Thermal destruction of bacterial spores immobilized in food/alginate particles

Spores of Clostridum sporogenes PA 3679 (NCIB 8053) and Bacillus stearothermophilus (NCIB 8919) were immobilized in large (0·8–2·4 cm) cubes consisting of alginate mixed with pureed potatoes, pea or meat. These were heated in experimental heating chambers at temperatures between 120 and 150°C. Theoretical predictions of the efficiency of the sterilization process were then compared with experimental data obtained from spore survival levels. The results indicate that this method may be used for the experimental substantiation of thermal processes received by large particulate foods.     

Optic disc pallor: a false localizing sign

A 20-year-old pregnant woman was referred with bilateral mild visual acuity loss and optic disc pallor. Because of profound color vision deficits out of proportion to her acuity loss, an abnormality of the cone photoreceptors was suspected. An electroretinogram confirmed the diagnosis of a cone dystrophy and precluded further costly and invasive testing. Cone dystrophy should be considered in the differential diagnosis of any patient with bilateral, nonrefractive visual loss, especially if color vision is disproportionately affected, even with a normal retinal appearance and no significant family history.     

Structural differences in the tars and chars from the pyrolysis of coals of different rank in hydrogen and in nitrogen

Two British coals—Linby high-volatile bituminous and Abernant anthracite — and an Australian brown coal were pyrolysed at 575 °C in hydrogen or nitrogen at 0.1, 5 and 30 MPa in an inclined, single-stage reactor. Hydrogen pressures of ? 5 MPa led to increased yields of tars which were more aromatic than those produced in nitrogen. The high-volatile bituminous coal fused under all conditions, whereas the anthracite and brown coal fused and agglomerated only in hydrogen at 30 MPa.     

Adhesive and signaling properties of a naturally occurring allele of glycoprotein IIIa with an amino acid substitution within the ligand binding domain-the Pena/Penb platelet alloantigenic epitopes

Platelet membrane glycoprotein IIIa (GPIIIa) is the most polymorphic integrin subunit in man, with at least seven recognized allelic isoforms present in the human gene pool. Whether these allelic variants of the GPIIb-IIIa complex differ in the ability to interact with the adhesive ligand fibrinogen (Fg) is still unknown. Since the Pena and Penb allelic forms of GPIIIa are distinguished by a single Arg143Gln amino acid substitution within the RGD binding domain of GPIIIa and anti-Pena human alloantibodies have been shown to bind GPIIb-IIIa on the platelet surface and inhibit ADP-induced platelet aggregation, we expressed both forms of this integrin in Chinese hamster ovary (CHO) cells and examined the relative adhesive properties. Both allelic forms of GPIIb-IIIa were expressed on the cell surface and were recognized by a well-characterized panel of murine and human monoclonal and polyclonal antibodies. Like Pena, the Penb form of GPIIb-IIIa could undergo conformational changes in response to RGD peptide binding, and could be induced by activating antibodies to bind Fg and the Fg mimetic antibody P1-55. The binding affinity for Fg of the Pena form of the GPIIb-IIIa complex was not significantly different from that of the Penb form, nor was its ability to signal to focal adhesion kinase, suggesting that Arg143Gln polymorphism has little or no effect on integrin function. Examination of the functional consequences of other integrin polymorphisms may be necessary to determine whether they constitute a risk factor for thrombosis or hemorrhage.     

Histamine induced contraction of human ciliary muscle cells

In cultured human ciliary muscle cells we previously showed that histamine, via an H1 receptor, stimulates the production of inositol phosphates and mobilization of intracellular calcium. We further investigated in this study whether histamine would cause contraction of human ciliary muscle cells. Photomicrographs were taken of the ciliary muscle cells before and after exposure to histamine. Cross sectional surface area of the cells was quantified using image analysis software. A decrease in cross sectional surface area was interpreted as an indication of cell contraction. The results of this study indicated that histamine (10(-6) M-10(-4) M) caused contraction of human ciliary muscle cells in a concentration-dependent fashion. The effect of histamine was mediated by the H1 receptor subtype since the histamine effect was antagonized by 10(-6) M chlorphentramine (an H1 receptor subtype selective antagonist) but not by 10(-6) M cimetidine (H2 antagonist) or thioperamide (H3 antagonist). The phospholipase C (PLC) inhibitor, U73122 (10(-6) M) and the intracellular calcium store depleting agent thapsigargin (10(-6) M) both prevented the histamine induced contraction, demonstrating that the activation of PLC and the intracellular calcium release were the key steps necessary for contraction. Our data indicate that in ciliary muscle cells, histamine, via an H1 receptor, activates PLC and increases intracellular calcium, which subsequently causes contraction of the cells.     

Failure of cytarabine in progressive multifocal leukoencephalopathy associated with human immunodeficiency virus infection. AIDS Clinical Trials Group 243 Team

BACKGROUND: Progressive multifocal leukoencephalopathy affects about 4 percent of patients with the acquired immunodeficiency syndrome (AIDS), and survival after the diagnosis of leukoencephalopathy averages only about three months. There have been anecdotal reports of improvement but no controlled trials of therapy with antiretroviral treatment plus intravenous or intrathecal cytarabine. METHODS: In this multicenter trial, 57 patients with human immunodeficiency virus (HIV) infection and biopsy-confirmed progressive multifocal leukoencephalopathy were randomly assigned to receive one of three treatments: antiretroviral therapy alone, antiretroviral therapy plus intravenous cytarabine, or antiretroviral therapy plus intrathecal cytarabine. After a lead-in period of 1 to 2 weeks, active treatment was given for 24 weeks. For most patients, antiretroviral therapy consisted of zidovudine plus either didanosine or stavudine. RESULTS: At the time of the last analysis, 14 patients in each treatment group had died, and there were no significant differences in survival among the three groups (P=0.85 by the log-rank test). The median survival times (11, 8, and 15 weeks, respectively) were similar to those in previous studies. Only seven patients completed the 24 weeks of treatment. Anemia and thrombocytopenia were more frequent in patients who received antiretroviral therapy in combination with intravenous cytarabine than in the other groups. CONCLUSIONS: Cytarabine administered either intravenously or intrathecally does not improve the prognosis of HIV-infected patients with progressive multifocal leukoencephalopathy who are treated with the antiretroviral agents we used, nor does high-dose antiretroviral therapy alone appear to improve survival over that reported in untreated patients.