Inter-chip input-output (I/O) communication bandwidth demand, which rapidly scaled with integrated circuit scaling, has leveraged equalization techniques to operate reliably on band-limited channels at additional power and area complexity. High-bandwidth inter-chip optical interconnect architectures have the potential to address this increasing I/O bandwidth. Considering future tera-scale systems, power dissipation of the high-speed I/O link becomes a significant concern. This work presents a design flow for the power optimization and comparison of high-speed electrical and optical links at a given data rate and channel type in 90 nm and 45 nm CMOS technologies. The electrical I/O design framework combines statistical link analysis techniques, which are used to determine the link margins at a given bit-error rate (BER), with circuit power estimates based on normalized transistor parameters extracted with a constant current density methodology to predict the power-optimum equalization architecture, circuit style, and transmit swing at a given data rate and process node for three different channels. The transmitter output swing is scaled to operate the link at optimal power efficiency. Under consideration for optical links are a near-term architecture consisting of discrete vertical-cavity surface-emitting lasers (VCSEL) with p-i-n photodetectors (PD) and three long-term integrated photonic architectures that use waveguide metal-semiconductor-metal (MSM) photodetectors and either electro-absorption modulator (EAM), ring resonator modulator (RRM), or Mach-Zehnder modulator (MZM) sources. The normalized transistor parameters are applied to jointly optimize the transmitter and receiver circuitry to minimize total optical link power dissipation for a specified data rate and process technology at a given BER. Analysis results shows that low loss channel characteristics and minimal circuit complexity, together with scaling of transmitter output swing, allows electrical links to achieve excellent power efficiency at high data rates. While the high-loss channel is primarily limited by severe frequency dependent losses to 12 Gb/s, the critical timing path of the first tap of the decision feedback equalizer (DFE) limits the operation of low-loss channels above 20 Gb/s. Among the optical links, the VCSEL-based link is limited by its bandwidth and maximum power levels to a data rate of 24 Gb/s whereas EAM and RRM are both attractive integrated photonic technologies capable of scaling data rates past 30 Gb/s achieving excellent power efficiency in the 45 nm node and are primarily limited by coupling and device insertion losses. While MZM offers robust operation due to its wide optical bandwidth, significant improvements in power efficiency must be achieved to become applicable for high density applications.

The thesis focuses on a higher order noise-shaping Δ ADC architecture which employs filtered quantization error as a dither signal. Furthermore, the work studies implementation challenges using Switched-Capacitor and Switched-Current techniques. Digitization in an IF conversion receiver can be accomplished either with a wide band Nyquist rate ADC or a BandPass Δ ADC. The use of the latter is the optimum solution since the bandwidth of the IF signals is typically much smaller than the carrier frequency and reducing the quantization noise in the entire nyquist band becomes superfluous. Instead by using BandPass Δ ADCs the quantization noise power is reduced only in a narrow band around IF location. We study state-of-the-art high dynamic range Δ data converter topologies suited for wide-band radio receivers. We propose a topology which achieves higher order noise shaping by employing filtered quantization error as a dither signal. We study implementation challenges for Δ converters in digital technology. Traditionally, Δ ADCs used Switched-Capacitor (SC) circuits to realize their building blocks. This analog sample-data technique is based on the idea that a periodically switched capacitor can emulate a resistor. The limiting factor that degrades the performance of SC circuits implemented in standard VLSI technologies is the continuous reduction of supply voltages, prompted by the continuous scaling-down process. This fact, which is advantageous for digital circuitry, makes the design of SC circuits difficult, which are forced to use clock boosting strategies for switches and to increase the power consumption in order to obtain high-speed and high dynamic range opamps with low voltage operation. In this scenario, the use of current-domain sampled data technique, also named Switched-Current (SI), instead of voltages results advantageous for several reasons. As the signal carriers are currents, the supply voltage does not limit the signal range as much as in SC circuits. Therefore, SI circuits are more suitable than SC for low-voltage operation. This work studies the feasibility and bottlenecks of implementing Δ modulator building blocks using SI technique. A BandPass filter, DAC and 1-bit quantizer have been designed in 0.18µm technology using SI technique. (For mathematical equations pl refer the pdf file)

Thesis (PhD)--Stellenbosch University, 2015. / ENGLISH ABSTRACT: In this work we investigate a new method to measure the electric field of ultrafast laser pulses by extending a known measurement technique, ptychography, in the spatial domain to the time domain which we call time domain ptychography. The technique requires the measurement of intensity spectra at different time delays of an unknown temporal object and a known probe pulse. We show for the first time by measurement and calculation that this technique can be applied with excellent results to recover both the amplitude and phase of a temporal object. This technique has several advantages, such as fast convergence, the resolution is limited by the usable measured spectral bandwidth and the recovered phase has no sign ambiguity. We then extend the technique to pulse characterization where the probe is derived form the temporal object by filtering meaning the probe pulse is also unknown, but the spectrum of the probe pulse must be the same as the spectrum of the temporal object before filtering. We modify the reconstruction algorithm, now called ptychographic iterative reconstruction algorithm for time domain pulses (PIRANA), in order to also reconstruct the probe and we show for the first time that temporal objects, a.k.a laser pulses, can be reconstructed with this new modality. / AFRIKAANSE OPSOMMING: In hierdie werk het ons ’n nuwe metode ondersoek om die elektriese veld van ’n ultravinnige laser puls te meet deur ’n bekende meettegniek wat gebruik word in die ruimtelike gebied, tigografie, aan te pas vir gebruik in die tyd gebied genaamd tyd gebied tigografie. Die tegniek vereis die meting van ’n reeks intensiteit spektra by verskillende tyd intervalle van ’n onbekende ‘tyd voorwerp’ en ’n bekende monster puls. Ons wys vir die eerste keer deur meting en numeriese berekening dat hierdie tegniek toegepas kan word met uitstekende resultate, om die amplitude en fase van ’n ‘tyd voorwerp’ te meet. Hierdie tegniek het verskeie voordele, die iteratiewe proses is vinnig, die resolusie van die tegniek word bepaal deur die spektrale bandwydte gemeet en die fase van die ‘tyd voorwerp’ word met die korrekte teken gerekonstrueer. Ons het hierdie tegniek uitgebrei na puls karakterisering waar die monster pulse afgelei word, deur ’n bekende filter te gebruik, van die onbekende ‘tyd voorwerp’ nl. die inset puls. Ons het die iteratiewe algoritme wat die ‘tyd voorwerp’ rekonstrueer aangepas om ook die monster puls te vind en ons wys dat ons hierdie metode suksesvol kan gebruik om laser pulse te karakteriseer

The α7 nicotinic acetylcholine receptor (nAChR) subtype is abundantly expressed in the central nervous system (CNS) and in the periphery. Positive allosteric modulators (PAMs) of the α7 increase the response to an agonist and are divided into two types depending on whether they also decrease desensitization of the receptor (type II) or not (type I). Therefore, this study aims to investigate whether the enhancement of endogenous α7 nAChR function will result in a beneficial effect in nociceptive, inflammatory and chronic neuropathic pain models. While NS1738 and PNU-120596 were not active to reduce acute thermal pain, measured by hot-plate and tail-flick tests, only PNU-120596 dose-dependently attenuated paw-licking behavior in the formalin test. Our results with selective (MEK) inhibitor U0126 argues for an important role of extracellular signal-regulated kinase (ERK1/2) pathways activation in PNU-120596’s antinociceptive effects in formalin-induced pain. The α7 antagonist MLA, via intrathecal and intraplantar administration, reversed PNU-120596’s effects, confirming PNU-120596’s action through central and peripheral α7 nAChRs. Tolerance to PNU-120596 was not developed after chronic treatment of the drug. Furthermore, mixtures of PNU-120596 and choline, an endogenous α7 nAChR agonist, synergistically reduced formalin-induced pain, while interactions of non-antinociceptive doses of PNU-120596 and PHA-543613, a selective α7 nAChR agonist, or nicotine resulted in antinociception. In contrast, PNU-120596 failed to enhance nicotine-induced convulsions, -hypomotility and –antinociception in acute pain models. Surprisingly, it enhanced nicotine-induced hypothermia via α7 nAChRs. In the carrageenan inflammatory test both NS1738 and PNU-120596 significantly reduced thermal hyperalgesia, while only PNU-120596 significantly reduced edema. Importantly, PNU-120596 reversed established thermal hyperalgesia and edema induced by carrageenan. In the chronic neuropathic pain (CCI) model, PNU-120596 had long-lasting (up to 6 hrs), dose-dependent anti-hyperalgesic and anti-allodynic effects after a single injection, while NS1738 was inactive. Subcutaneous and intrathecal administration of MLA reversed PNU-120596’s effects, suggesting the involvement of α7 nAChRs. Finally, PNU-120596 enhanced an ineffective dose of selective agonist PHA-543613 to produce anti-allodynic effects in the CCI model. Our results show a fundamental in vivo difference between type I and II α7 nAChR PAMs, and demonstrate type II’s potential for the treatment of chronic inflammatory pain.

des-Formylflustrabromine (dFBr), isolated from the marine organism Flustra foliacea, is the first selective, positive allosteric modulator (PAM) of α4β2 nicotinic acetylcholine receptors that potentiates the action of the neurotransmitter acetylcholine (ACh). Most agonists for this receptor population are not selective and can activate other nACh receptors. A selective PAM, which activates α4β2 nACh receptors only in the presence of ACh, might find application in the treatment of of various neurological diseases such as Alzheimer’s disease or autism. dFBr was examined and found to produce a biphasic dose-response curve over a wide concentration range (i.e., potentiation at low concentration, but inhibition of the ACh-induced response at high concentrations). Our goal was to examine various structural features of dFBr required for potentiation; a secondary goal was to examine the same for inhibition. To understand the structural requirements of dFBr, a systematic ‘deconstruction reconstruction and elaboration’ approach (see p. 48) was employed to determine the contribution of various structural components of dFBr to its activity at α4β2 nACh receptors. Novel compounds were synthesized and characterized. Human α4β2 nACh receptors were expressed in Xenopus oocytes and the actions of dFBr and its analogs were measured using a two-electrode voltage clamp technique. Dose-response curves were obtained for the compounds in the absence and presence of 100 μM ACh. Structural features of dFBr optimal and/or required for PAM action at 42 nACh receptors were identified. A novel reconstructed analog with all the essential features for PAM action was synthesized and submitted for biological testing. Elaborated analogs of dFBr further helped in identification of various structural features important for PAM action and the inhibition of action of ACh. The ‘deconstruction reconstruction and elaboration’ approach (see p.48) identified important structural features of dFBr that modify its actions as a PAM or an antagonist (NAM? or channel blocker?) at α4β2 nACh receptors. This information should be useful for the subsequent design of novel analogs to evaluate their potential for the treatment of neurological disorders associated with ACh.

No description available.

Ce travail vise à concevoir un modulateur optique assisté par plamsons, compatible CMOS et à faible consommation électrique. L’électro-absorption, basée sur l’effet Franz-Keldysh dans le germanium, a été choisie comme principe de modulation pour réduire la taille du dispositif et la consommation d'énergie électrique associée. L’effet Franz-Keldysh se traduit par un changement du coefficient d'absorption du matériau près du bord de bande sous l'application d'un champ électrique statique, d'où la production d'une modulation directe de l'intensité lumineuse. L'utilisation de plasmons permet en principe d’augmenter l'effet électro-optique en raison du fort confinement du mode optique. Un outil de simulation électro-optique intégré a été développé pour concevoir et optimiser le modulateur. Le modulateur plasmonique proposé a un taux d'extinction de 3.3 dB avec des pertes d'insertion de 11.2 dB et une consommation électrique de seulement 20 fJ/bit, soit la plus faible consommation électrique décrite pour les modulateurs photoniques sur silicium. Le couplage du modulateur à un guide silicium standard en entrée et en sortie a également été optimisé par l’introduction d'un adaptateur de mode Si-Ge optimisé, réduisant les pertes de couplage à seulement 1 dB par coupleur. Par ailleurs, un travail expérimental a été effectué pour tenter de déplacer l'effet Franz-Keldysh, maximum à 1650 nm, à de plus faibles longueurs d'onde proches de 1.55 μm pour des applications aux télécommunications optiques. / This work aims to design a CMOS compatible, low-electrical power consumption modulator assisted by plasmons. For compactness and reduction of the electrical power consumption, electro-absorption based on the Franz-Keldysh effect in Germanium was chosen for modulation. It consists in the change of the absorption coefficient of the material near the band edge under the application of a static electric field, hence producing a direct modulation of the light intensity. The use of plasmons allows enhancing the electro-optical effect due to the high field confinement. An integrated electro-optical simulation tool was developed to design and optimize the modulator. The designed plasmonic modulator has an extinction ratio of 3.3 dB with insertion losses of 13.2 dB and electrical power consumption as low as 20 fJ/bit, i.e. the lowest electrical power consumption reported for silicon photonic modulators. In- and out-coupling to a standard silicon waveguide was also engineered by the means of an optimized Si-Ge taper, reducing the coupling losses to only 1 dB per coupler. Besides, an experimental work was carried out to try to shift the Franz-Keldysh effect, which is maximum at 1650 nm, to lower wavelength close to 1.55 μm for telecommunication applications.

This thesis details the design, construction and characterisation of an ultracold atoms system, developed in conjunction with a flexible optical trapping scheme which utilises a Liquid Crystal Spatial Light Modulator (LC SLM). The ultracold atoms system uses a hybrid trap formed of a quadrupole magnetic field and a focused far-detuned laser beam to form a Bose-Einstein Condensate of 2×105 87Rb atoms. Cold atoms confined in several arbitrary optical trapping geometries are created by overlaying the LC SLM trap on to the hybrid trap, where a simple feedback process using the atomic distribution as a metric is shown to be capable of compensating for optical aberrations. Two novel methods for creating flexible optical traps with the LC SLM are also detailed, the first of which is a multi-wavelength technique which allows several wavelengths of light to be smoothly shaped and applied to the atoms. The second method uses a computationally-efficient minimisation algorithm to create light patterns which are constrained in both amplitude and phase, where the extra phase constraint was shown to be crucial for controlling propagation effects of the LC SLM trapping beam.

by Cheung Tak Chi. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 117-123). / Abstract also in Chinese. / Acknowledgeements --- p.i / Abbreviations --- p.ii / Abstract --- p.v / List of Figures --- p.viii / List of Tables --- p.xiv / Contents --- p.xv / Contents / Chapter 1. --- Introduction --- p.1 / Chapter 1.1 --- Epidemiological Risk Factors --- p.1 / Chapter 1.1.1 --- Age --- p.1 / Chapter 1.1.2 --- Race --- p.2 / Chapter 1.1.3 --- Environmental or Migratory Factor --- p.2 / Chapter 1.1.4 --- Diet --- p.2 / Chapter 1.1.5 --- Genetics --- p.3 / Chapter 1.2 --- Regulation of Normal Prostate Development and Function --- p.4 / Chapter 1.3 --- Biochemistry and Development of Prostate Cancer --- p.6 / Chapter 1.3.1 --- Androgen-Dependent Prostate Cancer --- p.6 / Chapter 1.3.2 --- Androgen-Independent Prostate Cancer --- p.8 / Chapter 1.4 --- Classification of Prostate Cancer --- p.9 / Chapter 1.4.1 --- Stage A Prostate Cancer --- p.10 / Chapter 1.4.2 --- Stage B Prostate Cancer --- p.10 / Chapter 1.4.3 --- Stage C Prostate Cancer --- p.11 / Chapter 1.4.4 --- Stage D Prostate Cancer --- p.11 / Chapter 1.5 --- Methods for Early Detection of Prostate Cancer --- p.12 / Chapter 1.6 --- Clinical Treatment of Prostate Cancer --- p.12 / Chapter 1.6.1 --- Surgery --- p.12 / Chapter 1.6.2 --- Radiotherapy --- p.13 / Chapter 1.6.3 --- Chemotherapy --- p.13 / Chapter 1.6.4 --- Hormonal Therapy --- p.13 / Chapter 1.7 --- Objective --- p.14 / Chapter 1.8 --- Estrogen and Its Related Compounds --- p.16 / Chapter 1.8.1 --- 17β-Estradiol --- p.16 / Chapter 1.8.2 --- Tamoxifen --- p.18 / Chapter 1.8.3 --- Aromatase Inhibitor --- p.20 / Chapter 1.9 --- Anticancer Drugs --- p.23 / Chapter 1.9.1 --- Doxorubicin --- p.23 / Chapter 1.9.2 --- cis-Platinum --- p.24 / Chapter 1.10 --- Apoptotic Pathways --- p.25 / Chapter 1.10.1 --- BCL-2 /BAD Pathway --- p.26 / Chapter 1.10.2 --- FADD Pathway --- p.27 / Chapter 1.10.3 --- CAS Pathway --- p.27 / Chapter 2. --- Materials and Methods --- p.28 / Chapter 2.1 --- Materials --- p.28 / Chapter 2.2 --- Cell Lines --- p.32 / Chapter 2.3 --- Preparation of Drugs --- p.32 / Chapter 2.4 --- Drug Sensitivity Assay --- p.33 / Chapter 2.5 --- Cell Cycle Analysis --- p.35 / Chapter 2.6 --- DNA Fragmentation Assay --- p.36 / Chapter 2.7 --- Annexin Binding Assay --- p.37 / Chapter 2.8 --- Western Blot Analysis --- p.38 / Chapter 2.9 --- Data Analysis --- p.41 / Chapter 3. --- Results --- p.42 / Chapter 3.1 --- Response of Human Androgen-Independent Prostate Cancer Cells to Doxorubicin and cis-Platinum --- p.42 / Chapter 3.2 --- The Effect of 17p-Estradiol on the Growth and Anticancer Drug Sensitivity of Human Androgen-Independent Prostate Cancer Cells --- p.45 / Chapter 3.2.1 --- 17β-Estradiol on Cell Growth --- p.45 / Chapter 3.2.2 --- 17β-Estradiol on Anticancer Drug Sensitivity --- p.45 / Chapter 3.2.3 --- 17β-Estradiol and Doxorubicin on Cell Cycle Progression --- p.51 / Chapter 3.2.4 --- 17β-Estradiol and Doxorubicin Induced DNA Fragmentation --- p.57 / Chapter 3.2.5 --- 17β-Estradiol and Doxorubicin on Annexin Staining --- p.59 / Chapter 3.2.6 --- 17β-Estradiol and Doxorubicin on Apoptotic Protein Expression --- p.62 / Chapter 3.3 --- The Effect of Tamoxifen on the Growth and Anticancer Drug Sensitivity of Human Androgen-Independent Prostate Cancer Cells --- p.64 / Chapter 3.3.1 --- Tamoxifen on Cell Growth of Human --- p.65 / Chapter 3.3.2 --- Tamoxifen on Anticancer Drug Sensitivity --- p.65 / Chapter 3.3.3 --- Tamoxifen and Doxorubicin on Cell Cycle Progression --- p.71 / Chapter 3.3.4 --- Tamoxifen and Doxorubicin Induced DNA Fragmentation --- p.76 / Chapter 3.3.5 --- Tamoxifen and Doxorubicin on Annexin Staining --- p.78 / Chapter 3.3.6 --- Tamoxifen and Doxorubicin on Apoptotic Protein Expression --- p.79 / Chapter 3.4 --- The Effect of Aromatase Inhibtiors on the Growth and Anticancer Drug Sensitivity of Human Androgen-Independent Prostate Cancer Cells --- p.81 / Chapter 3.4.1 --- Aromatase Inhibitors on Cell Growth --- p.81 / Chapter 3.4.2 --- Aromatase Inhibitors on Anticancer Drug Sensitivity --- p.83 / Chapter 3.4.3 --- 4-AcA and Doxorubicin on Cell Cycle Progression --- p.93 / Chapter 3.4.4 --- 4-AcA and Doxorubicin Induced DNA Fragmentation --- p.99 / Chapter 3.4.5 --- 4-AcA and Doxorubicin on Annexin Staining --- p.100 / Chapter 3.4.6 --- 4-AcA and Doxorubicin on Apoptotic Protein Expression --- p.102 / Chapter 4. --- Discussion --- p.105 / Chapter 4.1 --- 17 β-Estradiol and Anticancer Drug Sensitivity --- p.106 / Chapter 4.2 --- Tamoxifen and Anticancer Drug Sensitivity --- p.109 / Chapter 4.3 --- Aromatase Inhibitors and Anticancer Drug Sensitivity --- p.112 / Chapter 4.4 --- DU145 Cells vs PC3 Cells --- p.115 / Chapter 5. --- Conclusion and Perspectives --- p.116 / Chapter 6. --- References --- p.117

FtsZ é homóloga de tubulina, presente em quase todas as bactérias, que se autoassocia em filamentos que formam uma estrutura chamada anel Z dentro das células. O anel Z quando formado recruta de um macrocomplexo proteico chamado divisomo, que é responsável pela síntese do septo de divisão, formando duas células filhas. Diversos moduladores se ligam diretamente a FtsZ regulam sua polimerização, controlando o momento e o local onde o anel Z é formado. MciZ é um peptídeo de 40 aminoácidos expresso durante a esporulação de Bacillus subtilis e inibe a formação do do anel Z na célula mãe. O objetivo do presente trabalho foi estudar a interação entre as proteínas FtsZ e MciZ e investigar os mecanismos envolvidos na inibição da polimerização de FtsZ por MciZ. Através de uma triagem genética, usando uma biblioteca de mutantes de ftsZ, identificamos treze mutações em ftsZ que conferiram resistência à superexpressão de MciZ in vivo. Sete delas eram capazes de crescer na presença e na ausência da superexpressão de MciZ e as outras seis se mostraram dependentes da superexpressão de MciZ. A partir da coexpressão e copurificação do complexo FtsZ:MciZ, observamos que todas as proteínas mutantes ainda continuavam interagindo com MciZ in vitro. O Kd estimado para a interação entre as proteínas foi de 150±50nM, e mostrou-se que MciZ não se liga nem ao CTP (C-Terminal Peptide) de FtsZ, nem compete com GTP para a ligação no mesmo sítio. Usando construções truncadas de MciZ, determinou-se que o N-terminal da proteína (resíduos 1 ao 27) é suficiente para inibição. A partir das estruturas tridimensionais de MciZ (RMN) e do complexo FtsZ:MciZ (cristalografia de raios x), determinou-se que MciZ é um peptídeo desenovelado, que assume uma estrutura terciária ao interagir através da sua α-hélice H2 e folha-β B2 com a α-hélice H10 e a folha-β S9 de FtsZ. MciZ mostrou-se capaz de reduzir o tamanho dos protofilamentos de FtsZ de forma subestequiométrica, gerando fragmentos menores de filamentos. Proporções de MciZ:FtsZ de 1:10 foram suficientes para extinguir completamente o anel Z, confirmando a inibição subestequiométrica também in vivo. A conservação da inibição da fusão FtsZ-MciZ e a cinética de despolimerização de FtsZ induzida por MciZ provaram que MciZ não é um simples sequestrador. Marcações fluorescentes de MciZ sugeriram que o peptídeo é capaz de interagir com o anel Z in vivo, e também decorar feixes de FtsZ in vitro, formando focos localizados frequentemente na ponta dos filamentos. Cossedimentações com polímeros de FtsZ mostraram a presença de MciZ ou da fusão FtsZ-MciZ. Apesar de MciZ induzir o aumento da atividade GTPáscia específica de FtsZ, a ausência de hidrólise de GTP não eliminou o efeito subestequiométrico de MciZ. Nossos resultados em conjunto mostram que MciZ é um capeador dos filamentos de FtsZ, bloqueando a elongação pela ponta menos e bloqueando o anelamento entre protofilamentos / FtsZ is a tubulin-like protein present in most bacteria, that self-assembles into filaments forming a structure known as Z-ring in the cells. Following formation, the Z- ring recruits a protein macrocomplex, the divisome, which is responsible by the division septum synthesis, resulting in two daughter cells. Many modulators interact directly to FtsZ, regulating its polymerization and controlling the time and place of the Z-ring formation. MciZ is a 40-amino-acid peptide that is expressed during sporulation in Bacillus subtilis and inhibits the formation of the Z-ring in the mother-cell. The aim of this work was to study the interaction between FtsZ and MciZ proteins, and to investigate the mechanisms involved in FtsZ inhibition by MciZ. Applying a genetic screening, using an ftsZ mutant library, we identified 13 mutations on ftsZ that conferred resistance to MciZ overexpression in vivo. Seven of them were able to grow either in the presence or absence of MciZ overexpression, and the other six showed to be dependent on it. With the co-expression and co-purification of the FtsZ:MciZ complex, we observed all mutant proteins still interact with MciZ in vitro. Estimated Kd for the interaction was 150±50nM, and it was demonstrated that MciZ does not bind to FtsZ CTP (C-Terminal Peptide), nor does it compete with GTP for the same binding site. Using truncated versions of MciZ, it was determined that its N-terminal (residues 1 to 27) is sufficient for the inhibition. Based on the tridimensional structure of MciZ (NMR) and of the FtsZ:MciZ complex (x- ray crystallography), it was determined that MciZ is an unstructured peptide that assumes a tertiary structure by interacting with FtsZ α-helix H10 and β-sheet S9 through its α-helix H2 and β-sheet B2. MciZ was able to reduce the size of FtsZ protofilaments in a substoichiometric manner, generating smaller fragmented filaments. 1:10 ratios of MciZ:FtsZ were sufficient to completely extinguish the Z-ring, thus confirming the substoichiometric inhibition in vivo as well. The inhibition of FtsZ polymerization by the FtsZ-MciZ fusion and the FtsZ depolymerization kinetics induced by MciZ proved that MciZ is not a simple sequesterer. Fluorescent dyeing of MciZ suggests the peptide is able to interact with the Z-ring in vivo, as well as decorate FtsZ bundles in vivo, forming localized spots frequently at the filaments\' ends. Co- sedimentations with FtsZ polymers showed the presence of MciZ or of the FtsZ-MciZ fusion. Despite MciZ-induced increase in specific GTPase activity of FtsZ, the lack of GTP hydrolysis did not eliminate the substoichiometric effect of MciZ. Combined, our results show that MciZ is an FtsZ filament capper, blocking elongation at the minus end and blocking the annealing between protofilaments