The giant isopod genus
Bathynomus
A. Milne-Edwards, 1879, is recorded for the first time in Indonesian waters, from deep waters off southern Java in the Indian Ocean.
Bathynomus raksasa
sp. nov.
is ...described and notes on juvenile specimens of an unidentified species found in the same locality are also provided.
Bathynomus raksasa
sp. nov.
is characterized by the large size (averaging at 330 mm), narrowly rounded clypeus apex, prominent longitudinal carina on the clypeus, convex lateral margins of the uropodal exopod and endopod, produced distolateral corners of the uropodal exopod and endopod which have acute ends, an uropodal exopod with a setal fringe of medium length (69%), a pleotelson 1.6 times wider than long with the posterior margin medially concave, and the large number (11–13) of spines on the pleotelson.
EGFR signaling pathway and microRNAs (miRNAs) are two important factors for development and treatment in non-small cell lung cancer (NSCLC). Microarray analysis enables the genome-wide expression ...profiling. However, the information from microarray data may not be fully deciphered through the existing approaches. In this study we present an mRNA:miRNA stepwise regression model supported by miRNA target prediction databases. This model is applied to explore the roles of miRNAs in the EGFR signaling pathway. The results show that miR-145 is positively associated with epidermal growth factor (EGF) in the pre-surgery NSCLC group and miR-199a-5p is positively associated with EGF in the post-surgery NSCLC group. Surprisingly, miR-495 is positively associated with protein tyrosine kinase 2 (PTK2) in both groups. The coefficient of determination (R2) and leave-one-out cross-validation (LOOCV) demonstrate good performance of our regression model, indicating that it can identify the miRNA roles as oncomirs and tumor suppressor mirs in NSCLC.
•We construct mRNA:miRNA regression models exploring mRNA and miRNA relationship.•R2 and LOOCV demonstrate good performances of these models.•The model is suitable for predicting the expression level of mRNA using miRNA(s).•The model is able to identify miRNA roles as tumor suppressor mirs or oncomirs.•The mode can also be used to explore the underlying mechanisms of NSCLC.
Gout is one of the most common noncommunicable diseases in Hong Kong. Although effective treatment options are readily available, the management of gout in Hong Kong remains suboptimal. Like other ...countries, the treatment goal in Hong Kong usually focuses on relieving symptoms of gout but not treating the serum urate level to target. As a result, patients with gout continue to suffer from the debilitating arthritis, as well as the renal, metabolic, and cardiovascular complications associated with gout. The Hong Kong Society of Rheumatology spearheaded the development of these consensus recommendations through a Delphi exercise that involved rheumatologists, primary care physicians, and other specialists in Hong Kong. Recommendations on acute gout management, gout prophylaxis, treatment of hyperuricemia and its precautions, co-administration of non-gout medications with urate-lowering therapy, and lifestyle advice have been included. This paper serves as a reference guide to all healthcare providers who see patients who are at risk and are known to have this chronic but treatable condition.
Natural killer (NK) cell cytotoxic function is critical in guarding an organism against viral infections and malignantly transformed cells. Although the 51Chromium (51Cr)-release assay is regarded as ...the gold standard for assessing NK cell cytolytic activity, this method is associated with a number of technical problems including the use of radioactive reagents and inconsistent assay performance, due to the lack of assay standardisation across laboratories. Here we describe the setup of a flow cytometry (FC) based method for the measurement of NK cell cytotoxicity, suitable for patient testing. The FC protocol was assessed using four normal samples, and reference values for NK activity of the local Hong Kong population were defined by 40 peripheral blood samples from healthy volunteers. For method validation, we tested a total of 13 specimens including nine healthy individuals and four patients with clinical conditions that were expected to have NK cell dysfunction. We directly compared those results between FC and the 51Cr-release assay and we were able to demonstrate that FC is a clinically valid method for measuring NK cell function in a clinical setting.
Stress has been implicated in the development of cancers. Adrenaline levels are increased in response to stress. The effects of adrenaline on colon cancer are largely unknown. The aims of the study ...are to determine the effects of adrenaline in human colon adenocarcinoma HT-29 cells and the possible underlying mechanisms involved.
The effect of adrenaline on HT-29 cell proliferation was determined by
3H thymidine incorporation assay. Expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) were detected by Western blot. Matrix metalloproteinase-9 (MMP-9) activity and prostaglandin E
2 (PGE
2) release were determined by zymography and enzyme immunoassay, respectively.
Adrenaline stimulated HT-29 cell proliferation. This was accompanied by the enhanced expression of COX-2 and VEGF in HT-29 cells. Adrenaline also upregulated MMP-9 activity and PGE
2 release. Adrenaline stimulated HT-29 cell proliferation which was reversed by COX-2 inhibitor sc-236. COX-2 inhibitor also reverted the action of adrenaline on VEGF expression and MMP-9 activity. Further study was performed to determine the involvement of β-adrenoceptors. The stimulatory action of adrenaline on colon cancer growth was blocked by atenolol and ICI 118,551, a β
1- and β
2-selective antagonist, respectively. This signified the role of β-adrenoceptors in this process. In addition, both antagonists also abrogated the stimulating actions of adrenaline on COX-2, VEGF expression, MMP-9 activity and PGE
2 release in HT-29 cells.
These results suggest that adrenaline stimulates cell proliferation of HT-29 cells via both β
1- and β
2-adrenoceptors by a COX-2 dependent pathway.
Probiotics are widely used as functional foods which have been advocated for the maintenance of gastrointestinal microflora equilibrium and treatment of gastrointestinal disorders. However, studying ...the role of probiotics in peptic ulcer disease is limited. The aim of the present study is to investigate the effect of a probiotic strain
Lactobacillus rhamnosus GG on gastric ulcer and to elucidate the mechanisms involved. Gastric kissing ulcers were induced in rats by acetic acid (60% v/v).
L. rhamnosus GG was given intragastrically at 10
8 cfu/day or 10
9 cfu/day for three consecutive days after ulcer induction.
L. rhamnosus GG successfully colonized in the gastric mucosa especially at the ulcer margin. It also significantly and dose-dependently reduced gastric ulcer area. Cell apoptosis to cell proliferation ratio was strongly decreased and accompanied by significant up-regulation of ornithine decarboxylase (ODC) and B-cell lymphoma 2 (Bcl-2) protein expression at the ulcer margin. Angiogenesis was also significantly stimulated together with the induction of vascular endothelial growth factor (VEGF) expression. Furthermore,
L. rhamnosus GG up-regulated the phosphorylation level of epidermal growth factor receptor (EGF receptor) without altering the total EGF receptor expression. These findings suggested that
L. rhamnosus GG enhanced gastric ulcer healing via the attenuation of cell apoptosis to cell proliferation ratio and increase in angiogenesis. Regulators of these processes such as ODC, Bcl-2, VEGF and EGF receptor are likely to be involved in the healing action of
L. rhamnosus GG for gastric ulcer.
Cathelicidin, an antimicrobial peptide of the innate immune system, modulates microbial growth, wound healing, and inflammation. However, its association with inflammatory bowel diseases (IBDs) is ...unknown. Our objective was to determine whether cathelicidin would exert a modulatory effect on the progression of IBD and, if so, investigate the mechanism of action through which this effect occurred. We evaluated the potential for a synthetic cathelicidin, the mouse cathelin-related antimicrobial peptide (mCRAMP), to prevent the initiation and promote the healing of lesions from inflammatory colitis that was experimentally induced in mice with dextran sulfate sodium (DSS). During the experiment, mCRAMP was given: (i) as a parallel treatment starting together with 3% DSS feeding, and (ii) as a posttreatment starting 7 days after 3% DSS feeding. The body weight, fecal microflora populations, clinical symptoms, and histologic findings of colonic tissues were measured. Relative gene expression of mucins (MUC1, MUC2, MUC3, and MUC4) in colonic tissues was determined by real-time polymerase chain reaction. Intrarectal administration of mCRAMP ameliorated DSS-induced colitis with negligible effects on mucosal healing. The peptide also significantly reduced the increased number of fecal microflora in colitis animals. It reversed the decline of colonic mucus thickness during colitis through upregulation of the expression of mucin genes. Treatment with mCRAMP also prevented colitis development by suppressing the induction of apoptosis by DSS. The current study demonstrates for the first time that intrarectal administration of cathelicidin may be a novel therapeutic option for IBDs.
PurposeIn an attempt to create national harmonisation of legislation, a set of model Work Health and Safety (WHS) Regulations were developed in Australia. These regulations require principal ...contractors to undertake specific WHS planning and coordination activities if the construction works to be completed cost AU $250,000 or more. However, there are some doubts about the usefulness of this monetary threshold. This study aimed to investigate how effective this threshold can be in Australia.Design/methodology/approachTo evaluate the performance and operation of this threshold in the Australian construction industry, this study modelled the costs of construction for four construction project scenarios – small classroom, two-storey home renovation with adjacent pool, small commercial warehouse and single-storey house (volume home builder) – under various conditions based on historical data (2011–2017) and in eight Australian jurisdictions.FindingsAmong the six study factors (i.e. the types for construction, geographical location, design specification, delivery method, contracting approach and inflation), the research found considerable variation in the operation and performance of the monetary threshold.Originality/valueThe research highlights some potential challenges associated with the use of a monetary threshold in the regulation of WHS planning in construction projects. Thus, the results are expected to contribute to addressing these challenges, leading to the development of an appropriate balance to achieve efficient and effective WHS regulation in Australia.
Cigarette smoking is a risk factor for colorectal cancer. It is suggested that 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific nitrosamine, mediates the carcinogenic action ...of cigarette smoking by promoting cancer growth. In the present study, the proliferative response of a cultured colon cancer cell line HT-29 to NNK was determined. It was found that NNK dose-dependently stimulated HT-29 cell proliferation. In this regard, the stimulatory action of NNK was abolished by atenolol and ICI 118,551, a beta1- and beta2-selective antagonist, respectively. In addition, cell growth was stimulated by the nonselective adrenergic agonist, noradrenaline, and more effectively by the beta-selective agonist, isoproterenol. The second message cyclic AMP level for beta-adrenoceptor activation was elevated by isoproterenol and NNK treatment. These agents also up-regulated cyclooxygenase-2 expression, cytosolic phospholipase A2 expression, and prostaglandin E2 release. Beta2-adrenoceptor blockade with ICI 118,551, in contrast, significantly decreased cyclooxygenase-2 expression, cytosolic phospholipase A2 expression and prostaglandin E2 release induced by NNK and isoproterenol. To conclude, it is proposed that NNK stimulates HT-29 cell proliferation through beta-adrenoceptors, preferentially beta2 receptors. Activation of the beta-adrenoceptors, and the consequent cyclic AMP elevation coupled with the downstream arachidonic acid pathway, is perhaps an important mechanistic cascade in the promotion of colon cancer growth. These findings partly elucidate the carcinogenic actions of cigarette smoke and shed new light on the novel modulatory role of beta-adrenoceptors in the development of colon cancer.
Blockade of angiogenesis is a promising strategy to suppress tumor growth, invasion, and metastasis. Vascular endothelial growth factor (VEGF), which binds to tyrosine kinase receptors VEGF receptors ...(VEGFR) 1 and 2, is the mediator of angiogenesis and mitogen for endothelial cells. Cyclooxygenase-2 (COX-2) plays an important role in the promoting action of nicotine on gastric cancer growth. However, the action of nicotine and the relationship between COX-2 and VEGF/VEGFR system in tumorigenesis remain undefined. In this study, the effects of nicotine in tumor angiogenesis, invasiveness, and metastasis were studied with sponge implantation and Matrigel membrane models. Nicotine (200 microg/mL) stimulated gastric cancer cell proliferation, which was blocked by SC-236 (a highly selective COX-2 inhibitor) and CBO-P11 (a VEGFR inhibitor). This was associated with decreased VEGF levels as well as VEGFR-2 but not VEGFR-1 expression. Topical injection of nicotine enhanced tumor-associated vascularization, with a concomitant increase in VEGF levels in sponge implants. Again, application of SC-236 (2 mg/kg) and CBO-P11 (0.4 mg/kg) partially attenuated vascularization by approximately 30%. Furthermore, nicotine enhanced tumor cell invasion through the Matrigel membrane by 4-fold and promoted migration of human umbilical vein endothelial cells in a cocultured system with gastric cancer cells. The activity of matrix metalloproteinases 2 and 9 and protein expressions of plasminogen activators (urokinase-type plasminogen activator and its receptor), which are the indicators of invasion and migration processes, were increased by nicotine but blocked by COX-2 and VEGFR inhibitors. Taken together, our results reveal that the promoting action of nicotine on angiogenesis, tumor invasion, and metastasis is COX-2/VEGF/VEGFR dependent.
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