Small samples of tobacco powder, prepared by grinding the dried tobacco leaves, were heated in a micro-thermo-balance in different atmospheres and at different heating rates. The size distribution and the mass concentration of the smoke particles produced were measured simultaneously with a laser particle counter and a piezo balance mass monitor. In addition, the change of weight loss with time was also measured during each experiment. It was found that a larger amount of smoke particles was produced when tobacco was heated in the atmosphere of inert gas and/or at higher heating rates. Furthermore, comparison of measured and calculated size distributions showed that the particle size distribution was governed mainly by coagulation.
The effect of water vapour on the growth of cigarette smoke particles was investigated by a light-scattering method which can measure the particle size distribution and the refractive index. The particle growth, below 90 % relative humidity, was less than 10 % for both main and side-stream smoke. The results were discussed with equations derived from the weight changes of smoke condensate in moist air, and with the changes of the refractive index. Calculations showed that the cigarette smoke particle reaches equilibrium very quickly and that it doubles its radius at about 99.5 % relative humidity.
Objective: To study maternal lipoprotein(a) levels in
normal pregnancy and in pregnancy with evidence of
vascular disease in the maternal uteroplacental circulation
defined by Doppler ultrasound study.
Samples: Maternal venous blood was collected from
75 normal pregnant women and 68 pregnant women
with evidence of potential uteroplacental vascular disease
identified by Doppler ultrasound study.
Methods: Plasma lipoprotein(a) levels in maternal blood
were measured using an enzyme-liked immunosorbent
Main outcome measures: Plasma lipoprotein(a) levels
and pregnancy outcome were examined.
Results: None of the normal group had lipoprotein(a)
levels greater than 30 mg/dl, a cutoff level which has
been associated with increased risk of atherosclerosis.
28 of the 68 women with uteroplacental insufficiency
had lipoprotein(a) levels greater than this cutoff level.
In this group there was a statistically significant higher
prevalence of preeclampsia in comparison with women
with a normal lipoprotein(a) level (p < 0.001). The
lipoprotein(a) level was significantly higher in severe
(n = 13, median 60.5 mg/dl, P < 0.001] than in mild
preeclampsia (n = 5, median 34 mg/dl). Those with high
levels (> 30 mg/dl) exhibited significantly more adverse
indices of fetal outcome.
Conclusion: This study has demonstrated that high levels
of lipoprotein(a) interfere with uteroplacental circulation
and play a role in the pathophysiology of preeclampsia.
Lipoprotein(a) concentrations are associated
with the severity of the disease. We suggest that high levels
of lipoprotein(a) might affect the placenta and fetus.
We have studied the serological relationship among the human immunodeficiency virus type 1 (HIV-1), and three simian immunodeficiency viruses (SIV). SIVagm was isolated from African green monkeys (Cercopithecus aethiops), and compared with the previously described isolates of SIVmac from a rhesus macaque (Macaca mulatta) and SIVsm from a sooty mangabey (Cercocebus atys). With respect to the glycoproteins, the simian viruses represent a subgroup apparently different from HIV . To classify HIV and SIV isolates further, we compared tryptic peptide maps of the core polypeptides p18 and p24 of HIV-2, three HIV-1 and five SIV isolates. Each peptide map was distinguishable, and differences are most prominent between the HIV-1 group and the SIVmac/SIVsm group. HIV-2 is very similar to SIVmac and SIVsm. The three SIVagm isolates form a more heterogeneous group. The p24s of all SIVagms are more similar to the p24s of HIV-1, but with respect to p18, one isolate is similar to HIV-1, while the two others are more related to SIVmac, SIVsm, and HIV-2.