Methods: We have selected a total of nine Asian nations, based on the strength of their economic output and long-term real GDP growth rates. The OECD members included Japan and the Republic of Korea, while the seven non-OECD nations were China, India, Indonesia, Malaysia, Pakistan, the Philippines, and Thailand. Healthcare systems efficiency was analyzed over the period 1996-2017. To assess the effectiveness of healthcare expenditure of each group of countries, the two-way fixed effects model (country- and year effects) was used.
Results: Quality of governance and current health expenditure determine healthcare system performance. Population density and urbanization are positively associated with a healthy life expectancy in the non-OECD Asian countries. In this group, unsafe water drinking has a statistically negative effect on healthy life expectancy. Interestingly, only per capita consumption of carbohydrates is significantly linked with healthy life expectancy. In these non-OECD Asian countries, unsafe water drinking and per capita carbon dioxide emissions increase infant mortality. There is a strong negative association between GDP per capita and infant mortality in both sub-samples, although its impact is far larger in the OECD group. In Japan and South Korea, unemployment is negatively associated with infant mortality.
Conclusion: Japan outperforms other countries from the sample in major healthcare performance indicators, while South Korea is ranked second. The only exception is per capita carbon dioxide emissions, which have maximal values in the Republic of Korea and Japan. Non-OECD nations' outcomes were led by China, as the largest economy. This group was characterized with substantial improvement in efficiency of health spending since the middle of the 1990s. Yet, progress was noted with remarkable heterogeneity within the group.
Objective: The current study was conducted to evaluate acute oral toxicity of LA on normal rats.
Methods: The study was conducted in accordance with the Organization for Economic Co-operation and Development guidelines (OECD 423) with slight modifications. LA was administered orally to female Sprague Dawley (SD) rats (n = 6/group) at a single dose of 300 and 2,000 mg/kg body weight, respectively, while normal control received vehicle only. Animals from all the three groups were monitored for any behavioural and toxicological changes and mortality for two weeks. Food and fluid consumption, body weight was monitored on daily basis. At the end (on day 15th) of the experimental period, blood was collected for haematological and biochemical analysis. Further, all the animals were euthanized, and internal organs were harvested for histopathological investigation using four different stainings; haematoxylin and eosin, Masson trichrome, Periodic Acid Schiff and Picro Sirius Red for gross pathology through microscopical observation.
Results: The study results showed no LA treatment-related mortality and morbidity at two different dosages. Daily food and water consumption, body weight, relative organ weight, haematological, and biochemical analysis were observed to be normal with no severe alterations to the internal tissues.
Conclusion: The current finding suggests that single oral administration of LA, even up to 2,000 mg/kg body weight, did not exhibit any signs of toxicity in SD rats; thus, it was safe to be used on disease models in animals.
METHOD: Cleistanthins A and B were isolated from the leaves of Cleistanthus collinus. Both the compounds were administered orally for 90 days at the concentration of 12.5, 25 and 50 mg/kg, and the effects on blood pressure, biochemical parameters and histology were assessed. The dose for sub-chronic toxicology was determined by fixed dose method according to OECD guidelines.
RESULT: Sub-chronic toxicity study of cleistanthins A and B spanning over 90 days at the dose levels of 12.5, 25 and 50 mg/kg (once daily, per oral) revealed a significant dose dependant toxic effect in lungs. The compounds did not have any effect on the growth of the rats. The food and water intake of the animals were also not affected by both cleistanthins A and B. Both the compounds did not have any significant effect on liver and renal markers. The histopathological analysis of both cleistanthins A and B showed dose dependent morphological changes in the brain, heart, lung, liver and kidney. When compared to cleistanthin A, cleistanthin B had more toxic effect in Wistar rats. Both the compounds have produced a dose dependent increase of corpora amylacea in brain and induced acute tubular necrosis in kidneys. In addition, cleistanthin B caused spotty necrosis of liver in higher doses.
CONCLUSION: The present study concludes that both cleistanthin A and cleistanthin B exert severe toxic effects on lungs, brain, liver, heart and kidneys. They do not cause any significant pathological change in the reproductive system; neither do they induce neurodegenerative changes in brain. When compared to cleistanthin A, cleistanthin B is more toxic in rats.