ESTIMATING RELATIVE MAGNITUDES OF COMPONENTS OF FARM PRODUCTION IN SEMI-SUBSISTENCE FARMING: THE CASE OF KAVANGO

Output from the non-formal, traditional or semi-subsistence sector is usually estimated on the basis-marketed production only. It is therefore often underestimated in national statistics and information on the relative importance of different sources of farm-household production is either not attempted or is unreliable. This paper provides an estimation of the magnitude and relative contribution of different production and consumption components for different farm-household types in Kavango. Some of the practical and conceptual issues involved are discussed, as well as the implications of the results obtained for development planning.Farm Management,

Establishment and characterisation of chemoresistant osteosarcoma cell lines by single and multi-agent induced strategies

Osteosarcoma is a rare malignant bone tumour that occurs primarily in adolescents and young adults. Prior to the adoption of chemotherapy in mid 1970s, more than 85% if post-surgery osteosarcoma patients developed metastasis. Nowadays, standard osteosarcoma treatment of osteosarcoma includes neo-adjuvant chemotherapy followed by surgical removal and adjuvant multi-drug chemotherapy. The combination of cisplatin, doxorubicin and high-dose methotrexate is the standard treatment for most patients. Surgery combined with chemotherapy has improved the survival rate for osteosarcoma patients to 60% - 70%. However, most of the patients with metastatic or recurrent osteosarcoma have poor prognosis due to the development of chemotherapeutic drug resistance. Developing drug-resistant cancer cell models is one approach to study the mechanisms of chemoresistance in cancer cells. In this study, clinically relevant chemoresistant osteosarcoma cell models were developed from the cell lines MG-63 and HOS-143B. One of the strategies used the current study includes a multiple drugs combination approach, where cisplatin, doxorubicin, and methotrexate are combined in one treatment. The purpose of this method is to simulate a similar experience with osteosarcoma patients who are receiving clinical chemotherapy treatment and therefore, to establish a clinically relevant osteosarcoma-resistant model to study the mechanisms of drug resistance. Cisplatin, doxorubicin, and methotrexate were used as single agents and in triple combination. The highest level of resistance to cisplatin was observed in MG-63/CISR8 (3.56 ± 0.43-fold; p=0.001), doxorubicin in HOS-143B/DOXR8 (1.99 ± 0.20; p=0.0002), and methotrexate in HOS-143B/MTXR8 (3.77 ± 0.90-fold; p=0.046). The MG-63/TRIR8 and HOS-143B/TRIR8 triple-resistance models showed lower levels of resistance, 2.28 ± 0.63-fold (p=0.032) and 2.17 ± 0.13-fold resistant (p=0.0004) to combination treatment; and were not resistant to the drugs individually. Apoptosis assays suggest that the resistance in MG-63/TRIR8 is mainly from cisplatin and methotrexate and not doxorubicin. In contrast, the resistance in HOS-143B/TRIR8 is mainly from doxorubicin and methotrexate instead of cisplatin. Upregulation of P-glycoprotein was seen in all resistant models except those developed with single-agent methotrexate. The P-glycoprotein inhibitor elacridar reversed the resistance of doxorubicin on MG-63/DOXR8 (0.36 ± 0.06-fold, p=0.003), MG-63/TRIR8 (0.72 ± 0.07-fold, p=0.04), HOS-143B/CISR8 (0.47 ± 0.09-fold, p=0.009), and HOS-143B/TRI (0.45 ± 0.03-fold, p=0.0005). The migration rate of the MG-63 resistant models was significantly increased by 2.12 – 2.46-fold, their invasion rate tended to increase, and RT-PCR showed a switch from epithelial to mesenchymal gene signalling. In contrast, a significant decrease in migration was seen in HOS-143B resistant models with 0.39 – 0.43-fold, their invasion rate tended to decrease and a switch from mesenchymal to epithelial gene signalling occurred.SPHK1 and HIF1A were upregulated in most of the resistant models from the PCR array analysis and SPHK1 protein level was also determined to increase in MG-63/CISR8 (2.03 ± 0.08-fold, p=0.034), MG-63/DOXR8 (1.77 ± 0.24-fold, p=0.02), and HOS-143B/CISR8 (3.55 ± 0.84-fold, p=0.0459). A strong correlation (r=0.726) was shown between the gene expression of SPHK1 and HIF1A in HOS-143B resistant sublines. Currently, there is also a lack of effective treatments for patients who experience relapsed osteosarcoma. One treatment for relapsed patients is gemcitabine and docetaxel combination chemotherapy (GEMDOX). A systematic review was performed in this study to investigate the efficacy of combination therapy of gemcitabine and docetaxel on relapsed osteosarcoma patients. The results showed the age and gender of the patients would have a prognostic effect on the GEMDOX regimen as the second-line treatment for relapsed osteosarcoma, whereas the GEMDOX therapy was determined to have a higher efficacy on male patients and with age <18. There was no difference in toxicities between different doses (675 mg/m2 and 1,000 mg/m2) of the GEMDOX regimen, age, or gender of patients. A preclinical in vitro study was performed by investigating the sensitivity of GEMDOX therapy on the established resistant sublines. The established resistant osteosarcoma sublines were used to investigate the efficacy of the GEMDOX treatment in the relapsed setting. Out of 8 of the resistant models, MG-63/DOXR8 was significantly resistant to gemcitabine (2.44 ± 0.26-fold, p=0.001) compared to MG-63 and HOS-143B/MTXR8 was significantly resistant to docetaxel (2.32 ± 0.17-fold, p=0.005) compared to HOS-143B. These two resistant sublines were also significantly resistant to the combination of gemcitabine and docetaxel with 2.50 ± 0.53-fold (p=0.04) and 2.09 ± 0.32-fold (p=0.017) respectively. However, the rest of the 6 resistant sublines were not resistant to GEMDOX treatment, which indicates GEMDOX regimen as a potential therapeutic treatment for relapsed osteosarcoma. This project is the first to develop chemoresistant osteosarcoma cell lines with a triple combination of drugs. The characteristics of these resistant models also provide a better understanding of the resistant mechanisms in osteosarcoma cells. Lastly, these developed single and multi-agents induced clinically-relevant osteosarcoma cell lines could act as an invaluable tool for future studies of drug resistant mechanisms in osteosarcoma cells

Effect of a 6-week yoga intervention on swing mechanics during the golf swing:a feasibility study

Recent evidence suggests that participating in physical conditioning programmes can improve golf performance, however, the effectiveness of a yoga intervention has yet to be investigated. The aim of the current study was to investigate the effectiveness of a six-week yoga intervention on golf swing mechanics. Ten male golfers participated in the laboratory-based-study. Golf swing mechanics were collected from two testing sessions, before and after the six-week yoga intervention, using the Vicon motion capture system. Following the six-week yoga intervention, significant changes were observed between the yoga and control group in X-Factor (P ≤ 0.05) and a medium effect (d ≥ 0.50) observed. No significant changes (P &gt; 0.05) and no effect (d &lt; 0.20) were observed in the X-Factor stretch. Significant changes (P ≤ 0.05) and a medium effect (d &gt; 0.50) were observed for the pelvis rotations following the yoga intervention, however, no differences were observed in torso rotations or hand velocities (P &gt; 0.05). The findings of this feasibility study suggest that yoga may be a promising intervention in helping to improve golf swing mechanics, however, future research is required to confirm the effect of the use of yoga during the golf swing due to the sample size

Magnetohydrodynamic Model of Equatorial Plasma Torus in Planetary Nebulae

Some basic structures in planetary nebulae are modeled as self-organized magnetohydrodynamic (MHD) plasma configurations with radial flow. These configurations are described by time self-similar dynamics, where space and time dependences of each physical variable are in separable form. Axisymmetric toroidal MHD plasma configuration is solved under the gravitational field of a central star of mass $M$. With an azimuthal magnetic field, this self-similar MHD model provides an equatorial structure in the form of an axisymmetric torus with nested and closed toroidal magnetic field lines. In the absence of an azimuthal magnetic field, this formulation models the basic features of bipolar planetary nebulae. The evolution function, which accounts for the time evolution of the system, has a bounded and an unbounded evolution track governed respectively by a negative and positive energy density constant $H$.Comment: 14 figure

Nearby Clumpy, Gas Rich, Star Forming Galaxies: Local Analogs of High Redshift Clumpy Galaxies

Luminous compact blue galaxies (LCBGs) have enhanced star formation rates and compact morphologies. We combine Sloan Digital Sky Survey data with HI data of 29 LCBGs at redshift z~0 to understand their nature. We find that local LCBGs have high atomic gas fractions (~50%) and star formation rates per stellar mass consistent with some high redshift star forming galaxies. Many local LCBGs also have clumpy morphologies, with clumps distributed across their disks. Although rare, these galaxies appear to be similar to the clumpy star forming galaxies commonly observed at z~1-3. Local LCBGs separate into three groups: 1. Interacting galaxies (~20%); 2. Clumpy spirals (~40%); 3. Non-clumpy, non-spirals with regular shapes and smaller effective radii and stellar masses (~40%). It seems that the method of building up a high gas fraction, which then triggers star formation, is not the same for all local LCBGs. This may lead to a dichotomy in galaxy characteristics. We consider possible gas delivery scenarios and suggest that clumpy spirals, preferentially located in clusters and with companions, are smoothly accreting gas from tidally disrupted companions and/or intracluster gas enriched by stripped satellites. Conversely, as non-clumpy galaxies are preferentially located in the field and tend to be isolated, we suggest clumpy, cold streams, which destroy galaxy disks and prevent clump formation, as a likely gas delivery mechanism for these systems. Other possibilities include smooth cold streams, a series of minor mergers, or major interactions.Comment: 22 pages, 5 figure

Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells

Copyright @ 2010 Gopalakrishnan et al; licensee BioMed Central Ltd.Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide (H2O2). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards H2O2-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to H2O2-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following H2O2 treatment. Conclusions Taken together, our data implicate a role for the NER in H2O2-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to H2O2-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence.This research is supported by the Defence Innovative Research Programme, Defence Science and Technology Agency, Singapore (POD: 0613592) and the Academic Research Fund, Ministry of Education, Singapore (T206B3108). Supported in part by a grant from British Council, PMI2 Connect (Grant Number: RC134)