The occurrence of “wasting disease” of Zostera in Ireland in the 1930's

There is only one publication quoted in connection with “wasting disease” of Zostera marina L. in Ireland. This was examined and it was concluded that in fact, it did not describe “wasting disease”, but merely the normal seasonal changes of Zostera. However, another report which has not been quoted before did give an account of the disease in County Down. Evidence that the disease occurred in County Mayo is presented for the first time.     

Muscle wasting in the presence of disease,why is it so variable?

Skeletal muscle wasting is a common clinical feature of many chronic diseases and also occurs in response to single acute events. The accompanying loss of strength can lead to significant disability, increased care needs and have profound negative effects on quality of life. As muscle is the most abundant source of amino acids in the body, it appears to function as a buffer for fuel and substrates that can be used to repair damage elsewhere and to feed the immune system. In essence, the fundamentals of muscle wasting are simple: less muscle is made than is broken down. However, although well‐described mechanisms modulate muscle protein turnover, significant individual differences in the amount of muscle lost in the presence of a given severity of disease complicate the understanding of underlying mechanisms and suggest that individuals have different sensitivities to signals for muscle loss. Furthermore, the rate at which muscle protein is turned over under normal conditions means that clinically significant muscle loss can occur with changes in the rate of protein synthesis and/or breakdown that are too small to be measurable. Consequently, the changes in expression of factors regulating muscle turnover required to cause a decline in muscle mass are small and, except in cases of rapid wasting, there is no consistent pattern of change in the expression of factors that regulate muscle mass. MicroRNAs are fine tuners of cell phenotype and are therefore ideally suited to cause the subtle changes in proteome required to tilt the balance between synthesis and degradation in a way that causes clinically significant wasting. Herein we present a model in which muscle loss as a consequence of disease in non‐muscle tissue is modulated by a set of microRNAs, the muscle expression of which is associated with severity of disease in the non‐muscle tissue. These microRNAs alter fundamental biological processes including the synthesis of ribosomes and mitochondria leading to reduced protein synthesis and increased protein breakdown, thereby freeing amino acids from the muscle. We argue that the variability in muscle loss observed in the human population arises from at least two sources. The first is from pre‐existing or disease‐induced variation in the expression of microRNAs controlling the sensitivity of muscle to the atrophic signal and the second is from the expression of microRNAs from imprinted loci (i.e. only expressed from the maternally or paternally inherited allele) and may control the rate of myonuclear recruitment. In the absence of disease, these factors do not correlate with muscle mass, since there is no challenge to the established balance. However, in the presence of such a challenge, these microRNAs determine the rate of decline for a given disease severity. Together these mechanisms provide novel insight into the loss of muscle mass and its variation in the human population. The involvement of imprinted loci also suggests that genes that regulate early development also contribute to the ability of individuals to resist muscle loss in response to disease.     

Investigation of EEG abnormalities in the early stage of Parkinson’s disease

The objective of the present study was to investigate brain activity abnormalities in the early stage of Parkinson’s disease (PD). To achieve this goal, eyes-closed resting state electroencephalography (EEG) signals were recorded from 15 early-stage PD patients and 15 age-matched healthy controls. The AR Burg method and the wavelet packet entropy (WPE) method were used to characterize EEG signals in different frequency bands between the groups, respectively. In the case of the AR Burg method, an increase of relative powers in the δ- and θ-band, and a decrease of relative powers in the α- and β-band were observed for patients compared with controls. For the WPE method, EEG signals from patients showed significant higher entropy over the global frequency domain. Furthermore, WPE in the γ-band of patients was higher than that of controls, while WPE in the δ-, θ-, α- and β-band were all lower. All of these changes in EEG dynamics may represent early signs of cortical dysfunction, which have potential use as biomarkers of PD in the early stage. Our findings may be further used for early intervention and early diagnosis of PD.     

Effect of the rootstock on the occurrence of lime-induced chlorosis of potted Vitis vinifera L. cv. ‘Pinot blanc’

The chlorosis susceptible Vitis vinifera L. cv. Pinot blanc was grafted on two hybrid rootstocks with different iron efficiency, as follows: V. Berlandieri × V. rupestris 140 Ru (iron-efficient) and V. riparia × V. rupestris 101-14 (iron-inefficient). The grafted vines were grown in pots of a calcareous and a non-calcareous soil. The shoot growth was periodically checked and leaves, selected at two different times (at the middle of the annual growing period), were assayed for total chlorophyll, ferrous iron, ash alkalinity, percentage of dry matter and chlorosis score. At the end of the growing cycle the roots were oven-dried and weighed. The most significant findings of the trial were: (a) the soil strongly affected the shoot growth, with canes about twice as long in the non-calcareous soil; (b) the iron-efficient rootstock (140 Ru) did not induce chlorosis when growing on the calcareous soil, while the opposite occurred with the iron-inefficient rootstock (101=14); and (c) a high ash alkalinity occurred in light chlorotic leaves compared to green ones, under the same iron concentration.     

Does magnesium dysbalance participate in the development of insulin resistance in early stages of renal disease?

We investigated the potential role of magnesium (Mg) dysbalance in the pathogenesis of insulin resistance (IR) in patients with mildly-to-moderately decreased renal function (creatinine: 142.8+/-11.0 mmol/l). The data were compared to those of 8 age- and sex-matched healthy controls (CTRL). The standard oral glucose tolerance test (oGTT) was performed in 61 patients. Twenty-two patients were classified as IR according to their values on fasting and after-load immunoreactive insulin concentrations. Serum and total erythrocyte Mg (tErMg) (atomic absorption spectro-photometry) and free erythrocyte Mg (fErMg) concentrations ((31) P NMR spectroscopy) were determined prior to and two hours after the glucose load. Ten out of 39 insulin-sensitive (IS) patients, but only one out of 22 insulin-resistant (IR) patients, had a low basal fErMg concentration (<162.2 micromol/l, chi2, p<0.01). IR patients had higher serum Mg, total erythrocyte Mg and bound erythrocyte Mg (bErMg) concentrations (both before and after glucose load) when compared with the IS group. Both groups responded to the glucose load with a significant decrease in serum Mg concentration (within the normal range), while the IR group also exhibited a decline in tErMg and bErMg. The mean sum of insulin needed to metabolize the same glucose load correlated positively with tErMg (r=0.545, p<0.01) and bErMg (r=0.560, p<0.01) in the IR patients. It is concluded that, at an early stage of renal dysfunction, IR is not associated with the decline in free erythrocyte Mg concentration, but the magnesium handling in red blood cells is altered.     

Aspects of early arthritis. Biological therapy in early arthritis--overtreatment or the way to go?

The availability of newer, and more expensive, therapies for patients with rheumatoid arthritis has changed treatment beyond recognition. Disease remission is the goal for all new patients. Studies have shown that a combination of tumour necrosis factor (TNF)-blocking drugs and methotrexate produces superior outcomes over monotherapy alone; however, use is limited by cost and potential side-effects. Currently, anti-TNF therapy is normally reserved for patients who have failed traditional disease-modifying anti-rheumatic drugs. The question that remains is whether TNF-blocking drugs are better used if given early; the high direct costs are countered by both direct and indirect savings in healthcare costs from optimal control of disease, and the benefits of early control outweigh the increased risk of infection and malignancy.     

How to assess the pathogenicity of mutations in Charcot-Marie-Tooth disease and other diseases?

Knowledge whether a certain DNA variant is a pathogenic mutation or a harmless polymorphism is a critical issue in medical genetics, in which results of a molecular analysis may serve as a basis for diagnosis and genetic counseling. Due to its genetic heterogeneity expressed at the levels of loci, genes and mutations, Charcot-Marie-Tooth (CMT) disease can serve as a model group of clinically homogenous diseases for studying the pathogenicity of mutations. Close to a 17p11.2-p12 duplication occurring in 70% of patients with the demyelinating form of CMT disease, numerous mutations have been identified in poorly characterized genes coding for proteins of an unknown function. Functional analyses, segregation analyses of large pedigrees, and inclusion of large control groups are required to assess the potential pathogenicity of CMT mutations. Hence, the pathogenicity of numerous CMT mutations remains unclear. Some variants detected in the CMT genes and originally described as pathogenic mutations have been shown to have a polymorphic character. In contrast, polymorphisms initially considered harmless were later reclassified as pathogenic mutations. However, the process of assessing the pathogenicity of mutations, as presented in this study for CMT disorders, is a more general issue concerning all disorders with a genetic background. Since the number of DNA variants is still growing, in the near future geneticists will increasingly have to cope with the problem of pathogenicity of identified genetic variants.     

How do avian embryos breathe? Oxygen transport in the blood of early chick embryos

1. Chick embryos with primary circulation, up to about 3 days of development, show no hemoglobin-mediated transport of oxygen. 2. In embryos with secondary circulation, between 3 and 6 days of incubation, the vascular area acts as the respiratory organ. Its efficiency in the oxygen uptake is less than that of the chorioallantois of later embryos. On the contrary, oxygen release to the tissues is highly efficient. 3. A full efficient hematic uptake of oxygen is reached at about the 6th incubation day, when chorioallantois acts as the embryonic respiratory organ. 4. The different respiratory mechanisms of developing chick embryo are closely related to the functional properties of the various hemoglobins which are produced during the embryonic life.