Cementoblastoma related to a primary tooth: a case report

Cementoblastomas are benign lesions of the odontogenic ectomesenchyme that rarely occur related to the primary dentition, especially on the left side of the mandible. This study describes a case of a true cementoblastoma related to the left second primary mandibular molar in a 7-year-old child (the largest one seen in the left side of the mandible). Additionally, the radiographic and histologic findings of the lesion are described in details.     

Increase in membrane uptake of long-chain fatty acids early during preadipocyte differentiation.

An increase in early rates of oleate uptake, which reflected fatty acid (FA) entry into the cells, was apparent 2-3 days after confluence of differentiating BFC-1 preadipocytes. The increase was measured in cells kept without glucose and with arsenate, where greater than 95% of intracellular radioactivity was recovered as free unesterified oleate. Uptake of retinoic acid, a molecule structurally similar to long-chain FA, remained unaltered during cell differentiation. Increase in oleate transport was related to increase in transport Vmax (determined under arsenate treatment) from 0.2 to 2 nmol/min per 10(6) cells, whereas Km remained unchanged (2 x 10(-7) M). Oleate transport was maximal at about day 6 after cell confluence (day 0), as FA metabolism (incorporation into lipids) began to gradually increase. The increase in transport preceded induction of mRNAs for both cytosolic FA-binding protein, which appeared at day 6, and for the FA synthase, which appeared at day 10. Data indicated that increases in activities of FA transport and of lipoprotein lipase, early during cell differentiation, favored increased availability of exogenous FA at a stage when endogenous FA synthesis is limited. This result would promote FA esterification and lipid deposition by supplying a rate-limiting substrate. Furthermore, oleate addition to BFC-1 preadipocytes at confluence potentiated the effect of dexamethasone in inducing mRNA for cytosolic FA-binding protein. In adipocytes, FA from exogenous or endogenous sources was necessary to maintain levels of cytosolic FA-binding protein mRNA. Thus, the increase in FA availability might contribute to, or modulate, induction of proteins necessary for preadipocyte differentiation.     

Comparative effects of quinolones on human mononuclear leucocyte functions

The effects of three quinoline derivatives--pefloxacin, ciprofloxacin and ofloxacin--were investigated in mitogen-stimulated human peripheral blood mononuclear leucocytes (MNL). At concentrations of 50 mg/l or more, pefloxacin, ciprofloxacin or ofloxacin significantly inhibited MNL proliferation in response to phytohaemagglutinin. This inhibition was more marked with ciprofloxacin than pefloxacin or ofloxacin. To determine the possible mechanism(s) involved in the inhibition of MNL proliferation following exposure to pefloxacin, ciprofloxacin or ofloxacin, we assessed (1) interleukin-1 (IL-1) activity in supernatants from monocytes treated with the quinolones and (2) the effects of 2-mercaptoethanol (2-ME) a thiol compound which acts as an antioxidant agent and the effect of indomethacin (INDO) an inhibitor of prostaglandin E2 synthesis. 2-ME and INDO did not prevent the decrease in the proliferation. IL-1 activity was shown to be decreased for the same range of antibiotic concentrations as observed for the inhibition of MNL proliferation. Cellular viability of the MNL or monocytes was not modified by any of the quinolones at the concentrations tested. Taken together, these results suggest that pefloxacin, ciprofloxacin and ofloxacin act as immunomodulators. The mechanism involved with the cascade of events that leads to the lymphocyte proliferation and the clinical relevance need further investigation.     

Early-onset gastric carcinomas display molecular characteristics distinct from gastric carcinomas occurring at a later age

Gastric cancer is thought to result from a combination of environmental factors and accumulation of specific genetic alterations, and consequently mainly affects older patients (>50 years of age). Fewer than 10% of patients present with the disease before 45 years of age and these young patients are thought to develop carcinomas with a different molecular genetic profile from that of sporadic carcinomas occurring at a later age. Forty early-onset gastric carcinoma resection specimens were characterized for microsatellite instability (MSI) and loss of heterozygosity status using 22 polymorphic microsatellite markers. Twenty-four biopsies were additionally evaluated for the presence of MSI. No MSI was observed in any of the cases analysed. Losses were infrequent, but were most common for the D1S234 (26.1%) and D1S1676 (17.4%) markers, flanking the RUNX3 gene; for the p53ALU (23.1%) and TP53 (15.4%) markers, near the TP53 gene; and for the D16S2624 (17.2%) marker, near the E-cadherin (CDH1) gene. All cases with loss of CDH1, as well as 6/7 cases with loss of TP53, displayed aberrant staining of the corresponding proteins, pointing to a functional role for these proteins in early-onset gastric carcinogenesis. No germline CDH1, TP53 or RUNX3 mutations were detected in any of the cases analysed. No correlation was observed between non-functional E-cadherin and the histological type of the tumours analysed. Finally, Epstein-Barr virus was not detected in any of the cases analysed. On the basis of these results, early-onset gastric carcinomas appear to have characteristics distinct from gastric carcinomas occurring at a later age.     

Determination of free thyroxine by adsorption on Sephadex gel

The authors describe a simplified method for the measurement of free thyroxine based on the affinity of Sephadex gel for thyroxine. Radiolabeled thyroxine added to diluted serum is adsorbed by the gel proportionally to the free thyroxine concentration of the sample. The concentration of binding proteins present in the sample does not affect the adsorption of free thyroxine on the gel. The adsorbed thyroxine is separated by centrifugation and filtration using a rigid filter. Calibration is made against the equilibrium dialysis method. The intra (CV of 4.9 p. cent, 6.1 p. cent, 10.2 p. cent for concentrations of free thyroxine of 14.1, 27.1 and 67.6 pmol/l respectively) and interassay (CV of 5.3 p. cent, 8.2 p. cent, 9.2 p. cent at 9.4, 23.0 and 83.1 pmol/l respectively) imprecisions are comparable to equilibrium dialysis. The results obtained with this method show a good correlation with those of a two-step radioimmunoassay for patients without non-thyroidal diseases or pregnancy (r2 = 0.85, n = 50). The reference range (mean +/- two standard deviations) determined in 108 euthyroid adults is 10.3 to 21.9 pmol/l. Results obtained for hypothyroid patients (7.7 +/- 2.3 pmol/l, mean +/- one standard deviation, n = 26), hyperthyroid patients (47.4 +/- 22.9 pmol/l, n = 32), patients with non-thyroidal illnesses (18.7 +/- 4.9 pmol/l, n = 35) and pregnant women (10.8 +/- 1.7 pmol/l, n = 20) are in good agreement with those reported using equilibrium dialysis or ultrafiltration. Our method offers an alternative to more tedious techniques of free thyroxine determination in the hospitalized population for which the use of analog methods has been criticized.     

Partial androgen insensitivity with phenotypic variation caused by androgen receptor mutations that disrupt activation function 2 and the NH(2)- and carboxyl-terminal interaction

Partial androgen insensitivity with sex phenotype variation in two unrelated families was associated with missense mutations in the androgen receptor (AR) gene that disrupted the AR NH(2)-terminal/carboxy terminal interaction. Each mutation caused a single amino acid change within the region of the ligand-binding domain that forms activation function 2 (AF2). In one family, the mutation I737T was in alpha helix 4 and in the other F725L was between helices 3 and 4. Neither mutation altered androgen binding as determined by assays of mutant AR in the patient's cultured genital skin fibroblasts or of recombinant mutant receptors transfected into COS cells. In transient cotransfection assays in CV1 cells, transactivation with the AR mutants at low concentrations of DHT was reduced several fold compared with wild-type AR but increased at higher concentrations. Defects in NH(2)-terminal/carboxy terminal interactions were identified in mammalian two hybrid assays. In similar assays, there was reduced binding of the p160 coactivators TIF2/SRC2 and SRC1 to the mutant AR ligand binding domains (LBD). In the family with AR I737T, sex phenotype varied from severely defective masculinization in the proband to a maternal great uncle whose only manifestation of AIS was severe gynecomastia. He was fertile and passed the mutation to two daughters. The proband of the F725L family was also incompletely masculinized but was raised as a male while his half-sibling by a different father was affected more severely and reared as a female. These studies indicate that the function of an AR AF2 mutant in male development can vary greatly depending on the genetic background.     

Structural organization of the neutrophil NADPH oxidase: phosphorylation and translocation during priming and activation

The reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is part of the microbicidal arsenal used by human polymorphonuclear neutrophils (PMNs) to eradicate invading pathogens. The production of a superoxide anion (O2-) into the phagolysosome is the precursor for the generation of more potent products, such as hydrogen peroxide and hypochlorite. However, this production of O2- is dependent on translocation of the oxidase subunits, including gp91phox, p22phox, p47phox, p67phox, p40phox, and Rac2 from the cytosol or specific granules to the plasma membrane. In response to an external stimuli, PMNs change from a resting, nonadhesive state to a primed, adherent phenotype, which allows for margination from the vasculature into the tissue and chemotaxis to the site of infection upon activation. Depending on the stimuli, primed PMNs display altered structural organization of the NADPH oxidase, in that there is phosphorylation of the oxidase subunits and/or translocation from the cytosol to the plasma or granular membrane, but there is not the complete assembly required for O2- generation. Activation of PMNs is the complete assembly of the membrane-linked and cytosolic NADPH oxidase components on a PMN membrane, the plasma or granular membrane. This review will discuss the individual components associated with the NADPH oxidase complex and the function of each of these units in each physiologic stage of the PMN: rested, primed, and activated.