Foot fractures and complex trauma of the foot: a case series.

Foot fractures are common injuries. This retrospective study evaluates their frequency, incidence, treatment and outcomes with emphasis on complex trauma of the foot (CTF), an injury that affects soft tissue as well as bone. From 2005 to 2015, 506 patients with foot fractures were treated at our institution; of these, 27 had CTF.

Double Up Food Bucks Participation is Associated with Increased Fruit and Vegetable Consumption and Food Security Among Low-Income Adults.

Objective: To evaluate the effect of the Utah Double Up Food Bucks (DUFB) program on fruit and vegetable (F&V) intake and food security status among Supplemental Nutrition Assistance Program (SNAP) recipients.

Methods: Data were collected in 2015, using a before-and-after study design. At the farmers' market, a convenience sample of SNAP recipients was recruited for a survey and a 4-week telephone follow-up survey.

Spherical bodies present within the germinal vesicle of Podarcis sicula previtellogenic oocyte derive from the temporaneous inactivation of ribosomal genes.

In the present paper we have investigated the origin of the spherical bodies (SBs) present within the germinal vesicle of about 400 microm previtellogenic oocytes in the lizard Podarcis sicula. In particular, we have attempted to clarify whether they derive from the single, large nucleolus present in early diplotenic oocyte as a consequence of ribosomal gene inactivation. We have, therefore, experimentally induced a decrease in rRNA synthesis by injecting animals with D-galactosamine or by exposing them to low temperatures.

A novel 7-modified camptothecin analog overcomes breast cancer resistance protein-associated resistance in a mitoxantrone-selected colon carcinoma cell line.

We selected a mitoxantrone-resistant HT29 colon carcinoma cell line (HT29/MIT) that exhibited a very high degree of resistance to the selecting agent and marked resistance to topotecan and SN38, but limited resistance to doxorubicin. The development of drug resistance was independent of expression of P-glycoprotein or multidrug resistance-associated protein but was associated with high up-regulation of the breast carcinoma resistance protein (BCRP) as shown by Western blot analysis. BCRP overexpression was associated with a reduced intracellular accumulation of topotecan, a known substrate for BCRP.

Physicochemical properties, cytotoxic activity and topoisomerase II inhibition of 2,3-diaza-anthracenediones.

The physicochemical, cytotoxic and pharmacological properties of 2,3-diaza-anthracenedione derivatives were examined to gain insight into the structure-activity relationships in this class of compounds. Spectrophotometric, chiroptical and voltammetric measurements were performed, along with cell cytotoxicity, alkaline elution, topoisomerase II-mediated DNA cleavage and cellular drug-uptake determination. In comparison with classic anthracenediones such as mitoxantrone and ametantrone, the aza derivatives were characterized by less negative reduction potentials, lower affinity for DNA and modified geometry of intercalation.

Topoisomerase II DNA cleavage stimulation, DNA binding activity, cytotoxicity, and physico-chemical properties of 2-aza- and 2-aza-oxide-anthracenedione derivatives.

The cytotoxic activity of mitoxantrone and related anthracenediones has been ascribed to the ability of these compounds to interfere with DNA topoisomerase II function, resulting in DNA cleavage stimulation. The molecular details of enzyme inhibition by these intercalating agents remain to be defined. In an attempt to identify the structural determinants for optimal activity, the molecular and cellular effects of a series of heteroanalogues bearing different side-chains were examined in relation to the physico-chemical and DNA binding properties of these compounds.

Base sequence determinants of amonafide stimulation of topoisomerase II DNA cleavage.

A number of antitumor drugs including naphthalimides, a new class of intercalating agents, interfere with the DNA breakage-reunion activity of mammalian DNA topoisomerase II resulting in DNA cleavage stimulation. In this work, the sequence specificity of a lead compound of this series, amonafide, in stimulating DNA cleavage by murine topoisomerase II has been studied. Amonafide-stimulated cleavage intensity patterns were markedly different from those of other antitumor drugs by using pBR322 and SV40 DNAs.

Correlates of successful breastfeeding: a study of social and personal factors.

This study examined the degree to which first-time mothers' perceptions of their marital relationships, various support systems, and adjustment to pregnancy and motherhood were associated with success at initiating and maintaining lactation during the first year postpartum. Additionally, the incidence and duration of breastfeeding, feeding problems encountered, as well as the sources and quality of feeding-related help received by these mothers were examined. Mothers in this study showed a pattern of breastfeeding incidence and duration similar to that established statewide and nationwide.

Sequence selectivity of topoisomerase II DNA cleavage stimulated by mitoxantrone derivatives: relationships to drug DNA binding and cellular effects.

Mitoxantrone, a DNA intercalator, is an effective antitumor drug known to interfere with topoisomerase II function through stimulation of enzyme-mediated DNA cleavage. To clarify the drug structural requirements for stimulation of topoisomerase II DNA cleavage, the cytotoxic activity and molecular effects of mitoxantrone, ametantrone, and a new derivative (BBR2577), bearing a modification on one of the side chains, were examined in relation to their DNA binding affinities and modes of drug-DNA interaction. The results showed a good correlation between cytotoxicity and topoisomerase II DNA cleavage.

Similar sequence specificity of mitoxantrone and VM-26 stimulation of in vitro DNA cleavage by mammalian DNA topoisomerase II.

The molecular mechanism of topoisomerase II trapping by antitumor drugs probably involves the formation of a ternary complex DNA-drug-topoisomerase II. Recent studies support the view that a drug molecule might be placed at the DNA cleavage site interacting with the two flanking base pairs and amino acid residues of the enzyme. In this work, the DNA sequence-dependent action of mitoxantrone on topoisomerase II DNA cleavage was investigated in SV40 DNA fragments and short oligonucleotides, in comparison to VM-26, 4-demethoxydaunorubicin, and mAMSA.

Characterization of a topoisomerase II gene rearrangement in a human small-cell lung cancer cell line.

Background: Small-cell lung cancer (SCLC) is a highly chemosensitive tumor, but the recurrent disease that is common after initial response is often unresponsive to further chemotherapy. Although the mechanisms of drug resistance in SCLC have not been established, studies suggest that alterations of the nuclear enzyme DNA topoisomerase II may reduce the sensitivity of the cell to drug action. This enzyme is recognized as a primary target for cytotoxic activity of important antitumor agents.

The role of topoisomerase II in drug resistance.

The conventional laboratory approach to study the mechanisms of drug resistance has been the selection of drug-resistant cell lines by continuous exposure to cytotoxic agents. Such lines, which are selected for resistance to a single agent, frequently display cross-resistance to a number of cytotoxic agents that are unrelated in both structure and proposed mechanism of action. Multidrug-resistant cells display reduced drug accumulation, which is the result of overexpression of a surface glycoprotein (P170).

Relationships among tumor responsiveness, cell sensitivity, doxorubicin cellular pharmacokinetics and drug-induced DNA alterations in two human small-cell lung cancer xenografts.

In an attempt to understand the underlying cellular/biochemical factors of sensitivity/resistance in human small-cell lung cancer (SCLC), 2 SCLC tumor lines were compared with respect to tumor responsiveness to drug treatment, cell sensitivity, cellular doxorubicin accumulation, and DNA topoisomerase-II-mediated DNA cleavage. The tumor lines growing in nude mice with similar growth characteristics (doubling time around 10 days) were selected since one (POCI tumor) was found to be hypersensitive and the other (POSG tumor) resistant to doxorubicin treatment. The pattern of anti-tumor drug response of the doxorubicin-resistant tumor was atypical (i.

Comparison of DNA cleavage induced by etoposide and doxorubicin in two human small-cell lung cancer lines with different sensitivities to topoisomerase II inhibitors.

In an attempt to clarify the role of drug-induced protein-associated DNA breaks (i.e., DNA topoisomerase II-mediated DNA cleavage) in the cytotoxic activity of doxorubicin and etoposide, their cellular effects were compared in 2 human small-cell lung cancer (SCLC) lines, characterized by differential sensitivity to DNA topoisomerase II inhibitors.

Evidence of DNA topoisomerase II-dependent mechanisms of multidrug resistance in P388 leukemia cells.

A multidrug-resistant variant of the P388 leukemia cell line exhibits multiple biochemical changes, including reduced drug accumulation and markedly reduced DNA strand breakage induced by anthracyclines. To investigate whether the reduced formation of drug-induced DNA breaks was due to alteration of DNA topoisomerase II activity, nuclear extracts and partially purified enzymes from the sensitive line and the resistant subline were compared. DNA topoisomerase II activity in 0.

P-glycoprotein gene amplification and expression in multidrug-resistant murine P388 and B16 cell lines.

P-glycoprotein gene (mdrl) amplification and expression were examined in murine leukaemia P388/DX and melanoma B16VDXR cell lines, which exhibit a high level of resistance to a selecting agent, doxorubicin, and express a multidrug-resistant phenotype because they are cross-resistant to multiple cytotoxic drugs. The multidrug-resistant phenotype was obtained in different conditions of selection (in vivo and in vitro for P388/DX and B16VDXR, respectively). In both multidrug-resistant cell lines, an increased expression of P-glycoprotein gene (5 kb transcript detected in Northern blots) was observed and the level of P-glycoprotein mRNA correlated with the degree of resistance.

Role of DNA breakage in cytotoxicity of doxorubicin, 9-deoxydoxorubicin, and 4-demethyl-6-deoxydoxorubicin in murine leukemia P388 cells.

Formation and persistence of DNA single- and double-strand breaks stimulated by doxorubicin, 9-deoxydoxorubicin, or 4-demethyl-6-deoxydoxorubicin in murine leukemia P388 cells were compared in relation to drug DNA affinity, cellular pharmacokinetics, and cytotoxicity. Although cellular uptake and retention and DNA affinity of the anthracycline derivatives were similar to those of the parent drug, cytotoxic potency was quite different, 9-deoxydoxorubicin being much less cytotoxic than doxorubicin, and 4-demethyl-6-deoxydoxorubicin the most effective agent. After 1-h exposure of cells to cytotoxic drug levels, the extent of DNA strand breaks produced by 4-demethyl-6-deoxydoxorubicin was greater than that produced by doxorubicin, whereas 9-deoxydoxorubicin induced very few DNA breaks.