Improved Growth and Colchicine Concentration in Gloriosa Superba on Mycorrhizal Inoculation Supplemented with Phosphorus-Fertilizer

Background

Gloriosa superba produces an array of alkaloids including colchicine, a compound of interest in the treatment of various diseases. The tuber of Gloriosa superba is a rich source of colchicine which has shown anti-gout, anti-inflammatory, and anti-tumor activity. However, this promising compound remains expensive and Gloriosa superba is such a good source in global scale. Increase in yield of naturally occurring colchicine is an important area of investigation.

Materials and Methods

The effects of inoculation by four arbuscular mycorrhizal (AM), fungi, Glomus mossae, Glomus fasciculatum, Gigaspora margarita and Gigaspora gilmorei either alone or supplemented with P-fertilizer, on colchicine concentration in Gloriosa superba were studied. The concentration of colchicine was determined by high-performance thin layer chromatography.

Results

The four fungi significantly increased concentration of colchicine in the herb. Although there was significant increase in concentration of colchicine in non-mycorrhizal P-fertilized plants as compared to control, the extent of the increase was less compared to mycorrhizal plants grown with or without P-fertilization. This suggests that the increase in colchicine concentration may not be entirely attributed to enhanced P-nutrition and improved growth. Among the four AM fungi Glomus mossae was found to be best. The total colchicine content of plant (mg / plant) was significantly high in plants inoculated with Glomus mossae and 25 mg kg⁻¹phosphorus fertilizer (348.9 mg /plant) while the control contain least colchicine (177.87 mg / plant).

Conclusion

The study suggests a potential role of AM fungi in improving the concentration of colchicine in Gloriosa superba tuber.     

Mitochondrial dysfunction in ataxia-telangiectasia

Ataxia-telangiectasia mutated (ATM) plays a central role in DNA damage responses, and its loss leads to development of T-cell malignancies. Here, we show that ATM loss also leads to intrinsic mitochondrial abnormalities in thymocytes, including elevated reactive oxygen species, increased aberrant mitochondria, high cellular respiratory capacity, and decreased mitophagy. A fraction of ATM protein is localized in mitochondria, and it is rapidly activated by mitochondrial dysfunction. Unexpectedly, allelic loss of the autophagy regulator Beclin-1 significantly delayed tumor development in ATM-null mice. This effect was not associated with rescue of DNA damage signaling but rather with a significant reversal of the mitochondrial abnormalities. These data support a model in which ATM plays direct roles in modulating mitochondrial homeostasis and suggest that mitochondrial dysfunction and associated increases in mitochondrial reactive oxygen species contribute to the cancer-prone phenotype observed in organisms lacking ATM. Thus, ataxia-telangiectasia should be considered, at least in part, as a mitochondrial disease.     

Global Health and Emergency Care: A Resuscitation Research Agenda—Part 2

At the 2013 Academic Emergency Medicine global health consensus conference, a breakout session to develop a research agenda for resuscitation was held. Two articles are the result of that discussion. This second article addresses data collection, management, and analysis and regionalization of postresuscitation care, resuscitation programs, and research examples around the world and proposes a strategy to strengthen resuscitation research globally. There is a need for reliable global statistics on resuscitation, international standardization of data, and development of an electronic standard for reporting data. Regionalization of postresuscitation care is a priority area for future research. Large resuscitation clinical research networks are feasible and can give valuable data for improvement of service and outcomes. Low‐cost models of population‐based research, and emphasis on interventional and implementation studies that assess the clinical effects of programs and interventions, are needed to determine the most cost‐effective strategies to improve outcomes. The global challenge is how to adapt research findings to a developing world situation to have an effect internationally.     

Peripheral arterial disease and renal transplantation

It was hypothesized that peripheral arterial disease (PAD) is less frequent after kidney transplantation than among comparable patients who are on the deceased-donor waiting list. The cumulative incidences and risk factors for PAD were compared among 43,427 adult transplant recipients and 53,309 adults who were placed on the renal transplant waiting list between 1995 and 2003. All patients had Medicare primary insurance coverage, and Medicare claims were used to identify PAD. For patients with diabetes, the 3-yr cumulative incidence of de novo PAD was 24% on the waiting list versus 20% after transplantation. For patients without diabetes, the 3-yr cumulative incidence was 9% on the waiting list versus 5% after transplantation. The adjusted relative risk (RR) for PAD among patients without diabetes was 0.73 (95% confidence interval [CI] 0.66 to 0.80; P < 0.0001) in the transplant population versus the waiting list population, whereas among patients with diabetes, it was 0.88 (95% CI 0.82 to 0.96; P = 0.0024). A diagnosis of PAD on the waiting list was associated with an almost three-fold increase in the RR for death for patients without diabetes (2.98; 95% CI 2.71 to 3.27; P < 0.0001) and with diabetes (2.92; 95% CI 2.71 to 3.15; P < 0.0001). After transplantation, de novo PAD increased the RR for death almost two-fold in patients without diabetes (1.92; 95% CI 1.63 to 2.26; P < 0.0001) and with diabetes (1.83; 95% CI 1.58 to 2.12; P < 0.0001). The incidence of PAD is higher on the waiting list than after transplantation and is associated with an increased risk for death among patients with and without diabetes.