Solar Energy Harvesting in WSN with Development Tool

The aim of this thesis was to introduce a solar energy and wsn, as well as to introduce how the solar energy harvesting development tool helps create a perpetually powered wireless sensor network and provides enough power to run a wireless sensor application with no additional batteries. Solar energy is radiant light and heat from the sun. WSN is widely used in modern society. In this project these two areas were combined and it was studied to use the solar energy harvesting in a wireless sensor network with the development tool. As a result of this thesis, the SEH module's solar panel was optimized for operating lights, which provides enough power to run a wireless sensor application with no additional batteries

Small molecule-mediated tribbles homolog 3 promotes bone formation induced by bone morphogenetic protein-2.

Although bone morphogenetic protein-2 (BMP2) has demonstrated extraordinary potential in bone formation, its clinical applications require supraphysiological milligram-level doses that increase postoperative inflammation and inappropriate adipogenesis, resulting in well-documented life-threatening cervical swelling and cyst-like bone formation. Recent promising alternative biomolecular strategies are toward promoting pro-osteogenic activity of BMP2 while simultaneously suppressing its adverse effects. Here, we demonstrated that small molecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat critical size mandibular defect model. Moreover, we successfully elicited the BMP2 adverse outcomes (i.e. adipogenesis and inflammation) in the mandibular defect by applying high dose BMP2. Phenamil treatment significantly improves the quality of newly formed bone by inhibiting BMP2 induced fatty cyst-like structure and inflammatory soft-tissue swelling. The observed positive phenamil effects were associated with upregulation of tribbles homolog 3 (Trib3) that suppressed adipogenic differentiation and inflammatory responses by negatively regulating PPARγ and NF-κB transcriptional activities. Thus, use of BMP2 along with phenamil stimulation or Trib3 augmentation may be a promising strategy to improve clinical efficacy and safety of current BMP therapeutics

Enhanced Osteogenesis of Adipose-Derived Stem Cells by Regulating Bone Morphogenetic Protein Signaling Antagonists and Agonists.

UnlabelledAlthough adipose-derived stem cells (ASCs) are an attractive cell source for bone tissue engineering, direct use of ASCs alone has had limited success in the treatment of large bone defects. Although bone morphogenetic proteins (BMPs) are believed to be the most potent osteoinductive factors to promote osteogenic differentiation of ASCs, their clinical applications require supraphysiological dosage, leading to high medical burden and adverse side effects. In the present study, we demonstrated an alternative approach that can effectively complement the BMP activity to maximize the osteogenesis of ASCs without exogenous application of BMPs by regulating levels of antagonists and agonists to BMP signaling. Treatment of ASCs with the amiloride derivative phenamil, a positive regulator of BMP signaling, combined with gene manipulation to suppress the BMP antagonist noggin, significantly enhanced osteogenic differentiation of ASCs through increased BMP-Smad signaling in vitro. Furthermore, the combination approach of noggin suppression and phenamil stimulation enhanced the BMP signaling and bone repair in a mouse calvarial defect model by adding noggin knockdown ASCs to apatite-coated poly(lactic-coglycolic acid) scaffolds loaded with phenamil. These results suggest novel complementary osteoinductive strategies that could maximize activity of the BMP pathway in ASC bone repair while reducing potential adverse effects of current BMP-based therapeutics.SignificanceAlthough stem cell-based tissue engineering strategy offers a promising alternative to repair damaged bone, direct use of stem cells alone is not adequate for challenging healing environments such as in large bone defects. This study demonstrates a novel strategy to maximize bone formation pathways in osteogenic differentiation of mesenchymal stem cells and functional bone formation by combining gene manipulation with a small molecule activator toward osteogenesis. The findings indicate promising stem cell-based therapy for treating bone defects that can effectively complement or replace current osteoinductive therapeutics

Design and implementation of LTE-A and 5G kernel algorithms on SIMD vector processor

With the wide spread of wireless technology, the time for 4G has arrived, and 5G will appear not so far in the future. However, no matter whether it is 4G or 5G, low latency is a mandatory requirement for baseband processing at base stations for modern cellular standards. In particular, in a future 5G wireless system, with massive MIMO and ultra-dense cells, the demand for low round trip latency between the mobile device and the base station requires a baseband processing delay of 1 ms. This is 10 percentage of today’s LTE-A round trip latency, while at the same time massive MIMO requires large-scale matrix computations. This is especially true for channel estimation and MIMO detection at the base station. Therefore, it is essential to ensure low latency for the user data traffic. In this master’s thesis, LTE/LTE-A uplink physical layer processing is examined, especially the process of channel estimation and MIMO detection. In order to analyze this processing we compare two conventional algorithms’ performance and complexity for channel estimation and MIMO detection. The key aspect which affects the algorithms’ speed is identified as the need for “massive complex matrix inversion”. A parallel coding scheme is proposed to implement a matrix inversion kernel algorithm on a single instruction multiple data stream (SIMD) vector processor. The major contribution of this thesis is implementation and evaluation of a parallel massive complex matrix inversion algorithm. Two aspects have been addressed: the selection of the algorithm to perform this matrix computation and the implementation of a highly parallel version of this algorithm.Med den breda spridningen av trådlös teknik, har tiden för 4G kommit, och 5G kommer inom en överskådlig framtid. Men oavsett om det gäller 4G eller 5G, låg latens är ett obligatoriskt krav för basbandsbehandling vid basstationer för moderna mobila standarder. I synnerhet i ett framtida trådlöst 5G-system, med massiva MIMO och ultratäta celler, behövs en basbandsbehandling fördröjning på 1 ms för att klara efterfrågan på en låg rundresa latens mellan den mobila enheten och basstationen. Detta är 10 procent av dagens LTE-E rundresa latens, medan massiva MIMO samtidigt kräver storskaliga matrisberäkningar. Detta är särskilt viktigt för kanaluppskattning och MIMO-detektion vid basstationen. Därför är det viktigt att se till att det är låg latens för användardatatrafik. I detta examensarbete, skall LTE/LTE-A upplänk fysiska lagret bearbetning undersökas, och då särskilt processen för kanaluppskattning och MIMO-detektion. För att analysera denna processing jämför vi två konventionella algoritmers prestationer och komplexitet för kanaluppskattning och MIMO-detektion. Den viktigaste aspekten som påverkar algoritmernas hastighet identifieras som behovet av "massiva komplex matrisinversion". Ett parallellt kodningsschema föreslås för att implementera en "matrisinversion kernel-algoritmen" på singelinstruktion multidataström (SIMD) vektorprocessor. Det största bidraget med denna avhandling är genomförande och utvärdering av en parallell massiva komplex matrisinversion kernel-algoritmen. Två aspekter har tagits upp: valet av algoritm för att utföra denna matrisberäkning och implementationen av en högst parallell version av denna algoritm

TLR1/2 Specific Small‐Molecule Agonist Suppresses Leukemia Cancer Cell Growth by Stimulating Cytotoxic T Lymphocytes

Abstract Toll‐like receptor 2 (TLR2) expressed on antigen presenting cells evokes a series of critical cytokines, which favor the development of tumor‐specific cytotoxic T lymphocytes (CTLs). Therefore, TLR2 represents an attractive cancer immunotherapeutic target. Here, a synthetic library of 14 000 compounds together with a series of newly developed compounds for NF‐κB activation using HEK‐Blue hTLR2 cells is initially screened. Following further screening in a variety of cells including HEK‐Blue hTLRs reporter cells, murine, and human macrophage cell lines, a potent small molecule agonist 23 (SMU‐Z1) is identified, which specifically activates TLR2 through its association with TLR1, with a EC50 of 4.88 ± 0.79 × 10−9 m. Toxicology studies, proinflammatory cytokines (e.g., TNF‐α, IL‐1β, IL‐6, and nitric oxide) and target‐protein based biophysical assays demonstrate the pharmacologically relevant characteristics of SMU‐Z1. In addition, SMU‐Z1 promotes murine splenocyte proliferation and upregulates the expression of CD8+ T cells, NK cells and DCs, which results in a significant antitumor effect in a murine leukemia model. Finally, the induced tumors in three out of seven mice disappear after administration of SMU‐Z1. Our studies thus identify a novel and potent TLR1/2 small molecule agonist, which displays promising immune adjuvant properties and antitumor immunity

Enhanced Mandibular Bone Repair by Combined Treatment of Bone Morphogenetic Protein 2 and Small-Molecule Phenamil.

Growth factor-based therapeutics using bone morphogenetic protein 2 (BMP-2) presents a promising strategy to reconstruct craniofacial bone defects such as mandible. However, clinical applications require supraphysiological BMP doses that often increase inappropriate adipogenesis, resulting in well-documented, cyst-like bone formation. Here we reported a novel complementary strategy to enhance osteogenesis and mandibular bone repair by using small-molecule phenamil that has been shown to be a strong activator of BMP signaling. Phenamil synergistically induced osteogenic differentiation of human bone marrow mesenchymal stem cells with BMP-2 while suppressing their adipogenic differentiation induced by BMP-2 in vitro. The observed pro-osteogenic and antiadipogenic activity of phenamil was mediated by expression of tribbles homolog 3 (Trb3) that enhanced BMP-smad signaling and inhibited expression of peroxisome proliferator-activated receptor gamma (PPARγ), a master regulator of adipogenesis. The synergistic effect of BMP-2+phenamil on bone regeneration was further confirmed in a critical-sized rat mandibular bone defect by implanting polymer scaffolds designed to slowly release the therapeutic molecules. These findings indicate a new complementary osteoinductive strategy to improve clinical efficacy and safety of current BMP-based therapeutics

Sustainable Radical Cascades to Synthesize Difluoroalkylated Pyrrolo[1,2‑<i>a</i>]indoles

We disclose herein a photocatalytic difluoroalkylation and cyclization cascade reaction of <i>N</i>-(but-2-enoyl)­indoles with broad substrate scopes in up to 90% isolated yield. This method provides sustainable and efficient access to synthesize difluoroalkylated pyrrolo­[1,2-<i>a</i>]­indoles with a quaternary carbon center under mild conditions

Small molecule-mediated tribbles homolog 3 promotes bone formation induced by bone morphogenetic protein-2.

Although bone morphogenetic protein-2 (BMP2) has demonstrated extraordinary potential in bone formation, its clinical applications require supraphysiological milligram-level doses that increase postoperative inflammation and inappropriate adipogenesis, resulting in well-documented life-threatening cervical swelling and cyst-like bone formation. Recent promising alternative biomolecular strategies are toward promoting pro-osteogenic activity of BMP2 while simultaneously suppressing its adverse effects. Here, we demonstrated that small molecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat critical size mandibular defect model. Moreover, we successfully elicited the BMP2 adverse outcomes (i.e. adipogenesis and inflammation) in the mandibular defect by applying high dose BMP2. Phenamil treatment significantly improves the quality of newly formed bone by inhibiting BMP2 induced fatty cyst-like structure and inflammatory soft-tissue swelling. The observed positive phenamil effects were associated with upregulation of tribbles homolog 3 (Trib3) that suppressed adipogenic differentiation and inflammatory responses by negatively regulating PPARγ and NF-κB transcriptional activities. Thus, use of BMP2 along with phenamil stimulation or Trib3 augmentation may be a promising strategy to improve clinical efficacy and safety of current BMP therapeutics

Trb3 controls mesenchymal stem cell lineage fate and enhances bone regeneration by scaffold-mediated local gene delivery

Aberrant lineage commitment of mesenchymal stem cells (MSCs) in marrow contributes to abnormal bone formation due to reduced osteogenic and increased adipogenic potency. While several major transcriptional factors associated with lineage differentiation have been found during the last few decades, the molecular switch for MSC fate determination and its role in skeletal regeneration remains largely unknown, limiting creation of effective therapeutic approaches. Tribbles homolog 3 (Trb3), a member of tribbles family pseudokinases, is known to exert diverse roles in cellular differentiation. Here, we investigated the reciprocal role of Trb3 in the regulation of osteogenic and adipogenic differentiation of MSCs in the context of bone formation, and examined the mechanisms by which Trb3 controls the adipo-osteogenic balance. Trb3 promoted osteoblastic commitment of MSCs at the expense of adipocyte differentiation. Mechanistically, Trb3 regulated cell-fate choice of MSCs through BMP/Smad and Wnt/β-catenin signals. Importantly, in vivo local delivery of Trb3 using a novel gelatin-conjugated caffeic acid-coated apatite/PLGA (GelCA-PLGA) scaffold stimulated robust bone regeneration and inhibited fat-filled cyst formation in rodent non-healing mandibular defect models. These findings demonstrate Trb3-based therapeutic strategies that favor osteoblastogenesis over adipogenesis for improved skeletal regeneration and future treatment of bone-loss disease. The distinctive approach implementing a scaffold-mediated local gene transfer may further broaden the translational use of targeting specific therapeutic gene related to lineage commitment for clinical bone treatment

Statistics of the seed weight, seed size and fresh seed weight at different periods of development.

<p>Statistics of the seed weight, seed size and fresh seed weight at different periods of development.</p