Natural silicate materials, including zeolite clinoptilolite, have been shown to exhibit diverse biological activities and have been used successfully as a vaccine adjuvant and for the treatment of diarrhea. We report a novel use of finely ground clinoptilolite as a potential adjuvant in anticancer therapy. Clinoptilolite treatment of mice and dogs suffering from a variety of tumor types led to improvement in the overall health status, prolongation of life-span, and decrease in tumors size. Local application of clinoptilolite to skin cancers of dogs effectively reduced tumor formation and growth. In addition, toxicology studies on mice and rats demonstrated that the treatment does not have negative effects. In vitro tissue culture studies showed that finely ground clinoptilolite inhibits protein kinase B (c-Akt), induces expression of p21WAF1/CIP1 and p27KIP1 tumor suppressor proteins, and blocks cell growth in several cancer cell lines. These data indicate that clinoptilolite treatment might affect cancer growth by attenuating survival signals and inducing tumor suppressor genes in treated cells.

Recent studies have indicated that the interleukin-12/interferon-g (IFN-g) axis is important in mycobacterial infection susceptibility. Using an intronic (CA) n polymorphic microsatellite marker within the IFN-g receptor-1 (IFNGR1) gene, we have compared the allelic frequencies of this marker in hospitalized tuberculosis patients (n ¼ 120) with that of controls (n ¼ 87) from Rijeka, Croatia. We identified 13 (CA) n alleles in the tuberculosis patients, whereas only 10 were found in the controls. A significant difference between one allelic marker and the control group was observed (P ¼ 0.02, 95% confidence interval 0.14-0.94), suggesting a possible protective association. In contrast, several other allelic markers showed a trend towards association with the disease. We also found a trend towards an increased frequency in homozygosity of one allelic marker in patients (11.7%) as compared with controls (4.6%). We conclude that there is no evidence for disease association of the IFNGR1 gene marker in Mendeliantype (single-allele) inheritance. However, our results also suggest that unidentified allelic variations in the IFNGR1 gene might elevate or decrease the risk in this ethnic population, as a part of the multigenic predisposition to tuberculosis.

Genetic susceptibility to tuberculosis includes several unknown yet different loci each contributing to a small extent. Intronic polymorphisms within the interferon-g (IFN-g) gene IFNG Tþ874A and IFNG Gþ2109A correlate with the IFN-g production in vitro, and the frequency of potential high IFN-g producers was previously reported by others to be lower in patients than in controls from Sicily. The aim of this study was to determine whether there is an association between polymorphisms in the IFN-g gene and predisposition to tuberculosis. We analysed two IFNG SNPs (Tþ874A and Gþ2109A) in patients (n ¼ 253) hospitalized in Rijeka (Croatia) and controls (n ¼ 519) from the same area. Onefifth of the controls were healthy contacts of the diseased, and the rest were blood donors. IFNG alleles, their predicted haplotypes or genotypes were not associated with disease susceptibility. Thus, we could not reproduce results from Sicilian case-control study. However, T/Tþ874 (possible high IFN-g producer) and þ874A/A (putative low producer) genotypes were associated with microscopically positive-negative forms of disease. Haplotypes (Tþ874A and Gþ2109A) based on a prediction by software PHASE and subsequent genotype analysis corroborated these findings. Patients had significantly higher frequency of genotypes without T at þ874 (AA/AA; AA/AG and AG/AG) in microscopyor bacterial culture-positive groups compared with their negative counterparts. These data suggest an association with disease severity rather than susceptibility to tuberculosis in Croatian Caucasian population.

Rett syndrome (RTT, MIM No. 312750) is a progressive neurodevelopmental disorder and one of the most common causes of mental retardation. It is transmitted as an X-linked dominant trait, therefore almost exclusively affecting females. About 80% of RTT cases are sporadic caused by mutations in the MECP2 gene located on Xq28. The gene codes for two isoforms of the methyl-CpG-binding protein (MeCP2, MeCP2B) which are involved in transcriptional silencing through DNA methylation. The gene has 4 exons. The fourth one is the largest. Almost all mutations in MECP2 occur de novo. Although mutations are dispersed throughout the gene, about 67% of all MECP2 mutations, caused by C>T transitions at 8 CpG dinucleotides, are located in the third and fourth exon. The most common mutation is R168X. So far, there is no clear evidence on genotype-phenotype correlations. There are also reports claiming that the same mutation can provoke different phenotypes. It was shown that MeCP2 can silence certain genes. One of them, brain-derived neurotrophic factor, is essential for neural plasticity, learning and memory. This discovery revealed the role of MeCP2 in the control of neuronal activity-dependent gene regulation and suggested that the pathology of RTT may result from deregulation of this process.

Mravak‐Stipetic M, Gall‐Troselj K, Lukac J, Kusic Z, Pavelic K, Pavelic J: Detection of Helicobacter pylori in various oral lesions by nested polymerase chain reaction (PCR). J Oral Pathol Med 1998; 27: 1–3. © Munksgaard, 1998. Nested PCR was used for the detection of Helicobacter pylori DNA in specimens collected from seven different topographic sites in the oral cavity. Out of 161 patients, only 21 (13.04%) were positive. There was no correlation between H. pylori status and patient diagnosis and age. No preferential site for bacterial colonization was found in the oral cavity, nor was an association established between a bacterial presence and ulcerated versus non‐ulcerated lesions. The results indicate that the oral mucosa does not appear to represent a preferred site of colonization for H. pylori. Furthermore, the evidence presented in this paper suggests that H. pylori is not pathogenic in the oral cavity, nor is it associated with common oral pathologic processes.