Distribution of whaleworm (Anisakis simplex,Nematoda, Ascaridoidea) L3 larvae in three species of marine fish; saithe (Pollachius virens (L.)), cod (Gadus morhua L.) and redfish (Sebastes marinus (L.)) from Norwegian waters

The frequency distribution of Anisakis simplex L3 larvae between host tissues was investigated in three host species: saithe, cod and redfish. Fish were sampled from Norwegian coastal waters and examined for the presence of A. simplex in muscle and viscera. In all three of the host species, A. simplex larvae were most frequently detected in the viscera; the percentages of total infection for saithe, cod and redfish were 99.6%, 97.8% and 88.0%, respectively. In general, the distribution patterns of A. simplex L3 between muscle and viscera were not significantly affected by host size. The observations that distributions vary between species and are not affected by host size do not support an earlier hypothesis which states that A. simplex L3 distributions are determined by an optimal pre-encapsulation migratory distance within host tissues. In contrast, it is suggested that A. simplex L3 distributions are governed by the conditions encountered within host tissues, and are possibly related to the availability of nutrients. Received: 9 July 1997 / Accepted: 15 September 1997     

Muscle fibre type,efficiency, and mechanical optima affect freely chosen pedal rate during cycling

This study investigated the variation in freely chosen pedal rate between subjects and its possible dependence on percentage myosin heavy chain I (%MHC I) in m. vastus lateralis, maximum leg strength and power, as well as efficiency. Additionally, the hypothesis was tested that a positive correlation exists between percentage MHC I and efficiency at pre-set pedal rates but not at freely chosen pedal rate. Twenty males performed cycling at low and high submaximal power output ( approximately 40 and 70% of the power output at which maximum oxygen uptake (VO(2max)) was attained at 80 r.p.m.) with freely chosen and pre-set pedal rates (61, 88, and 115 r.p.m.). Percentage MHC I as well as leg strength and power were determined. Freely chosen pedal rate varied considerably between subjects: 56-88 r.p.m. at low and 61-102 r.p.m. at high submaximal power output. This variation was only partly explained by percentage MHC I (21-97%) as well as by leg strength and power. Interestingly, %MHC I correlated significantly with the pedal rate at which maximum peak crank power occurred (r = -0.81). As hypothesized, %MHC I and efficiency were unrelated at freely chosen pedal rate, which was in contrast to a significant correlation found at pre-set pedal rates (r = 0.61 and r = 0.57 at low and high power output, respectively). Conclusions: Subjects with high percentage MHC I chose high pedal rates close to the pedal rates at which maximum peak crank power occurred, while subjects with low percentage MHC I tended to choose lower pedal rates, favouring high efficiency. Nevertheless, the considerable variation in freely chosen pedal rate between subjects was neither fully accounted for by percentage MHC I nor by leg strength and power. Previously recognized relationships between percentage Type I ( approximately %MHC I) and efficiency as well as between pedal rate and efficiency were confirmed for pre-set pedal rates, but for freely chosen pedal rate, these variables were unrelated.     

Long QT syndrome with a high mortality rate caused by a novel G572R missense mutation in KCNH2

In a four-generation family with long QT syndrome, syncopes and torsades de pointes ventricular tachycardia (TdP) were elicited by abrupt awakening in the early morning hours. The syndrome was associated with a novel KCNH2 missense mutation, G572R, causing the substitution of a glycine residue at position 572, at the end of the S5 transmembrane segment of the HERG K(+)-channel, with an arginine residue. This segment is involved in the channel pore and the mutation may cause a reduction in the rapidly activating delayed rectifier K+ current (Ikr), or changed gating properties of the ion channel, leading to prolonged cardiac repolarization. The electrocardiograms of affected persons showed prolonged QT interval and notched T waves. Despite treatment with atenolol, 200 mg twice daily, the proband still experienced TdP episodes. Three untreated relatives of the proband died suddenly, and unexpectedly, at 18, 32, and 57 years of age. The G572R mutation is thus associated with a high mortality rate, and the clinical presentation illustrates that some mutations may not be controllable by just beta-blockade.     

Quantitative determination of cell surface β-adrenoceptors in different rat skeletal muscles

In the present study, the density of cell surface beta-adrenergic receptors was determined in different skeletal muscles using the hydrophilic ligand [3H]CGP 12177. The density of beta-adrenergic receptors was highest in the slow-twitch soleus muscle (32.8+/-0.9 fmol mg dw(-1)) and lowest in the fast-twitch glycolytic white gastrocnemius (10.4+/-0.5 fmol mg dw(-1)) beta-Adrenoceptor density correlated closely with the percentage of type-I fibres (r=0.979; P<0.0001) and inversely with the percentage of type-IIB fibres (r=696; P<0.03). Incubation with isoprenaline (10 microM) for 30 min decreased the density of beta-adrenergic receptors in the cell surface from 32.9+/-0.8 to 19.3+/-0.7 fmol mg dw(-1) in the soleus and from 16.8+/-1.0 to 12.0+/-0.7 fmol mg dw(-1) in the epitrochlearis. Internalisation appeared rapid (half-time less than 5 min). To study externalisation of beta-adrenergic receptors, soleus strips were incubated 30 min with 10 microM isoprenaline and then transferred to buffer without agonist. The first incubation reduced the density to approximately 50%, the subsequent incubation without agonist increased cell surface receptor density to approximately 80% of the initial density after 1 h. No further increase was observed over the next 2 h, suggesting that some of the receptors had been degraded. Insulin or contractile activity did not influence rate of externalisation.     

Neurotoxicity associated with neuroleptic-induced oral dyskinesias in rats. Implications for tardive dyskinesia?

Tardive dyskinesia is a serious motor side effect of long-term treatment with neuroleptics, with an unknown pathophysiologic basis. Brain damage and aging are prominent risk-factors, and together with the persistent character of the disorder, it is likely that long-lasting neuronal changes are involved in the pathogenesis. It has been hypothesized that striatal neurodegeneration caused by excitotoxic mechanisms and oxidative stress may play an important role in the development of the disorder, and the scope of the present work is to review the evidence supporting this hypothesis. The rat model of tardive dyskinesia has been used extensively in the field, and the usefulness of this model will be discussed. Neuroleptics are able to induce oxidative stress in vitro and increase striatal glutamatergic activity in rats, which may lead to toxic effects in the striatum. Drugs that block excitotoxicity inhibit the development of persistent oral dyskinesia in the rat model, and impaired energy metabolism leads to increased frequency of oral dyskinesia. There are also signs of altered striatal histology in rats with high frequency of oral dyskinesia. Furthermore, markers of increased oxidative stress and glutamatergic neurotransmission have been found in the cerebrospinal fluid of patients with tardive dyskinesia. In conclusion, several lines of evidence implicate neurotoxic events in the development of neuroleptic induced tardive dyskinesia.     

Effects of oxytocin in normal man during low and high sodium diets

AIM: We tested the hypothesis that oxytocin in normal man causes natriuresis by means of nitric oxide and/or atrial natriuretic peptide. METHODS: Normal male subjects were investigated after 4 days of sodium controlled diets (30 mmol sodium chloride day(-1), n = 8 or 230 mmol sodium chloride day(-1), n = 6). Oxytocin was infused intravenously (1 pmol kg(-1) min(-1) for 240 min). RESULTS: Mean arterial blood pressure, heart rate and glomerular filtration rate by clearance of chromium-labelled ethylenediaminetetraacetate remained stable. Plasma oxytocin increased from 2 to 3 pg mL(-1) to around 50 pg mL(-1). Oxytocin decreased urine flow (4.2 +/- 0.2--0.75 +/- 0.11 and 4.6 +/- 1.3-1.4 +/- 0.6 mL min(-1), low- and high-salt diet, respectively). During low-salt conditions, oxytocin reduced sodium and potassium excretion (11 +/- 2--4 +/- 2 and 93 +/- 19--42 +/- 3 micromol min(-1), respectively). Plasma renin, angiotensin II, aldosterone and renal excretion of metabolites of nitric oxide (nitrate and nitrite) all decreased. Plasma atrial natriuretic peptide and cyclic guanosine monophosphate were unchanged. A similar pattern was obtained during high-salt conditions but in this case the antinatriuresis was not different from that occurring during the corresponding time control series. CONCLUSIONS: The data reject the hypothesis. In contrast, we found significant antinatriuretic, antikaliuretic and antidiuretic effects, which were not mediated by the renin-angiotensin-aldosterone system, atrial natriuretic peptide, systemic haemodynamics, or processes increasing urinary excretion of metabolites of nitric oxide. The natriuretic effect of oxytocin found in laboratory animals is species-specific.     

Evaluation of calibrated 1 and 10 microl loops and dipslide as compared to pipettes for detection of low count bacteriuria in vitro

Criteria for defining urinary tract infection have changed as the importance of low count bacteriuria in patients with symptoms of infection has been recognized. Little has been published, however, regarding the ability of routine laboratory methods to meet this new challenge. We compared 1 microl and 10 microl calibrated plastic loops (Nunc, Denmark), to a commonly used dipslide method (Uricult, Orion, Finland) using a 0.1 ml pipette as the gold standard. Four typical uropathogens, E. coli, P. aeruginosa, S. saprophyticus and E. faecalis, were mixed in pooled human urine in numbers representing low counts, i.e. 10(2), 10(3), and 10(4), together with 10(5) colony-forming units (cfu)/ml, and sampling with the four methods was performed 20 times for each with each bacterium and each dilution. Colony counts showed that in many cases the 1 microl loop did not deposit any bacteria on the agar plate when colony counts were lower than 10(4) cfu/ml. The 10 microl loop constantly deposited 1.5 times higher numbers of bacteria than predicted, which correlated with the results of weighing the amount of water sampled, i.e. 15.24 (1.55) microg (mean (SD)). The dipslide counts correlated with the 10 microl loop although the agar mounts on the slides absorbed water equal to about 200 microl. There were no significant differences in the counts of the four different bacteria. Variation coefficients increased with decreasing volumes sampled, but the 10 microl loop was found sufficiently exact to detect counts from 10(3) to 10(4), since only 10-fold multiples are usually reported for urine cultures.