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J Kowalski

Publications and source records attributed to J Kowalski.

At least 19 recordsLinked to original sources
PubMed2007

Power analyses for longitudinal study designs with missing data.

Existing methods for power analysis for longitudinal study designs are limited in that they do not adequately address random missing data patterns. Although the pattern of missing data can be assessed during data analysis, it is unknown during the design phase of a study. The random nature of the missing data pattern adds another layer of complexity in addressing missing data for power analysis. In this paper, we model the occurrence of missing data with a two-state, first-order Markov process and integrate the modelling information into the power function to account for random missing data patterns. The Markov model is easily specified to accommodate different anticipated missing data processes. We develop this approach for the two most popular longitudinal models: the generalized estimating equations (GEE) and the linear mixed-effects model under the missing completely at random (MCAR) assumption. For GEE, we also limit our consideration to the working independence correlation model. The proposed methodology is illustrated with numerous examples that are motivated by real study designs.

Adolescent↗
PubMed2006

Power analyses for correlations from clustered study designs.

Power analysis constitutes an important component of modern clinical trials and research studies. Although a variety of methods and software packages are available, almost all of them are focused on regression models, with little attention paid to correlation analysis. However, the latter is arguably a simpler and more appropriate approach for modelling concurrent events, especially in psychosocial research. In this paper, we discuss power and sample size estimation for correlation analysis arising from clustered study designs. Our approach is based on the asymptotic distribution of correlated Pearson-type estimates. Although this asymptotic distribution is easy to use in data analysis, the presence of a large number of parameters creates a major problem for power analysis due to the lack of real data to estimate them. By introducing a surrogacy-type assumption, we show that all nuisance parameters can be eliminated, making it possible to perform power analysis based only on the parameters of interest. Simulation results suggest that power and sample size estimates obtained under the proposed approach are robust to this assumption.

Clinical Trials as Topic↗
PubMed2006

Seroprevalence of human granulocytic anaplasmosis in Berlin/Brandenburg, Germany: an 8-year survey.

This study investigated the seroprevalence of antibodies against Anaplasma phagocytophilum in Berlin/Brandenburg, north-eastern Germany. During 1994-2001, 422 sera from patients with proven tick-exposure (specimens with antibodies against Borrelia burgdorferi) were compared with 249 control sera. Using indirect fluorescent antibody testing, significantly more positive samples were detected among Borrelia antibody-positive specimens (4.5%, 95% CI 2.5-6.5%) than among controls (1.2%, 95% CI 0.5-1.9%; p < 0.05). While six (2.2%, 95% CI 1.3-3.1%) samples were positive among Borrelia antibody-positive sera between 1994 and 1997, 13 (8.7%, 95% CI 6.9-10.5%) were positive between 1998 and 2001 (p < 0.01), indicating an uneven annual seroprevalence.

Adolescent↗
PubMed2006

Effect of Epilobium angustifolium L. extracts and polyphenols on cell proliferation and neutral endopeptidase activity in selected cell lines.

The ability of Epilobium extracts and polyphenols to induce neutral endopeptidase (NEP) activity and to inhibit the proliferation in cell lines with high NEP expression (SK-N-SH) and with low NEP expression (PC-3) was investigated. Epilobium extracts enhanced in a dose-depend manner NEP activity in both cell lines with additional inhibition of cell proliferation. The sensitivity of cells depended on basal enzyme activity. SK-N-SK cells were much more sensitive than PC-3 cells. Oenothein B enhanced NEP activity at a concentration of 5-40 microM while quercetin-3-glucuronide and quercetin-3-O-(6"-gal-loyl) galactoside showed slight or no activity at a concentration of 100 microM. The comparison of activities of the extracts with oenothein B, a dimeric macrocyclic ellagitannin, suggests that the latter is mostly responsible for the observed effects. Taking into account the role of NEP in the homeostasis of signalling peptides, Epilobium angustifolium extracts may be a potential herbal remedy in diseases connected with the disturbed metabolism of signaling peptides caused by an unbalanced neutral endopeptidase activity.

Cell Line, Tumor↗
PubMed2005

Induction of neutral endopeptidase activity in PC-3 cells by an aqueous extract of Epilobium angustifolium L. and oenothein B.

An aqueous extract of Epilobium angustifolium and its main compound oenothein B (OeB), a dimeric macrocyclic ellagitannin, are specifically able to induce the neutral endopeptidase (NEP) in prostate cancer cells. The angiotensin-converting enzyme (ACE) is not influenced. Additionally, a weak but statistically significant inhibition of cell proliferation is observed. Simultaneous treatment of the cells with arabinosylcytosine and the extract as well as the OeB, leads to an additional enhancement of NEP activity. Taking into account the role of this peptidase in prostate cancer progression, our results might offer a pharmacological explanation for the use of Epilobium in folk medicine.

Cell Line, Tumor↗
PubMed2004

Power analyses for longitudinal trials and other clustered designs.

Existing methods for power and sample size estimation for longitudinal and other clustered study designs have limited applications. In this paper, we review and extend existing approaches to improve these limitations. In particular, we focus on power analysis for the two most popular approaches for clustered data analysis, the generalized estimating equations and the linear mixed-effects models. By basing the derivation of the power function on the asymptotic distribution of the model estimates, the proposed approach provides estimates of power that are consistent with the methods of inference for data analysis. The proposed methodology is illustrated with numerous examples that are motivated by real study designs.

Clinical Trials as Topic↗
PubMed2003

Effects of atorvastatin, simvastatin, and fenofibrate therapy on monocyte chemoattractant protein-1 secretion in patients with hyperlipidemia.

OBJECTIVE: Monocytes that migrate into the arterial wall participate in the development and, eventually, rupture of the atherosclerotic plaque. The aim of this study was to evaluate the secretion of monocyte chemoattractant protein-1 (MCP-1) by monocytes from hyperlipidemic patients treated with hypolipidemic drugs, namely fenofibrate, simvastatin, or atorvastatin to determine what role is played by these drugs in the development and stabilization of the atherosclerotic plaque. METHODS: Fifty-four hyperlipidemic patients, who did not respond to a low-fat diet, were treated with fenofibrate, simvastatin, or atorvastatin (18 patients in each group) for 1 month. The control group included 18 normolipidemic, healthy, age-matched participants. Ten hyperlipidemic patients were effectively treated with hypolipidemic diet alone for 1 month. This group was compared with a control group of ten healthy subjects. To accurately evaluate the adhesion molecule levels, we excluded hyperlipidemic patients and control subjects with any inflammatory disease. Before and after treatment, monocytes were isolated from peripheral blood. After stimulation with lipopolysaccharide (LPS), MCP-1 secretion was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: MCP-1 levels were significantly higher in hyperlipidemic patients than controls: 15.8+/-0.47, 16.7+/-0.23, and 14.9+/-0.45 compared with 12.36+/-0.42 ng/ml. Fenofibrate, atorvastatin, and simvastatin significantly decreased MCP-1 levels from 15.8+/-0.47 to 8.79+/-0.89, from 16.7+/-0.23 to 7.46+/-0.73, and from 14.9+/-0.45 to 10.3+/-0.8 ng/ml, respectively. In the diet-treated group of hyperlipidemic patients, the level of MCP-1 before therapy was significantly higher than in controls (16.89+/-0.31 vs 12.45+/-0.36 ng/ml). The diet therapy caused a significant decrease in levels of MCP-1 to 15.1+/-0.36 ng/ml. There was a correlation between the decreased levels of lipids and the decreased release of MCP-1 in the patients treated with hypolipemic drugs. CONCLUSION: The drug-induced decrease in MCP-1 secretion in hyperlipidemic patients suggests that, apart from acting on lipids, the hypolipidemic drugs studied may directly inhibit the activity of monocytes.

Atorvastatin↗
PubMed2003

Generalized covariance-adjusted canonical correlation analysis with application to psychiatry.

The lack of control over covariates in practice motivates the need for their adjustment when measuring the degree of association between two sets of variables, for which canonical correlation is traditionally used. In most studies however, there is also a lack of control over the attributes of responses for the sets of variables of interest. In particular, a portion of the response variable may be continuous and the other discrete. For such settings, the traditional partial canonical correlation approach is restrictive, since a covariate-adjustment for a set of continuous variables is assumed. By ignoring the assumption of continuous variates and proceeding with a partial canonical correlation analysis in the presence of continuous and discrete variates, results in canonical correlation estimates that are not consistent. In this paper we generalize the traditional partial canonical correlation approach to covariate-adjustment by allowing the response variables to contain continuous, as well as discrete, variates. The methodology is illustrated with a psychiatric application for examining which sleep variables relate to which depressive symptoms, as measured by commonly used constructs that presents with both continuous and discrete outcomes.

Analysis of Variance↗
PubMed2003

Effects of fenofibrate and simvastatin on plasma sICAM-1 and MCP-1 concentrations in patients with hyperlipoproteinemia.

OBJECTIVE: The most important mechanism through which high plasma lipid levels trigger the formation of atherosclerotic lesions involves a change in the expression of adhesion molecules on endothelial and smooth muscle cells. The aim of this study was to evaluate an extralipid effect of fenofibrate and simvastatin by examination of MCP-1 and ICAM-1 plasma concentration after 1-month hypolipemic therapy as well as MCP-1 and ICAM-1 plasma concentration after 1-month therapy with low-fat diet alone. METHODS: Twenty patients with HLPIIb or HLPIIa, who did not respond to a low-fat diet, were treated with micronized fenofibrate or simvastatin, respectively, for 1 month. The control group included 18 normo-lipidemic, healthy age-matched participants; 10 patients with HLPIIa were effectively treated with a low-fat diet for 1 month. This group was compared to a control group of 10 healthy subjects. The plasma adhesion molecule levels were measured by an ELISA method before and after the treatment. To accurately evaluate the adhesion molecule levels, we excluded hyperlipidemic patients and control subjects with any inflammatory disease. RESULTS: sICAM-1 levels were significantly higher in HLPIIa and HLPIIb patients (331 +/- 19 ng/ml and 423 +/- 23 ng/ml, respectively) compared with the control group (236 +/- 12 mg/ml). MCP-1 levels were also significantly higher in HLPIIa and HLPIIb patients (170 +/- 9 pg/ml and 183 +/- 15 pg/ml, respectively) compared with the control group (100 +/- 4 pg/ml). Fenofibrate (200 mg daily) significantly decreased sICAM-1 (by 17%) and MCP-1 levels (by 12.5%). Simvastatin (20 mg daily) caused a significant decrease (by 10.5%) in sICAM-1 levels only. Restriction in dietary lipids resulted in a significant decrease in the levels of cholesterol (8%), LDL cholesterol (14.9%) and ApoB (12.7%), which was accompanied by a significant decrease in the levels of sICAM-1 (8.7%) and MCP-1 (16.1%). CONCLUSION: The results of this study suggest that high lipid levels are accompanied by increased levels of sICAM-1 and MCP-1 and that hypolipidemic therapy only slightly decreases the levels of these molecules compared with plasma lipids. The hypolipidemic diet-related decrease in the levels of lipids, ICAM-1 and MCP-1 suggests that it is a drug-induced decrease in lipid levels but not a direct action of the drugs on endothelial cells, smooth muscle cells or macrophages that leads to a decrease in the levels of adhesion molecules.

Chemokine CCL2↗
PubMed2003

The risk of atherosclerosis in patients with impaired glucose tolerance.

OBJECTIVES: Glucose metabolism disorders usually coexist with dyslipidemia and coagulation/fibrinolysis disturbances. Increase of insulin resistance followed by hyperinsulinemia leads to enhanced protein synthesis, including production of apolipoproteins. As a result, the structure of Low Density Lipoprotein (LDL) becomes small and dense. This augments lipid infiltration into the arterial wall. Following this process monocyte adhesion to endothelium initiates atherosclerotic injury. One of the markers of this inflammatory reaction is Monocyte Chemoattractant Peptide-1 (MCP-1). A lot of inflammatory mediators affect both oxidative modification of LDL and coagulation processes being responsible for anti-fibrinolytic predominance. Plasminogen Activator Inhibitor-1 (PAI-1) is a marker of this state. Therefore the aim of this study is to evaluate the marker of the oxidation processes (oxLDL) as well as prothrombotic (PAI-1) and inflammatory state (MCP-1) markers in patients with Impaired Glucose Tolerance (IGT). METHODS: The study was carried out on 16 subjects: 10 with biochemically confirmed IGT and 6 age-matched healthy persons without such disorders. Following tests were performed: OGTT, HbA(1c) level as well as TCh, HDL, LDL and TG. Plasma concentrations of oxLDL, PAI-1 and MCP-1 were measured using ELISA method. RESULTS: In patients with Impaired Glucose Tolerance plasma levels of oxLDL were significantly higher compared to control group (67.6 +/- 0.9 U/l vs. 57.8 +/- 4.0 U/l; p < 0.01) in spite of LDL levels, which did not reveal such difference. MCP-1 plasma concentration compared to control group occurred to be significantly increased in experimental group as well (156.4 +/- 9.2 ng/ml vs. 125.4 +/- 1.9 ng/ml; p < 0.05). PAI-1 level revealed most significant difference (84.0 +/- 1.8 ng/ml vs. 43.7 +/- 2.7 ng/ml; p < 0.0001). CONCLUSIONS: It is concluded that patients with Impaired Glucose Tolerance should be considered as a group in which atherogenic modification of lipoproteins occurred. Also plasma inflammatory as well as prothrombotic markers concentration was elevated.

Adult↗
PubMed2002

Double-blind, randomized, placebo-controlled study of topical 5% acyclovir-1% hydrocortisone cream (ME-609) for treatment of UV radiation-induced herpes labialis.

Immunopathology is recognized as an important component of infectious disease manifestations, and corticosteroids have been used as an adjunct to antimicrobial therapy for a variety of conditions. Antiviral therapy of herpes labialis has been shown to result in only a small reduction in the time to healing and the duration of pain. To determine if topical application of a combination product containing 5% acyclovir and 1% hydrocortisone (ME-609) could provide benefit to herpes labialis patients, 380 immunocompetent adults with a history of herpes labialis were exposed to experimental UV radiation (UVR) to induce a recurrence. On day 2, just before the appearance of the majority of lesions ("delayed" lesions), subjects were randomized to receive active medication or vehicle control six times per day for 5 days. Overall, 120 of 380 patients developed delayed classical lesions, of whom 50 of 190 (26%) had been treated with ME-609 and 70 of 190 (37%) had received placebo (a reduction of 29% [P = 0.02]). Healing time, measured as the time to normal skin, was reduced by treatment with ME-609 (9.0 days for treated patients versus 10.1 days for the controls [P = 0.04]). There was a trend toward a reduction in the maximum lesion size in the ME-609 recipients compared to that in the controls (43 versus 60 mm(2), respectively [P = 0.07]). The treatment had no effect on lesion pain, but ME-609 treatment reduced the number of patients with moderate or severe tenderness. Compared to treatment with a placebo, treatment with the combination antiviral-immunomodulatory cream provided benefit to patients with experimental UVR-induced herpes labialis, reducing classical lesion incidence, healing time, lesion size, and lesion tenderness. ME-609 is a novel product that merits further evaluation as a treatment for cold sores.

Acyclovir↗
PubMed2002

Plasma cytokines as predictors of coronary heart disease.

BACKGROUND AND OBJECTIVE: Growing body of evidence explicitly suggests the significant role of inflammatory processes in vascular diseases related to atherosclerosis. Monocytes, present in every phase of atherogenesis, are the principal cells accumulating in atherosclerotic plaque. Monocyte Chemotactic Protein 1 (MCP-1) seems to influence firm adherence of rolling monocytes and infiltration into the artery wall. Although the significant meaning of inflammation in atherogenesis has been proved, potential role of antiinflammatory cytokines remains unknown. Interleukin 10 (IL-10) is a major cytokine of pleiotropic antiinflammatory function known to exert inhibitory effects on monocytes. Recent data emerging from clinical and pathological studies suggest important role of thrombosis and fibrinolytic disorders in atherosclerosis complications especially in coronary heart disease (CHD). Individuals with greater Plasminogen Activator Inhibitor 1 (PAI-1) level are believed to be more susceptible to cardiovascular disease. METHODS: In our study we measured the plasma levels of MCP-1, IL-10 and PAI-1 in 10 patients with stable angina and 10 healthy subjects. We also estimated its mutual correlations. The plasma levels of MCP-1, IL-10 and PAI-1 were determined with R&D kits (ELISA). RESULTS: Plasma levels of MCP-1 were significantly higher (261.5+/-40.7 pg/mL vs 73.3+/-3.05 pg/mL; p<0.0002) and also levels of PAI-1 were higher (79.36+/-5.8 ng/mL vs 35.88+/-1.38 ng/mL; p<0.0001) in patients with SA compared with the healthy control subjects. Whereas plasma levels of IL-10 were lower (11.6+/-0.5 pg/mL vs 16.5+/-0.4 pg/mL; p<0.0001) compared with control group and correlated with both MCP-1 plasma level (r=-0.67; p<0.0015) and PAI-1 concentration (r=-0.69; p<0.0008). CONCLUSION: The data obtained confirm the predictive role of cytokines in patients with stable coronary heart disease. The negative correlation of anti-inflammatory IL-10 and PAI-1 was also found.

Adult↗
PubMed2001

Identification of an angiogenic mitogen selective for endocrine gland endothelium.

The known endothelial mitogens stimulate growth of vascular endothelial cells without regard to their tissue of origin. Here we report a growth factor that is expressed largely in one type of tissue and acts selectively on one type of endothelium. This molecule, called endocrine-gland-derived vascular endothelial growth factor (EG-VEGF), induced proliferation, migration and fenestration (the formation of membrane discontinuities) in capillary endothelial cells derived from endocrine glands. However, EG-VEGF had little or no effect on a variety of other endothelial and non-endothelial cell types tested. Similar to VEGF, EG-VEGF possesses a HIF-1 binding site, and its expression is induced by hypoxia. Both EG-VEGF and VEGF resulted in extensive angiogenesis and cyst formation when delivered in the ovary. However, unlike VEGF, EG-VEGF failed to promote angiogenesis in the cornea or skeletal muscle. Expression of human EG-VEGF messenger RNA is restricted to the steroidogenic glands, ovary, testis, adrenal and placenta and is often complementary to the expression of VEGF, suggesting that these molecules function in a coordinated manner. EG-VEGF is an example of a class of highly specific mitogens that act to regulate proliferation and differentiation of the vascular endothelium in a tissue-specific manner.

Amino Acid Sequence↗
PubMed2001

Neuroleptics normalize increased release of interleukin- 1 beta and tumor necrosis factor-alpha from monocytes in schizophrenia.

Some recent reports show that schizophrenia is accompanied by changes in lymphocyte activity. This study investigated the activity of monocytes by determining their release of interleukin- 1 beta (IL- 1 beta) and tumor necrosis factor-alpha (TNF-alpha). Monocytes were immunomagnetically isolated from the peripheral blood of schizophrenic patients before and after neuroleptic medication and stimulated by lipopolisaccharide (LPS) in vitro. The monocytes of schizophrenic patients released significantly higher amounts of IL- 1 beta and TNF-alpha than those of healthy controls. Treatment with the typical neuroleptics haloperidol and perazine decreased the release of IL- 1 beta and TNF-alpha to the control levels. The study has shown that the activity of monocytes is increased in schizophrenia and that neuroleptic treatment normalizes this activity.

Adult↗
PubMed2001

Development of poly-(D,L-lactide--coglycolide) microsphere formulations containing recombinant human vascular endothelial growth factor to promote local angiogenesis.

Although preclinical animal studies have demonstrated the utility of recombinant human vascular endothelial growth factor (rhVEGF) in promoting neovascularization in regions of ischemia, rhVEGF systemic administration did not provide clinical benefit to patients in recent placebo-controlled Phase II clinical trials. The amount of rhVEGF localized in the ischemic region after systemic administration is minimal and does not persist for more than 1 day. A greater persistence of rhVEGF at the region of ischemia may provide an increased angiogenesis with the eventual formation of patent blood vessels to restore nourishment to the tissues. We sought to develop a formulation of rhVEGF in poly(D,L-lactide--co-glycolide) (PLG) microspheres that would provide a continuous local delivery of intact protein. A stable formulation of rhVEGF for encapsulation contained a small amount of a stabilizing sugar, trehalose. Addition of excess trehalose increased the rate of release from the PLG. In addition, PLG with free acid end groups appeared to retard the initial release of rhVEGF by associating with it through ionic interactions at the positively charged heparin binding domain. rhVEGF was released continuously for 21 days with a very low (less than 10%) initial burst. The released rhVEGF aggregated and hydrolyzed over time and lost heparin affinity but not receptor affinity. The compression molding of rhVEGF PLG microspheres into disks yielded formulations with a low initial release and a lag of 10 days followed by complete release. The PLG microsphere formulations were assessed in the corneal implant model of angiogenesis and generated a dose-dependent angiogenic response. These formulations were also administered intravitreally and subretinally, generating local neovascularization comparable to the human disease states, vitroretinopathy and age-related macular degeneration, respectively. The rhVEGF PLG formulations may increase local angiogenesis without systemic side effects and may also be useful in the development of ocular disease models.

Animals↗
PubMed2001

Hepatocyte growth factor enhances vascular endothelial growth factor-induced angiogenesis in vitro and in vivo.

Vascular endothelial growth factor (VEGF) is an important mediator of angiogenesis in both physiological and pathological processes. Hepatocyte growth factor (HGF) is a mesenchyme-derived mitogen that also stimulates cell migration, and branching and/or tubular morphogenesis of epithelial and endothelial cells. In the present study, we tested the hypothesis that simultaneous administration of HGF and VEGF would synergistically promote new blood vessel formation. HGF acted in concert with VEGF to promote human endothelial cell survival and tubulogenesis in 3-D type I collagen gels, a response that did not occur with either growth factor alone. The synergistic effects of VEGF and HGF on endothelial survival correlated with greatly augmented mRNA levels for the anti-apoptotic genes Bcl-2 and A1. Co-culture experiments with human neonatal dermal fibroblasts and human umbilical vein endothelial cells demonstrated that neonatal dermal fibroblasts, in combination with VEGF, stimulated human umbilical vein endothelial cells tubulogenesis through the paracrine secretion of HGF. Finally, in vivo experiments demonstrated that the combination of HGF and VEGF increased neovascularization in the rat corneal assay greater than either growth factor alone. We suggest that combination therapy using HGF and VEGF co-administration may provide a more effective strategy to achieve therapeutic angiogenesis.

Animals↗