breastfeeding duration.</p> <p>Conclusion</p> <p>The lack of effect of our PC intervention may reflect the low baseline breastfeeding rate and low value placed on breastfeeding in our population, the type of PC intervention or group allocation biases.</p> <p>Trial registration</p> <p>ISRCTN93605280.</p

Age composition and survival of public housing stock in Hong Kong

Emerging notably in more developed regions, building stock ageing which is characterised by shrinking new completions and falling “mortality” has been posing challenges to various stakeholders in built environment. To find way out of this transition, we need to know how long buildings will last these days and the factors leading to their “mortality”. By using data from 1950s till to date, a comprehensive investigation is conducted to analyse the age composition and life expectancy of public housing stock in Hong Kong. What comes after are survival analysis and empirical analysis of those demolished to identify the key factors leading to demolition. Presented in this paper are the preliminary findings as well as the research agenda on the theme to model age composition and survival of both private and public building stocks in Hong Kong and other similar cities in Asia Pacific Rim such as Adelaide and Singapore, together with research activities to formulate policies for sustainable urban management

Determinants of personal exposure to fine particulate matter (PM2.5) adult subjects in Hong Kong

Personal monitoring for fine particulate matter (PM2.5) was conducted for adults (48 subjects, 18-63 years of age) in Hong Kong during the summer and winter of 2014-2015. All filters were analyzed for PM2.5 mass and constituents (including carbonaceous aerosols, water-soluble ions, and elements). We found that season (p = 0.02) and occupation (p &lt; 0.001) were significant factors affecting the strength of the personal-ambient PM2.5 associations. We applied mixed-effects models to investigate the determinants of personal exposure to PM2.5 mass and constituents, along with within- and between-individual variance components. Ambient PM2.5 was the dominant predictor of (R-2 = 0.12-0.59, p &lt; 0.01) and the largest contributor (&gt;37.3%) to personal exposures for PM2.5 mass and most components. For all subjects, a one-unit (2.72 mu g/m(3)) increase in ambient PM2.5 was associated with a 0.75 mu g/m(3) (95% CI: 0.59-0.94 mu g/m(3)) increase in personal PM2.5 exposure. The adjusted mixed-effects models included information extracted from individual&#39;s activity diaries as covariates. The results showed that season, occupation, time indoors at home, in transit, and cleaning were significant determinants for PM2.5 components in personal exposure (R-beta(2) = 0.06-0.63, p &lt; 0.05), contributing to 3.0-70.4% of the variability. For onehour extra time spent at home, in transit; and cleaning an average increase of 1.7-3.6% (ammonium, sulfate, nitrate, sulfur), 2.7-12.3% (elemental carbon, ammonium, titanium, iron), and 8.7-19.4% (ammonium, magnesium ions, vanadium) in components of personal PM2.5 were observed, respectively. In this research, the within-individual variance component dominated the total variability for all investigated exposure data except PM2.5 and EC. Results from this study indicate that performing long-term personal monitoring is needed for examining the associations of mass and constituents of personal PM2.5 with health outcomes in epidemiological studies by describing the impacts of individual-specific data on personal exposures. (C) 2018 Elsevier B.V. All rights reserved

Cigarette Smoking Accelerated Brain Aging and Induced Pre-Alzheimer-Like Neuropathology in Rats

Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD). To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD) rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP) processing by increasing the production of sAPPβ and accumulation of β–amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia