Ameliorative effects of ascorbic acid on tolerance to drought stress on pepper (Capsicum annuum L) plants.

Drought stress is an important environmental stress that clearly affect biological systems of plants. There is a possibility that growth regulators are able to protect plants under drought conditions. Ascorbic acid (AsA) plays a particular role on growth of plants and protects cells from oxidative damage caused by environmental stresses. This study emphasized the impacts of AsA on improving the drought tolerance of the pepper plants. Based on a factorial arrangement in a completely randomized design, the experiment had two factors. The first factor was drought: irrigation within the field capacity, moderate stress (irrigation within the 60% field capacity) and severe stress (irrigation within the 30% field capacity). The second factor was AsA: 0 mM sprayed with distilled water, 0.5 mM and 1 mM. The experiment had three replications. Drought stress inhibited plant growth parameters including fruit number, height, weight, yield, chlorophyll a and b, total chlorophyll, carotenoid contents, it caused improvement in activity of catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), proline content, anthocyanins, soluble sugars, malondialdehyde (MDA) and H2O2 in the leaves of sweet pepper. Application of AsA contributes to an increase in antioxidant enzymes activity such as SOD, CAT, POD and proline contents, chlorophyll a and b, total chlorophyll, carotenoids, soluble carbohydrates. However, it reduced the content of anthocyanins, MDA and H2O2. Based on this study, it can be suggested that ascorbic acid adjusted antioxidant activity, especially after it has been subjected to drought stress.

Bridging the Gap Between Ethical Theory and Practice in Medicine: A Constructivist Grounded Theory Study.

Physicians try hard to alleviate mental and physical ailments of their patients. Thus, they are heavily burdened by observing ethics and staying well-informed while improving health of their patients. A major ethical concern or dilemma in medication is that some physicians know their behavior is unethical, yet act against their moral compass. This study develops models of theory-practice gap, offering optimal solutions for the gap. These solutions would enhance self-motivation or remove external obstacles to stimulate ethical practices in medicine. The Constructivist Grounded Theory Methodology is applied here where the participants and the main researcher mutually interacted with each other. Data collection was performed through qualitative methods including observation and semi-structured interviews with 21 physicians and medical students. Initial and focused coding was done, from which principal concepts were later extracted. MAXQDA software was used for analyzing data. Analysis of twelve major concepts in the study resulted in two factors and solution groups, from which four general notions influencing the ethical theory and practice gap in medicine were extracted: (1) providing effective education to change attitude and behavior; (2) considering motivational and emotional factors; (3) reconstructing regulations and processes to facilitate ethical practice; (4) conducting comprehensive and systematic studies. The existing medical educational system needs to be reconsidered to add to individual internal motivation, including optimizing persuasion strategies, maximizing participation of students, adhering to virtuous ethical theories, and fostering emotions. Additionally, regulations and processes can be reconstructed to remove practical obstacles and promote ethical practice with insignificant damages to individual self-motivation.

The Relationship of CXCR1, IκBα and HIF-1α Expression Levels with Clinicopathological Parameters in Colorectal Cancer.

BACKGROUND: The role of C-X-C motif chemokine receptor 1 (CXCR1), inhibitor of kappa B (IκBα), and hypoxia-inducible factor 1 alpha (HIF-1α) have been reported to promote tumorigenesis and progression in colorectal cancer (CRC). This study is to evaluate the expression of CXCR1, IκBα, and hypoxia-inducible factor 1 alpha (HIF-1α), in combination, in CRC tissues. It also aims to analyze the relationship of these three factors with clinico-pathological characteristics. METHODS: CRC and tumor-adjacent tissues were surgically collected from CRC patients. All patients were diagnosed by pathological examination, and none of the patients had received preoperative chemotherapy or radiotherapy. RNA extraction and cDNA synthesis were performed, and the transcription of CXCR1, IκBα, HIF-1α, and ß-actin was quantified by RT-qPCR. RESULTS: The significant increase of CXCR1, HIF-1α, and decrease of IκBα mRNA expression level were observed in tumor samples of CRC patients (p < 0.05). In addition, CXCR1 expression level was correlated with lymph node metastasis (p = 0.013). Also, results demonstrated a relationship between HIF-1α expression and TNM stage and lymph node metastasis (p = 0.047 and p = 0.005, respectively). CXCR1 and HIF-1α simultaneous expression demonstrated the significant relationship with lymph node metastasis in CRC. CONCLUSIONS: Our findings indicated that CXCR1, HIF-1α, and IκBα can be used as potential prognostic factors indicating tumors in the advanced stage in patients with CRC.

Microarray-based long oligonucleotides probe designed for Brucella Spp. detection and identification of antibiotic susceptibility pattern.

Brucella spp. is a common zoonotic infection referred to as Brucellosis, and it is a serious public health problem around the world. There are currently six classical species (pathogenic species in both animals and humans) within the genus Brucella. The ability and practicality facilitated by a microarray experiment help us to recognize Brucella spp. and its antibiotic resistant gene. Rapid phenotypic determination of antibiotic resistance is not possible by disk diffusion methods. Thus, evaluating antibiotics pattern and Brucella detection appear necessary technique by molecular methods in brucellosis. So, the aim of this study was to design a microarray long oligonucleotides probe and primer for the complete diagnosis of Brucella spp. and obtaining genetic profiles for antibiotic resistance in bacteria at the same time. In this study, we designed 16 antibiotic-resistant gene solid-phase primers with similar melting temperatures of 60 °C and 16 long oligonucleotide probes. These primers and probes can identify tetracycline-, chloramphenicol-, and aminoglycoside-resistant genes, respectively. The design of microarray probes is a versatile process that be done in a wide range of selections. Since the long oligo microarray probes are the best choices for specific diagnosis and definite treatment, this group of probes was designed in the present survey.

Lack of Association between the CDH1 -160C>A Polymorphism and Risk of Gastrointestinal Cancer - a Meta-Analysis.

E-cadherin (CDH1) genetic variations alter gene transcriptional activity of epithelial cells in vitro and may cause susceptibility to various cancers. Associations of CDH1 -160C>A polymorphism with various cancers have been widely reported. However, the results are controversial and inconsistent. To derive a more accurate estimation of the relationship, a meta-analysis was performed with regard to gastrointestinal (GI) cancer risk. Eligible studies were identified through a search of PubMed database until December 2015. Associations between the CDH1 -160C>A polymorphism and GI cancer risk was considered by odds ratios (ORs) together with their 95% confidence intervals (CIs). A total of 31 studies including 11,606 cases and 12,655 controls were involved in this meta-analysis. Overall, this meta-analysis showed no association between CDH1 -160C>A polymorphism and GI cancer risk (A vs. C: OR = 1.08, 95%CI = 0.98-1.18, P = 0.086;CA vs. CC: OR = 1.09, 95%CI = 0.97- 1.22, P = 0.118; AA vs. CC: OR = 1.10, 95%CI = 0.89-1.35, P = 0.356; AA vs. CC + CA: OR = 1.06, 95%CI = 0.96-1.18, P = 0.207; CA+AA vs. CC: OR = 1.01, 95%CI = 0.84-1.22, P = 0.89). In subgroup analysis, similar results were found. In conclusion, this meta-analysis has demonstrated that there is a lack of association of the CDH1-160C>A polymorphism with GI cancer susceptibility.