bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Critical Appraisal of the Continuous Glucose–Error Grid Analysis
Authors: Wentholt Iris M. , Hoekstra Joost B. , DeVries J. Hans 
Published: July 2006

OBJECTIVE—There is no consensus on how to optimally assess the accuracy of continuous glucose sensors. We examined the continuous glucose–error grid analysis (CG-EGA) and compared it with classical accuracy assessment methods, using data from a previously reported study comparing two different continuous glucose sensors in type 1 diabetic patients.
RESEARCH DESIGN AND METHODS—Drift, delay, mean absolute difference (MAD), sensitivity, and specificity for detecting hypo- and hyperglycemia were calculated, and a Clarke error grid and a CG-EGA were constructed for both sensors, also including an examination of the influence of choosing different time intervals for paired sensor and reference glucose values.
RESULTS—For sensor II, there was a delay between blood glucose and sensed glucose (7.1 min, P &lt; 0.001). Sensor II was more accurate than sensor I during hypo- and hyperglycemia (e.g., smaller MAD, P = 0.011 and P = 0.024, respectively; better sensitivity for detecting hypoglycemia, P = 0.018). Correction for the 7-min delay improved sensor II MAD with 2.2% in every range. In contrast, CG-EGA did not reveal a difference in accuracy between the sensors. Paradoxically, CG-EGA results for sensor II deteriorated when corrected for the delay. CG-EGA calculated with shorter time intervals resulted in worsening accuracy for both sensors.
CONCLUSIONS—CG-EGA did not detect differences in accuracy whereas conventional methods did. CG-EGA is time demanding; results are hard to interpret and seem to vary with chosen time intervals. At present, CG-EGA does not contribute to a combination of various established assessment methods.
A Clinico-microbiological Study of Diabetic Foot Ulcers in an Indian Tertiary Care Hospital
Authors: Gadepalli Ravisekhar , Dhawan Benu , Sreenivas Vishnubhatla , Kapil Arti , Ammini A.C. , Chaudhry Rama 
Published: July 2006

OBJECTIVE—To determine the microbiological profile and antibiotic susceptibility patterns of organisms isolated from diabetic foot ulcers. Also, to assess potential risk factors for infection of ulcers with multidrug-resistant organisms (MDROs) and the outcome of these infections.
RESEARCH DESIGN AND METHODS—Pus samples for bacterial culture were collected from 80 patients admitted with diabetic foot infections. All patients had ulcers with Wagner’s grade 3–5. Fifty patients (62.5%) had coexisting osteomyelitis. Gram-negative bacilli were tested for extended spectrum β-lactamase (ESBL) production by double disc diffusion method. Staphylococcal isolates were tested for susceptibility to oxacillin by screen agar method, disc diffusion, and mec A–based PCR. Potential risk factors for MDRO-positive samples were explored.
RESULTS—Gram-negative aerobes were most frequently isolated (51.4%), followed by gram-positive aerobes and anaerobes (33.3 and 15.3%, respectively). Seventy-two percent of patients were positive for MDROs. ESBL production and methicillin resistance was noted in 44.7 and 56.0% of bacterial isolates, respectively. MDRO-positive status was associated with presence of neuropathy (P = 0.03), osteomyelitis (P = 0.01), and ulcer size &gt;4 cm2 (P &lt; 0.001) but not with patient characteristics, ulcer type and duration, or duration of hospital stay. MDRO-infected patients had poor glycemic control (P = 0.01) and had to be surgically treated more often (P &lt; 0.01).
CONCLUSIONS—Infection with MDROs is common in diabetic foot ulcers and is associated with inadequate glycemic control and increased requirement for surgical treatment. There is a need for continuous surveillance of resistant bacteria to provide the basis for empirical therapy and reduce the risk of complications.
Evidence for Independent Heritability of the Glycation Gap (Glycosylation Gap) Fraction of HbA1c in Nondiabetic Twins
Authors: Cohen Robert M. , Snieder Harold , Lindsell Christopher J. , Beyan Huriya , Hawa Mohammed I. , Blinko Stuart , Edwards Raymond , Spector Timothy D. , Leslie R. David G. 
Published: July 2006

OBJECTIVE—HbA1c (A1C) is substantially determined by genetic factors not shared in common with glucose. Fractions of the variance in A1C, the glycation gap (GG; previously called the glycosylation gap) and the hemoglobin glycosylation index, correlate with diabetes complications. We therefore tested whether GG (measured A1C − A1C predicted from glycated serum proteins [GSPs]) was genetically determined and whether it accounted for the heritability of A1C.
RESEARCH DESIGN AND METHODS—We conducted a classic twin study on A1C and GSP collected in 40 and 46 pairs of monozygotic and dizygotic healthy female twins, respectively. The predicted A1C was based on the regression line between A1C and GSP in a separate population spanning the pathophysiologic range.
RESULTS—GG was more strongly correlated between monozygotic (r = 0.65) than dizygotic (r = 0.48) twins, adjusted for age and BMI. The best-fitting quantitative genetic model adjusted for age and BMI showed that 69% of population variance in GG is heritable, while the remaining 31% is due to unique environmental influences. In contrast, GSP was similarly correlated between monozygotic (r = 0.55) and dizygotic (r = 0.49) twins, hence not genetically determined. GG was strongly correlated to A1C (r = 0.48), attributable mostly to genetic factors. About one-third of the heritability of A1C is shared with GG; the remainder is specific to A1C.
CONCLUSIONS—Heritability of the GG accounts for about one-third of the heritability of A1C. By implication, there are gene(s) that preferentially affect erythrocyte lifespan or glucose and/or nonenzymatic glycation or deglycation in the intracellular, rather than extracellular, compartment.
Assessing the Outcome of the Management of Diabetic Foot Ulcers Using Ulcer-Related and Person-Related Measures
Authors: Jeffcoate William J. , Chipchase Susan Y. , Ince Paul , Game Fran L. 
Published: July 2006

OBJECTIVE—The purpose of this study was to compare different outcome measures in the audit of management of diabetic foot ulcersRESEARCH DESIGN AND METHODS—Data collected prospectively in a consecutive cohort of patients referred to a specialist multidisciplinary foot care clinic between 1 January 2000 and 31 December 2003 were analyzed. A single index ulcer was selected for each patient and classified according to both the Size (Area and Depth), Sepsis, Arteriopathy, and Denervation [S(AD)SAD] and University of Texas (UT) systems. Ulcer-related outcomes (healing, resolution by ipsilateral amputation or by death, and persisting unhealed) were determined at 6 and 12 months and compared with patient-related outcomes (survival, any amputation, and being free from any ulcer) at 12 months.RESULTS—In 449 patients (63.7% male, mean age 66.7 ± 13.2 years), 352 (78.4%) ulcers were superficial [S(AD)SAD/UT grade 1] and 134 of these (38.1% of 352) were neither ischemic nor infected. A total of 183 (40.8% of 449) ulcers were clinically infected, and peripheral arterial disease was present in 216 patients (48.1%). Seventeen patients (3.8%) were lost to follow-up and were excluded from analysis. Of the ulcers, 247 (55.0% of 449) and 295 (65.7%) healed without amputation by 6 and 12 months, respectively. Median (range) time to healing was 78 (7–364) days. Of all index ulcers, 5.8 and 8.0% were resolved by amputation, and 6.2 and 10.9% by death by the same time points; 27.8 and 11.6% persisted unhealed. In contrast, patient-related outcomes revealed that of 449 patients only 202 (45.0%) were alive, without amputation, and ulcer free at 12 months. This group had had 272 (1–358) days without any ulcer. A total of 48 (10.7%) patients had undergone some form of amputation, and 75 (16.7%) had died.CONCLUSIONS—These data illustrate the extent to which ulcer-related outcomes may underestimate the true morbidity and mortality associated with diabetic foot disease. It is suggested that when attempts are made to compare the effectiveness of management in different centers, greater emphasis should be placed on patient-related outcome measures.
Prevalence of Cardiovascular Disease Risk Factors in U.S. Children and Adolescents With Diabetes
Authors: Rodriguez Beatriz L. , Fujimoto Wilfred Y. , Mayer-Davis Elizabeth J. , Imperatore Giuseppina , Williams Desmond E. , Bell Ronny A. , Wadwa R. Paul , Palla Shana L. , Liu Lenna L. , Kershnar Ann , Daniels Stephen R. , Linder Barbara ,   for the SEARCH for Diabetes in Youth Study Group
Published: July 2006

OBJECTIVE—The purpose of this study was to determine the prevalence and correlates of selected cardiovascular disease (CVD) risk factors among youth aged &lt;20 years with diabetes.
RESEARCH DESIGN AND METHODS—The analysis included 1,083 girls and 1,013 boys examined as part of the SEARCH for Diabetes in Youth study, a multicenter, population-based study of youth 0–19 years of age with diabetes. Diabetes type was determined by a biochemical algorithm based on diabetes antibodies and fasting C-peptide level. CVD risk factors were defined as follows: HDL cholesterol &lt;40 mg/dl; age- and sex-specific waist circumference &gt;90th percentile; systolic or diastolic blood pressure &gt;90th percentile for age, sex, and height or taking medication for high blood pressure; and triglycerides &gt;110 mg/dl.
RESULTS—The prevalence of having at least two CVD risk factors was 21%. The prevalence was 7% among children aged 3–9 years and 25% in youth aged 10–19 years (P &lt; 0.0001), 23% among girls and 19% in boys (P = 0.04), 68% in American Indians, 37% in Asian/Pacific Islanders, 32% in African Americans, 35% in Hispanics, and 16% in non-Hispanic whites (P &lt; 0.0001). At least two CVD risk factors were present in 92% of youth with type 2 and 14% of those with type 1A diabetes (P &lt; 0.0001). In multivariate analyses, age, race/ethnicity, and diabetes type were independently associated with the odds of having at least two CVD risk factors (P &lt; 0.0001).
CONCLUSIONS—Many youth with diabetes have multiple CVD risk factors. Recommendations for weight, lipid, and blood pressure control in youth with diabetes need to be followed to prevent or delay the development of CVD as these youngsters mature.
Isn’t This Just Bedtime Snacking?
Authors: Morse Shereen A. , Ciechanowski Paul S. , Katon Wayne J. , Hirsch Irl B. 
Published: July 2006

OBJECTIVE—Night-eating syndrome is characterized by excessive eating in the evening and nocturnal awakening with ingestion of food. Psychosocial variables and emotional triggers may be associated with these behaviors. In patients with diabetes, such behaviors may lead to glucose dysregulation and contribute to obesity and complications.
RESEARCH DESIGN AND METHODS—In 714 tertiary care patients with type 1 and 2 diabetes, we determined the proportion of patients reporting eating &gt;25% of their daily food intake after regular suppertime. We also screened patients for major depression, childhood maltreatment histories, nonsecure attachment styles, and emotional eating triggers. We examined whether patients reporting night-eating behaviors had greater psychosocial distress, higher HbA1c (A1C) levels, more obesity, and more diabetes complications compared with patients without night-eating behaviors.
RESULTS—Night-eating behaviors were reported in 9.7% of patients. Compared with patients without night-eating behaviors, those with these behaviors were less adherent with diet, exercise, and glucose monitoring and more likely to be depressed, to report childhood maltreatment histories, to have nonsecure attachment styles, and to report eating in response to anger, sadness, loneliness, worry, and being upset. Controlling for age, sex, race, and major depression, patients with night-eating behaviors, compared with patients without night-eating behaviors, were more likely to be obese (odds ratio 2.6 [95% CI 1.5–4.5]), to have A1C values &gt;7% (2.2 [1.1–4.1]) and to have two or more diabetes complications (2.6 [1.5–4.5]).
CONCLUSIONS—Night-eating behaviors are associated with adverse outcomes in patients with diabetes. Use of clinical screening tools may help identify patients with night-eating behaviors.
Advantage of Premeal-Injected Insulin Glulisine Compared With Regular Human Insulin in Subjects With Type 1 Diabetes
Authors: Rave Klaus , Klein Oliver , Frick Annke D. , Becker Reinhard H.A. 
Published: July 2006

OBJECTIVE—Insulin glulisine, a rapid-acting insulin analog, provides prandial insulin replacement. In this study, we compared postprandial blood glucose control after pre- and postmeal insulin glulisine with regular human insulin (RHI).
RESEARCH DESIGN AND METHODS—In a single-dose, randomized, four-way complete cross-over study, subjects received standardized, 15-min meals, covered by subcutaneous injections of either insulin glulisine (immediately premeal or 15 min postmeal; 0.15 unit/kg per injection) or RHI (30 min or immediately premeal; 0.15 unit/kg per injection). Twenty-one patients with type 1 diabetes (mean age 36.4 years; mean BMI 26.0 kg/m2) were enrolled; 20 patients completed the study. Postprandial baseline-subtracted blood glucose exposure, maximum excursion, maximum and minimum blood glucose concentrations, and time to the maximum excursion and minimum concentration were assessed, along with serum insulin concentrations.
RESULTS—Lower maximum blood glucose excursion (65 vs. 89 mg/dl), total blood glucose exposure within 2 h (279 vs. 334 mg · h/dl, maximum blood glucose concentration (180 vs. 209 mg/dl), and less time to maximum blood glucose excursion (48 vs. 70 min) were seen with immediately premeal insulin glulisine versus immediately premeal RHI. The maximum serum concentration of insulin glulisine was almost double that of RHI (82 vs. 45 μU/ml), achieved in approximately half the time (55 vs. 97 min). Conversely, insulin glulisine (15 min postmeal) versus RHI (immediately premeal) and RHI (30 min premeal) versus insulin glulisine (immediately premeal) resulted in comparable blood glucose control.
CONCLUSIONS—Insulin glulisine renders postprandial glucose disposal closer to physiologic requirements compared with RHI and enables appropriate timing of prandial insulin administration.
Different Mechanisms for Impaired Fasting Glucose and Impaired Postprandial Glucose Tolerance in Humans
Authors: Meyer Christian , Pimenta Walkyria , Woerle Hans J. , Van Haeften Timon , Szoke Ervin , Mitrakou Asimina , Gerich John 
Published: July 2006

OBJECTIVE—To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done.
RESEARCH DESIGN AND METHODS—We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of β-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations.
RESULTS—Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased ∼30% (P &lt; 0.05), but clamp-determined insulin sensitivity was normal (P &gt; 0.8). HOMA-%B and first-phase insulin responses were reduced ∼35% (P &lt; 0.002) and ∼30% (P &lt; 0.02), respectively, but second-phase insulin responses were normal (P &gt; 0.5). NFG/IGT had normal HOMA-IR but ∼15% decreased clamp-determined insulin sensitivity (P &lt; 0.03). Furthermore, HOMA-%B was normal but both first-phase (P &lt; 0.0003) and second-phase (P &lt; 0.0001) insulin responses were reduced ∼30%. IFG/NGT differed from NFG/IGT by having ∼40% lower HOMA-%B (P &lt; 0.012) and ∼50% greater second-phase insulin responses (P &lt; 0.005).
CONCLUSIONS—Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity.
Harmful or Not: Trichostatin A treatment of embryos generated by ICSI or ROSI
Authors: Kishigami Satoshi , Ohta Hiroshi , Mizutani Eiji , Wakayama Sayaka , Bui Hong-Thuy , Thuan Nguyen , Hikichi Takafusa , Suetsugu Rinako , Wakayama Teruhiko 
Published: July 2006

AbstractTrichostatin A (TSA), a histone deacetylase inhibitor, is a known teratogen causing malformations such as vertebral fusions when applied during the postimplantation period; TSA also causes developmental arrest when applied during the preimplantation period. Regardless of these hindrances, we have succeeded in the establishment of an efficient somatic cloning method for the mouse where reconstructed embryos are treated with TSA. To elucidate this apparent discrepancy, we treated fertilized mouse embryos generated either by intracytoplasmic sperm injection (ICSI) or round spermatid injection (ROSI) with 50 nM TSA for 20 h after fertilization as well as parthenogenetic embryos and found that TSA treatment inhibited the preimplantation development of ICSI embryos but not ROSI or parthenogenetic embryos. And, although we often observed hypomorphism following TSA treatment in embryos grown to full term produced by both ICSI (av. of body weight: 1.7 g vs. 1.5 g) and ROSI (1.6 g vs. 1.2 g), TSA treatment reduced the offspring production rate for ICSI from 57% to 34% but not for ROSI from 30% to 36%. Thus, these data indicate that the effects, harmful or not, of TSA treatment on embryonic development depend on their nuclear derivations. Also, the resulting hypomorphism after TSA treatment is a caveat for this procedure in current Assisted Reproductive Technologies.
Enhanced expression of selenocysteine lyase in acute glomerulonephritis and its regulation by AP-1
Authors: Jafari Claudia , Panzer Ulf , Steinmetz Oliver , Zahner Gunther , Stahl Rolf , Harendza Sigrid 
Published: July 2006

AbstractAcute glomerulonephritis can lead to chronic glomerulonephritis or resolve without permanent damage to the kidneys. Differential gene expression was studied in a model of acute and chronic glomerulonephritis to identify factors influencing the course of glomerulonephritis towards healing or chronification. One of the differentially expressed genes was identified as SCL, encoding selenocysteine lyase. Its expression was higher in acute glomerulonephritis and lower in chronic glomerulonephritis. The transcriptional regulation of SCL was studied in vitro in rat mesangial cells (MC). SCL RNA expression increased eight-fold compared to the baseline after stimulation with interleukin-1β (IL-1β) for three hours. Luciferase expression and gel shift experiments revealed an enhancer element between bp −152 and −298 of the SCL 5’-regulatory region, with protein binding to an AP-1 binding site that may be involved in the regulation of SCL-RNA in vivo in an endogenous feedback mechanism to the inflammatory reaction in acute glomerulonephritis, leading to resolution of this disease.
Quantum Dots in Biological and Biomedical Research: Recent Progress and Present Challenges
Authors: Klostranec J. M. , Chan W. C. W. 
Published: July 2006

AbstractThe marriage of nanomaterials with biology has produced a new generation of technologies that can profoundly impact biological and biomedical research. Quantum dots (Qdots) are an archetype for this hybrid research area and have gained popularity and interest from diverse research communities because of their unique and tunable optical properties. In this Review, we will describe their history and development, optical and electronic properties, and applications in biology and medicine. A critical evaluation of barriers impacting current Qdot technologies will be discussed and insights into the future outlook of the field will be explored.
Inside Front Cover: Direct Printing of 3D and Curvilinear Micrometer‐Sized Architectures into Solid Substrates with Sub‐micrometer Resolution (Adv. Mater. 15/2006)
Authors: Campbell C. J. , Smoukov S. K. , Bishop K. J. M. , Baker E. , Grzybowski B. A. 
Published: July 2006

AbstractThe inside cover shows a hexagonal array of convex microlenses etched directly into glass using a reaction‐diffusion process initiated from a hydrogel stamp. The technique, reported by Grzybowski and co‐workers on p. 2004, allows for direct printing of complex microarchitectures into a variety of materials with sub‐micrometer resolution. The images were generated by longtime exposure of slowly rotating patterns. Cover design by Christopher J. Campbell.
Durometry for the assessment of skin disease in systemic sclerosis
Authors: Kissin Eugene Y. , Schiller Aileen M. , Gelbard Rondi B. , Anderson Jennifer J. , Falanga Vincent , Simms Robert W. , Korn Joseph H. , Merkel Peter A. 
Published: July 2006

AbstractObjectiveTo examine the validity of a durometer to objectively measure skin hardness in systemic sclerosis (SSc), and to compare digital durometry with the modified Rodnan skin score (MRSS) and ultrasonography.MethodsPatients with SSc and healthy controls underwent durometry measurements in 3 assessments: a Latin square experiment to establish durometry's intra‐ and interobserver reliability compared with skin scoring (5 SSc, 1 control); a longitudinal cohort to assess sensitivity to change in skin hardness (13 SSc, 5 controls); and an ultrasound cohort to evaluate correlation between durometry, ultrasound‐measured skin thickness, and clinical skin scoring (30 SSc, 12 controls).ResultsIntraobserver reproducibility was higher for durometry than for clinical skin scoring (intraclass correlation coefficient [ICC] 0.97 versus 0.85), whereas interobserver reproducibility was similar (0.75 versus 0.73). Interobserver reproducibility of durometry was good for all body areas (ICC 0.61–0.85), but for skin scoring it was moderate in the legs (0.51) and poor in the abdomen (0.08), feet (0.09), and fingers (0.27). Durometry scores correlated with clinical skin scores (Latin square: r = 0.44, P = 0.03; longitudinal cohort: r = 0.81, P < 0.001) and ultrasound‐measured skin thickness (hands: r = 0.58, forearms: r = 0.63, upper arms: r = 0.40; P ≤ 0.001 for all). Uninvolved skin in patients with SSc was harder than skin from controls (mean ± SD 23 ± 7 durometer units [DU] versus 19 ± 6 DU; P < 0.0001). Finally, there was a strong correlation between change in MRSS and change in durometry score (r = 0.77, P = 0.002).ConclusionDurometer‐measured skin hardness correlates well with MRSS and ultrasound‐measured skin thickness, provides greater reliability than MRSS, and is sensitive to changes in skin hardness over time. Durometry should be considered for use in clinical therapeutic SSc trials.