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The global epidemiology of HIV/AIDS and malaria overlap because a significant number of HIV-infected individuals live in regions with different levels of malaria transmission. Although the consequences of co-infection with HIV and malaria parasites are not fully understood, available evidence suggests that the infections act synergistically and together result in worse outcomes. The importance of understanding chemotherapeutic interactions during malaria and HIV co-infection is now being recognized. We know that some antimalarial drugs have weak antiretroviral effects; however, recent studies have also demonstrated that certain antiretroviral agents can inhibit malaria-parasite growth. Here, we discuss recent findings on the impact of HIV/AIDS and malaria co-infection and the possible roles of chemotherapy in improving the treatment of these diseases.

The propensity of isolates of the malaria parasite Plasmodium falciparum to delete a segment of chromosome 9 has provided positional information that has allowed us to identify a gene necessary for cytoadherence. It has been termed the cytoadherence-linked asexual gene (clag9). clag9 encodes at least nine exons and is expressed in blood stages. The hydrophobicity profile of the predicted CLAG9 protein identifies up to four transmembrane domains. We show here that targeted gene disruption of clag9 ablated cytoadherence to C32 melanoma cells and purified CD36. DNA-induced antibodies to the clag9 gene product reacted with a polypeptide of 220 kDa in the parental malaria clone but not in clones with a disrupted clag9 gene.

The binding of erythrocytes infected with Plasmodium falciparum to the endothelium lining the small blood vessels of the brain and other organs can mediate severe pathology. A region at the right end of chromosome 9 has been implicated in the binding of parasitised erythrocytes to the endothelial receptor CD36. A gene expressed in asexual erythrocytic stage parasites has been identified in this region and termed the cytoadherence linked asexual gene (clag). Antisense RNA production and targeted gene disruption of clag resulted in greatly reduced binding to CD36. Hybridisation to 3D7 chromosomes showed clag to be a part of a gene family of at least nine members. All members analysed so far have a conserved gene structure of at least nine exons, as well as putative transmembrane domains. The possible functions of the gene family are discussed.

The M-protein genes (emm genes) of 103 separate impetiginous Streptococcus pyogenes isolates were sequenced and the sequence types were compared to the types obtained by Vir typing. Vir typing is based on restriction fragment length polymorphism (RFLP) analysis of a 4- to 7-kb pathogenicity island encoding emm and other virulence genes. By using both HaeIII and HinfI to generate RFLP profiles, complete concordance between Vir type and emm sequence type was found. Comparison of the emm sequences with those in GenBank revealed new sequence types sharing less than 90% identity with known types. Diversity in the emm sequence was generated by corrected frameshift mutations, point mutations, and small in-frame mutations.

This review of the current periodontal literature evaluates clinical regeneration with guided tissue barriers in infrabony defects and furcations. A meta-analysis was conducted by calculating weighted means with confidence intervals for each treatment group. Clinical improvement in infrabony defects was best for polylactic acid/polyglactin (PLA/PGA) barriers, with a mean pocket reduction of 5.3 mm and a mean gain in clinical probing attachment level of 4.7 mm. For furcations, special attention was given to the frequency of either complete or partial (> or = 50%) furcation closure. Complete furcation closure was an infrequent result of guided tissue regeneration, occurring in only 7% to 19% of furcations treated with barriers. For the time period reported, the best clinical results in furcations and infrabony defects occurred with PLA/PGA-type barriers. However, there were no statistically significant differences among the various barriers in infrabony defects or furcations.

The authors surveyed 360 general dentists and 291 endodontists to obtain information on routine, nonemergency endodontic treatments adapted to clinical practice. Frequent practices and recent advances in treatment modalities-including instrumentation, obturation, intracanal preparations, medications and restorations-are highlighted.

A review of the literature was performed related to the frequency of closure of Grade II furcations with various regenerative therapies such as bone replacement grafts (BRG), coronally positioned flaps (CPF), guided tissue regeneration barriers (GTR), or open flap debridement (OFD). Fifty papers involving 1,016 furcations were evaluated. Complete furcation closure was reported only 20% of the time. Clinical change from Grade II to Grade I (partial furcation fill) was found in an additional 33% of the cases. Therefore, general improvement in clinical furcation status has been reported only about 50% of the time. The most effective furcation regenerative therapy was the combination of GTR plus BRG (91% overall positive). Similar overall positive results (88%) were achieved with nondemineralized allogeneic freeze-dried bone plus tetracycline without a barrier. The least effective therapy for regeneration in furcations was OFD (2% complete furcation closures and 13% partial furcation closures). If complete furcation closure is a primary goal of regenerative therapy, that goal would not appear to be commonly met.