Some nutritional properties of unrefined sugar and its promotion of the survival of new-born rats.

1. The claims that rats fed on diets with ‘brown sugar’ (unrefined muscovado) perform better in a number of ways than do rats fed on refined white sugar (sucrose) have been examined. 2. Male Wistar rats were fed on purified diets from weaning, in which the carbohydrate component was either maize starch or unrefined sugar or sucrose. The sugars produced no differences in growth rate, body composition, or the weights of liver or kidneys. Compared with sucrose, unrefined sugar produced an increase in blood cholesterol and in the activity of hepatic fatty acid synthetase, and a greater increase in blood triglyceride. In confirmation of earlier results, rats fed on either sugar had heavier livers and kidneys, increased activity of hepatic glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and a higher concentration of plasma triglyceride compared with rats fed on maize starch. 3. Female Sprague-Dawley rats were fed on the same three diets as the male rats, and mated when they weighed about 200 g. No difference was seen in their ability to mate, the progress of pregnancies, or the sizes of the litters. Does fed on unrefined sugar produced litters of higher viability than did does fed on starch or sucrose. Survival was between 85 and 100% with unrefined sugar and between 30 and 75% with starch or sucrose. 4. Unrefined muscovado sugar has thus been shown to contain a factor required by female rats for the proper viability of their pups. This may be the same ‘Reproductive Factor R’ as that described by Wiesner & Yudkin (1951). In certain circumstances, unrefined muscovado sugar might therefore contribute to the nutritional value of a human diet, although in what circumstances, in what respect and to what extent it might do so, is by no means clear

Assessing health systems for type 1 diabetes in sub-Saharan Africa: developing a 'Rapid Assessment Protocol for Insulin Access'

BACKGROUND: In order to improve the health of people with Type 1 diabetes in developing countries, a clear analysis of the constraints to insulin access and diabetes care is needed. We developed a Rapid Assessment Protocol for Insulin Access, comprising a series of questionnaires as well as a protocol for the gathering of other data through site visits, discussions, and document reviews. METHODS: The Rapid Assessment Protocol for Insulin Access draws on the principles of Rapid Assessment Protocols which have been developed and implemented in several different areas. This protocol was adapted through a thorough literature review on diabetes, chronic condition management and medicine supply in developing countries. A visit to three countries in sub-Saharan Africa and meetings with different experts in the field of diabetes helped refine the questionnaires. Following the development of the questionnaires these were tested with various people familiar with diabetes and/or healthcare in developing countries. The Protocol was piloted in Mozambique then refined and had two further iterations in Zambia and Mali. Translations of questionnaires were made into local languages when necessary, with back translation to ensure precision. RESULTS: In each country the protocol was implemented in 3 areas – the capital city, a large urban centre and a predominantly rural area and their respective surroundings. Interviews were carried out by local teams trained on how to use the tool. Data was then collected and entered into a database for analysis. CONCLUSION: The Rapid Assessment Protocol for Insulin Access was developed to provide a situational analysis of Type 1 diabetes, in order to make recommendations to the national Ministries of Health and Diabetes Associations. It provided valuable information on patients' access to insulin, syringes, monitoring and care. It was thus able to sketch a picture of the health care system with regards to its ability to care for people with diabetes. In all countries where this tool was used the involvement of local stakeholders resulted in the process acting as a catalyst in bringing diabetes to the attention of the health authorities

Hypothesis: ‘Vasocrine’ signalling from perivascular fat - a mechanism linking insulin resistance and vascular disease

Adipose tissue expresses cytokines which inhibit insulin signalling pathways in liver and muscle. Obesity also results in impairment of endothelium-dependent vasodilatation to insulin. We propose a vasoregulatory role for local deposits of fat around the origin of arterioles supplying skeletal muscle. Isolated first order arterioles from rat cremaster muscle are under dual regulation by insulin, which activates both endothelin-1 mediated vasoconstriction and nitric oxide mediated vasodilatation. In obese rat arterioles, insulin-stimulated nitric oxide synthesis is impaired, resulting in unopposed vasoconstriction. We propose this to be the consequence of production of the adipocytokine tumour necrosis factor-α from the cuff of fat seen surrounding the origin of the arteriole in obese rats – a depot to which we ascribe a specialist vasoregulatory role. We suggest that this cytokine accesses the nutritive vascular tree to inhibit insulin-mediated capillary recruitment – a mechanism we term ‘vasocrine’ signalling. We also suggest a homology between this vasoactive periarteriolar fat and both periarterial and visceral fat, which may explain relationships between visceral fat, insulin resistance and vascular disease

The influence of dietary carbohydrate and fat on kidney calcification and the urinary excretion of N-acetyl-beta-glucosaminidase (EC 3.2.1.30).

1. Male Sprague-Dawley rats were fed on diets containing either sucrose or starch as the carbohydrate component. In one experiment, the diets also contained 200 g either butter or polyunsaturated margarine/kg; in a second experiment, the diets contained less fat in the form of 20 g maize oil/kg. 2. Over a period of 11 months assays were made in the urine of several ions and of the activity of the enzyme N-acetyl-β-glucosaminidase (β-2-acetamido-2-deoxy-β-D glucoside acetamidodeoxygluco-hydrolase; EC 3.2.1.30); at 13 months, examination was made of some of the abdominal viscera, especially of the kidneys. 3. In rats fed on the higher amount of fat, dietary sucrose produced a higher activity of the enzyme than did dietary starch, and a greater excretion of inorganic phosphate. 4. With both the higher and lower amounts of dietary fat, sucrose led to an increase in the weight of the liver and of the kidneys, and an increase in the concentration of calcium and of phosphate in kidney tissue. With the higher amount of fat, sucrose also produced an increase in the concentration of magnesium in the kidney. There was no difference in the concentration of any of the ions assayed in the plasma or, apart from inorganic phosphate, in the urine. 5. The kidneys of the sucrose-fed rats showed nephrocalcinosis, mostly in the cortico-medullary region, and basophilic deposits in the tubules. Attention is drawn to this unusual occurrence of nephrocalcinosis in male rats

Volume 9. Article 1. Tetrodon poisoning.

https://elischolar.library.yale.edu/bulletin_yale_bingham_oceanographic_collection/1131/thumbnail.jp

Cyanobacteria blooms cannot be controlled by effective microorganisms (EM) from mud- or Bokashi-balls

In controlled experiments, the ability of ‘‘Effective Microorganisms (EM, in the form of mudballs or Bokashi-balls)’’ was tested for clearing waters from cyanobacteria. We found suspensions of EM-mudballs up to 1 g l-1 to be ineffective in reducing cyanobacterial growth. In all controls and EM-mudball treatments up to 1 g l-1 the cyanobacterial chlorophyll-a (Chl-a) concentrations increased within 4 weeks from&120 to 325–435 lg l-1. When pieces of EM-mudballs (42.5 g) were added to 25-l lake water with cyanobacteria, no decrease of cyanobacteria as compared to untreated controls was observed. In contrast, after 4 weeks cyanobacterial Chl-a concentrations were significantly higher in EM-mudball treatments (52 lg l-1) than in controls (20 lg l-1). Only when suspensions with extremely high EM-mudball concentrations were applied (i.e., 5 and 10 g l-1), exceeding the recommended concentrations by orders of magnitude, cyanobacterial growth was inhibited and a bloom forming concentration was reduced strongly. In these high dosing treatments, the oxygen concentration dropped initially to very low levels of 1.8 g l-1. This was most probably through forcing strong light limitation on the cyanobacteria caused by the high amount of clay and subsequent high turbidity of the water. Hence, this study yields no support for the hypothesis that EM is effective in preventing cyanobacterial proliferation or in terminating blooms. We consider EM products to be ineffective because they neither permanently bind nor remove phosphorus from eutroficated systems, they have no inhibiting effect on cyanobacteria, and they could even be an extra source of nutrients