This doctoral research by Jane Whynot explores how Gender-based Analysis/Plus (GBA/+), has been integrated into the Canadian federal government’s evaluation function. This research has been supervised by Dr. Caroline Andrew at the University of Ottawa. Efforts presented in this dissertation have been profoundly influenced by political leadership, and their efforts to reprioritize gender equality and other elements of diversity across the bureaucracy. Presumably, employing this mechanism across the policy cycle will provide information to decision-makers that will ultimately impact diversity, equity, and inclusion (EDI) outcomes. Canada is unique amongst governments worldwide in its efforts to so comprehensively consider personal identity elements in policy discourse. Sadly, however, the federal government’s evaluation function is lagging. Both domestic and international cues prompting the integration of gender and other elements of diversity into evaluation efforts have fallen unheard despite official domestic commitments formalizing these linkages. Theories of intersectionality, and how intersectional analysis is undertaken are at the core of this research. The “+” in GBA was intended to represent all elements of personal identity beyond gender such as but not limited to race, language, sexuality, geographic location, disability, and Aboriginal status. The federal government’s lead agency for gender equality does not explicitly reference details on any of these components in their publicly facing materials. These elements are embedded in this research’s conceptual framework and subsequent lines of evidence. Michie, VanStalen, and West’s (2012) theory of behavioural change provides the foundational structure for this research. These authors suggest that (c)apacity change only occurs when (m)otivations, (o)opportunities, and c(apabilities) are simultaneously present. Mayne (2016, 2017, 2018) was responsible for integrating this model of behavioural change into program theory; it is this COM-B theory of change (ToC) that has been used as the conceptual framework for this research. In Mayne’s COM-B ToC, capacity change outcomes are situated mid-results chain and are accompanied by both precedent and antecedent outcomes. A tailored ToC for integrating GBA+ in the federal government’s evaluation function is presented in the thesis that aligns with the changing state of GBA+ implementation across the policy cycle, honing in on the federal government evaluation function. This research was initiated before the specific articulation of GBA+ as a federal government priority in the Policy on Results (Treasury Board Secretariat, 2016); the conceptual framework serves to capture the dynamic nature of the state of GBA/+ implementation across the federal government’s policy cycle. This research adopted a mixed-methods approach involving qualitative and quantitative lines of evidence as recognized by Greene (2007). Supporting lines of evidence included: • A survey was administered to the Heads of Evaluation (HoE) who are senior level decision-makers responsible for the evaluation function within each federal government organization. Survey questions posed addressed the entire tailored ToC. Responses were intentionally designed to solicit binary responses; • A critical review of all publicly accessible federal government produced resources exploring the linkage between gender mainstreaming, GBA and GBA+ and evaluation; • Key informant interviews comprised of representatives from various federal government organizations including leads from central agencies and those responsible for gender mainstreaming, academics with expertise in feminist evaluation, Equity Diversity and Inclusion (EDI), and • Case studies of federal government evaluation functions exploring the integration of GBA+ in evaluation efforts (n=6). Each case study focused on a different element of GBA+ evaluation integration. Focus areas of each case study included: 1 organization focused on building evaluation function capacity to integrate GBA+, 1 organization focused on building capacity to integrate GBA+ amongst the evaluation and performance measurement and/or results unit, and 4 organizations focused on a single program. Each case study included the following lines of evidence: a literature review, a review of evaluations for GBA+ since 2016, a review of organizational documentation, key informant interviews, and for 3 case studies, a combination of focus groups/information exchange sessions. The COM-B tailored ToC for integrating GBA/+ in the federal government’s evaluation function encompasses a causal outcome pathway represented by a results chain. These pathways map a series of outcomes extending from activities and outputs, stakeholder reach/reaction, capacity change, behaviour change, direct benefits, and improved well-being. Each of these outcomes has multiple accompanying assumptions. Data from the tailored ToC is presented across thesis chapters. Despite widespread recognition of nascent GBA+ policy requirements and the federal government’s GBA+ tool, little GBA+ instrumental evaluation use has resulted. A wide interval exists however between awareness and use. Nestled between building GBA+ capacity and instrumental use within evaluation functions, are multiple examples of GBA+ conceptual and process use. Many organizations are aware of the federal government’s GBA+ tool, but there is inconsistent uptake of related training opportunities to build this capacity. Many federal organizations have undertaken only comparative or additive intersectional analysis and indicated limited intention to progress to interactional or truly intersectional integration analysis. To some extent, evaluation functions must navigate their course in this uncharted territory. Federal government organizations identifying as having established some capacity for GBA+ integration have developed unique GBA+ evaluation tools specific to their organizations in the absence of central agency guidance materials and a lack of evaluation function engagement of Gender Champions (GC) and Gender Focal Points (GFP). This research provided the first examination within the governmental contexts of efforts to integrate intersectional research within evaluation functions. While providing answers to many questions, many more arise – consequently providing the foundation for a potential future research program.

Market research reports by In-Stat, Gartner, and the Swedish Post and Telecom Agency (PTS) reveal a growing worldwide demand for Voice over IP (VoIP) and smartphones. This trend is expected to continue over the coming years and there is wide scope for mobile VoIP solutions. Nevertheless, with this growth in VoIP adoption come challenges related with quality of service and security. Most consumer VoIP solution, even in PCs, analog telephony adapters, and home gateways, do not yet support media encryption and other forms of security. VoIP applications based on mobile platforms are even further behind in adopting media security due to a (mis-)perception of more limited resources. This thesis explores the alternatives and feasibility of achieving VoIP security for mobile devices in the realm of the IP Multimedia Subsystem (IMS).

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第22001号 / 医博第4515号 / 新制||医||1038(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 井上 治久, 教授 林 康紀, 教授 高橋 淳 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

The applications based on social networking have brought revolution towards social life and are continuously gaining popularity among the Internet users. Due to the advanced computational resources offered by the innovative hardware and nominal subscriber charges of network operators, most of the online social networks are transforming into the mobile domain by offering exciting applications and games exclusively designed for users on the go. Moreover, the mobile devices are considered more personal as compared to their desktop rivals, so there is a tendency among the mobile users to store sensitive data like contacts, passwords, bank account details, updated calendar entries with key dates and personal notes on their devices. The Project Social Wireless Network Secure Identification (SWIN) is carried out at Swedish Institute of Computer Science (SICS) to explore the practicality of providing the secure mobile social networking portal with advanced security features to tackle potential security threats by extending the existing methods with more innovative security technologies. In addition to the extensive background study and the determination of marketable use-cases with their corresponding security requirements, this thesis proposes a secure identification design to satisfy the security dimensions for both online and offline peers. We have implemented an initial prototype using PHP Socket and OpenSSL library to simulate the secure identification procedure based on the proposed design. The design is in compliance with 3GPP’s Generic Authentication Architecture (GAA) and our implementation has demonstrated the flexibility of the solution to be applied independently for the applications requiring secure identification. Finally, the thesis provides strong foundation for the advanced implementation on mobile platform in future.

Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro / A doença de Parkinson (DP) é a segunda doença neurodegenerativa mais frequente, depois da doença de Alzheimer, com uma incidência de aproximadamente 3,3% na população brasileira acima dos 60 anos. Ela é caracterizada por uma perda dos neurônios dopaminérgicos da parte compacta da substância negra e pela presença de inclusões protéicas intracelulares denominadas corpúsculos de Lewy nos neurônios sobreviventes. A DP tem uma etiologia complexa que envolve interações genes-ambiente e múltiplos genes de susceptibilidade. Nesse contexto, mutações de perda de função no gene da glicocerebrosidase (GBA) têm sido bem validadas como importantes fatores de risco para a DP. Esse gene está localizado na região 1q21 e compreende 11 exons que codificam a enzima lisossômica glicocerebrosidase. O principal objetivo deste estudo foi investigar se alterações no gene GBA constituem um fator de predisposição para o desenvolvimento da DP na população brasileira. Para isso, um grupo de 126 pacientes brasileiros, não-aparentados, com DP (24 casos familiares e 102 isolados; idade média 66,4 11,4) foram analisados para mutações no GBA através do seqüenciamento completo de todos os exons e alguns íntrons. Sete alterações e um alelo recombinante, anteriormente encontrados em pacientes com a DP analisados em outros estudos, foram detectados (K(-)27R, IVS2+1G>A, N370S, L444P, T369M, A456P, E326K e RecNciI), assim como, uma variante nunca antes identificada associada à DP (G325G) e uma nova mutação (W378C), num total de 18 pacientes (14,3%). Além disso, foram encontradas três alterações intrônicas (c.454+47G>A, c.589-86A>G e c.1225-34C>A), que constam do banco de SNPs, entretanto, não foram associadas a nenhuma doença. Dentre todas as variantes identificadas, três são comprovadamente patogênicas (IVS2+1G>A, L444P e N370S) e foram encontradas em 5,5% da amostra, não sendo detectadas na amostra controle, indicando uma freqüência significativamente alta dessas mutações em pacientes com DP quando comparadas aos controles (P=0,0033). Esses resultados reforçam a associação entre o gene GBA e a DP na população brasileira, além de apoiar a hipótese de que alterações nesse gene representam um importante fator de susceptibilidade ao desenvolvimento da DP / Parkinsons disease is the second most common neurodegenerative disorder, after Alzheimers disease, with an incidence of 3.3% in Brazilian population over the age of 60 years. Its characterized by the degeneration of dopaminergic neurons within the substantia nigra pars compacta and the presence of intracellular protein inclusions called Lewy bodies in the surviving neurons. PD has a complex etiology which may involve gene-environment interactions and multiple susceptibility genes. In this context, loss-of-function mutations in the glucocerebrosidase gene (GBA) have been well-validated as important susceptibility factors for PD. This gene is located on 1q21 and comprises 11 exons that encode them lysosomal enzyme glucocerebrosidase. The main objective of our study was to investigate if alterations in the GBA gene constitute a predisposing factor for the development of PD in the Brazilian population. For this, a Brazilian cohort of 126 unrelated PD patients (24 familial and 102 sporadic cases; mean age: 66.4 11.4) were screened for GBA mutations by complete sequencing of the genes exons and some introns. Seven alterations and one recombinant allele, previously found in PD patients performed in other studies, were detected (K(-)27R, IVS2+1G>A, N370S, L444P, T369M, A456P, E326K e RecNciI), as well as, a variant never identified in PD patients (G325G) and one newly identified variant (W378C), in a total of 18 patients (14.3%). In addition, were found three intronic changes (c.454 +47 G>A, c.589- 86A>G and c.1225-34C>A), which are present in the database of SNPs, however, were not associated with any disease. Among all the variants identified, three are proven pathogenic (IVS2 +1 G>A, N370S and L444P) and were found in 5.5% of the sample and not detected in the control sample, indicating a significantly higher frequency of these mutations in patients with PD compared to controls (P = 0.0033). Our results, have strengthened the association between the GBA gene and PD in the Brazilian population, in addition to support the hypothesis that alterations in this gene represent a significant genetic susceptibility factor for the development of PD

Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro / A doença de Parkinson (DP) é a segunda doença neurodegenerativa mais frequente, depois da doença de Alzheimer, com uma incidência de aproximadamente 3,3% na população brasileira acima dos 60 anos. Ela é caracterizada por uma perda dos neurônios dopaminérgicos da parte compacta da substância negra e pela presença de inclusões protéicas intracelulares denominadas corpúsculos de Lewy nos neurônios sobreviventes. A DP tem uma etiologia complexa que envolve interações genes-ambiente e múltiplos genes de susceptibilidade. Nesse contexto, mutações de perda de função no gene da glicocerebrosidase (GBA) têm sido bem validadas como importantes fatores de risco para a DP. Esse gene está localizado na região 1q21 e compreende 11 exons que codificam a enzima lisossômica glicocerebrosidase. O principal objetivo deste estudo foi investigar se alterações no gene GBA constituem um fator de predisposição para o desenvolvimento da DP na população brasileira. Para isso, um grupo de 126 pacientes brasileiros, não-aparentados, com DP (24 casos familiares e 102 isolados; idade média 66,4 11,4) foram analisados para mutações no GBA através do seqüenciamento completo de todos os exons e alguns íntrons. Sete alterações e um alelo recombinante, anteriormente encontrados em pacientes com a DP analisados em outros estudos, foram detectados (K(-)27R, IVS2+1G>A, N370S, L444P, T369M, A456P, E326K e RecNciI), assim como, uma variante nunca antes identificada associada à DP (G325G) e uma nova mutação (W378C), num total de 18 pacientes (14,3%). Além disso, foram encontradas três alterações intrônicas (c.454+47G>A, c.589-86A>G e c.1225-34C>A), que constam do banco de SNPs, entretanto, não foram associadas a nenhuma doença. Dentre todas as variantes identificadas, três são comprovadamente patogênicas (IVS2+1G>A, L444P e N370S) e foram encontradas em 5,5% da amostra, não sendo detectadas na amostra controle, indicando uma freqüência significativamente alta dessas mutações em pacientes com DP quando comparadas aos controles (P=0,0033). Esses resultados reforçam a associação entre o gene GBA e a DP na população brasileira, além de apoiar a hipótese de que alterações nesse gene representam um importante fator de susceptibilidade ao desenvolvimento da DP / Parkinsons disease is the second most common neurodegenerative disorder, after Alzheimers disease, with an incidence of 3.3% in Brazilian population over the age of 60 years. Its characterized by the degeneration of dopaminergic neurons within the substantia nigra pars compacta and the presence of intracellular protein inclusions called Lewy bodies in the surviving neurons. PD has a complex etiology which may involve gene-environment interactions and multiple susceptibility genes. In this context, loss-of-function mutations in the glucocerebrosidase gene (GBA) have been well-validated as important susceptibility factors for PD. This gene is located on 1q21 and comprises 11 exons that encode them lysosomal enzyme glucocerebrosidase. The main objective of our study was to investigate if alterations in the GBA gene constitute a predisposing factor for the development of PD in the Brazilian population. For this, a Brazilian cohort of 126 unrelated PD patients (24 familial and 102 sporadic cases; mean age: 66.4 11.4) were screened for GBA mutations by complete sequencing of the genes exons and some introns. Seven alterations and one recombinant allele, previously found in PD patients performed in other studies, were detected (K(-)27R, IVS2+1G>A, N370S, L444P, T369M, A456P, E326K e RecNciI), as well as, a variant never identified in PD patients (G325G) and one newly identified variant (W378C), in a total of 18 patients (14.3%). In addition, were found three intronic changes (c.454 +47 G>A, c.589- 86A>G and c.1225-34C>A), which are present in the database of SNPs, however, were not associated with any disease. Among all the variants identified, three are proven pathogenic (IVS2 +1 G>A, N370S and L444P) and were found in 5.5% of the sample and not detected in the control sample, indicating a significantly higher frequency of these mutations in patients with PD compared to controls (P = 0.0033). Our results, have strengthened the association between the GBA gene and PD in the Brazilian population, in addition to support the hypothesis that alterations in this gene represent a significant genetic susceptibility factor for the development of PD

<p>The purpose of this study is to provide a simple user interface with which everyone can</p><p>design his/her own game, and play it on Game Boy Advance console. This project helps</p><p>people develop games without having programming knowledge. Everything is done by means of a user interface and without any programming knowledge. It is magic, isn’t it?</p><p>Game Boy Advance is a game console developed by Nintendo. In order to market their</p><p>products, they must also develop games running on their products. Every time they develop a game for the Game Boy Advance console, they have to implement a low level C++ application over and over again. This makes things more complicated. However, if this software is used, everything becomes easier.</p><p>This project can be seen as an interpreter that interprets the designed game, which is</p><p>very high level, and converts it to a Game Boy Advance game. If this project is finished</p><p>successfully, game design for Game Boy Advance will experience a revolution in its history.</p><p>In brief, it is required to develop a visual, GUI‐based system that allows people to develop games for the Game Boy Advance console. This GUI system is required to</p><p>implement and use the API (Game Engine) developed by Lypson.</p>

<p>   This bachelor thesis describes the development of a MOD music player to run on GBA (Game Boy Advance) for Lypson Game Engine. GBA is a basic platform for embedded development, and the stereo system makes it possible to use the platform as a music player. The sound players of the GBA for Lypson Game Engine were designed to play wave files and the size of typical wave files is in the order of megabytes. MOD files are much smaller when compared with wave ones. Therefore, to avoid consuming the resources of the CPU and memory to process and store wave files, the use of MOD files represents a better alternative.The development took C++ as programming language and the development platform used was HAM. The first step was to obtain samples of music, and then control the hardware of GBA to play sound. After that, came the phase of combining it with Lipson Game Engine. These tasks enabled the acquisition of knowledge about the frame of MOD files; learning how to make the GBA play sound and mastering the operating instruction of GBA hardware by the process of development. In addition, it provided a chance to learn about embedded development, which represented a starting point to learn about embedded programming in general.As for the main result, it was achieved by the successful development of the MOD Player, which is now running on the Lypson Game Engine. As the MOD files are of small size, the music player is more efficient when compared with those previously used.</p>

The purpose of this study is to provide a simple user interface with which everyone can design his/her own game, and play it on Game Boy Advance console. This project helps people develop games without having programming knowledge. Everything is done by means of a user interface and without any programming knowledge. It is magic, isn’t it? Game Boy Advance is a game console developed by Nintendo. In order to market their products, they must also develop games running on their products. Every time they develop a game for the Game Boy Advance console, they have to implement a low level C++ application over and over again. This makes things more complicated. However, if this software is used, everything becomes easier. This project can be seen as an interpreter that interprets the designed game, which is very high level, and converts it to a Game Boy Advance game. If this project is finished successfully, game design for Game Boy Advance will experience a revolution in its history. In brief, it is required to develop a visual, GUI‐based system that allows people to develop games for the Game Boy Advance console. This GUI system is required to implement and use the API (Game Engine) developed by Lypson.

La malaltia de Gaucher és una malaltia d'herència autosòmica recessiva, causada per mutacions en el gen GBA, o en alguns pocs casos, per mutacions en el gen PSAP. El gen GBA codifica la hidrolasa lisosòmica Glucocerebrosidasa i el gen PSAP codifica la proteïna activadora de l'enzim anterior, la Saposina C.Fins al moment s'han descrit més de 200 mutacions en el gen GBA causants de la malaltia de Gaucher, que han permès desenvolupar un diagnòstic molecular de la malaltia, i unes poques en el gen PSAP.Aquestes mutacions produeixen una deficiència en alguna d'aquestes dues proteïnes, la Glucocerebrosidasa o la Saposina C, que estan implicades en la via de degradació dels glicoesfingolípids.Algunes de les mutacions descrites en el gen GBA són al·lels complexos, que són portadors de diferents mutacions, produïts per processos de recombinació entre el gen i el seu pseudogèn.En aquest treball presentem el cas d'un individu que va ser dignosticat erròneament com a homozigot per a la mutació N370S, quan realment era portador d'un al·lel complex no descrit fins al moment.A més, hem volgut caracteritzar millor l'al·lel mutant RecNciI i per a això hem analitzat aquesta mutació en població espanyola i argentina, ja que és molt freqüent en aquesta última població, utilitzant diferents mètodes. D'aquesta manera també hem pogut trobar nous individus que tenien al·lels Rec i no s'havien pogut detectar, i entendre millor els mecanismes mitjançant els quals es produeixen aquests al·lels.També s'han analitzat mostres de pacients de la malaltia de Gaucher que eren candidats de ser portadors de mutacions en el gen PSAP. Aquest anàlisi ens ha permès decriure una mutació en la Saposina D que juntament amb una altra mutació ja descrita prèviament és la causant de la patologia.Fins al moment s'han desenvolupat diferents tècniques de teràpia gènica, però en general tenen moltes limitacions. Per una banda els vectors utilitzats poden generar reaccions immunes (adenovirus) o integracions a l'atzar en el genoma (retrovirus). Per altra banda, el gen forani deixa d'expressar-se després d'un cert temps. Per tot això és lògic que s'hagin desenvolupat noves estratègies per a la teràpia de malalties genètiques. Una d'aquestes aproximacions és l'utilització de quimeraplasts, molècules quimèriques de RNA-DNA capaces de promoure la correcció d'una mutació mitjançant els mecanismes de reparació de la cèl·lula. En la malaltia de Gaucher una de les mutacions més freqüents és la L444P. Hem intentat corregir aquesta mutació utilitzant quimeraplasts en fibroblasts d'un pacient de la malaltia de Gaucher homozigot per la mutació L444P.Els resultats obtinguts mostren una molt baixa, o nul·la, eficiència de correcció. Recentment s'han publicat diferents treballs on descriuen també resultats negatius per altres malalties utilitzant aquesta tècnica, deixant en entredit l'eficàcia d'aquesta tècnica.Una de les teràpies que actualment s'està utlitzant en la malaltia de Gaucher és la teràpia de reducció de substrat com a complement o alternativa a la teràpia de reemplaçament enzimàtic. La teràpia de reducció de substrat es basa en la inhibició parcial de la glucosilceramida sintasa (GCS), enzim encarregat de sintetitzar glucosilceramida a partir de ceramida i glucosa. D'aquesta manera s'evita l'acúmul de glucosilceramida que provoca la malaltia.En els darrers anys, els siRNAs (small interference RNAs) s'han utilitzat en diferents tipus d'experiments per inhibir l'expressió gènica. L'objectiu d'aquest treball és la inhibició de la expressió del gen de la GCS mitjançant siRNAs com una possible alternativa terapèutica per a la malaltia de Gaucher.Vam dissenyar quatre siRNAs per a inhibir el gen GCS humà i els vam transfectar en cèl·lules HeLa. Amb dos d'aquests siRNAs vam aconseguir reduir la expressió de GCS a nivell de RNA. També vam comprovar la reducció tant a nivell d'activitat enzimàtica com de formació de glucosilceramida.Després d'aconseguir silenciar el gen de la GCS utilitzant siRNAs, vam decidir probar-ho utilitzant shRNAs (short-hairpin RNAs). Els shRNAs són siRNAs generats per un plasmidi on se li ha insertat la seqüència que s'ha de transcriure per formar aquest shRNA. Vam generar dos shRNAs diferents aconseguint inhibir també l'expressió de GCS. / "Characterization of mutations causing Gaucher disease. Gene therapy approach."The glycosphingolipid (GSL) lysosomal storage disorders are a group of inherited genetic diseases caused by mutations in the genes coding for enzymes involved in GSL catabolism. These diseases are characterised by the accumulation of the GSL substrates within lysosomes of cells, which results in cellular dysfunction and damage. The most common of the glycosphingolipidoses is Gaucher disease (GD), an autosomal recessive trait due to the accumulation of glucosylceramide caused by deficient activity of the enzyme glucocerebrosidase (EC 3.2.1.45).The glucocerebrosidase gene, lies on a gene-rich region which includes the metaxin gene and the glucocerebrosidase and metaxin highly homologous pseudogenes. The presence of these repetitions leads to DNA rearrangements. Some of these rearrangements give rise to complex alleles that cause the disease, of which RecNciI is the most prevalent. We analysed Gaucher disease patients from Argentina and Spain bearing this allele, and patients who carried mutation L444P, one of the three changes present in the RecNciI allele. Only two patients bearing mutations in the PSAP gene, and not in the GBA gene, have been reported. In both cases, one mutant allele remained unidentified. We report here the identification of the second mutation in one of these patients, being the first complete genotype described so far in a SAP-C deficient-GD patient. This mutation, p.Q430X, is the first one reported in the saposin D domain and probably produces a null allele by nonsense mediated mRNA decay.A number of gene therapy approaches have been developed for the treatment of genetic diseases, most of them based on the use of viral vectors. However, in general they have not been successful and some complications. To overcome these limitations, novel strategies have recently emerged. One of them is chimeraplasty, based on the correction of single-base mutations by mismatch repair mechanisms using chimeric RNA/DNA oligonucleotides, named chimeraplasts. Mutation L444P is one of the most common mutations in many populations. We have attempted to correct mutation L444P in fibroblasts from a Gaucher disease patient using a chimeraplast approach. Our results show a very low efficiency (if any) of chimeraplast correction. In the last few years, small interference RNAs (siRNAs) have been used in a number of different experimental settings to silence gene expression. Enzyme replacement and substrate deprivation therapies are the current approaches to treat Gaucher disease. We present here a new approach based on the inhibition of the GCS gene using siRNAs as a possible future therapeutic strategy for Gaucher disease. A clear reduction in GCS RNA levels, enzyme activity and glucosylceramide synthesis was achieved. Similar results were obtained when using plasmids expressing shRNAs. Also, siRNAs to inhibit the mouse homolog Ugcg gene were successfully assayed.