Ugandan HIV-1 V3 loop sequences closely related to the U.S./European consensus.

The third variable (V3) loop of the human immunodeficiency virus type 1 (HIV-1) envelope protein is an important determinant for virus neutralization and cell tropism. V3 loop sequences from uncultured lymphocytes obtained in 1990 from 22 Ugandan HIV-1-infected patients could, with the exception of two patients' sequences, be divided into two groups (A and B) on the basis the V3 loop size and sequence. The V3 loop consensus sequences from both groups showed a high degree of homology to a U.S./European consensus, a characteristic also reflected by the results of peptide serology. In the case of group B the difference in sequence was only five amino acids. In contrast, the V3-flanking regions for both groups showed greater homology to an earlier (1986/1987) Ugandan consensus. The discovery of these two new Ugandan V3 loop genotypes, which are closely related to the U.S./European consensus, has implications for the understanding of the evolution of HIV-1 and for the future design of a vaccine for use in Africa.     

Subcapital callus resection for slipped capital femoral epiphysis

Surgical Principles The lateral approach is routinely combined with an osteotomy of the greater trochanter. We resect the newly formed callus located at the anterior, posterior and caudal aspect of the femoral neck distal to the epiphysis. No shortening of the femoral neck results from this procedure. One can safely avoid a vascular injury by performing a careful dissection, since the posteriorly reflected articular capsule containing the nutrient vessels to the head is detached from the femoral neck like a banana peel. The resection manoeuvre is performed next to the physeal plate of the slipped epiphysis. After callus resection, reduction of the femoral head by longitudinal traction and internal rotation of the limb is easy. The aim is complete correction of the slippage. When there is excess physeal cartilage, we resect it with a curette and then the head is fixed using 2 screws. Revised Version from: Operat. Orthop. Traumatol. 4 (1992), 77–85 (German Edition).     

A simple model describes large individual differences in simultaneous colour contrast

We report experimental evidence for substantial individual differences in the susceptibility to simultaneous colour contrast. Interestingly, we found that not only the general amount of colour induction varies across observers, but also the general shape of the curves describing asymmetric matching data. A simple model based on von Kries adaptation and crispening describes the data rather well when we regard its free parameters as observer specific. We argue that the von Kries component reflects the action of a temporal adaptation mechanism, while the crispening component describes the action of the instantaneous, purely spatial mechanism most appropriately labeled simultaneous colour contrast. An interesting consequence of this view is that traditional ideas about the general characteristics of simultaneous contrast must be considered as misleading. According to Kirschmann’s 4th law, for instance, the simultaneous contrast effect should increase with increasing saturation of the surround, but crispening predicts the converse. Based on this reasoning, we offer a plausible explanation for the mixed evidence on the validity of Kirschmann’s 4th law. We also argue that simultaneous contrast, the crispening effect, Meyer’s effect and the gamut expansion effect are just different names for the same basic phenomenon.     

Metabolic activation to a mutagen of 3-hydroxy-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene, a secondary metabolite of benzo[a]pyrene

3-Hydroxy-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (3-OH-BP-7,8-diol)wag isolated from arylsulfatase/ß-glucuronidase-treatedbile of rats to which 3-hydroxybenzo[a]pyrene (3-OH-BP) hasbeen administered. This triol was investigated for mutagenicityin Salmonella typhimurium (reversion to histidine prototrophyof strains TA 97, TA 98, TA 100 and TA 1537) and in V79 Chinesehamster cells (acquisition of resistance to 6-thioguanine).When no exogenous metabolizing system was added the triol wasinactive, while 3-OH-BP showed weak mutagenic effects with allfour bacterial strains. In the presence of NADPH-fortified postmitochondrialsupernatant fraction (S9 mix) of liver homogenate from Aroclor1254-treated rats, the mutagenicity of 3-OH-BP was potentiated,and the triol was activated to a mutagen(s). In the presenceof S9 mix, the triol was 5—18 times more mutagenic than3-OH-BP in strains TA 97, TA 100 and TA 1537, but both compoundsshowed similar mutagenic potencies with strain TA 98. Thesestrain differences strongly suggest that the mutagenicity of3-OH-BP in the S9 mix-mediated test was not exclusively dueto metabolites of 3-OH-BP-7, 8-diol. Trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene(BP-7,8-diol), like the triol, showed mutagenic effects onlyin the presence of S9 mix. Strain TA 1537 was reverted by thetriol but not by the diol. In the other bacterial strains thediol was more mutagenic than the triol, the difference in potencybeing largest in strain TA 100 (2.5-to 10-fold, depending onthe experimental conditions). In V79 cells, the diol was a potentmutagen, while the triol showed only very weak mutagenic effects.However the triol was more cytotoxic than the diol. High cytotoxicityof the triol was observed even in the absence of S9 mix. Theresults of the present study demonstrate that metabolites of3-OH-BP-7, 8-diol) are biologically-active derivatives of benzo[a]pyrene.Comparison of the mutagenic effectiveness in different bacterialstrains also reveals that metabolites of 3-OH-BP-7, 8-diol andof BP-7, 8-diol substantially differ in the kind of geneticalterations they evoke.