Measurements of tooth wear among Australian Aborigines: I. Serial loss of the enamel crown

The dental casts made from Aboriginal children during the course of a longitudinal growth study in Central Australia provided material for analyzing tooth wear under known environmental conditions. The wear facets produced on the occlusal surfaces were clearly preserved on the dental stone casts and recorded the progress of enamel attrition from ages 6 to 18. These casts were photographed and traced by electronic planimetric methods that automatically recorded the location and size of wear facets on the first and second permanent molars. These areas of worn tooth surface were compared to the total tooth surface. The worn surface was regressed on age to calculate wear rates of each tooth. Discriminant analyses were also performed to determine the significance of dental attrition differences between the sexes at each age group. The total wear on each tooth was highly correlated with age as expected but females wore their teeth at a significantly higher rate than males. The mandibular molars wore more rapidly than maxillary teeth in both sexes. The discriminant analysis successfully grouped 91% of the cases according to age and sex. Pattern of wear, the location, and size of wear facets also differed between age groups and sex. The questions of why there is a difference between male and female wear or why there is greater wear on one arch or arch region have no ready answers. The differing rates and pattern of dental wear do suggest that arch shape and growth rates may be the answer though it has yet to be tested. However, the occlusal surface wear is useful for age estimation in a population and provides a record of shifting masticatory forces during growth.     

Differences in sexual functioning between patients with benign and malignant breast tumors

The aim of this study was to compare differences in sexual behavior between patients with benign and malignant breast tumors. A total of 187 patients treated for breast tumors (benign or malignant) at the General Hospital >Pozega<, Croatia, filled in the questionnaire between January 2001 and May 2003. Patients were asked to fill in the questionnaire one to ten years after treatment of breast tumor, while they were on their regular control visit. Deterioration in sexual life experienced 36.27% of patients with benign tumors and 51.76% of patients with malignant tumor (p<0.01). The main reason of sex life impairment in both groups was distortion of body image perception. Most of partners did not change their behavior toward women with breast tumors (48.72% for benign group and 41.82% or malignant group, p>0.05). A great amount of women in both groups felt certain change in her >body image<, but in greater extent in malignant group (41.18% vs. 25.49%), (p<0.05). From our results we can see that patients in this study do not recognize need for consultation with their physician regarding sex life after treatment of tumor (41.18% for benign and 35.29% in malignant group). It can be concluded that considerable amount of attention should be given to psychological aspects of recovery which can improve prognosis and quality of life in general.     

The inhibitory effect of HMGB-1 protein on the repair of cisplatin-damaged DNA is accomplished through the acidic domain

The well established inhibitory effect of HMGB-1 on repair of cisplatin-damaged DNA has been studied with two modified forms of the protein, shown to bind platinated DNA with higher affinity than the original protein: in vivo acetylated HMGB-1 and HMGB-1 lacking its C-terminal domain. The native and the modified proteins were assayed for their effects on adduct removal by using cell-free extract capable of repairing cisplatinated DNA in vitro. The inhibition observed with the native HMGB-1 was reduced in the presence of acetylated HMGB-1 and completely abolished when the assay was carried out with the truncated protein. When the repair assay was performed in the presence of a synthetic polypeptide identical to the C-terminal tail, either alone or together with the truncated protein, the inhibitory effect was partially recovered in a concentration-dependent manner. These findings strongly suggest that the HMGB-1-induced inhibition of cisplatin-DNA adduct repair is accomplished through the acidic domain. The results obtained are discussed in terms of the repair events that may occur in the presence of HMGB-1 protein.     

Estimates of African, European and Native American ancestry in Afro-Caribbean men on the island of Tobago

BACKGROUND/AIMS: The Tobago Afro-Caribbean population is a valuable resource for studying the genetics of diseases that show significant differences in prevalence between populations of African descent and populations of other ancestries. Empirical confirmation of low European and Native American admixture may help in clarifying the ethnic variation in risk for such diseases. We hypothesize that the degree of European and Native American admixture in the Tobago population is low. METHODS: Admixture was estimated in a random sample of 220 men, from a population-based prostate cancer screening survey of 3,082 Tobago males, aged 40 to 79 years. We used a set of six autosomal markers with large allele frequency differences between the major ethnic populations involved in the admixture process, Europeans, Native Americans and West Africans. RESULTS: The ancestral proportions of Tobago population are estimated as 94.0+/-1.2% African, 4.6+/-3.4% European and 1.4+/-3.6% Native American. CONCLUSIONS: We conclude that Tobago Afro-Caribbean men are predominantly of West African ancestry, with minimal European and Native American admixture. The Tobago population, thus, may carry a higher burden of high-risk alleles of African origin for certain diseases than the more admixed African-American population. Conversely, this population may benefit from a higher prevalence of protective alleles of African origin.     

Glycation-induced inactivation of aspartate aminotransferase, effect of uric acid

Glycation is common posttranslational modification of proteins impairing their function, which occurs during diabetes mellitus and aging. Beside extracellular glycation of long-lived proteins, intracellular modifications of short-lived proteins by more reactive sugars like fructose are possible. The process includes free oxygen radicals (glycoxidation). In an attempt to reduce glycoxidation and formation of advanced glycation products (AGE), influence of 0.2–1.2 mM uric acid as endogenous antioxidant on glycoxidation of purified pig heart aspartate aminotransferase (AST) by 50 mM and 500 mM D-fructose in vitro was studied. Uric acid at 1.2 mM concentration reduced AST activity decrease and formation of total AGE products caused by incubation in vitro of the enzyme with sugar up to 25 days at 37 °C. The results thus support the hypothesis that uric acid has beneficial effects in controlling protein glycoxidation. The in vitro system AST-fructose proved to be a useful tool for investigation of glycation process. (Mol Cell Biochem 278: 85–92, 2005)     

LIN-12/Notch trafficking and regulation of DSL ligand activity during vulval induction in Caenorhabditis elegans

A novel mode of crosstalk between the EGFR-Ras-MAPK and LIN-12/Notch pathways occurs during the patterning of a row of vulval precursor cells (VPCs) in Caenorhabditis elegans: activation of the EGFR-Ras-MAPK pathway in the central VPC promotes endocytosis and degradation of LIN-12 protein. LIN-12 downregulation in the central VPC is a prerequisite for the activity of the lateral signal, which activates LIN-12 in neighboring VPCs. Here we characterize cis-acting targeting sequences in the LIN-12 intracellular domain and find that in addition to a di-leucine motif, serine/threonine residues are important for internalization and lysine residues are important for post-internalization trafficking and degradation. We also identify two trans-acting factors that are required for post-internalization trafficking and degradation: ALX-1, a homolog of yeast Bro1p and mammalian Alix and the WWP-1/Su(dx)/Itch ubiquitin ligase. By examining the effects of mutated forms of LIN-12 and reduced wwp-1 or alx-1 activity on subcellular localization and activity of LIN-12, we provide evidence that the lateral signal-inhibiting activity of LIN-12 resides in the extracellular domain and occurs at the apical surface of the VPCs.     

Possible involvement of 4-hydroxynonenal in splenocyte regulated liver regeneration

Liver regeneration is a complex, systemic process regulated by humoral and cellular mechanisms. Inflammatory response to the extensive tissue damage, as in partial hepatectomy, plays important role during regeneration. Hence, it is assumed that the spleen might play a role in systemic inflammatory response involved in liver regeneration. On the other hand, liver damage and consequential regeneration are often associated with oxidative stress and lipid peroxidation. One of the end products of lipid peroxidation, 4-hydroxynonenal (HNE), is nowadays considered not only as a "second toxic messenger of free radicals" but also as a growth-regulating factor. We therefore studied in vitro interactions of the HNE-treated murine liver cells and autologous spleen cells. The spleen cells supported recovery of liver cells from the HNE cytotoxicity although spleen cells themselves exerted cytotoxic effects against the proliferating liver cells that were not treated with HNE. Our results imply that the cytokines secreted by activated immunocompetent cells may be responsible for the observed recovery of the HNE-damage liver cells, suggesting that HNE might be an important factor regulating cellular and cytokine mediated mechanisms of liver regeneration control.     

Viruses activate a genetically conserved cell death pathway in a unicellular organism

Given the importance of apoptosis in the pathogenesis of virus infections in mammals, we investigated the possibility that unicellular organisms also respond to viral pathogens by activating programmed cell death. The M1 and M2 killer viruses of Saccharomyces cerevisiae encode pore-forming toxins that were assumed to kill uninfected yeast cells by a nonprogrammed assault. However, we found that yeast persistently infected with these killer viruses induce a programmed suicide pathway in uninfected (nonself) yeast. The M1 virus-encoded K1 toxin is primarily but not solely responsible for triggering the death pathway. Cell death is mediated by the mitochondrial fission factor Dnm1/Drp1, the K+ channel Tok1, and the yeast metacaspase Yca1/Mca1 encoded by the target cell and conserved in mammals. In contrast, cell death is inhibited by yeast Fis1, a pore-forming outer mitochondrial membrane protein. This virus-host relationship in yeast resembles that of pathogenic human viruses that persist in their infected host cells but trigger programmed death of uninfected cells.