NO2 gas sensing performance enhancement based on reduced graphene oxide decorated V2O5 thin films.

Here, we demonstrate improved NO2 gas sensing properties based on reduced graphene oxide (rGO) decorated V2O5 thin film. Excluding the DC sputtering grown V2O5 thin film, rGO was spread over V2O5 thin film by the drop cast method. The formation of several p-n heterojunctions was greatly affected by the current-voltage relation of the rGO-decorated V2O5 thin film due to the p-type and n-type nature of rGO and V2O5, respectively. Initially with rGO decoration on V2O5 thin film, current decreased in comparison to the pristine V2O5 thin film, whereas depositing rGO film on a glass substrate drastically increased current. Among all sensors, only the rGO-decorated V2O5 sensor revealed a maximum NO2 gas sensing response for 100 ppm at 150 °C, and it achieved an approximately 61% higher response than the V2O5 sensor. The elaborate mechanism for an extremely high sensing response is attributed to the formation and modulation of p-n heterojunctions at the interface of rGO and V2O5. In addition, the presence of active sites like oxygenous functional groups on the rGO surface enhanced the sensing response. On that account, sensors based on rGO-decorated V2O5 thin film are highly suitable for the purpose of NO2 gas sensing. They enable the timely detection of the gas, further protecting the ecosystem from its harmful effects.

(D-π-A)2-π-D-A type ferrocenyl bisthiazole linked triphenylamine based molecular systems for DSSC: synthesis, experimental and theoretical performance studies.

We have designed and synthesized ferrocenyl (donor) bisthiazole linked triphenylamine (donor) based donor-π-acceptor-π-donor-acceptor (D-π-A)2-π-D-A type dyes D1 and D2 by using Pd-catalyzed Sonogashira cross-coupling and Knoevenagel condensation reactions. Their photophysical, electrochemical and computational studies reveal strong donor-acceptor interaction. Dye sensitized solar cells (DSSCs) based on D1 and D2 exhibit power conversion efficiencies (PCE) of 6.33% and 5.03%, respectively. The higher PCE value of the D1 based DSSC is attributed to its enhanced short-circuit current (Jsc) and open-circuit current (Voc) and fill factor (FF) values because of the strong binding of the anchoring cyanoacrylic acid with the TiO2 surface as compared to the dicyanovinyl unit in D2. Time dependent density functional theory (TD-DFT) calculations at B3LYP level on dyes D1 and D2 were performed, which reveal that both dyes show HOMO-1 → LUMO as a major transition. Computational photovoltaic calculations also reveal that dye D1 has better electron injection (ΔGinject) from ELUMO to the conduction band (CB) of TiO2 as compared to dye D2, which is in good agreement with experimental results.

HLA class II gene associations in African American type 1 diabetes reveal a protective HLA-DRB1*03 haplotype.

AIMS: Owing to strong linkage disequilibrium between markers, pinpointing disease associations within genetic regions is difficult in European ancestral populations, most notably the very strong association of the HLA-DRB1*03-DQA1*05:01-DQB1*02:01 haplotype with Type 1 diabetes risk, which is assumed to be because of a combination of HLA-DRB1 and HLA-DQB1. In contrast, populations of African ancestry have greater haplotype diversity, offering the possibility of narrowing down regions and strengthening support for a particular gene in a region being causal. We aimed to study the human leukocyte antigen (HLA) region in African American Type 1 diabetes. METHODS: Two hundred and twenty-seven African American patients with Type 1 diabetes and 471 African American control subjects were tested for association at the HLA class II genes, HLA-DRB1, HLA-DQA1, HLA-DQB1 and 5147 single nucleotide polymorphisms across the major histocompatibility complex region using logistic regression models. Population admixture was accounted for with principal components analysis. RESULTS: Single nucleotide polymorphism marker associations were explained by the HLA associations, with the major peak over the class II loci. The HLA association overall was extremely strong, as expected for Type 1 diabetes, even in African Americans in whom diabetes diagnosis is heterogeneous. In addition, there were unique features: the HLA-DRB1*03 haplotype was split into HLA-DRB1*03:01, which confers greatest susceptibility in these samples (odds ratio 3.17, 95% CI 1.72-5.83) and HLA-DRB1*03:02, an allele rarely observed in Europeans, which confers the greatest protection in these African American samples (odds ratio 0.22, 95% CI 0.09-0.55). CONCLUSIONS: The unique diversity of the African HLA region we have uncovered supports a specific and major role for HLA-DRB1 in HLA-DRB1*03 haplotype-associated Type 1 diabetes risk.

Six-year incidence of lower extremity arterial disease and associated risk factors in Type 1 diabetic African-Americans.

AIMS: To report the 6-year incidence of, and risk factors for, lower extremity arterial disease (LEAD) in African-Americans with Type 1 diabetes mellitus. METHODS: African-Americans (n = 483) with Type 1 diabetes were re-examined 6 years after an original visit. At both visits, patients underwent a structured clinical interview which included history of amputation or leg angioplasty because of poor circulation in lower extremities; ocular examination; masked grading of seven stereoscopic fundus photographs; and blood pressure measurements. Biological tests included blood and urine assays. RESULTS: Of the 483 patients who had a 6-year follow-up, 457 had no LEAD at the baseline examination. Of these 457 patients, 26 (5.7%) developed LEAD over the 6-year follow-up. Six-year incidence of LEAD was significantly associated with baseline older age (P = 0.0002) and longer duration of diabetes (P < 0.0001). Multiple logistic regression analysis showed that baseline longer duration of diabetes, male gender, higher systolic blood pressure, retinopathy severity, and presence of foot ulcers were significant and independent risk factors for incidence of LEAD. CONCLUSIONS: Blood pressure control and prevention and treatment of foot ulcers may be helpful in reducing the morbidity associated with LEAD in African-Americans with Type 1 diabetes.

Light induces peroxidation in retina by activating prostaglandin G/H synthase.

Prostaglandin G/H synthase (PGHS) has been shown to generate peroxides to a significant extent in the retina and absorbs light at the lower end of the visible spectrum. We postulated that PGHS could be an important initial source of peroxidation in the retina exposed to light, which would in turn alter retinal function. Exposure of pig eyes (in vivo) to light (350 fc/3770 lx) caused after 3 h a 50% increase and by 5 h a 30% decrease in a- and b-wave amplitudes of the electroretinogram (ERG) which were comparable at 380-650 nm and 380-440 nm but were not observed at wavelengths > 450 nm. These effects of light were prevented by free radical scavengers (dimethylthiourea and high-dose allopurinol) and PGHS inhibitors (naproxen and diclofenac), but stable analogs of prostaglandins did not affect the ERG. Both increases and subsequent decreases in ERG wave amplitudes following light exposure in vivo were associated with increases in retinal prostaglandin and malondialdehyde (peroxidation product) levels, which were inhibited by the nonselective PGHS blockers, naproxen and diclofenac. Similar observations were made in vitro on isolated porcine eyecups as well as on retinal membranes exposed to light (250 fc/ 2700 lx) 380-650 nm and 380-440 nm but not at > 500 nm. Both PGHS-1 and PGHS-2 contributed equivalently to light-induced prostaglandin synthesis, as shown after selective PGHS-2 blockers, but mRNA expression of PGHS-1 and 2 was not affected by light. Finally, light stimulated activities of pure PGHS-1 and PGHS-2 isozymes, and these were also shown to produce superoxide radical (detected with fluorogenic spin trap, proxyl fluorescamine). Taken together, data suggest that PGHS- (1 and 2) is activated by short wavelength visible light, and in the retina is an important source of reactive oxygen species which in turn alter retinal electrophysiological function. PGHS thus seems a likely chromophore in setting forth photic-induced retinal injury. Findings provide an explanation for increased sensitivity of the retina to visible light predominantly at the far blue range of its spectrum.

Nutritional factors in diabetics with and without retinopathy.

We used 3-d food-record-keeping techniques to examine nutritional factors in diabetic patients with and without retinopathy. Patients without retinopathy had significantly higher daily intakes of total carbohydrate, water-soluble dietary fibers, insoluble dietary fibers, and glucose than did patients with retinopathy. Also, patients without retinopathy took a significantly lower proportion of their total daily calories as protein.

Plasma fibrinopeptide A, beta-thromboglobulin, and platelet factor 4 in diabetic retinopathy.

We examined plasma levels of fibrinopeptide A, beta-thromboglobulin, and platelet factor 4 in diabetic patients. Among diabetic patients (n = 33) plasma levels of fibrinopeptide A, beta-thromboglobulin and platelet factor 4 were significantly higher than in controls (n = 41). In the subgroups of diabetic patients with (1) minimal (n = 13), and (2) moderate-severe (n = 14) retinopathy only plasma fibrinopeptide A levels were significantly higher than in controls. Among the total group of diabetic patients plasma levels of fibrinopeptide A increased significantly with increasing severity of retinopathy. These results suggest that diabetic retinopathy is associated with in vivo activation of blood coagulation factors and that this activation increases with advancing retinopathy.

Evidence of a human-mediated invasion of the tropical western Atlantic by the 'world's most common brittlestar'.

Approximately three million years ago the Isthmus of Panama formed an impenetrable land barrier between the tropical eastern Pacific Ocean and the tropical western Atlantic Ocean. Since this time, isolated geminate species have evolved from once contiguous populations, either side of the barrier. One such organism whose distribution is divided by the Isthmus is the tropical brittlestar Ophiactis savignyi, once suggested to be the most common brittlestar in the world. Rather than showing a genetic pattern consistent with a history of isolation, we show that this species has recently dispersed between the Pacific Ocean and the western Atlantic Ocean. This conclusion is based upon a phylogenetic analysis using sequences of the COI mitochondrial DNA gene from these populations. Identical haplotypes between oceans, and a genetic signature of population expansion, provide compelling evidence that the western Atlantic contains at least one cluster of haplotypes recently derived from the Indo-Pacific. Inadvertent human-aided translocation of individuals, presumably in ballast water or fouling communities, is strongly implicated as a mechanism for dispersal between oceans. We believe that cryptic marine invasions are likely to be common and our awareness of them will rapidly increase as systematic and phylogeographic knowledge of marine taxa grow.

Diabetic retinopathy in African Americans with type 1 diabetes: The New Jersey 725: I. Methodology, population, frequency of retinopathy, and visual impairment.

OBJECTIVE: To determine the frequency and severity of diabetic retinopathy, as well as associated visual impairment, among African Americans with type 1 diabetes. METHODS: A total of 725 African Americans with type 1 diabetes were enrolled in the study (The New Jersey 725). Clinical evaluations included structured clinical interview, ocular examination, stereoscopic fundus photography, and blood pressure measurements. Severity of retinopathy was determined via masked grading of fundus photographs. Biological evaluations included blood and urine assays. RESULTS: Of the 725 patients, 463 (63.9%) presented with any diabetic retinopathy and 137 (18.9%) with proliferative diabetic retinopathy. The frequency and severity of retinopathy were both significantly associated with older age at examination. Visual impairment (visual acuity in the better eye < or =20/40) was present in 79 (11.0%) and legal blindness in 22 (3.1%) of the patients. Diabetic retinopathy was responsible for 90.9% of the blindness. Frequency of visual impairment was significantly associated with older age and female sex, and only weakly with lower education. CONCLUSIONS: Diabetic retinopathy in African Americans with type 1 diabetes is common, being found in almost two thirds of the patients studied. Its frequency and severity increase with age. Visual impairment is common, increasing with age and duration of diabetes and is more frequent in women than in men.

Diabetic retinopathy in African Americans with type 1 diabetes: The New Jersey 725: II. Risk factors.

OBJECTIVE: To determine whether diabetic retinopathy in African Americans with type 1 diabetes is associated with the following 6 putative risk factors: duration of diabetes, glycemic control, systemic hypertension, renal disease, socioeconomic status, and male sex. METHODS: Patients in The New Jersey 725 study underwent detailed ocular evaluation, a structured clinical interview, blood pressure measurements, and assays of blood and urine samples. RESULTS: Glycemic control was poor; 89.8% of the patients had glycosylated hemoglobin values of more than 0.08. Renal disease and systemic hypertension were present in 49.8% and 34.3% of patients, respectively. Frequency and severity of retinopathy were significantly associated with longer duration of diabetes (P<.001). After adjusting for duration of diabetes and other confounding variables, on average, patients with total glycosylated hemoglobin values in the highest quartile were 3 times more likely to have any retinopathy than those in the lowest quartile; patients with renal disease, 3 times more likely to have any retinopathy and 10 times more likely to have proliferative retinopathy than patients without renal disease; and patients in the highest quartile of systolic sitting blood pressure, 3 times more likely to have proliferative retinopathy than patients in the lowest quartile. CONCLUSIONS: Risk factors for diabetic retinopathy in African Americans with type 1 diabetes include presence of renal disease, poor glycemic control, high systolic blood pressure, and long duration of diabetes.

Macular edema and retinal hard exudates in African Americans with type 1 diabetes: the New Jersey 725.

OBJECTIVE: To determine frequency and associated risk factors for macular edema and retinal hard exudates in hospitalized African Americans with type 1 diabetes. SUBJECTS AND METHODS: Included were 725 African Americans with type 1 diabetes who participated in the New Jersey 725. Clinical evaluations consisted of a structured clinical interview, ocular examination, stereoscopic fundus photographs, and blood pressure measurements. Presence of macular edema and hard exudates was determined via masked grading of fundus photographs. Biological evaluations included blood and urine assays. RESULTS: Of the 725 patients, 89 (12.3%) had macular edema and 149 (20.6%) had retinal hard exudates in at least 1 eye. The presence of macular edema and hard exudates was significantly associated with older age at examination, longer duration of diabetes, and severity of diabetic retinopathy. Presence of proteinuria, missing insulin injections at least once a week, and longer duration of diabetes were significantly and independently associated with macular edema. Presence of proteinuria, male sex, higher low-density lipoprotein cholesterol levels, and longer duration of diabetes were significantly and independently associated with severity of retinal hard exudates. CONCLUSION: Macular edema and hard exudates are common in African Americans with type 1 diabetes, particularly in patients with evidence of renal disease.

Color vision defects in early diabetic retinopathy.

Four color vision tests were used to assess color vision in 51 insulin-dependent diabetic patients and 41 normal controls. Right and left eyes of diabetic patients, selected because they had minimal retinopathy, had significantly more color vision defects than controls on Lanthony desaturated D-15, Farnsworth-Munsell 100-Hue, and chromagraph tests. The 100-Hue scores were significantly higher in both right and left eyes of diabetic patients than in controls. There were no significant associations between presence or absence of a color vision defect and age, sex, age at onset, duration of diabetes, or its metabolic control.

Color vision defects in sickle cell anemia.

The Farnsworth-Munsell 100-hue test was used to compare color vision in patients with sickle cell anemia, 20/20 visual acuity, and mild to severe peripheral retinopathy, but without posterior retinal vessel involvement, with matched normal controls. Patients with sickle cell anemia had significantly more blue-yellow and mixed color vision defects and significantly higher Farnsworth-Munsell 100-hue scores than did controls. There were no significant associations between color vision defects and the severity of peripheral retinal findings or the diameter of the foveal avascular zone. These results suggest that color vision defects may exist in patients with sickle cell anemia in the absence of ophthalmoscopic retinal changes in the posterior fundus.

Posterior vitreous fluorophotometry. II. Comparison of diabetic patients and controls with the use of a new analysis procedure.

We used a new computerized procedure to analyze posterior vitreous fluorophotometry scans, obtained with a commercial fluorophotometer (Fluorotron Master Coherent, Palo Alto, Calif), in insulin-dependent diabetic patients and controls. Diabetic patients with minimal retinopathy had significantly higher effective fluorescein vitreous diffusivity and 30-minute 3-mm vitreous fluorescence values than either controls or diabetic patients with no retinopathy. However, there was no significant difference between the groups for the apparent permeability of the blood-retinal barrier to fluorescein. These results suggest the possibility that the higher 3-mm fluorescence levels found in the diabetic patients with minimal retinopathy may result in part from enhanced movement of fluorescein through the vitreous.

Posterior vitreous fluorophotometry. I. Description of a new analysis procedure and results in normal subjects.

A new automated analysis procedure was used to evaluate the apparent blood-retinal barrier permeability (mean +/- SD = 1.31 = 0.31 X 10(-7) cm/s at 60 minutes after intravenous dye administration) and the effective diffusivity (mean +/- SD = 0.88 +/- 0.40 X 10(-5) cm2/s) for fluorescein in the vitreous of 21 normal subjects. The analysis improvements include (1) use of an individualized convolution (spread) function for each eye in comparing simulated and experimental scans, (2) separation of vitreous and chorioretinal fluorescence, and (3) precise determination of vitreous position relative to the retina. The average reproducibility in six subjects was 23% for permeability and 22% for diffusivity based on repeated determinations separated in time by at least a week. Diffusivity values, but not permeability values, significantly associated in comparisons of first and second determinations, suggesting permeability may fluctuate in time while diffusivity remains relatively constant. The fluorescence at 3 mm anterior to the retina (commonly employed as a measure of blood-retinal barrier leakiness) was strongly associated with diffusivity. In contrast, the anticipated association between permeability and 3-mm fluorescence was weak or absent.

Posterior vitreous fluorophotometry in normal subjects.

We performed vitreous fluorophotometry using the Fluorotron Master and intravenous fluorescein injection of 14 mg/kg of body weight in 22 normal subjects. Various methods of analysis were used to evaluate vitreous fluorescein concentration at 3 mm from the retina as well as averaged over the posterior 6 mm. The various methods of calculation yielded mean (+/- SD) postinjection values ranging from 1.7 +/- 1.4 to 4.3 +/- 2.3 ng/mL at 30 minutes and from 7.1 +/- 2.4 to 10.8 +/- 2.7 ng/mL at 60 minutes. The permeability index determined 60 minutes after injection ranged from 0.92 +/- 0.40 X 10(-7) to 1.19 +/- 0.30 X 10(-7) cm/s, according to the protocol used. Replicate pairs of measurements in six subjects demonstrated that the procedure was reproducible to within 17% to 49%, depending on the analysis. The results suggest that if the current methods of data analysis are used, fluorescein leakage might be considered abnormally high if at 60 minutes the 3-mm posterior vitreous fluorescein concentration corrected for background fluorescence exceeds 14.3 ng/mL and/or the permeability index exceeds 2 X 10(-7) cm/s.

Temporary loss of foveal contrast sensitivity associated with panretinal photocoagulation.

Snellen visual acuity and spatial contrast sensitivity measurements were used to monitor changes in foveal vision in two patients undergoing argon laser panretinal photocoagulation (PRP) in both eyes for proliferative diabetic retinopathy. Foveal edema developed in one of the four eyes. The remaining three eyes showed no signs of foveal edema, but developed temporary losses in high spatial frequency contrast sensitivity during the closely spaced PRP treatments. Since Snellen visual acuity remained stable at the prelaser level, these results indicate the need for more sensitive measures of visual resolution to monitor foveal integrity in patients undergoing PRP.

The ovine corticotropin-releasing hormone-stimulation test in type I diabetic patients and controls: suggestion of mild chronic hypercortisolism.

We examined hypothalamic-pituitary-adrenal (HPA) axis function in insulin-dependent diabetic outpatients (N = 22) and age-, sex-, and weight-matched normal controls (N = 22). The evaluation included measurements of 9:00 AM fasting plasma cortisol and cortisol-binding globulin (CBG) levels, 24-hour urinary free cortisol (UFC) excretion, and plasma corticotropin and cortisol responses to intravenously administered ovine corticotropin-releasing hormone ([CRH] 1 microgram/kg given as a bolus at 8:00 PM). Diabetic patients had significantly elevated 9:00 AM plasma cortisol levels (mean +/- SE, 300.7 +/- 99.3 v 237.3 +/- 99.3 nmol/L, P < .04), higher 24-hour UFC excretion (313.2 +/- 112.6 v 244.2 +/- 69.3 nmol/24 h, P < .02), and greater cortisol responses to CRH infusion (time-integrated values: 49,408.2 +/- 11,289.8 v 40,217.9 +/- 7,228.6 nmol/L.120 min, P < .004; peak cortisol values: 529.7 +/- 107.6 v 438.7 +/- 77.3 nmol/L, P < .002) than controls. UFC excretion values were positively correlated with both 5-year averaged hemoglobin A1c level (P = .03) and total number of insulin units administered per day (P = .03). These results suggest that insulin-dependent diabetic outpatients have mild chronic hypercortisolism, which might influence the control of the disease and play a role in the development of its chronic complications.

Preservation of neural function in the perinate by high PGE(2) levels acting via EP(2) receptors.

Despite increasingly frequent and longer lasting hypoxic episodes during progressive labor, the neonate is alert and vigorous at birth. We investigated whether high levels of PGs during the perinatal period assist in preserving neural function after such "stressful" hypoxic events. Visual evoked potentials (VEPs) and electroretinograms (ERGs) were recorded before and 45 min after mild moderate asphyxic hypoxia (two 4-min asphyxic-hypoxic periods induced by interrupting ventilation at 8-min intervals) in newborn piglets <12 h old treated or not treated with inhibitors of PG synthase (ibuprofen or diclofenac) with or without PG analogs. At 45 min after the hypoxic episode, P2 and b-wave amplitudes were slightly decreased and latencies were delayed. These changes in the VEP and ERG returned to near normal by 120 min. Ibuprofen and diclofenac decreased brain and retinal PG levels and markedly intensified 45 min after hypoxia-induced changes in VEP and ERG, but cerebral and retinal blood flows improved. Combined treatment with PG synthase inhibitor in combination with 16,16-dimethyl-PGE(2) (a PGE(2) analog), but not with PGI(2) and PGF(2alpha) analogs, and in combination with the EP(2) receptor agonist butaprost (but not EP(1) or EP(3) agonists), prevented ibuprofen- and diclofenac-aggravated postasphyxia electrophysiological changes. In conclusion, high levels of PGE(2) in nervous tissue, via actions on EP(2) receptors, seem to contribute to preservation of neural function in the perinate subjected to frequent hypoxic events.

Human strabismus: evaluation of the interhemispheric transmission time and hemiretinal differences using a reaction time task.

Experimentally induced strabismus in visually immature cats leads to abnormal development of the posterior corpus callosum. This, in turn, should lead to abnormal interhemispheric integration of unilaterally presented visual information. To test whether strabismus produces deficits in the human commissural visual system, the interhemispheric transmission time (ITT) was compared in strabismic and normal subjects. Simple unimanual reaction times (RT) were tested in 30 subjects in response to a lateralized target presented monocularly at 4 degrees and 35 degrees nasally and temporally from the fovea along the horizontal meridian. This method was also used to examine the effect of strabismus on the central and peripheral portions of each hemiretina. The results showed that in strabismic subjects with or without amblyopia, the ITT did not differ significantly from normals at both eccentricities. In non-amblyopic strabismic patients, RTs in the central and peripheral portions of hemiretina were comparable to normals. However, a reduced speed of response was found in the central visual field (4 degrees) in the amblyopic eye. Our results suggest that the ITT is normal in strabismic subjects and that the longer RTs in the central portion of the nasal and temporal hemiretina of the amblyopic eye may be associated with the severe amblyopic condition.