PI and RI correlated to the severity of the renal disease, as reflected by the rate of decline in reciprocal serum creatinine during antihypertensive treatment. The median RI or PI value could separate the patients into groups one of slow and another of fast progression.

A new autosomal-recessive mouse mutant with progressive motor neuronopathy (pmn) is described. Homozygotes develop paralysis of the hindlimbs during the third week of life. Soon thereafter the forelimbs also become weak, and all mice die six to seven weeks after birth. Heterozygotes are normal. Skeletal muscles show neurogenic atrophy without histological signs of reinnervation. Axonal degeneration apparently starts at the endplates and is prominent in the sciatic nerve and its branches and the phrenic nerve. Axonal sprouts are abundant. There is no evidence of demyelination, and unaffected nerve fibers are normally myelinated. Sensory axons are spared. Almost all distal motor axons have disappeared in four to five weeks after birth. Ventral nerve roots show a reduced diameter of the largest fibers but no fiber deficits. The ventral horn cells show slight chromatolysis. The corticospinal tract is normal, but in terminally ill animals the fasciculus gracilis, the rubrospinal tract and possibly also reticulospinal fibers degenerate. The brain is histologically normal. The disease manifests itself in a dying-back fashion in the distal portion of the motor neurons and may represent an animal model of hereditary motor neuron diseases in man.

The limit of agreement between GFR(DTPA) and GFR(EDTA) are acceptable and, therefore, GFR estimated from 99mTc-DTPA renography is acceptable for clinical use in patients with reduced renal function. Furthermore, the method is simple and less time consuming compared with renal clearance techniques.

No abstract

We describe a patient with bilateral extreme microphthalmia with bilateral congenital glaucoma, bilateral medial oblique facial cleft ending in lid colobomas, bilateral stenosis of the choanae, bifid uvula, frontal encephalocele, and premature craniosynostosis. The cause is unknown, but the phenotype resembles the Fryns anophthalmia-plus syndrome, which may be a recessive trait, although intrauterine environmental factors cannot be excluded.

In 69 patients on chronic haemodialysis, blood sampled randomly during dialysis was analyzed for carboxyhaemoglobin (COHb). The median value was 1.40% (range 0.9-2.3) in non-smoking patients and (1.4-7.5) in smokers. In non-smokers treated with erythropoietin (EPO) correlation was found between COHb and the weekly EPO dose (r = 0.57, p = 0.007). In smoking patients not given EPO, the COHb correlated well with the number of cigarettes smoked (r = 0.84, p = 0.003). The COHb values did not correlate to the haemoglobin values. It is concluded that COHb levels in uraemic non-smokers are elevated because of increased endogenous CO production from the enhanced erythrocyte turnover. As even low COHb levels may negatively influence the oxygen status of the uraemic patient, the addition of exogenous CO from cigarette smoking should be avoided.

SummaryAttempts were made to clarify whether laboratory guineapigs may harbour a poliovirus which, in 1911, was described as the cause of a disease called guineapig lameness. By the use of ELISA for antibodies against the poliovirus, Theiler's murine encephalomyelitis virus (TMEV), it was shown that two pet shop guineapigs suffering from lameness had extremely high titres against poliovirus, while healthy guineapigs from the same pet shop were negative. Clearly positive results were also found in 35 out of 152 laboratory guineapig sera. Positive results were found in only two out of six breeding centres, but in three out of three experimental units, all of which purchased guineapigs from one of the seropositive breeding colonies. The diseased guineapigs recovered fully after treatment with vitamins in the drinking water, a treatment used for guineapig lameness by small animal practitioners. A theory that vitamin C deficient guineapigs are, due to an impaired steroid secretion, predisposed to succumbing to infection and develop demyelinating disease similar to that in TMEV infected mice is discussed briefly. Guineapig sera were also tested serologically for other infections. Antibodies against lymphocytic choriomeningitis virus, Clostridium piliforme and Toxoplasma gondii were not found, but one breeding colony was infected with adenovirus, pneumonia virus of mice, reovirus type 3, Sendai virus, parainfluenza (simianl virus type 5 and Encephalitozoon cuniculi. Two other breeding colonies were infected with both reovirus type 3 and E. cuniculi. In all three experimental units infection with adenovirus was observed, and in two of these Sendai virus and E. cuniculi antibodies were also found. The pet shop guineapigs were infected with adenovirus, reovirus type 3 and E. cuniculi. Keywords Guineapigs; Cavia porcellusj virusj poliovirus; enterovirusj encephalomyelitisj guineapig lamenessj TMEV The possible existence and research interference of a guinea pig poliovirus has received little attention in laboratory animal health monitoring. This virus may be the cause of an enzootic disease, guineapig lameness, which in 1911 was described by Romer as aCorrespondence to:

No abstract