Advances in Bragg stack quantum well solar cells Johnson, D.C.; Ballard, I.; Barnham, K.W.J. ...
Solar energy materials and solar cells,
05/2005, Volume:
87, Issue:
1
Journal Article, Conference Proceeding
Peer reviewed
Strain-balanced quantum well solar cells (SB-QWSC) extend the photon absorption edge beyond that of bulk GaAs by incorporation of quantum wells in the i-region of a p–i–n device. The addition of a ...distributed Bragg reflector (DBR) can substantially increase the photocurrent with little or no detriment to the dark-current. Experimental results are presented that show improvements of DBR cell efficiencies over SB-QWSC's without DBR's. In addition, at high dark-current levels appropriate to high concentration, we observe that the dark-currents of the SB-QWSC's exhibit ideal diode behaviour. We present evidence that the ideality
n
=
1
dark-current is reduced in the DBR cells and discuss the possible efficiency improvements if the dark-current is radiatively dominant.
In diet studies, stomach contents from predatory fish may be difficult to identify due to digestion. The Gizzard Shad Dorosoma cepedianum is an important prey species for sport fish; thus, ...determining the size of ingested shad can assist with evaluating competitive interactions, bioenergetic patterns, and niche partitioning and can add precision to predictive models. The gizzard organ of clupeids appears to be more resistant to digestion compared to other tissues and can often be found in the stomachs of predatory fish after other tissues from Gizzard Shad are digested. If the gizzard diameter is proportional to Gizzard Shad weight or length, it could be a useful structure for estimating the size of partially digested Gizzard Shad when other structures that are traditionally used to estimate weight or length (e.g., backbones) are damaged due to advanced digestion. For this reason, we evaluated the allometry relating gizzard diameter and Gizzard Shad weight and TL. We sampled a total of 936 Gizzard Shad from nine Oklahoma reservoirs. Fish were frozen and later thawed; they were measured for weight (±0.01 g) and TL (±1 mm), and the gizzard was then removed. Gizzard diameter was measured (±0.1 mm) at its widest point using calipers. Eight different equations were evaluated to find the best relationship (lowest Akaike’s information criterion) between gizzard diameter and weight or length. The relationship between gizzard diameter and fish weight was best modeled as a second‐order polynomial, whereas the relationship between gizzard diameter and fish TL was best described by a five‐parameter Richard’s equation. Both relationships explained over 80% of the variation in Gizzard Shad size. The 95% CIs for weight (±4–7%) and TL (±2–7%) indicated good overall precision for mean fish size based on gizzard diameter. Therefore, we recommend using gizzard diameter to determine weight and TL from diet samples when advanced digestion of Gizzard Shad limits the use of more traditional metrics (TL, backbone length, etc.).
While hemorrhagic shock might be the result of various conditions, hemorrhage control and resuscitation are the corner stone of patient management. Hemorrhage control can prove challenging in both ...the acute care and surgical settings, especially in the abdomen, where no direct pressure can be applied onto the source of bleeding. Resuscitative endovascular balloon occlusion of the aorta (REBOA) has emerged as a promising replacement to resuscitative thoracotomy (RT) for the management of non-compressible torso hemorrhage in human trauma patients. By inflating a balloon at specific levels (or zones) of the aorta to interrupt blood flow, hemorrhage below the level of the balloon can be controlled. While REBOA allows for hemorrhage control and augmentation of blood pressure cranial to the balloon, it also exposes caudal tissue beds to ischemia and the whole body to reperfusion injury. We aim to introduce the advantages of REBOA while reviewing known limitations. This review outlines a step-by-step approach to REBOA implementation, and discusses common challenges observed both in human patients and during translational large animal studies. Currently accepted and debated indications for REBOA in humans are discussed. Finally, we review possible applications for veterinary patients and how REBOA has the potential to be translated into clinical veterinary practice.
Platelets have long been proposed to play a role in fostering neoplasias, ranging from tissue repair to cancer, but clinical evidence remains limited. Since available therapautics antagonizing ...hemostatic platelet functions lead to bleeding, the concept of targeting platelets in the context of cancer prevention or treatment has not been pursued in controlled clinical trials. To address this, we developed a novel antiplatelet strategy by partial inhibition of thrombopoiesis.
We hypothesized that if platelets played a key role in fostering neoplastic malignancies, controlled platelet count reduction within a safe range would slow platelet-dependent cancer progression without adversely affecting hemostasis. Since the MPL ligand megakaryocyte growth and development factor (thrombopoietin, MGDF) is required for maintenance of normal platelet count, and the liver is responsible only for a portion of thrombopoietin synthesis, we tested this hypothesis by targeted knock-down of hepatic thrombopoietin synthesis using an antisense oligonucleotide (ASO) in mammary cancer-prone transgenic mice. We investigated whether partial reduction of thrombopoietin sythesis through ASO knock-down was hemostatically safe and impacted kinetics or penetrance of neoplastic progression in de novo mammary carcinogenesis in MMTV-PyMT mice.
We designed and generated thrombopoietin ASO-s (TPO ASO) to achieve about 50% platelet count reduction in mice by inhibition of hepatic thrombopoietin gene expression. Then MMTV-PyMT transgenic mice were subcutaneously administered one of the effective TPO ASO-s, with treatment initiated at 40 days of age and before appearance of palpable (>2.0 mm) mammary tumors. We assessed the impact of saturating dose TPO ASO, including platelet count, plasma TPO level, and number of megakaryocytes in the femoral bone marrow. Mammary tumor growth, pulmonary metastases, and overall survival (fixed end-point study based on total tumor burden) of TPO ASO-treated mice were compared with untreated controls. At study endpoints, mammary carcinomas, platelet deposition, intra-tumoral vessel density, and Ki-67 positive cells were quantitatively evaluated.
As anticipated from the drug screen, TPO ASO treatment at saturating effect reduced plasma thrombopoietin levels and blood platelet count by ~50% within 4 weeks, and the number of megakaryocytes in femoral bone marrow. TPO ASO also suppressed primary tumor growth (attached figure) and impaired development of pulmonary metastases (p<0.05), resulting in increased overall survival (p<0.001). Histological analysis of primary tumors revealed that TPO ASO significantly reduced mean platelet deposition in tumor vessels (from 54% to 26%; p<0.001), reduced vessel density (from 3.1% area to 1.5% area; p<0.05) and Ki-67 positive cells (from 62/field to 36/field; p<0.05) in primary tumors. Together, these results support the notion that strategies that safely reduce platelet presence or activity within developing mammary tumors, may limit neoplastic progression coincident with reduced angiogenesis.
In summary, we found that TPO ASO reduces thrombopoietin levels and platelet count within the hemostatically safe range and significantly slows neoplastic progression of spontaneous mammary carcinomas in MMTV-PyMT mice. Overall, pharmacological knockdown of hepatic TPO synthesis is a new antiplatelet strategy that may be reasonably safe and effective in various platelet-driven disorders, including cancer.
Revenko:Ionis Pharmaceuticals, Inc: Employment, Other: Intellectual property rights. Monia:Ionis Pharmaceuticals, Inc: Employment, Other: Intellectual property rights. Gruber:Aronora, Inc: Employment, Other: Intellectual property rights.
The purpose of this review is to assess the relationship between mood disorders and development, course, and associated morbidity and mortality of selected medical illnesses, review evidence for ...treatment, and determine needs in clinical practice and research.
Data were culled from the 2002 Depression and Bipolar Support Alliance Conference proceedings and a literature review addressing prevalence, risk factors, diagnosis, and treatment. This review also considered the experience of primary and specialty care providers, policy analysts, and patient advocates. The review and recommendations reflect the expert opinion of the authors.
Reviews of epidemiology and mechanistic studies were included, as were open-label and randomized, controlled trials on treatment of depression in patients with medical comorbidities. Data on study design, population, and results were extracted for review of evidence that includes tables of prevalence and pharmacological treatment. The effect of depression and bipolar disorder on selected medical comorbidities was assessed, and recommendations for practice, research, and policy were developed.
A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between mood disorders and many medical illnesses. In addition, there is evidence to suggest that mood disorders affect the course of medical illnesses. Further prospective studies are warranted.
Background: One limitation of resuscitative endovascular balloon occlusion of the aorta (REBOA) is hemodynamic instability upon balloon deflation due to distal hyperemia and washout of ischemic ...metabolites. We sought to determine whether stepwise reperfusion after supraceliac (Zone 1) REBOA by transitioning to infrarenal (Zone 3) occlusion would mitigate the physiologic consequences of balloon deflation and decrease hemodynamic instability.
Methods: Twelve anesthetized swine underwent controlled hemorrhage of 25% blood volume, 45 minutes of Zone 1 REBOA, then resuscitation with shed blood. Standardized critical care began with deflation of the Zone 1 balloon in all animals, and continued for six hours. Half of the animals were randomly assigned to Zone 3 REBOA for an additional 55 minutes following Zone 1 balloon deflation.
Results: There were no differences in physiology at baseline, during the initial 30 minutes of hypotension, or during the 45 minutes of Zone 1 occlusion. After Zone 1 balloon deflation, there was no difference in proximal mean arterial pressure (pMAP) with or without Zone 3 occlusion or percentage of critical care time spent within the target pMAP range between 65 and 75 mm Hg. There were also no significant differences in peak lactate concentration or resuscitation requirements.
Conclusions: In an animal model of hemorrhagic shock and Zone 1 REBOA, subsequent Zone 3 aortic occlusion did not add a significant ischemic burden, but it also did not provide significant hemodynamic support. The effect of this strategy on functional outcomes warrants further study. Continued investigation is necessary to determine optimal resuscitative support strategies during reperfusion following Zone 1 REBOA
In this paper, a detailed analysis on the radiation response of solar cells with multi quantum wells (MQW) included in the quasi-intrinsic region between the emitter and the base layer is presented. ...While the primary source of radiation damage of photovoltaic devices is minority carrier lifetime reduction, we found that in the case of MQW devices, carrier removal (CR) effects are also observed. Experimental measurements and numerical simulations reveal that with increasing radiation dose, CR can cause the initially quasi-intrinsic background doping of the MQW region to become specifically n- or p-type. This can result in a significant narrowing and even the collapse of the electric field between the emitter and the base where the MQWs are located. The implications of the CR-induced modification of the electric field on the current-voltage characteristics and on the collection efficiency of carriers generated within the emitter, the MQW region, and the base are discussed for different radiation dose conditions. This paper concludes with a discussion of improved radiation hard MQW device designs.
The cardiac troponin C (cTnC) mutation, L29Q, has been found in a patient with familial hypertrophic cardiomyopathy. We previously showed that L29, together with neighboring residues, Asp2, Val28, ...and Gly30, plays an important role in determining the Ca(2+) affinity of site II, the regulatory site of mammalian cardiac troponin C (McTnC). Here we report on the Ca(2+) binding characteristics of L29Q McTnC and D2N/V28I/L29Q/G30D McTnC (NIQD) utilizing the Phe(27) --> Trp (F27W) substitution, allowing one to monitor Ca(2+) binding and release. We also studied the effect of these mutants on Ca(2+) activation of force generation in single mouse cardiac myocytes using cTnC replacement, together with sarcomere length (SL) dependence. The Ca(2+)-binding affinity of site II of L29Q McTnC(F27W) and NIQD McTnC(F27W) was approximately 1.3- and approximately 1.9-fold higher, respectively, than that of McTnC(F27W). The Ca(2+) disassociation rate from site II of L29Q McTnC(F27W) and NIQD McTnC(F27W) was not significantly different than that of control (McTnC(F27W)). However, the rate of Ca(2+) binding to site II was higher in L29Q McTnC(F27W) and NIQD McTnC(F27W) relative to control (approximately 1.5-fold and approximately 2.0-fold respectively). The Ca(2+) sensitivity of force generation was significantly higher in myocytes reconstituted with L29Q McTnC (approximately 1.4-fold) and NIQD McTnC (approximately 2-fold) compared with those reconstituted with McTnC. Interestingly, the change in Ca(2+) sensitivity of force generation in response to an SL change (1.9, 2.1, and 2.3 mum) was significantly reduced in myocytes containing L29Q McTnC or NIQD McTnC. These results demonstrate that the L29Q mutation enhances the Ca(2+)-binding characteristics of cTnC and that when incorporated into cardiac myocytes, this mutant alters myocyte contractility.
In humans, platelet count within the normal range is required for physiological hemostasis, but, adversely, platelets also support pathological thrombosis. Moreover, by releasing growth factors, they ...may enhance neoplastic proliferation. We hypothesize that platelet count correlates with platelet-dependent pathologies, even within the range of hemostatic competence. Because platelet production is promoted by thrombopoietin signaling through the myeloproliferative leukemia virus oncogene (cMPL), a receptor expressed on megakaryocytes, we evaluated the feasibility of selective targeting of hepatic thrombopoietin production to test this hypothesis. We synthesized murine- and primate-specific antisense oligonucleotides (THPO-ASO) that silence hepatic thrombopoietin gene (THPO) expression without blocking extrahepatic THPO. Repeated doses of THPO-ASO were administered to mice and a baboon, causing a sustained 50% decline in plasma thrombopoietin levels and platelet count within 4 weeks in both species. To investigate whether reducing platelet count within the translationally relevant hemostatic range could alter a neoplastic process, we administered THPO-ASO to 6-week-old transgenic MMTV-PyMT mice that develop early ductal atypia that progresses into cMPL-negative fatal metastatic breast cancer within 2 to 3 months. THPO-ASO treatment increased the average time to euthanasia (primary humane endpoint) at 2 cm3 combined palpable tumor volume. Our results show that THPO-ASO reduced blood platelet count, plasma platelet factor 4, vascular endothelial growth factor, thrombopoietin levels, bone marrow megakaryocyte density, tumor growth rate, proliferation index, vascularization, platelet and macrophage content, and pulmonary metastases vs untreated controls. These findings confirm that sustained and moderate pharmacological platelet count reduction is feasible with THPO-ASO administration and can delay progression of certain platelet-dependent pathological processes within a safe hemostatic platelet count range.
•Antisense oligonucleotide targeting of hepatic THPO gene expression reduces platelet count within the hemostatic range in mice and baboons.•THPO gene silencing suppresses spontaneous metastatic mammary gland carcinoma progression in transgenic MMTV-PyMT mice.
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