Tear buffering in contact lens wearers

The buffering capacity of tears collected from contact lens wearers was compared to that from non-contact lens wearers. Three groups of subjects were investigated: 6 subjects not wearing contact lenses, 3 subjects wearing rigid contact lenses, and 3 subjects wearing hydrogel contact lenses. Each of the 12 subjects provided, on 6 separate occasions, 100 microliters of tears. The pH of the tears was measured with a closed chamber, temperature stabilized micro-electrode system firstly on collection and then after titration with acid and base. In all, 28 titration steps across the acid-base spectrum were completed for each subject's tears on each occasion. These tear pH responses to acid-base challenge were compared to that of unbuffered distilled water for the same titration procedure. There was no statistically significant effect of contact lens wear on tear buffering capacity, but considerable inter-subject variability was noted.     

Determinants of symptom interval in childhood cancer.

The duration of symptoms before diagnosis (lag time) was defined for 184 of 236 children diagnosed as having a malignancy at the Royal Hospital for Sick Children, Edinburgh for the time period January 1982 until December 1990. The natural logarithm of the lag time was correlated with age, gender, diagnostic group, white cell count in acute leukaemia, clinical stage of disease in solid tumours, and event free survival. Age was significantly associated with lag time, older children presenting later. In the diagnostic groups, mean lag time ranged from 2.8 weeks in nephroblastoma to 13.3 weeks for brain tumours. Diagnostic group was predictive for lag time after adjustment for age, with for example, a significantly longer lag time for those with brain tumours. However lag time was not predictive of event free survival and it is likely that lag time has other major determinants. When compared with previous studies, there also appears to be a regional variation in lag time for diagnostic groups. It seems likely that this is a reflection of geographical difference in the structure of health systems and is therefore yet another important determinant.     

Prevention of murine graft-versus-host disease by inducing and eliminating ASGM1+ cells of donor origin

In this study anti-asialo GM1 antibodies (anti-ASGM1) were used to further characterize the effector cells responsible for graft-versus-host (GVH)-induced histopathological lesions: Two different types of ASGM1+ cells were identified: an endogenous ASGM1+ population and an induced ASGM1+ population. Both of the ASGM1+ cell populations exhibited natural killer (NK) cell activity, as assessed by their ability to lyse YAC tumor targets in vitro. Donor C57BL/6 (B6) mice were treated in vivo with anti-ASGM1 to eliminate endogenous ASGM1+ cells. ASGM1+ cells were induced in B6 donor mice by treating the animals with 15 x 10(6) B6 x AF1 (B6AF1) lymphoid cells for 44-48 hr. The induced ASGM1+ cells were eliminated by in vivo treatment with anti-ASGM1. GVH reactions were induced by injecting B6 lymphoid cells into B6AF1 mice. Prior to GVH induction the B6 donor cells were tested for NK cell activity against YAC tumor target cells in vitro and for T and B cell functions by mitogen responses in vitro. GVH reactions were determined by splenomegaly, suppression of the plaque-forming cell (PFC) response to sheep red blood cells (SRBC), suppression of the T and B cell mitogen responses, and the development of GVH-associated histopathological alterations in the thymus, liver, and pancreas. Donor lymphoid cells depleted of endogenous ASGM1+ cells were effective at inducing splenomegaly, severe suppression of immune functions, and histopathological lesions. Donor lymphoid cells depleted of both the endogenous and induced ASGM1+ cells displayed normal T cell mitogen responses and were capable of inducing splenomegaly and partial suppression of the PFC response to SRBC when injected into B6AF1 recipients, however, these lymphoid cells failed to induce both GVH-associated histopathological lesions and severe suppression of T and B cell mitogen responses. These results suggest that semiallogeneic stimulation induces an ASGM1+ population in the donor inoculum that displays NK cell-like function (YAC killing) and that plays a crucial role in inducing GVH-mediated histopathological lesions and severe immunosuppression of both T and B cell responses.     

An infertile man with a 45X karyotype

We describe an infertile man with normal secondary sexual characteristics and a 45X karyotype. Physical examination showed bilateral soft small testes and the semen contained no sperm. Serum testosterone, estrogen and gonadotropin levels were within normal range. Biopsy of the testis showed germinal aplasia.     

Reduction of infarct size and infiltration of polymorphonuclear leukocytes by a thromboxane synthetase inhibitor. Studies in a rabbit ischemic heart model.

The effect of sodium 6-(2-(1-(1H)-imidazolyl)methyl-4,5-dihydrobenzo(b) thiophene)carboxylate (RS-5186), a potent and long acting thromboxane synthetase inhibitor in vitro and in vivo, on infarct size and on the infiltration of polymorphonuclear leukocytes (PMNs), was studied in a rabbit coronary artery occlusion (1 h)--reperfusion (0.5 h or 3 h) model. The infarcted region was stained with triphenyltetrazolium, and the ratio of infarcted area/left ventricular area was calculated. The infiltration of PMNs into the infarcted region was determined by measuring the PMNs specific enzyme, myeloperoxidase (MPO) activity. In the vehicle treated group, infarct size and MPO activity were increased with increased reperfusion time from 0.5 h to 3 h (infarct size: 15.3 +/- 2.7 to 25.2 +/- 3.2%; MPO activity: 255 +/- 51 to 825.3 +/- 169.4 units/g wet weight). There was also a significant correlation (r = 0.90, p less than 0.01) between the infarct size and MPO activity. In contrast, in the RS-5186 treated group (2 mg/kg i.v.), both infarct size and MPO activity did not increase with prolongation of the reperfusion period (infarct size: 12.8 +/- 5.5 to 10.3 +/- 3.6%; MPO activity: 318.8 +/- 36.7 to 381.2 +/- 72.6 units/g wet weight). In 0.5 h reperfused samples, there was no significant difference in infarct size or in MPO activity between the vehicle treated group and RS-5186 treated group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum cholesterol and risk of cancer in a cohort of 39,000 men and women

Serum cholesterol concentration was studied for its prediction of cancer in 39,268 men and women aged 15-99 years and initially free from cancer. During a median follow-up of 10 years 1381 cancer cases were diagnosed. Serum cholesterol level was inversely associated with cancer incidence among non-smokers. Age-adjusted relative risks of cancer in quintiles of serum cholesterol were in male non-smokers 1.0, 0.81, 0.73, 0.69, and 0.46 and in female non-smokers 1.0, 0.75, 0.84, 0.78, and 0.70. The associations were not found to be confounded by serum vitamins A or E, serum selenium or several other factors. The association between serum cholesterol level and risk of cancer varied from strongly negative to slightly positive according to subpopulation and site of cancer. The strongest negative associations were found to appear during the first years of follow-up, especially for rapidly developing cancers. Thus the increased occurrence of cancer at low cholesterol levels seems mainly to be due to preclinical cancer.     

Respiratory syncytial virus

RSV is now understood to be the most significant viral respiratory pathogen of infants and is capable of causing both bronchiolitis and pneumonia. It is a particular risk to hospitalized infants as the virus is easily spread through close contact. The most vulnerable infants are those who suffer with either congenital heart disease or bronchopulmonary dysplasia who easily fall prey to pulmonary complications of infection. Strict environmental control and the use of protective clothing and eyewear should be implemented to decrease the nosocomial spread of RSV. Available diagnostic studies include viral isolation, fluorescent antibody stains, and enzyme immunoassays. Treatment of the disease is usually supportive but hospitalized patients frequently benefit from aerosolized ribavirin therapy. Hopefully, current vaccine trials will be successful and this pathogen will not only be treatable but will also be preventable.     

Blood pressure and excretion of sodium, potassium, calcium and magnesium in 8- and 9-year old boys from 19 European centres

We have measured systolic and diastolic blood pressure and excretions of sodium, potassium, calcium and magnesium in groups of about 50 8- and 9-year-old boys from 19 European centres using standardized methods for the measurement of blood pressure and collection of urine, and by carrying out all analyses in one laboratory. Weight, height, pulse rate and environmental temperature were also studied. Mean systolic blood pressure ranged from 91 to 105 mm Hg and diastolic blood pressure from 51 to 66 mm Hg. Mean 24-h excretion of sodium was between 91 and 146 mmol/d, that of potassium between 29 and 60 mmol/d, that of calcium between 1.5 and 2.6 mmol/d and that of magnesium between 2.7 and 4.2 mmol/d. Mean sodium excretion tended to be lower and potassium excretion tended to be higher in the boys from the north-western parts of Europe. Relations between either systolic or diastolic blood pressure and electrolyte excretions were generally weak or absent. Most remarkable is that only the association between mean diastolic blood pressure and 24-h magnesium excretion (partial regression coefficient (b +/- s.e., -5.04 +/- 2.08 mm Hg/mmol/d) was statistically significant after adjusting for differences in creatinine excretion and environmental temperature. Mean systolic blood pressure was not significantly related with any of the variables measured. The partial regression coefficient (b +/- s.e.) for diastolic blood pressure on weight was 0.186 +/- 0.062 mm Hg/kg, on height 0.165 +/- 0.056 mm Hg/cm, on pulse rate 0.364 +/- 0.100 mm Hg/beats per min and on outside temperature -0.25 +/- 0.07 mm Hg/degrees C.