Evaluation of peri-implant marginal bone loss using modified abutment connections at various crestal level placements

The purpose of this study was to evaluate crestal bone loss around 282 two-piece implants with straight (n = 193) and platform-switched (n = 89) abutment connections after placement at various crestal levels. Implants were assigned into two groups according to straight and platform-switched abutment connections. Each group was further subdivided into three groups depending on the location (supracrestal, crestal, or subcrestal) of the implant cervical platform. Linear measurements of bone resorption were made from the implant's platform to the first point of bone-to-implant contact at the time of implant placement and 2 years postrestoration. Data were statistically analyzed. Statistically significant differences were found between subgroups in both straight and platform-switched categories. The only nonstatistically significant difference (P = .341) arose when comparing the supra- and subcrestal locations in the straight abutment connection group. The platform-switched group exhibited significantly less bone loss (P = .046) only in subcrestal locations. The platform-switched concept was not beneficial during the overall comparison, but it was for the subcrestal location of the abutment connection. Crestal placement of the implant-abutment connection resulted in higher marginal bone resorption in both straight and platform-switched abutments.     

Huge intrathyroidal hematoma causing airway obstruction: a multidisciplinary challenge.

Thyroid hemorrhage is a relatively frequent event that in most cases causes pain and discomfort only, while rarely can cause significant neck swelling. Even more rarely, however, extensive thyroid hemorrhage can result in a rapidly expanding hematoma with airway compromise. We report a case of a rapidly expanding thyroid hemorrhage that occurred secondary to oral anticoagulation therapy in an 80-year-old patient with a previously existing goiter. The patient presented with acute onset of neck pain, dysphagia, and respiratory distress caused by tracheal compression from the thyroid mass. Computed tomography demonstrated a 6 x 9 x 10 cm mass consistent with an intrathyroidal hematoma projecting into the anterior mediastinum and displacing the trachea to the left. Rapid reversal of the coagulopathy was achieved with fresh frozen plasma and vitamin K. Consequently, the patient was managed conservatively with close observation, antibiotics, and steroids because no progression of airway compromise was manifested. Although the diagnosis can be easily established in these patients, no management guidelines of this condition exist. The potential of rapid airway compromise and the risk for exacerbation of bleeding in the light of significant elevation in the international normalized ratio (INR), make any airway management decisions very difficult. The importance of managing the airway and the haemostatic problem with the help of a multidisciplinary team is discussed.     

Haploinsufficiency for Pten and Serotonin transporter cooperatively influences brain size and social behavior

Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders that share deficits in sociability, communication, and restrictive and repetitive interests. ASD is likely polygenic in origin in most cases, but we presently lack an understanding of the relationships between ASD susceptibility genes and the neurobiological and behavioral phenotypes of ASD. Two genes that have been implicated as conferring susceptibility to ASD are PTEN and Serotonin transporter (SLC6A4). The PI3K and serotonin pathways, in which these genes respectively act, are both potential biomarkers for ASD diagnosis and treatment. Biochemical evidence exists for an interaction between these pathways; however, the relevance of this for the pathogenesis of ASD is unclear. We find that Pten haploinsufficient (Pten^+/−) mice are macrocephalic, and this phenotype is exacerbated in Pten^+/−; Slc6a4^+/− mice. Furthermore, female Pten^+/− mice are impaired in social approach behavior, a phenotype that is exacerbated in female Pten^+/−; Slc6a4^+/− mice. While increased brain size correlates with decreased sociability across these genotypes in females, within each genotype increased brain size correlates with increased sociability, suggesting that epigenetic influences interact with genetic factors in influencing the phenotype. These findings provide insight into an interaction between two ASD candidate genes during brain development and point toward the use of compound mutant mice to validate biomarkers for ASD against biological and behavioral phenotypes.     

Neuroprotection by lamotrigine in a rat model of neonatal hypoxic-ischaemic encephalopathy

Hypoxic-ischaemic (HI) encephalopathy is a severe complication of perinatal asphyxia and remains a frequent cause of a variety of brain disorders with long-term effects on the patients' life. The associated brain damage is strongly related to the toxic action of excitatory amino acids, especially glutamate and aspartate. Lamotrigine is an anti-epileptic drug that blocks the voltage-gated sodium channels of the presynaptic neuron and inhibits the release of glutamate. In the present study a well-established model of perinatal asphyxia in 7-d-old rats was used to investigate the effect of lamotrigine on HI-induced damage to different hippocampal brain structures, since disruption of this brain area is thought to play a key role in schizophrenia and epilepsy. Therefore, a combination of ischaemia, induced by unilateral occlusion of the left common carotid artery, followed by exposure to a 1-h period of hypoxia, was carried out in neonatal 7-d-old rats. Immediately after the insult, lamotrigine was given i.p. The histological outcome in the hippocampus was conducted and the tissue levels of glutamate, aspartate, GABA, and glutamine in the same area were determined. A remarkable reduction of HI-evoked damaged neurons in most of the investigated hippocampal regions was noted after lamotrigine administration. Furthermore, lamotrigine decreased the asphyxia-induced hippocampal tissue levels of glutamate and aspartate. Immediately after perinatal asphyxia GABA levels were enhanced, while levels of glutamine were decreased. Lamotrigine administration did not affect either GABA or glutamine levels. These results suggest a neuroprotective effect of lamotrigine in this particular animal model of neonatal HI encephalopathy.     

Effect of Moderate Wine Consumption on Oxidative Stress Markers in Coronary Heart Disease Patients

Evidence from research studies reports that wine consumption is associated with lower cardiovascular disease risk, partly through the amelioration of oxidative stress. The aim of the present study was to examine the effect of regular light to moderate wine consumption from coronary heart disease (CHD) patients compared to the effect induced by alcohol intake without the presence of wine microconstituents, on oxidation-induced macromolecular damage as well as on endogenous antioxidant enzyme activity. A randomized, single-blind, controlled, three-arm parallel intervention was carried out, in which 64 CHD patients were allocated to three intervention groups. Group A consumed no alcohol, and Group B (wine) and Group C (ethanol) consumed 27 g of alcohol/day for 8 weeks. Blood and urine samples were collected at baseline and at 4 and 8 weeks. Urine oxidized guanine species levels, protein carbonyls, thiobarbituric acid substances (TBARS) levels, as well as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, were measured. Oxidized guanine species and protein carbonyl levels were significantly increased in the ethanol group during the intervention and were significantly decreased in the wine group. These results support the idea that wine’s bioactive compounds may exert antioxidant actions that counteract the macromolecular oxidative damage induced by alcohol in CHD patients.     

Serum androgens and prostate cancer among 643 cases and 643 controls in the European Prospective Investigation into Cancer and Nutrition

We examined the hypothesis that serum concentrations of circulating androgens and sex hormone binding globulin (SHBG) are associated with risk for prostate cancer in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC). Concentrations of androstenedione, testosterone, androstanediol glucuronide and SHBG were measured in serum samples for 643 prostate cancer cases and 643 matched control participants, and concentrations of free testosterone were calculated. Conditional logistic regression models were used to calculate odds ratios for risk of prostate cancer in relation to the serum concentration of each hormone. After adjustment for potential confounders, there was no significant association with overall risk for prostate cancer for serum total or free testosterone concentrations (highest versus the lowest thirds: OR, 1.02; 95% CI, 0.73-1.41 and OR, 1.07, 95% CI, 0.74-1.55, respectively) or for other androgens or SHBG. Subgroup analyses showed significant heterogeneity for androstenedione by cancer stage, with a significant inverse association of androstenedione concentration and risk for advanced prostate cancer. There were also weak positive associations between free testosterone concentration and risk for total prostate cancer among younger men and risk for high-grade disease. In summary, in this large nested case-control study, concentrations of circulating androgens or SHBG were not strongly associated with risk for total prostate cancer. However, our findings are compatible with a positive association of free testosterone with risk in younger men and possible heterogeneity in the association with androstenedione concentration by stage of disease; these findings warrant further investigation.     

Elevated morning serum interleukin (IL)-6 or evening salivary cortisol concentrations predict posttraumatic stress disorder in children and adolescents six months after a motor vehicle accident

BACKGROUND: This study examined prospectively the activity of the hypothalamic-pituitary-adrenal axis, the sympathetic nervous system and inflammatory factors in children shortly after a motor vehicle accident (MVA) in relation to later posttraumatic stress disorder (PTSD) development. PATIENTS AND METHODS: Fifty six children, aged 7-18, were studied after an MVA and 1 and 6 months later; 40 subjects served as controls. Morning serum cortisol and interleukin (IL)-6 and plasma catecholamine concentrations were measured within 24h after the event. Salivary cortisol was measured 5 times at defined time points during the same day. PTSD diagnoses 1 and 6 months later were based on K-SADS interview. RESULTS: Morning serum IL-6 concentrations, measured within the first 24h after the accident, were higher in children that developed PTSD 6 months later than those who did not and those of the control group. Longitudinal IL-6 measurements revealed normalization of IL-6 in the PTSD group, while no differences between the three groups were detected 1 and 6 months later. Evening salivary cortisol and morning serum IL-6 after the accident were positively inter-related (r=0.54, p<0.001) and in separate regression analyses both predicted PTSD development 6 months later. In contrast, morning serum IL-6 did nor correlate with morning serum or salivary cortisol concentrations. CONCLUSIONS: Immediate posttraumatic alterations in neuroendocrine or inflammatory factors-increased evening salivary cortisol and/or increased morning serum IL-6 concentrations-are involved in subsequent PTSD development in children and adolescents.     

Presymptomatic molecular diagnosis of autosomal dominant polycystic kidney disease using PKD1-and PKD2-linked markers in Cypriot families

Autosomal dominant polycystic kidney disease (ADPKD), is a heterogeneous disorder, primarily characterized by the formation of cysts in the kidneys, and the late development in life of progressive chronic kidney failure. Three genes are implicated in causing ADPKD. One on chromosome 16, PKD1, accounts for 85–90% of all cases, and the PKD2 gene on chromosome 4 accounts for the remainder. A very rare third locus is still of unknown location. We used PKD1-and PKD2-linked polymorphic markers to make the diagnosis of ADPKD in young presymptomatic members in affected families. We showed that in young members of families where clinical diagnosis cannot be definitively established, molecular linkage analysis can assist clinicians in the diagnosis. In one family a 24-year old had one cyst on the right kidney; however, molecular analysis showed clearly that he had inherited the normal haplotype. In another family, in one part of the pedigree there was co-inheritance of the disease with a PKD1-linked haplotype which originated in a non-affected 78-year-old father. Analysis with PKD2-linked markers excluded this locus. The data can be explained in one of two ways. Either this family phenotype is linked to a third locus, or the proband was the first affected person, most probably because of a novel mutation in one of her father's chromosomes. In conclusion, the combined use of markers around the PKD1 and the PKD2 locus provides more definitive answers in cases where presymptomatic diagnosis is requested by concerned families.