Umbilical cord whole blood viscosity and the umbilical artery flow velocity time waveforms: a correlation

Summary. The possibility was examined of an association between umbilical cord whole blood viscosity and umbilical artery flow velocity time waveforms obtained with continuous wave Doppler ultrasound. The cord blood viscosity was measured at both high (100 s^−l) and low (0·1 s^−I) shear rates with a concentric cylinder viscometer. Plasma viscosity and fibrinogen were also measured. An abnormal pattern in the umbilical artery flow velocity waveform (high A/B ratio) indicative of high resistance was associated with an increase in whole blood viscosity at high shear (which may reflect a change in red cell rigidity). Viscosity at low shear (reflecting red cell aggregation and rouleaux formation) did not differ. There was a significant association between the small-for-gestational age fetus and abnormal umbilical artery waveform study ( P <0·002) but not abnormal whole blood viscosity at high ( P =0·09) or low ( P =0·08) shear.     

Modification of Retinyl Acetate Toxicity in Rats by Coadministration of Menhaden Oil

Modification of Retinyl Acetate Toxicity in Rats by Coadministrationof Menhaden Oil. LLN DAMOOD, C., III, THIGPEN, L. M., GILES,H. D., MAKOVEC, G. T., MCCARTHY, D. J., AND) HILL, D. L. (1989).Fundam. Appl. Toxicol. 12, 567–578. Menhaden oil, whichhas hypolipidemic and anticarcinogenic activity, reduces thehypertriglyceridemia caused by retinyl acetate. Male Sprague-Dawleyrats were dosed daily for 30 days by gavage with either cornoil (CO); menhaden oil (MO); 20, 80, and 250 mg/kg retinyl acetate(ROAc) in CO; or 20,80, or 250 mg/kg ROAc in MO. Hypertriglycendemiaby ROAc was reduced by coadministration of MO, and serum cholesterolvalues were reduced to levels similar to those for rats receivingMO alone. Coadministration of MO reduced the ROAc-induced fractureincidence at 80 mg/kg but not at 250 mg/kg; For groups dosedwith ROAc and CO or MO, there were no differences in weight-gaindepression, elevation of serum alkaline phosphatase, or reductionof food consumption, suggesting that reduced absorption of ROAcwas not the basis for the activity of MO. The reduction in retinoidtoxicity by MO suggests a need for further study of the toxicityand anticarcino genicity of retinoid/menhaden oil combinations.     

Hereditary complement factor I deficiency

We describe four cases (from three families) of hereditary factorI deficiency, bringing the total number of cases now reportedto 23. In one family there are two affected siblings: one hassuffered recurrent pyogenic infections; the other is asymptomatic.In the second family, the patient had recurrent pyogenic infectionsand a self-limiting vasculitic illness; in the third family,the patient suffered recurrent pyogenic and neisserial infections.All four patients had markedly reduced concentrations of C3in the serum (family 1 propositus: 28%; family 1 asymptomaticsibling: 15%; family 2: 31%; and family 3: 31 % normal humanserum) which was in the form of C3b. Low lgG₂ levels may occurin primary C3 deficiency, and reduction in lgG₂ concentrationto 1.14 g/l (normal: 1.30–5.90 g/l) was found in the patientfrom family 2. Using radioligand binding assays, we demonstratedincreased binding of C3b to erythrocytes in a patient with factorI deficiency. This C3b could not be cleaved by autologous serumbut could be cleaved by normal serum or purified factor I. Wereview and compare the published cases of C3, factor H and factorI deficiency.     

Psychophysiological insomnia: the behavioural model and a neurocognitive perspective

A number of paradoxes are apparent in the assessment and treatment of psychophysiological insomnia and sleep state misperception. Three of these paradoxes exist as discrepancies between polysomnographic (PSG) measures and the subjective impressions regarding sleep quality and quantity. The remaining incongruity exists largely within the objective domain. In the case of subjective–objective discrepancies, patients with insomnia: (1) frequently identify themselves as having been awake when awakened from PSG defined sleep; (2) tend to overestimate sleep latency and underestimate total sleep time as compared with PSG measures; (3) appear to derive more benefit from pharmacotherapy that can be explained by objective gains. The remaining paradox pertains to the observation that hypnotic medications, by and large, do not normalize sleep architecture or produce a more ‘sleep-like’ EEG. In this paper, we review possible explanations for these various paradoxes, introduce a new perspective and suggest possible research avenues. The model introduced is based on the observation that beta and/or gamma activity (which have been found to be associated with cognitive processes) is enhanced in insomnia at or around sleep onset. We propose that this kind of high frequency EEG activity may interfere with the normal establishment of sleep onset-related mesograde amnesia. As a result, the patient with insomnia maintains a level of information and/or memory processing that blurs the phenomenological distinction between sleep and wakefulness and influences retrospective judgments about sleep initiation and duration.