bluuebunny/crossref_metadata_2025_split huggingface dataset:
Duration of streptozotocin-induced diabetes differentially affects p38-mitogen-activated protein kinase (MAPK) phosphorylation in renal and vascular dysfunction
Authors: Chen Hongmei , Brahmbhatt Sachin , Gupta Akanksha , Sharma Avadhesh C 
Published: March 2005

Abstract
Background
In the present study we tested the hypothesis that progression of streptozotocin (STZ)-induced diabetes (14-days to 28-days) would produce renal and vascular dysfunction that correlate with altered p38- mitogen-activated protein kinase (p38-MAPK) phosphorylation in kidneys and thoracic aorta.

Methods
Male Sprague Dawley rats (350–400 g) were randomized into three groups: sham (N = 6), 14-days diabetic (N = 6) and 28-days diabetic rats (N = 6). Diabetes was induced using a single tail vein injection of STZ (60 mg/kg, I.V.) on the first day. Rats were monitored for 28 days and food, water intake and plasma glucose levels were noted. At both 14-days and 28-days post diabetes blood samples were collected and kidney cortex, medulla and aorta were harvested from each rat.

Results
The diabetic rats lost body weight at both 14-days (-10%) and 28-days (-13%) more significantly as compared to sham (+10%) group. Glucose levels were significantly elevated in the diabetic rats at both 14-days and 28-days post-STZ administration. Renal dysfunction as evidenced by renal hypertrophy, increased plasma creatinine concentration and reduced renal blood flow was observed in 14-days and 28-days diabetes. Vascular dysfunction as evidenced by decreased carotid blood flow was observed in 14-days and 28-days diabetes. We observed an up-regulation of inducible nitric oxide synthase (iNOS), prepro endothelin-1 (preproET-1) and phosphorylated p38-MAPK in thoracic aorta and kidney cortex but not in kidney medulla in 28-days diabetes group.

Conclusion
The study provides evidence that diabetes produces vascular and renal dysfunction with a profound effect on signaling mechanisms at later stage of diabetes.
Evaluation of a 7-Day Continuous Intravenous Infusion of Decitabine: Inhibition of Promoter-Specific and Global Genomic DNA Methylation
Authors: Samlowski Wolfram E. , Leachman Sancy A. , Wade Mark , Cassidy Pamela , Porter-Gill Patricia , Busby Leslie , Wheeler Richard , Boucher Kenneth , Fitzpatrick Frank , Jones David A. , Karpf Adam R. 
Published: March 2005

Purpose The nucleoside analog 5-aza-2′-deoxycytidine (5-aza-CdR, decitabine) is a potent inhibitor of DNA methylation in vitro. Cellular treatment with this agent induces the re-expression of methylation-silenced genes. It remains unclear to what extent this compound inhibits DNA methylation in vivo. A clinical study was designed to examine the molecular effects and toxicity of a continuous 1-week intravenous infusion of decitabine in solid tumor patients. Methods Ten patients with refractory solid tumors were included in this study. Decitabine was administered at 2 mg/m2/d via continuous infusion for 168 hours. Quantitative polymerase chain reaction and high performance liquid chromatography were utilized to measure promoter-specific and global DNA methylation in peripheral-blood cells before and after treatment. Results Transient grade III/IV neutropenia (two patients) and grade II thrombocytopenia (one patient) was observed at the lowest planned dose step (2 mg/m2/d for 7 days). Nonhematologic toxicities were not observed. Quantitative polymerase chain reaction demonstrated significant MAGE-1 promoter hypomethylation by 14 days after the start of treatment in all 13 treatment cycles examined. Significant genomic DNA hypomethylation was also seen by day 14 in 11 of 13 treatment cycles analyzed. Genomic DNA methylation reverted to baseline levels by 28 to 35 days after the start of treatment, demonstrating that inhibition of DNA methylation by decitabine is transient. Conclusion A 168-hour continuous infusion of decitabine is well tolerated and results in the inhibition of promoter-specific and genomic DNA methylation in vivo. This treatment schedule is suitable for evaluation of decitabine in combination with agents whose activity may be enhanced by the reversal of DNA methylation–mediated gene silencing.
Slow-moving predatory gastropods track prey odors in fast and turbulent flow
Authors: Ferner Matthew C. , Weissburg Marc J. 
Published: March 2005

SUMMARYOlfactory searching by aquatic predators is reliant upon the hydrodynamic processes that transport and modify chemical signals. Previous studies indicate that the search behavior of some benthic crustaceans is hindered by rapid water flow and turbulent mixing of prey chemicals, but different sensory strategies employed by other taxa might offset such detrimental effects. Using a laboratory flume, we investigated the odor-tracking behavior of a marine gastropod whelk (Busycon carica) to test the generalization that turbulence interferes with chemically mediated navigation. We exposed individual whelks to turbulent odor plumes in free-stream velocities of 1.5,5, 10 or 15 cm s–1, or with one of two obstructions placed upstream of the odor source in an intermediate flow of 5 cm s–1. Measurements of velocity and stimulus properties confirmed that obstruction treatments increased turbulence intensity and altered the fine-scale structure of downstream odor plumes. In all conditions tested, between 36–63% of test animals successfully located the odor source from 1.5 m downstream with no significant effect of flow treatment. Search behaviors, such as cross-stream meander were reduced at higher flow velocities and in the presence of obstructions, allowing whelks to reach the odor source significantly more quickly than in slower, less turbulent conditions. Our results demonstrate that whelks can respond to chemical information in fast and turbulent flow, and we suggest that these slow-moving predators can forage in hydrodynamic environments where the olfactory abilities of other taxa are limited.
Empirical estimation of free testosterone from testosterone and sex hormone-binding globulin immunoassays
Authors: Ly Lam P , Handelsman David J 
Published: March 2005

Background: The growing interest in measuring blood free testosterone (FT) is constrained by the unsuitability of the laborious reference methods for wider adoption in routine diagnostic laboratories. Various alternative derived testosterone measures have been proposed to estimate FT from either additional assay steps or calculations using total testosterone (TT) and sex hormone-binding globulin (SHBG) measured in the same sample. However, none have been critically validated in large numbers of blood samples.Methods: We analyzed a large dataset comprising over 4000 consecutive blood samples in which FT as well as TT and SHBG were measured. Dividing the dataset into samples with blood TT above and below 5 nM, using a bootstrap regression modeling approach guided by Akaike Information Criterion for model selection to balance parsimony against reduction of residual error, empirical equations were developed for FT in terms of TT and SHBG.Results: Comparison between the empirical FT equations with the laboratory FT measurements as well as three widely used calculated FT methods showed the empirical FT formulae had superior fidelity with laboratory measurements while previous FT formulae overestimated and deviated systematically from the laboratory FT values.Conclusion: We conclude that these simple, assumption-free empirical FT equations can estimate accurately blood FT from TT and SHBG measured in the same samples with the present assay methods and have suitable properties for wider application to evaluate the clinical utility of blood FT measurements.
Diabetes and premature menopause: is their co-existence detrimental to the skeleton?
Authors: Hadjidakis D J , Mylonakis A M , Sfakianakis M E , Raptis A E , Raptis S A 
Published: March 2005

Objective: Premature menopause is a known risk factor for osteoporosis, whilst the influence of type 2 diabetes on bone mineral density (BMD) is still controversial.
Design and methods: BMD values assessed by dual-energy X-ray absorptiometry (DXA) in L2–L4 vertebrae and the femoral neck (FN) of 40 diabetic women with premature menopause (D-EMP) were compared with those of 60 non-diabetic, prematurely menopausal women (EMP) and 60 diabetic women with normal menopause (D-NMP) who had been matched by age and body mass index (BMI). In all women, the time elapsed since menopause ranged between 10 and 25 years and the duration of diabetes exceeded 75% of the postmenopausal time period. The age of D-EMP women was 58.7±5 years (mean±1 s.d.), age at menopause 39.5±2.7, years since menopause 18.6±4.9, BMI 27.8±4.3 kg/m2 and duration of diabetes 13.9±3.9 years.
Results: Vertebral BMD values of D-EMP women were significantly higher than those of EMP women (0.908±0.135 vs. 0.817±0.14 g/cm2, P = 0.002), although there was no significant difference between D-EMP and D-NMP women (0.886±0.15 g/cm2). No significant differences were observed in FN BMD values between all groups. Age-adjusted BMD values (Z scores) of D-EMP women were higher than EMP women in both anatomic sites (P < 0.01), but did not differ from D-NMP women. In contrast to the other two groups, no statistically significant correlation was observed in D-EMP women between the BMD values of either anatomic area and the time elapsed since menopause. HbA1c values were positively correlated only to vertebral BMD values of the D-EMP group (P < 0.05). No correlation was observed between the BMD values and the duration of diabetes either in D-EMP or in D-NMP women.
Conclusions: Type 2 diabetes seems to positively affect the mineral density of the trabecular bone in women with premature menopause. The duration of diabetes does not appear to influence bone mass.
The natural history of post-traumatic neurohypophysial dysfunction
Authors: Agha Amar , Sherlock Mark , Phillips Jack , Tormey William , Thompson Christopher J 
Published: March 2005

Background and objectives: Posterior pituitary function remains poorly investigated after traumatic brain injury (TBI). We report the results of a study designed to prospectively define the natural history of post-traumatic diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone secretion (SIADH) using standard reliable methodology.Design and methods: 50 consecutive patients with severe or moderate TBI (initial Glasgow Coma Scale (GCS) score 3/15–13/15) were prospectively studied on three occasions: at the acute phase and at 6 months and at 12 months following TBI. In the acute phase, DI was diagnosed either by the presence of hypernatraemia in association with hypotonic polyuria or by the water-deprivation test (WDT) and, at 6 and 12 months by the WDT in all patients. Normative data on response to the WDT were obtained from healthy matched volunteers. Functional outcome was assessed using the Glasgow Outcome Scale (GOS).Results: 13 patients (26%) had DI in the acute post-TBI phase, of whom nine patients recovered by 6 months and one additional patient recovered by 12 months. Of the remaining three patients with permanent DI, two had partial vasopressin deficiency. Acute-phase peak plasma osmolality correlated negatively with the initial GCS scores (r= −0.39,P= 0.005) and with the GOS scores (r= −0.45,P= 0.001). Seven patients had SIADH in the acute phase of TBI but none did at 6 or 12 months. No new cases of DI or SIADH were noted after the acute phase.Conclusion: This prospective study shows that posterior pituitary dysfunction is common following TBI. Most cases recover completely but there is an appreciable frequency of long-term DI which can be subtle and should be recognized and managed appropriately.
Novel insecticides: Modes of action and resistance mechanism
Authors: Ishaaya Isaac 
Published: March 2005

AbstractEfforts have been made during the past three decades to develop insecticides with selective properties that act specifically on biochemical sites present in particular insect groups, but whose properties differ from other insecticides. This approach has led to the discovery of compounds that affect the hormonal regulation of molting and developmental processes in insects, e.g., ecdysone agonists (tebufenozide and methoxyfenozide), juvenile hormone mimics (pyriproxyfen and fenoxycarb), and chitin synthesis inhibitors (benzoylphenyl ureas and buprofezin). In addition, compounds that selectively interact with the insect nicotinic acetylcholine receptor such as imidacloprid, acetamiprid, and thiamethoxam have been introduced for the control of aphids, whiteflies, and other insect species.In this issue, we report on some new insecticides that fit the current approach of pest management programs, such as the new non‐steroidal ecdysone agonist THQ [1‐aroyl‐4‐(arylamino)1,2,3,4‐tetrahydroquinoline], which acts preferentially against mosquitoes with no appreciable effect on other insect groups or mammals. The mode of action of this compound, along with its selectivity, is discussed in detail in the report of Palli et al. Another novel compound reported in this issue is pyradalyl (S‐1812), which was found to act selectively on lepidopterans and thrips. In laboratory assays, pyradalyl was found to act on insect cell lines with no appreciable effect on mammal cell lines. The potential use of this compound in agricultural systems is discussed by Isayama et al.Three reports in this issue deal with resistance mechanisms and resistance management of novel insecticides. Nauen et al. present an up‐to‐date review on insect resistance mechanisms to neonicotinoids and ways to optimize their use in pest management programs. Horowitz et al. report on Bemisia tabaci biotypes B and Q and their resistance to neonicotinoids and pyriproxyfen. One of the most striking findings in their report is that the Q biotype develops resistance to pyriproxyfen and neoicotinopid faster than biotype B, while the latter exhibits better fitness. The practical implications of these findings are discussed. In another report, Ishaaya et al. present a study detailing the toxicity and cross‐resistance of selected biorational insecticides. Their findings indicate that no appreciable cross‐resistance was observed between the benzoylphenyl urea, novaluron, the juvenile hormone mimic, pyriproxyfen, and the neonicotinoids, acetamiprid and imidacloprid. Hence, these compounds could be used, in alternation, as components in insecticide resistance management programs.
Biotypes B and Q of Bemisia tabaci and their relevance to neonicotinoid and pyriproxyfen resistance
Authors: Horowitz A. Rami , Kontsedalov Svetlana , Khasdan Vadim , Ishaaya Isaac 
Published: March 2005

AbstractResistance monitoring for Bemisia tabaci field populations to the juvenile hormone mimic, pyriproxyfen, was conducted from 1996 to 2003 in commercial cotton fields in two areas of Israel: the Ayalon Valley (central Israel) and the Carmel Coast (northwestern Israel). Although the use of pyriproxyfen ceased in these areas in 1996–1997 (because of the resistance), resistance levels to pyriproxyfen declined to some extent in the fields but remained quite stable, and the susceptibility has not been totally restored. Two strains of B. tabaci collected from the Ayalon Valley in the late 1999 and 2002 cotton seasons (AV99L, AV02L) were assayed for their susceptibility to pyriproxyfen at F1, and subsequently a line of each strain was kept under controlled conditions without exposure to insecticides. After maintenance of more than 20 generations under laboratory conditions, the resistance to pyriproxyfen in the untreated strains substantially declined. This decline was concurrent with a replacement of Q biotype by B‐type under non‐insecticidal regimes; apparently B biotype was more competitive than the pyriproxyfen‐resistant Q‐type. Selection under controlled conditions with neonicotinoids on these B. tabaci strains resulted in continued pyriproxyfen resistance, predominantly of Q biotype. Based on our data, applications of either pyriproxyfen or neonicotinoids may select for biotype Q, which would survive to a greater degree where these insecticides are applied. Arch. Insect Biochem. Physiol. 58:216–225, 2005. © 2005 Wiley‐Liss, Inc.
Smart Polyion Complex Micelles for Targeted Intracellular Delivery of PEGylated Antisense Oligonucleotides Containing Acid‐Labile Linkages
Authors: Oishi Motoi , Nagatsugi Fumi , Sasaki Shigeki , Nagasaki Yukio , Kataoka Kazunori 
Published: March 2005

AbstractA novel pH‐sensitive and targetable antisense ODN delivery system based on multimolecular assembly into polyion complex (PIC) micelles of poly(L‐lysine) (PLL) and a lactosylated poly(ethylene glycol)–antisense ODN conjugate (Lac‐PEG–ODN) containing an acid‐labile linkage (β‐propionate) between the PEG and ODN segments has been developed. The PIC micelles thus prepared had clustered lactose moieties on their peripheries and achieved a significant antisense effect against luciferase gene expression in HuH‐7 cells (hepatoma cells), far more efficiently than that produced by the nonmicelle systems (ODN and Lac‐PEG–ODN) alone, as well as by the lactose‐free PIC micelle. In line with this pronounced antisense effect, the lactosylated PIC micelles showed better uptake than the lactose‐free PIC micelles into HuH‐7 cells; this suggested the involvement of an asialoglycoprotein (ASGP) receptor‐mediated endocytosis process. Furthermore, a significant decrease in the antisense effect (27 % inhibition) was observed for a lactosylated PIC micelle without an acid‐labile linkage (thiomaleimide linkage); this suggested the release of the active (free) antisense ODN molecules into the cellular interior in response to the pH decrease in the endosomal compartment is a key process in the antisense effect. Use of branched poly(ethylenimine) (B‐PEI) instead of the PLL for PIC micellization led to a substantial decrease in the antisense effect, probably due to the buffer effect of the B‐PEI in the endosome compartment, preventing the cleavage of the acid‐labile linkage in the conjugate. The approach reported here is expected to be useful for the construction of smart intracellular delivery systems for antisense ODNs with therapeutic value.
Tumor suppressor gene Runx3 sensitizes gastric cancer cells to chemotherapeutic drugs by downregulating Bcl‐2, MDR‐1 and MRP‐1
Authors: Guo Changcun , Ding Jie , Yao Liping , Sun Li , Lin Tao , Song Ying , Sun Lijun , Fan Daiming 
Published: March 2005

AbstractThe Runx3 gene is a member of the runt domain family transcription factors, key regulators of development and differentiation in metazoan. Recently, Runx3 was identified as a tumor suppressor gene. Loss of Runx3 was found to be associated with genesis and progression of gastric cancer. In this study, we transfected the gastric cancer cell line SGC7901 with eukaryotic expression vector of Runx3. In vitro drug sensitivity assay suggested that SGC7901/Runx3 cells were more sensitive to various chemotherapeutic drugs. Blocking Runx3 expression in immortalized stomach mucosal cells (GES‐1) or gastric cancer cells (SGC7901) by Runx3‐specific small interfering RNA conferred the cells resistance to chemotherapeutic drugs. Flow cytometry examination suggested that expression of Runx3 in gastric cancer cells increased the intracellular accumulation and retention of adriamycin. Semiquantitative RT‐PCR and Western blot suggested that Runx3 downregulated expression of Bcl‐2, MDR‐1 (P‐gp) and MRP‐1. Binding of Runx3 to promoter sequences of Bcl‐2, MDR‐1 and MRP‐1 gene was detected by eletrophoretic mobility shift assay (EMSA) and supershift EMSA. We cloned the MDR‐1 and MRP‐1 gene promoters containing Runx binding sites and constructed the luciferase reporter vectors of these 2 promoters. Luciferase reporter assay suggested that Runx3 inhibited the promoter activity of the MDR‐1 and MRP‐1 promoter in SGC7901 cells. Taken together, our findings suggested that overexpression of Runx3 could sensitize gastric cancer cells to chemotherapeutic drugs by downregulating the Bcl‐2, MDR‐1 and MRP‐1. © 2005 Wiley‐Liss, Inc.
Peripheral blood IFN‐γ‐secreting Vα24+Vβ11+ NKT cell numbers are decreased in cancer patients independent of tumor type or tumor load
Authors: Molling Johan W. , Kölgen Wendy , van der Vliet Hans J.J. , Boomsma Martijn F. , Kruizenga Hinke , Smorenburg Carolien H. , Molenkamp Barbara G. , Langendijk Johannes A. , Leemans C. René , von Blomberg B. Mary E. , Scheper Rik J. , van den Eertwegh Alfons J.M. 
Published: March 2005

AbstractNatural killer T (NKT) cells are CD1d‐restricted lymphoid cells and are characterized by an invariant T‐cell receptor, which in humans consists of a Vα24 chain paired with a Vβ11 chain. These cells are known for their rapid production of large amounts of cytokines (e.g., IFN‐γ and IL‐4), thereby modulating other cells of the immune system such as T cells, NK cells and dendritic cells. NKT cells have been reported to play important regulatory roles in many immune responses, including antitumor immune responses. Here, we demonstrate an age‐dependent decrease in circulating Vα24+Vβ11+ NKT cell numbers in both healthy controls and cancer patients and demonstrate that in both groups females have higher NKT cell levels compared to males. In a large group of 120 cancer patients, we show that circulating Vα24+Vβ11+ NKT cell numbers are about 50% lower than in age‐ and gender‐matched healthy controls and that this decrease is independent of tumor type or tumor load. This decrease was not restored upon tumor removal by means of surgery or radiotherapy. Even though the percentage of NKT cells that secrete IFN‐γ, as detected by ELISPOT, is normal in cancer patients, the absolute number of circulating IFN‐γ‐secreting NKT cells is reduced. Together, our results suggest that the reduced circulating Vα24+Vβ11+ NKT cell numbers in cancer patients are not affected by tumor load, but might actually reflect a risk factor for tumor development, e.g., by hampering efficient tumor immunosurveillance. © 2005 Wiley‐Liss, Inc.
Effect of diffuse fatty infiltration of the liver on hepatic artery resistance index
Authors: Mihmanli Ismail , Kantarci Fatih , Yilmaz Mehmet Halit , Gurses Bengi , Selcuk Dogan , Ogut Gunduz , Altug Ayca , Uysal Omer 
Published: March 2005

AbstractPurposeThis study was conducted to evaluate the effect of various degrees of diffuse fatty infiltration of the liver on the hepatic artery resistance index.MethodsOne‐hundred forty subjects were examined using standard color and spectral Doppler sonography protocols. Fatty infiltration of the liver was identified and graded sonographically. The patients were grouped (n = 35 in each of 4 groups) according to the degree of diffuse fatty infiltration of the liver as follows: normal (group 1), mild (group 2), moderate (group 3), and severe (group 4). The resistance index calculated for each patient was the mean of 3 measurements. Mean resistance index of the hepatic artery was then calculated for each group.ResultsThe mean resistance index was 0.81 ± 0.04 for group 1, 0.79 ± 0.06 for group 2, 0.75 ± 0.05 for group 3, and 0.73 ± 0.05 for group 4. We found a statistically significant (p < 0.05) decrease in resistance index when comparing groups 3 and 4 with groups 1 and 2 separately.ConclusionsHepatic artery resistance index decreases as the severity of diffuse fatty infiltration increases. © 2005 Wiley Periodicals, Inc. J Clin Ultrasound 33:95–99, 2005
Acid‐induced morphological transition of block copolymer brush adsorbed on mica surface
Authors: Cong Yang , Fu Jun , Li Jian , Han Yanchun 
Published: March 2005

AbstractThe morphology and morphological transformation of polystyrene‐block‐poly(4‐vinylpyridine) (PS‐b‐P4VP) brushes on mica surfaces have been investigated. PS‐b‐P4VP brushes were adsorbed onto mica surfaces when dip‐coated from dilute solutions because of the strong polar adhesive interaction between the mica surface and the 4VP segments. Porous, bicontinuous layers and isolated clusters were obtained, depending on the concentration of the copolymer solution. These brushes can respond to the acid treatment, adopting elongated conformation. As a result, the relative height of the brushes increased and the lateral dimension decreased. Copyright © 2005 Society of Chemical Industry