Evaluation of α-tubulin, detyrosinated α-tubulin, and vimentin in CTCs: identification of the interaction between CTCs and blood cells through cytoskeletal elements.

BACKGROUND: Circulating tumor cells (CTCs) are the major players in the metastatic process. A potential mechanism of cell migration and invasion is the formation of microtentacles in tumor cells. These structures are supported by α-tubulin (TUB), detyrosinated α-tubulin (GLU), and vimentin (VIM). In the current study, we evaluated the expression of those cytoskeletal proteins in CTCs. METHODS: Forty patients with breast cancer (BC) (16 early and 24 metastatic) were enrolled in the study. CTCs were isolated using the ISET platform and stained with the following combinations of antibodies: pancytokeratin (CK)/VIM/TUB and CK/VIM/GLU. Samples were analyzed with the ARIOL platform and confocal laser scanning microscopy. RESULTS: Fluorescence quantification revealed that the ratios CK/TUB, CK/VIM, and CK/GLU were statistically increased in MCF7 compared with more aggressive cell lines (SKBR3 and MDA-MB-231). In addition, all of these ratios were statistically increased in MCF7 cells compared with metastatic BC patients' CTCs (p = 0.0001, p = 0.0001, and p = 0.003, respectively). Interestingly, intercellular connections among CTCs and between CTCs and blood cells through cytoskeleton bridges were revealed, whereas microtentacles were increased in patients with CTC clusters. These intercellular connections were supported by TUB, VIM, and GLU. Quantification of the examined molecules revealed that the median intensity of TUB, GLU, and VIM was significantly increased in patients with metastatic BC compared with those with early disease (TUB, 62.27 vs 11.5, p = 0.0001; GLU, 6.99 vs 5.29, p = 0.029; and VIM, 8.24 vs 5.38, p = 0.0001, respectively). CONCLUSIONS: CTCs from patients with BC aggregate to each other and to blood cells through cytoskeletal protrusions, supported by VIM, TUB, and GLU. Quantification of these molecules could potentially identify CTCs related to more aggressive disease.

Dual-energy CT in patients with abdominal malignant lymphoma: impact of noise-optimised virtual monoenergetic imaging on objective and subjective image quality.

AIM: To investigate the impact of noise-optimised virtual monoenergetic imaging (VMI+) reconstructions on quantitative and qualitative image parameters in patients with malignant lymphoma at dual-energy computed tomography (DECT) examinations of the abdomen. MATERIALS AND METHODS: Thirty-five consecutive patients (mean age, 53.8±18.6 years; range, 21-82 years) with histologically proven malignant lymphoma of the abdomen were included retrospectively. Images were post-processed with standard linear blending (M_0.6), traditional VMI, and VMI+ technique at energy levels ranging from 40 to 100 keV in 10 keV increments. Signal-to-noise (SNR) and contrast-to-noise ratios (CNR) were objectively measured in lymphoma lesions. Image quality, lesion delineation, and image noise were rated subjectively by three blinded observers using five-point Likert scales. RESULTS: Quantitative image quality parameters peaked at 40-keV VMI+ (SNR, 15.77±7.74; CNR, 18.27±8.04) with significant differences compared to standard linearly blended M_0.6 (SNR, 7.96±3.26; CNR, 13.55±3.47) and all traditional VMI series (p<0.001). Qualitative image quality assessment revealed significantly superior ratings for image quality at 60-keV VMI+ (median, 5) in comparison with all other image series (p<0.001). Assessment of lesion delineation showed the highest rating scores for 40-keV VMI+ series (median, 5), while lowest subjective image noise was found for 100-keV VMI+ reconstructions (median, 5). CONCLUSION: Low-keV VMI+ reconstructions led to improved image quality and lesion delineation of malignant lymphoma lesions compared to standard image reconstruction and traditional VMI at abdominal DECT examinations.

Analysis of multiple physical parameters for mechanical phenotyping of living cells.

Since the cytoskeleton is known to regulate many cell functions, an increasing amount of effort to characterize cells by their mechanical properties has occured. Despite the structural complexity and dynamics of the multicomponent cytoskeleton, mechanical measurements on single cells are often fit to simple models with two to three parameters, and those parameters are recorded and reported. However, different simple models are likely needed to capture the distinct mechanical cell states, and additional parameters may be needed to capture the ability of cells to actively deform. Our new approach is to capture a much larger set of possibly redundant parameters from cells' mechanical measurement using multiple rheological models as well as dynamic deformation and image data. Principal component analysis and network-based approaches are used to group parameters to reduce redundancies and develop robust biomechanical phenotyping. Network representation of parameters allows for visual exploration of cells' complex mechanical system, and highlights unexpected connections between parameters. To demonstrate that our biomechanical phenotyping approach can detect subtle mechanical differences, we used a Microfluidic Optical Cell Stretcher to mechanically stretch circulating human breast tumor cells bearing genetically-engineered alterations in c-src tyrosine kinase activation, which is known to influence reattachment and invasion during metastasis.

Coil embolization of a fistula from the right inferior phrenic artery to the right pulmonary artery with involvement of further arteries: A rare case report.

A 51-year-old female patient was presenting dyspnea for more than a year with no previous lung infections or surgery. Initially, a diagnostic computed tomography was made, showing a rare arterio-arterial malformation between the right inferior phrenic and right pulmonary artery leading into a vascular bundle in the middle lung lobe. Due to the patients' dyspnea and massive extent of malformation, the indication for transcatheter arterial embolization was made. The first transcatheter arterial embolization procedure involved the inferior phrenic and a selective branch of the internal thoracic artery. Interventional angiography as well as computed tomography revealed further extend of the malformation showing a connection of right lateral thoracic, hepatic, and inferior epigastric artery to the fistula. After one month, a second transcatheter arterial embolization of these arteries as well as a second approach of the proximal internal thoracic artery was performed. In the follow-up the patient described a substantial improvement of her dyspnea and showed no signs of infections. A phrenic artery to pulmonary artery fistula is an extremely rare case occurring congenital or acquired. Patients may be asymptomatic or present, among others, dyspnea, hemoptysis, pulmonary infections and congestive heart failure. Symptomatic patients require treatment using transcatheter arterial embolization or surgical resection. The patient had dyspnea and a substantial extent of malformation with possibly complicated clinical course. The recommended less invasive treatment using transcatheter arterial embolization was successfully performed. In conclusion, our patient represented a rare congenital case of systemic and pulmonary artery communication, which we were able to treat sufficiently with coil embolization.

Computed Tomography Radiomics to Differentiate Intrahepatic Cholangiocarcinoma and Hepatocellular Carcinoma.

AIMS: Intrahepatic cholangiocarcinoma (iCCA) and hepatocellular carcinoma (HCC) differ in prognosis and treatment. We aimed to non-invasively differentiate iCCA and HCC by means of radiomics extracted from contrast-enhanced standard-of-care computed tomography (CT). MATERIALS AND METHODS: In total, 94 patients (male, n = 68, mean age 63.3 ± 12.4 years) with histologically confirmed iCCA (n = 47) or HCC (n = 47) who underwent contrast-enhanced abdominal CT between August 2014 and November 2021 were retrospectively included. The enhancing tumour border was manually segmented in a clinically feasible way by defining three three-dimensional volumes of interest per tumour. Radiomics features were extracted. Intraclass correlation analysis and Pearson metrics were used to stratify robust and non-redundant features with further feature reduction by LASSO (least absolute shrinkage and selection operator). Independent training and testing datasets were used to build four different machine learning models. Performance metrics and feature importance values were computed to increase the models' interpretability. RESULTS: The patient population was split into 65 patients for training (iCCA, n = 32) and 29 patients for testing (iCCA, n = 15). A final combined feature set of three radiomics features and the clinical features age and sex revealed a top test model performance of receiver operating characteristic (ROC) area under the curve (AUC) = 0.82 (95% confidence interval =0.66-0.98; train ROC AUC = 0.82) using a logistic regression classifier. The model was well calibrated, and the Youden J Index suggested an optimal cut-off of 0.501 to discriminate between iCCA and HCC with a sensitivity of 0.733 and a specificity of 0.857. CONCLUSIONS: Radiomics-based imaging biomarkers can potentially help to non-invasively discriminate between iCCA and HCC.

Changes in cortical bone response to high-fat diet from adolescence to adulthood in mice.

UNLABELLED: Diabetic obesity is associated with increased fracture risk in adults and adolescents. We find in both adolescent and adult mice dramatically inferior mechanical properties and structural quality of cortical bone, in agreement with the human fracture data, although some aspects of the response to obesity appear to differ by age. INTRODUCTION: The association of obesity with bone is complex and varies with age. Diabetic obese adolescents and adult humans have increased fracture risk. Prior studies have shown reduced mechanical properties as a result of high-fat diet (HFD) but do not fully address size-independent mechanical properties or structural quality, which are important to understand material behavior. METHODS: Cortical bone from femurs and tibiae from two age groups of C57BL/6 mice fed either HFD or low-fat diet (LFD) were evaluated for structural and bone turnover changes (SEM and histomorphometry) and tested for bending strength, bending stiffness, and fracture toughness. Leptin, IGF-I, and non-enzymatic glycation measurements were also collected. RESULTS: In both young and adult mice fed on HFD, femoral strength, stiffness, and toughness are all dramatically lower than controls. Inferior lamellar and osteocyte alignment also point to reduced structural quality in both age groups. Bone size was largely unaffected by HFD, although there was a shift from increasing bone size in obese adolescents to decreasing in adults. IGF-I levels were lower in young obese mice only. CONCLUSIONS: While the response to obesity of murine cortical bone mass, bone formation, and hormonal changes appear to differ by age, the bone mechanical properties for young and adult groups are similar. In agreement with human fracture trends, adult mice may be similarly susceptible to bone fracture to the young group, although cortical bone in the two age groups responds to diabetic obesity differently.

Localization of p21-activated kinase 1 (PAK1) to pinocytic vesicles and cortical actin structures in stimulated cells.

The mechanisms through which the small GTPases Rac1 and Cdc42 regulate the formation of membrane ruffles, lamellipodia, and filopodia are currently unknown. The p21-activated kinases (PAKs) are direct targets of active Rac and Cdc42 which can induce the assembly of polarized cytoskeletal structures when expressed in fibroblasts, suggesting that they may play a role in mediating the effects of these GTPases on cytoskeletal dynamics. We have examined the subcellular localization of endogenous PAK1 in fibroblast cell lines using specific PAK1 antibodies. PAK1 is detected in submembranous vesicles in both unstimulated and stimulated fibroblasts that colocalize with a marker for fluid-phase uptake. In cells stimulated with PDGF, in v-Src-transformed fibroblasts, and in wounded cells, PAK1 redistributed into dorsal and membrane ruffles and into the edges of lamellipodia, where it colocalizes with polymerized actin. PAK1 was also colocalized with F-actin in membrane ruffles extended as a response to constitutive activation of Rac1. PAK1 appears to precede F-actin in translocating to cytoskeletal structures formed at the cell periphery. The association of PAK1 with the actin cytoskeleton is prevented by the actin filament-disrupting agent cytochalasin D and by the phosphatidylinositol 3-kinase inhibitor wortmannin. Co-immunoprecipitation experiments demonstrate an in vivo interaction of PAK1 with filamentous (F)-actin in stimulated cells. Microinjection of a constitutively active PAK1 mutant into Rat-1 fibroblasts overexpressing the insulin receptor (HIRcB cells) induced the formation of F-actin- and PAK1-containing structures reminiscent of dorsal ruffles. These data indicate a close correlation between the subcellular distribution of endogenous PAK1 and the formation of Rac/Cdc42-dependent cytoskeletal structures and support an active role for PAK1 in regulating cortical actin rearrangements.

Mitochondrial autonomy: incorporation of monosaccharides into glycoprotein by isolated mitochondria.

Isolated intact mitochondria selectively incorporate monosaccharides from nucleotide diphosphate monosaccharides into protein. Fucose, mannose, glucose, and galactose were incorporated by the mitochondria into glycoprotein; xylose was not. Structural integrity of the mitochondria was not necessary for the incorporation of monosaccharide into glycoprotein; mitochondria broken by homogenization also incorporated monosaccharide. The monosaccharides incorporated into glycoprotein were localized in the inner mitochondrial membranes, the same membranes which contain the protein into which leucine is incorporated by the isolated mitochondria.

Human MCF10A mammary epithelial cells undergo apoptosis following actin depolymerization that is independent of attachment and rescued by Bcl-2.

Many tumor cells are impaired in adhesion-regulated apoptosis, which contributes to their metastatic potential. However, suppression of this apoptotic pathway in untransformed cells is not mediated only by adhesion to the extracellular matrix but also through the resulting ability to spread and adopt a distinct morphology. Since cell spreading is dependent on the integrity of the actin microfilament cytoskeleton, we sought to determine if actin depolymerization was sufficient to induce apoptosis, even in the presence of continuous attachment. For this study, we used a human mammary epithelial cell line (MCF10A), which is immortalized but remains adhesion dependent for survival. Treatment of MCF10A cells with latrunculin-A (LA), an inhibitor of actin polymerization, rapidly led to disruption of the actin cytoskeleton and caused cell rounding but preserved attachment. Initiation of apoptosis in LA-treated MCF10A cells was detected by mitochondrial localization of the Bax apoptotic protein, which was prevented by overexpression of Bcl-2. DNA fragmentation and poly(ADP-ribose) polymerase (PARP) cleavage in LA-treated MCF10A cells indicated progression to the execution phase of apoptosis. The MDA-MB-453 cell line, which was derived from a metastatic human mammary tumor, was resistant to PARP cleavage and loss of viability in response to actin depolymerization. Stable overexpression of Bcl-2 in the untransformed MCF10A cells was able to recapitulate the resistance to apoptosis found in the tumor cell line. We demonstrate that inhibition of actin polymerization is sufficient to stimulate apoptosis in attached MCF10A cells, and we present a novel role for Bcl-2 in cell death induced by direct disruption of the actin cytoskeleton.

An SH2 domain-containing 5' inositolphosphatase inhibits insulin-induced GLUT4 translocation and growth factor-induced actin filament rearrangement.

Tyrosine kinase receptors lead to rapid activation of phosphatidylinositol 3-kinase (PI3 kinase) and the subsequent formation of phosphatidylinositides (PtdIns) 3,4-P2 and PtdIns 3,4, 5-P3, which are thought to be involved in signaling for glucose transporter GLUT4 translocation, cytoskeletal rearrangement, and DNA synthesis. However, the specific role of each of these PtdIns in insulin and growth factor signaling is still mainly unknown. Therefore, we assessed, in the current study, the effect of SH2-containing inositol phosphatase (SHIP) expression on these biological effects. SHIP is a 5' phosphatase that decreases the intracellular levels of PtdIns 3,4,5-P3. Expression of SHIP after nuclear microinjection in 3T3-L1 adipocytes inhibited insulin-induced GLUT4 translocation by 100 +/- 21% (mean +/- the standard error) at submaximal (3 ng/ml) and 64 +/- 5% at maximal (10 ng/ml) insulin concentrations (P < 0.05 and P < 0.001, respectively). A catalytically inactive mutant of SHIP had no effect on insulin-induced GLUT4 translocation. Furthermore, SHIP also abolished GLUT4 translocation induced by a membrane-targeted catalytic subunit of PI3 kinase. In addition, insulin-, insulin-like growth factor I (IGF-I)-, and platelet-derived growth factor-induced cytoskeletal rearrangement, i.e., membrane ruffling, was significantly inhibited (78 +/- 10, 64 +/- 3, and 62 +/- 5%, respectively; P < 0.05 for all) in 3T3-L1 adipocytes. In a rat fibroblast cell line overexpressing the human insulin receptor (HIRc-B), SHIP inhibited membrane ruffling induced by insulin and IGF-I by 76 +/- 3% (P < 0.001) and 68 +/- 5% (P < 0.005), respectively. However, growth factor-induced stress fiber breakdown was not affected by SHIP expression. Finally, SHIP decreased significantly growth factor-induced mitogen-activated protein kinase activation and DNA synthesis. Expression of the catalytically inactive mutant had no effect on these cellular responses. In summary, our results show that expression of SHIP inhibits insulin-induced GLUT4 translocation, growth factor-induced membrane ruffling, and DNA synthesis, indicating that PtdIns 3,4,5-P3 is the key phospholipid product mediating these biological actions.

Membrane adenosine triphosphatase activities in rat pancreas.

The membrane ATPase activities present in rat pancreas were studied to investigate the possible role of ATPase enzymes in HCO3(-) secretion in the pancreas. It was found that all the HCO3(-)-sensitive (anion-sensitive) ATPase activity was accountable as pancreatic mitochondrial ATPase, thus supporting the view that a distinct plasma membrane 'bicarbonate-ATPase' is not involved in HCO3(-) secretion in pancreas. A remarkably high Mg+- and CA2+-requiring ATPase activity (30 mumol ATP hydrolysed/min per mg) was found in the plasma membrane fraction (rho = 1.10-1.13). This activity has been characterized in some detail. It is inhibited by p-fluorosulfonylbenzoyladenosine, an affinity label analogue of ATP and the analogue appears to label covalently a protein of Mr approximately 35 000. The (Ca2+ + Mg2+)-ATPase activity did not form a 'phosphorylated-intermediate' and was vanadate-insensitive. These and other tests have served to demonstrate that the (Ca2+ + Mg2+)-ATPase activity is different in properties from (Na+ + K+)-ATPase, Ca2+-ATPase, (H+ + K+)-ATPase or mitochondrial H+-ATPase. Apart from the (Ca2+ + Mg2+)-ATPase of plasma membrane and mitochondrial ATPase, the only other membrane ATPase activities noted were (Na+ + K+)-ATPase, which occurred in the same fractions as the (Ca2+ + Mg2+)-AtPase at rho = 1.10-1.13 and was of surprisingly low activity, and an ATPase activity in light membrane fractions (rho - 1.08-1.09) derived from zymogen granule membranes. At this time, therefore, there is no obvious candidate for an ATPase activity at the luminal surface of pancreatic cells which is directly involved in ion transport, but the results presented here direct attention to the high activity (Ca2+ + Mg2+)-ATPase in the plasma membrane fraction.

Quasi-equivalence in site-specific recombinase structure and function: crystal structure and activity of trimeric Cre recombinase bound to a three-way Lox DNA junction.

The crystal structure of a novel Cre-Lox synapse was solved using phases from multiple isomorphous replacement and anomalous scattering, and refined to 2.05 A resolution. In this complex, a symmetric protein trimer is bound to a Y-shaped three-way DNA junction, a marked departure from the pseudo-4-fold symmetrical tetramer associated with Cre-mediated LoxP recombination. The three-way DNA junction was accommodated by a simple kink without significant distortion of the adjoining DNA duplexes. Although the mean angle between DNA arms in the Y and X structures was similar, adjacent Cre trimer subunits rotated 29 degrees relative to those in the tetramers. This rotation was accommodated at the protein-protein and DNA-DNA interfaces by interactions that are "quasi-equivalent" to those in the tetramer, analogous to packing differences of chemically identical viral subunits at non-equivalent positions in icosahedral capsids. This structural quasi-equivalence extends to function as Cre can bind to, cleave and perform strand transfer with a three-way Lox substrate. The structure explains the dual recognition of three and four-way junctions by site-specific recombinases as being due to shared structural features between the differently branched substrates and plasticity of the protein-protein interfaces. To our knowledge, this is the first direct demonstration of quasi-equivalence in both the assembly and function of an oligomeric enzyme.

The small guanosine triphosphate-binding protein Rab4 is involved in insulin-induced GLUT4 translocation and actin filament rearrangement in 3T3-L1 cells.

Insulin's stimulation of glucose transport involves the translocation of vesicles containing the glucose transporter GLUT4 to the plasma membrane. Small GTP-binding proteins have been implicated in the regulation of vesicular traffic. We studied the effects of microinjection of wild-type Rab4 glutathione S-transferase fusion protein (WT Rab4), a GTP-binding defective mutant (Rab4 N121I), a guanosine triphosphatase-defective mutant (Rab4 Q67L), and a Rab4 antibody on insulin-induced GLUT4 translocation in 3T3-L1 adipocytes. Microinjection of Rab4 N121I and Rab4 antibodies had no effect on basal GLUT4 staining, but inhibited insulin-induced GLUT4 translocation by 50% compared with that in control IgG-injected cells. WT Rab4 and Rab4 Q67L microinjection had no effect on either basal or insulin-induced GLUT4 translocation. Premixing and coinjection of the Rab4 antibody with WT Rab4 almost completely abolished its inhibitory effect on insulin-induced GLUT4 translocation. In contrast, microinjection of an antibody directed against the highly conserved region of Rab3 proteins had no effect on insulin-induced GLUT4. These results point to a direct role of Rab4 in insulin-induced GLUT4 translocation, and that this effect is dependent on nucleotide binding to the protein. We also studied the effect of microinjection of the same proteins on insulin-induced actin filament rearrangement (membrane ruffling) in the same cell line. Microinjection of Rab4 N121I and Rab4 antibodies inhibited insulin-induced membrane ruffling by 40%, whereas WT Rab4 or a Rab3 antibody injection had no effect on cytoskeletal rearrangement. In summary, 1) Rab4 is a necessary component of the insulin/GLUT4 translocation signaling pathway; 2) the function of Rab4 in this pathway requires GTP binding; 3) Rab4 also participates in the process of insulin-induced membrane ruffling; and 4) Rab3 proteins do not seem to be involved in these processes.

Phosphatidylinositol 3-kinase is necessary and sufficient for insulin-stimulated stress fiber breakdown.

Rat-1 fibroblasts overexpressing the human insulin receptor undergo rapid actin rearrangement in response to insulin. Breakdown of stress fibers present in quiescent cells is followed by transient membrane ruffling and a return of stress fibers. We investigated the signaling pathways that mediate this insulin-stimulated reorganization of the actin cytoskeleton, which was visualized with rhodamine-phalloidin. Treatment of cells with the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor wortmannin prevented insulin action at the preliminary step of stress fiber breakdown. Cellular microinjection of a polyclonal antibody directed against the p85 subunit of PI3-kinase as well as a purified recombinant p85-SH2 domain protein also inhibited actin reorganization. Transient expression of a constitutively active form of PI3-kinase (p110*) was sufficient to cause both stress fiber breakdown and membrane ruffling in the absence of insulin. Microinjection of a polyclonal anti-Shc antibody or dominant negative N17-Ras protein did not affect actin dynamics, and although constitutively active V12-Ras caused modest cytoskeletal reorganization, this effect was blocked by pretreatment with wortmannin. In summary, activation of PI3-kinase is necessary and sufficient to stimulate actin rearrangement, indicating that PI3-kinase may initiate the only signaling cascade required for insulin to induce cytoskeletal restructuring.

Assessment of erythropoiesis activity during hemodialysis therapy by soluble transferrin receptor levels and ferrokinetic measurements.

The erythropoietic activity (EA) and degree of erythropoiesis attained by patients undergoing hemodialysis (HD) administered recombinant human erythropoietin (rHuEPO) were studied using ferrokinetic measurements and tests of soluble transferrin receptor (sTfR) levels, assessing which parameter is most useful for measurements in clinical practice. Plasma iron 59 ((59)Fe) clearance (half-life [T(1/2)] (59)Fe), plasma iron turnover (PIT), erythron transferrin uptake (ETU), and erythrocyte (59)Fe incorporation were determined in 23 patients before and at 4 months after administration of rHuEPO. sTfR levels, hematopoietic parameters, and iron metabolism parameters were measured periodically. T(1/2) (59)Fe was shortened (P: = 0.004), PIT and ETU were increased (P: = 0.032 and P: = 0.013, respectively), and the time taken by erythrocytes to incorporate 80% of the (59)Fe administered was reduced from 9.6 to 6.1 days. sTfR levels were increased by 15 days; this increase was significant (P: < 0.05) at 30 days, reaching a maximum of 3.22 mg/dL at day 45. A positive correlation was seen between sTfR levels and hemoglobin (Hb) (P: = 0.001), hematocrit (P: = 0.001), and reticulocytes (P: = 0.038) that was not found between ferrokinetic parameters and those evaluating efficient erythropoiesis (P: = 0.345 between ETU and Hb). In conclusion, EA is increased, shown by ETU and sTfR level. sTfR levels correlate with the parameters that evaluate efficient erythropoiesis, and their measurement does not involve the technical and/or ethical limitations of studies of ferrokinetics, making them the tool of choice in clinical practice for the evaluation of EA in patients undergoing HD administered rHuEPO.

Predictors of medication noncompliance in a sample of older adults.

The subjects were 1028 respondents from a randomly selected sample of independently living adults aged 55 years and older in the southeastern United States. Data on background characteristics, physical health, life satisfaction, psychological distress, and medication compliance were gathered from structured interviews. Among the 785 subjects in the analysis who were taking prescribed medications, 75% were women, 83% were white, their median income was $12,500 annually, 66% lived alone, their mean age was 73.9 years, and their mean number of years of education was 11.4. Twenty-one percent of all respondents taking medications had been noncompliant during the month preceding the study interview. Noncompliance with prescribed medications was significantly associated with higher socioeconomic status (P < 0.01), greater number of prescribed medications (P < 0.01), and higher psychological stress (P < 0.05). There was no relationship between compliance and living arrangements, health, life satisfaction, number of illnesses, age, or sex.

Sensation seeking needs among 8th and 11th graders: characteristics associated with cigarette and marijuana use.

This cross-sectional school-based study explored the relationship between adolescent use of cigarettes and marijuana and the sensation seeking personality factors of (1) Disinhibition and (2) Thrill and Adventure Seeking. The study population included a representative sample of both male and female 8th and 11th graders in the state of Delaware. Analytic methods utilized included correlational analysis and multivariate logistic regression. In the multivariate logistic regression models, the Disinhibition personality factor accounted for cigarette and marijuana using behaviors with odds ratios ranging between 2 and 3. Thrill and Adventure Seeking was not a significant explanatory variable in any of the final multivariate models. Potential confounders (age, gender and race) were considered in all analyses. Of all the two-way interactions assessed, none was significant. The findings from this study utilizing a large general community sample indicate that sensation seeking needs are a potential risk factor for adolescent substance use.

Postoperative inflammation following cataract extraction caused by bacterial contamination of the cleaning bath detergent.

Five of 16 patients who had uncomplicated cataract extraction with intraocular lens (IOL) implantation within a 2.5 day period experienced increased anterior segment inflammation on their first postoperative day. Four of these five patients had phacoemulsification and one a planned extracapsular cataract extraction. All had posterior chamber IOL implantation in the capsular bag. In all patients, this anterior segment inflammation cleared with topical steroids over two to three weeks with no evident residual ocular effects. A careful search for the possible cause of the inflammation showed that the ultrasonic cleaning bath and Weck liquid detergent used to clean the instruments contained Klebsiella pneumoniae bacteria. Further investigation demonstrated the presence of a heat-stable endotoxin produced by the bacteria. We postulate that endotoxin remaining on the instruments after cleaning and sterilization caused this postoperative anterior segment inflammation. To the best of our knowledge, these are the first reported cases caused by contaminated liquid detergent.

Social factors predicting postpartum choice of Norplant among African-American and non-Hispanic white adolescents.

PURPOSE: This study was designed to determine the factors associated with Norplant choice for postpartum teens. METHODS: A total of 151 teenagers, ages 12-20 years, who delivered at the Medical Center of Delaware from July to December 1992, were offered insertion of Norplant within 48 h postpartum. A structured interview was conducted in the postpartum period after nondirective counseling sessions including a physical demonstration using anatomical models of various contraceptive methods. Student's t-tests, chi-square, and multivariate analyses were used. RESULTS: Eighty-six teenagers were African-American (mean age = 17.3 +/- 1.9 years) and 65 non-Hispanic white (NHW) (mean age = 18.3 +/- 1.5 years). The NHW teenagers were older (p < 0.001); the African-American teenagers were more likely to have Medicaid (49% vs. 14%; p < 0.001) and to have one or more friends who use Norplant (62% vs. 34%; p < 0.001). In multivariate analyses, NHW teenagers were more likely to choose Norplant if they had discussed their choice with a parent or guardian [adjusted odds ratio (AOR) = 14.6, 95% confidence interval (CI), 2.12-100.57]; had Medicaid funding (AOR = 12.1; 95% (CI), 10.6-91.34); and had any friends who used Norplant (AOR = 6.3; 95% (CI), 1.38-28.40). However, for African-American teenagers, the strongest predictor for choice of Norplant was number of prior children delivered. After two deliveries, there was a better than four-fold likelihood (AOR = 4.8; 95% (CI), 1.47-15.94) that African-American teenagers would choose Norplant. For the African-American teenagers, parental discussion, Medicaid status, and friends' use of Norplant were not as important as family size, but far greater percentages of the African-American teenagers had access to Medicaid funding and peers who used Norplant. CONCLUSIONS: NHW and African-American teenagers choose Norplant for different reasons. Lack of funding may have been a barrier to choosing Norplant. Discussions with parents and friends have a positive influence on choosing Norplant for NHW teenagers. African-American teenagers were more likely than NHW to have Medicaid coverage, and more frequently choose Norplant if the current birth was their third child.

PIP: 151 youths, aged 12-20 years, who delivered at the Medical Center of Delaware from July to December 1992, were offered insertion of Norplant within 48 hours postpartum. These young women were subsequently interviewed to determine which factors are associated with choosing to accept or not accept Norplant. 86 Black teenagers of mean age 17.3 years and 65 non-Hispanic Whites of mean age 18.3 years participated. The White teenagers were significantly older, 49% of Blacks and 14% of Whites had Medicaid, and 62% of Blacks and 34% of Whites had one or more friends who use Norplant. In multivariate analyses, the White teens were more likely to choose Norplant if they had discussed their choice with a parent or guardian, if they received Medicaid funding, and if they had any friends who used Norplant. The strongest predictor for choice of Norplant among Black teens was the number of prior children delivered. After 2 deliveries, there was an almost 5-fold likelihood that Black teenagers would choose Norplant. For the Black teens, parental discussion, Medicaid status, and friends' use of Norplant were not as important as family size, but larger proportions of the Black teens had access to Medicaid funding and peers who used Norplant.