combine error detection and forward error correction to make more eﬃcient use of the channel. In type I HARQ, all the necessary parity bits are sent with each transmission. However, typeII HARQ sends only the error detection parity bits, while the error correction parity bits are retransmitted upon request if the decoder detects errors. Therefore, with typeII HARQ scheme a higher throughput can be achieved.
i−2,i:m:n , 3 ≤ i < m. Continuing this way, all the desired product moments and hence all covariances can be obtained.
5. Numerical results
The recurrence relations obtained in the preceding sections allow us to evaluate the means„variances and covairances of Erlang-truncated exponential progressive Type-II right censored order statistics for all sample sizes n and all censoring schemes (R 1 , R 2 ,..., Rm), m < n. These quantities can be used for various inferential purposes; for example, they are useful in determining BLUEs of location/scale parameters and BLUPs of censored failure times. In this section we compute the means and variances of Erlang-truncated exponential progressive Type-II right censored order statistics for sample sizes up to 20 and for different choices of m and progressive schemes (R1, R2,..., Rm), m < n.
Metabolic/hepatic encephalopathy is neuropathologically characterized by the presence of Alzheimer typeII astro- cytes (AA II) with large and clear nuclear morphology. To date, there is no good immunohistochemical marker to better identify these cells. Here, we assessed cases of hepatic encephalopathy of different etiologies by immuno- histochemistry using an anti-p62 antibody. We observed peripheral or diffuse nuclear staining of variable intensity in AA II in all cases but not in normal controls or reactive astrocytes. We conclude that p62 is a useful immunohisto-
This thesis aims at getting better insights in the theory and numerics of hyperbolic Maxwell variational inequalities of the second kind. Motivated by Bean’s critical state model for type-II (high-temperature) superconductivity replacing the classical Ohm’s law in Maxwell’s equations, we establish a novel well-posedness result for the concerned problem by means of a fully discrete scheme and a rigorous convergence analysis thereof. One major advantage of this approach is the natural derivation of a numerical algorithm to compute the corresponding solution based on the semismooth Newton method and a Moreau–Yosida penalization. Moreover, from a physical point of view, the problem features unknown interfaces between the superconducting and normal regions of the domain. Therefore, we propose an adaptive mesh refinement algorithm based on a posteriori error estimators in careful com- bination with the mentioned penalization. This results not only in an increased numerical accuracy, but it also provides a way to identify these unknown interfaces without any additional a priori as- sumption. The main results consist of the equivalence of the estimators to the actual error between the analytical solution and its penalized finite element approximation, as well as rigorous verification of the convergence of our novel algorithm. The final chapter is dedicated to a shape optimization problem subject to the variational inequality of the second kind. We compute the shape derivative of a penalized problem to cope with the low regularity of the dual variable mapping due to the under- lying variational inequality structure. Thereafter, a limiting analysis with respect to the penalization parameter yields the existence of a minimizer to the original shape optimization problem. Finally, we establish an efficient level set method where the shape derivative provides a descent direction. All our analytical results in this thesis are complemented by various numerical experiments.
We have investigated the temperature-dependent decay kinetics of typeII CdSe–CdTe and CdTe–CdSe core–lateral shell nano- platelets having quantum yields comparable to core-only plate- lets. A kinetic analysis of the photoluminescence (PL) decay and a measurement of the temperature dependent quantum yield are used to reveal for the first time the temperature dependence of the radiative and non-radiative lifetime of core only and hetero nanoplatelets. The observed increase of the radiative lifetime with temperature is in line with the predicted increase due to the giant oscillator strength effect in 2D and thus attributed to an increase of the homogeneous transition linewidth with tempera- ture, while we can exclude bimolecular e–h pair recombination by decay kinetics and its temperature dependence. Our findings are indicative of the presence of charge carriers in the form of excitons in the nanoplatelets. In comparison to core only platelets we observe a significant prolongation of the radiative lifetime by two orders of magnitude in typeII nanoplatelets, so that we expect that the radiative lifetime can be tuned by a heterojunction via confinement and band offsets. The analysis of the CdSe–CdTe and CdTe–CdSe hetero platelet PL decay shows that it is biexpo- nential. This again indicates that predominantly spatially indirect excitons are present at the hetero junction and not ionized e–h pairs. These findings suggest that hetero nanoplates are less suitable for applications in solarcells, since generated carriers are coulomb correlated. On the other hand lasing applications might strongly benefit from a broad gain spectrum generated by the excitonic typeII transition.
Abstract: β -Carotene has been shown to increase the risk of developing lung cancer in smokers and asbestos workers in two large scale trails, the Beta-Carotene and Retinol Efficacy Trial (CARET) and the Alpha-Tocopherol Beta-carotene Cancer Prevention Trial (ATBC). Based on this observation, it was proposed that genotoxic oxidative breakdown products may cause this effect. In support of this assumption, increased levels of sister chromatid exchanges, micronuclei, and chromosomal aberrations were found in primary hepatocyte cultures treated with a mixture of cleavage products (CPs) and the major product apo-8 0 carotenal. However, because these findings cannot directly be transferred to the lung due to the exceptional biotransformation capacity of the liver, potential genotoxic and cytotoxic effects of β-carotene under oxidative stress and its CPs were investigated in primary pneumocyte typeII cells. The results indicate that increased concentrations of β-carotene in the presence of the redox cycling quinone dimethoxynaphthoquinone (DMNQ) exhibit a cytotoxic potential, as evidenced by an increase of apoptotic cells and loss of cell density at concentrations > 10 µM. On the other hand, the analysis of micronucleated cells gave no clear picture due to the cytotoxicity related reduction of mitotic cells. Last, although CPs induced significant levels of DNA strand breaks even at concentrations ≥ 1 µM and 5 µM, respectively, β-carotene in the presence of DMNQ did not cause DNA damage. Instead, β-carotene appeared to act as an antioxidant. These findings are in contrast with what was demonstrated for primary hepatocytes and may reflect different sensitivities to and different metabolism of β-carotene in the two cell types.
5 number of human diseases related to these systems.  In recent years, subgroups of these enzymes have been identified, which are anchored directly to plasma membranes, either by a carboxy-terminal transmembrane domain (Type I), an amino-terminal transmembrane domain with a cytoplasmic extension (TypeII or TTSP), or through a GPI linkage. An additional mechanism is used by uPA (urokinase), which is fixed to the cell surface via binding to a specific uPA-receptor.  These trypsin-like serine proteases have a common catalytic mechanism for the cleavage of specific substrates and are frequently involved in consecutive proteolytic reactions or protease cascades, where one protease precursor (zymogen) is the substrate of an active protease. This shared mechanism confers the advantage that a single signal may be specifically and irreversibly amplified at each step, when a downstream zymogen is activated, providing the capacity for unleashing a burst of proteolytic potential. 
We included consecutive adult patients with a history of typeII diabetes for at least 6 months without fundoscopic signs of DR in this cross-sectional study. Exclusion criteria were other ocular diseases (e.g., glaucoma, retinal detachment, macular hole, age-related macular degeneration, retinal vascular occlu- sion, macular dystrophies), media opacities, structural damage to the center of the macula, active intraocular inflammation, and previous intraocular surgery. After Early Treatment Retinopathy Study (ETDRS) best-corrected visual acuity (BCVA) testing, a slit-lamp examination of the anterior segment, intraocular pressure measurement, and fundus biomicroscopy, ophthalmic imaging was performed as follows.
We developed colloidal synthesis to investigate the structural and electronic properties of CdSe –CdTe and inverted CdTe –CdSe heteronanoplatelets and experimentally demonstrate that the overgrowth of cadmium selenide or cadmium telluride core nanoplatelets with counterpartner chalcogenide wings leads to type-II heteronanoplatelets with emission energies de ﬁned by the bandgaps of the CdSe and CdTe platelets and the characteristic band o ﬀsets. The observed conduction and valence band oﬀsets of 0.36 eV and 0.56 eV are in line with theoretical predictions. The presented type-II heteronanoplatelets exhibit e ﬃcient spatially indirect radiative exciton recombination with a quantum yield as high as 23%. While the exciton lifetime is strongly prolonged in the investigated type-II 2D systems with respect to 2D type-I systems, the occurring 2D giant oscillator strength (GOST) e ﬀect still leads to a fast and eﬃcient exciton recombination. This makes type-II heteronanoplatelets interesting candidates for low threshold lasing applications and photovoltaics.
Moreover we found that light which was absorbed at a significant distance from the charge separating interface contributes similary to the charge separation signal as light absorbed in the adjacent CdTe-CdSe layers. This may be an indication of exciton diffusion or for photo-creation of free charge carriers in the nanocrystal layers (in analogy to reference ). Let us assume a significant creation of free charges in the multilayer part. Then electrons and holes may diffuse independently. Thus, when one of them reach the typeII interface, one type of charge carriers gets ”trapped” in the top layer. The diffusion of this trapped charge species is hence causing an SPV-signal. The other type of charge carrier continues its diffusion in the multilayers. If however charges created at the typeII interface diffuse, they get directly separated and it is the other type of charge carriers which enhances the SPV-signal due to diffusion. This would imply that electrons and holes diffuse at a comparable speed since we cannot distinguish a significant difference for excitation in the monolayers or in the multilayers. Ginger et al. however reported a strong difference between electrons and holes for diffusion.  Exciton diffusion on the other hand might transfer the excitons to the typeII interface where charge separation provides the free charge carriers for diffusion. Since the lifetime of bright excitons is typically below 1 ns this diffusion must be fast. However, initial preliminary experiments on exciton diffusion did not reveal fast exciton diffusion and no such indications have been found in existing literature. Diffusion of dark excitons is mentioned rarely in literature. However, it was reported that dark excitons could be recycled in energy transfer over CdTe nanocrystal layers. 
Interestingly, members of the polycistronic miR-17-92 cluster and its two mammalian paralogs miR-106a-363 cluster and miR-106b-25 cluster were highly represented in the ATII miRNAs. These clusters contain four seed families: miR-17, miR-18, miR-19 and miR-92 (Concepcion et al. 2012). In the present study, four miR-17-92 cluster members (miR-19a, miR-17, miR-20a, miR-18a) were detected. MiR-19a and miR-17- 5p were expressed at high levels with miR-17-5p having three targets within the canonical TGF-beta signaling pathway. Further, miR-106a from the miR-106a-363 cluster and all three members of miR-106b-25 cluster (miR-25, miR-93, miR-106b) were expressed at moderate levels. MiR-20b of the miR-106a-363 cluster was found at low level. So far, most studies have described the main role of the miR-17-92 cluster and its paralogs as oncogenes with upregulation in hematopoietic and solid cancers (Concepcion et al. 2012). However, there is growing evidence on its physiological function in normal development with loss of function of miR-17-92 cluster leading to early postnatal death (Ventura et al. 2008) and its potential role in tumor suppression. TGF-beta typeII transmembrane receptor was directly inhibited by miR-17, miR-20a and miR-20b and these miRNAs were upregulated in A549 with cisplatin sensitivity compared to cisplatin resistance (Jiang et al. 2014). Further, in oral squamous cell carcinoma miR-17 and miR-20a repressed tumor migration (Chang et al. 2013). Of special interest for the present study, in lung development miR-17, miR-20a and miR- 106b controlled E-cadherin expression and distribution, thus, provoking an epithelial phenotype. MiR-17 and miR-20a were expressed more highly during lung development than in adult lung, while miR-106b had even higher levels in adult lungs (Carraro et al. 2009). In the present study, miR-17, miR-20a and miR-106b were expressed above median levels in ATII cells in adult, healthy mice. These data suggest that not only during lung development, but also in adult mice all three miRNAs have a physiological role in maintaining epithelial homeostasis.
all x ∈ (0, 1). For convenience, let U 1 , . . . , U n always denote i.i.d. uniformly distributed
rv’s and U 1:n , . . . , U n:n their corresponding OS’s.
Theorem 2.2 shows that we can transform a Type-II right censored sample of uniformly distributed rv’s to a complete sample of ordered uniformly distributed rv’s of a smaller sample size. Now we study whether there is a transformation with this property such that the transformed rv’s are distributed as order statistics from i.i.d. rv’s even if the underlying distribution of the original sample is not U (0, 1) but possesses an arbitrary absolutely continuous cdf F . This issue is also discussed in Fischer and Kamps (2011), where some of the statements of this chapter can be found as well.
Star activity is often also observed at high enzyme con- centrations under optimum buffer conditions, and this re- flects the finite accuracy of these enzymes. By analyzing the rate of cleavage of star sites on a plasmid DNA by EcoRV it was possible to estimate the accuracy of a REase. The plasmid pAT153 contains 12 EcoRV* sites, each of which differs from the wild-type EcoRV sequence (GATATC) by one base pair. EcoRV showed a marked preference for one of these sites (GTTATC), which was cleaved (k cat /K m ) six orders of magnitude more slowly than the cognate site (GATATC). Nicked intermediate accumulates in the course of this cleavage. In vivo, this would enable DNA ligase to repair the single-strand breaks that arise at star sites (84). From cleavage studies with oligonucleotides, it was concluded that double-strand cleavage of non-cognate sub- strates is at least five orders of magnitude slower than cleav- age of the cognate substrate (85). While in the cognate sub- strate both strands of the DNA duplex are cleaved at the same rate, in non-cognate substrates one strand is cleaved faster than the other one. These studies showed that REases are among the most accurate enzymes known. This high accuracy is achieved by both preferential binding (ground state) and preferential catalysis (transition state). Cleavage at star sites by high concentrations of enzyme can be sup- pressed to some extent by spermidine (86), hydrostatic pres- sure (87) and, as shown recently, by mutations (88). The structural basis of specificity of REases: characteriza- tion of the REase–DNA interface using modified substrates. Because TypeII REases recognize their substrate sequences so accurately, they are attractive subjects for studying the mechanism of recognition. It was unclear at the begin- ning of these studies how recognition occurred, and it re- mains incompletely understood today. Initially, it was spec- ulated that recognition of symmetric (‘palindromic’) se- quences might depend on unusual structures such as open, partially single-stranded, sequences (38) or cruciforms (89). Although DNA is almost always distorted to some degree when bound by REases, these deformations are thermody- namically unstable, and aside from a few unusual occur- rences in recently solved crystal structures (e.g. PacI (22), and the EcoRII /PspGI/Ecl18kI/SsoII family ( 90)), they play little role in sequence recognition.
In conclusion, the results of this study demonstrate that carnitine supplementation to obese Zucker rats sig- nificantly improves carnitine status, counteracts the obesity-induced muscle fiber transition from type I to typeII and favors an oxidative metabolic phenotype of skeletal muscle which preferentially uses fatty acids as energy source. The enhanced capacity of skeletal muscle to utilize fatty acids was demonstrated by the carnitine- induced up-regulation of genes involved in fatty acid uptake and transport, carnitine uptake, fatty acid β- oxidation, mitochondrial fatty acid uptake (carnitine shuttle system) and tricarboxylic acid cycle. These meta- bolic changes in skeletal muscle are likely to contribute to the pronounced NEFA- and TG-lowering effects of carnitine supplementation in obese Zucker rats. There- fore, carnitine supplementation is supposed to be benefi- cial for the treatment of elevated levels of metabolic fuels (e.g., fatty acids) which are frequently found in sub- jects with obesity, insulin resistance, diabetes or meta- bolic syndrome.
(A) The representation of the stretch field imposed by the micro-spatula on the silastic membrane is simplified, since the stretch magnitude changes continuously and not discrete steps as shown here. The differently colored areas represent the length increase calculated by subtracting the displacement at the most far away distance from the micro-spatula (e.g. 50 µm) to the displacement at the closest distance from the micro-spatula (e.g. 30 µm) at each selected range. In the drawing, the micro-spatula is shown in blue at center top and membrane areas with different distances from the tip in yellow (10-30 µm from the tip); in green (30-50 µm) and in blue (50-70 µm). The left half of the scheme shows the horizontal displacement that the cells experience whereas the right half of the picture shows the displacement that the cells experience in the z-axis. (B) Horizontal stretch (average ± SD) shown in a histogram. The red bar represents the average stretch that cells experienced at 30-50 µm distance. (C) Two ATII cells before and after stretch. The cell membrane is highlighted by the solid lines. The dashed lines on the left panel show the outline of the cell before stretch. Abbreviation: ATII, alveolar typeII.
genes involved in muscle fiber switching, fatty acid utilization, oxidative phosphorylation, mitochondrial bio- genesis and function [4,5], and angiogenesis . Skeletal muscle contains two major types of muscle fibers which differ in their contractile proteins and their metabolic cap- acity . The typeII fibers (“glycolytic fibers”) have a little number of mitochondria and largely generate ATP through glycolytic metabolism, whereas type I fibers (“oxi- dative fibers”) are mitochondria-rich and thus utilize mainly oxidative phosphorylation [8,9]. Interestingly, the distribution of type I and typeII fibers of skeletal muscles shows high plasticity and can be altered by diverse factors, such as exercise, mechanical unloading, obesity or dia- betes, resulting in a change of the muscle’s functional and metabolic phenotype [10-13]. In an attempt to study whether the induction of PPARδ and PGC-1α in skeletal muscle by pharmacological niacin doses leads to a change of muscle fiber distribution and the muscle’s metabolic phenotype, we have previously tested the effect of niacin supplementation at a dose used for reduction of serum lipids in obese Zucker rats  and pigs . Both studies revealed that niacin supplementation induces muscle fiber transition from typeII to type I and increases the number of type I fibers in skeletal muscle [14,15]. Moreover, we found that the expression of genes involved in fatty acid transport, mitochondrial fatty acid import and oxidation, oxidative phosphorylation and angiogenesis and genes encoding PPARδ, PGC-1α and PGC-1β (encoded by PPARGC1B), which, like PGC-1α, is a key regulator of skeletal muscle’s oxidative and contractile phenotype , in skeletal muscle is elevated by niacin treatment [14,15]. Thus, these findings suggest that niacin induces a change in the muscle metabolic phenotype which is indicative of an increased capacity of muscle for oxidative utilization of fatty acids and which might be useful during metabolic states where TAG and NEFA are strongly elevated, such as during early lactation in high producing dairy cows . However, whether niacin treatment also causes typeII to type I muscle fiber switching and increases the type I fiber content of skeletal muscles in ruminants has not been investigated yet. Thus, the present study aimed to investigate whether niacin administration at a pharma- cological dose influences fiber distribution and the meta- bolic phenotype of different skeletal muscles in sheep as a model for ruminants. Niacin was administrated by drenching ensuring that the main part of the adminis- trated niacin bypasses the rumen and reaches the small intestine.
In this chapter, I recapitulate known mathematical facts that are needed as a basis for the following string theory constructions in the present work. In section 2.1, I intro- duce Calabi-Yau manifolds, which are usually the underlying mathematical objects for the six-dimensional internal space of string theory due to their special characteristics. The subsequent section 2.2 deals with concrete examples of manifolds that will all prove to be useful for the later discussions, and especially various descriptions of the torus will be considered in more detail in section 2.3. The next section 2.4 deals with the mathem- atical objects called orbifolds, which will reappear in section 3.1 in much more detail as concrete string theory backgrounds for the six-dimensional internal space. In section 2.5, the concepts of homology and cohomology are presented, which make it possible to define certain topological invariants on a manifold. In addition, one can build equivalence classes of closed subspaces of a manifold, the so-called cycles, that are used in order to build con- crete models in typeII string theories, and which reappear in this context in section 3.1.3. In the last part of this chapter, the ideas of the moduli space and metric deformations are introduced (section 2.6), which play a major role in my own analysis of string theory backgrounds.
The new ortho-implant typeII anchor system (Orthosys- tem ® , Straumann, Basel, Switzerland; Fig.1) available with
diameters of 4.1 mm and 4.8 mm, is a pure titanium 1- piece device. It consists of a endosseous implant body, a transmucosal implant neck, abutment, fixation cap and occlusal screw, all parts being made of pure titanium except the occlusal screw (stainless steal). The endosseous implant body has a self-tapping thread with a sand- blasted, large grit, acid-etched (SLA ® ) surface. A set of burs
For sample size calculation an implant failure rate of 5 % for group 1 (implant loading after a post-surgical healing period of 12 weeks) an implant failure rate of 25 % for group 2 (early implant loading within 1 week post implantation) was assumed. Based on 0.8 power to detect a significant difference at the two sided 5% level with an assumed loss to follow-up of 5 %, 62 patients in each group and 124 in total will be required. Sample size calcu- lation, which based on clinical experiences with the new Orthosystem typeII and early functional loading of con- ventional dental implants, was estimated with nQuery Advisor ® (Version 3.0) by the Institute of Medical Biosta- tistics, Epidemiology and Informatics (WH), University of Berlin, Germany.
had a BMI >= 25. In our BiDi sample, 78% of the participants had a BMI > 25. Taken together, we propose that overweight and obesity might be the mediating factors between BD and T2D, and that the risk for T2D in BD in comparison to the general population may not be increased in BD as such but rather the risk towards obesity. A previous Italian study and a follow-up study could also show that abdominal obesity as a major factor of the metabolic syndrome was associated with a higher rate of T2D in bipolar patients ( 54 , 55 ). The higher rate of obesity can be due to either lifestyle factors (food pattern, sedentary lifestyle), medication in ﬂuence (especially second-generation antipsychotics such as olanzapine and quetiapine) ( 56 ) as well as shared risk genes for BD and BMI ( 57 ). However, as a limiting factor in our study, we did not include other factors that, especially in men, have shown to increase the risk of T2D like smoking and arterial hypertension ( 58 , 59 ). In our sample, there was however no signi ﬁcant difference between the types of mood stabilizing medication in the diabetic vs. the nondiabetic group. But then, also valproate and lithium can lead to weight gain and not only atypical antipsychotics ( 19 , 60 ). Also, our sample size in the medication subgroups was too small to make de ﬁnite conclusions hereon. Interestingly, in a multivariate analysis comparing the nondiabetic and (pre-)diabetic bipolar groups, disease duration and number of depressive episodes, as well as BMI and age, remained statistically signi ﬁcant between the groups. Furthermore, metabolic parameters were signiﬁcantly correlated with the number of depressed episodes. There are previous studies that suggest that comorbid insulin resistance, diabetes mellitus typeII, and an increased BMI might lead to a more severe course in bipolar patients ( 61 – 63 ). From our data, we might conclude that increased BMI is the major contributor to an increased risk for T2D in BD in comparison to the general population; however, disease duration and depressive polarity might add to the risk of developing T2D in BD patients. However, as our study was a cross-sectional and not a longitudinal study, we cannot con ﬁrm the direction of the association of impaired metabolic parameters and a more severe course. Diagnosing and monitoring of overweight and prediabetes and T2DM in BD are furthermore of importance as there is growing evidence that impaired glucose metabolism and