The Czech Armed Forces (CAF) constitutes the most important element within defense system of Czech republic. Primary role of CAF is to defend country against foreign invasion to which purpose should its build-up and structure correspond. From the perspective of military theory defined by Carl von Clausewitz, there is pivotal component in case of composition of CAF which is porportion of individual arms and services. Proportion of military occupations matching these arms and services as well as combat and support parts of CAF is of primary concern in this work. This relationship is also compared with composition of United States Armed Forces due to fact that these are the most important and the most effective armed forces in the contemporary world. Based on this comparison, there can arise some of generally valid principles and procedures for developing the armed forces which can be also applied in case of CAF. Geopolitical position of Czech republic and its historical context is also taken into consideration in this work.

在後911時代，世界各國體認到國家安全的領域已從過去單純國防方面轉移到全方位的整體安全。單純的軍事力量已不足已維護國家安全，在面對各式挑戰和衝突時，必須以更全面的思考來應對。生物戰劑，在過去大多是在教科書和軍事準則上提到的可能威脅之一，但真正威脅到國家安全則是在911之後的炭疽信件。世人瞭解到我們是處於多麼真實且危險的世界。生物科技的進步一方面提昇人類的生活品質和生命長度，另一方面則是直接威脅到人類的生存。生物戰劑的運用方式可以相當多樣且多變，正是製造恐怖的最佳武器。 生物戰劑的目標可以從個人的暗殺、殺傷大量人員、影響農牧業及糧食供應、破壞經濟和社會秩序、影響政治選擇到製造動亂。而各種疾病和生物戰劑的散佈很難區分，更是增加防疫和應變上的困難。 我國在防疫措施上雖然在SARS之後已經有應變機制，但面對多樣的生物戰劑攻擊，仍然顯得捉襟見肘。吾人應分析可能的生物戰劑威脅並擬定相關應變措施，建立有關國家安全生物防護網，發揮全民國防之功能，維護整體國家安全。 關鍵詞：生物戰劑、應變機制、國家安全生物防護網、全民國防 / After 911-terrorism attack, nations all over the world finally realized that the national security field have transformed from national defense to full-spectrum national security. Military force cannot defense national security alone. When face kinds of challenges and threatens, we should think and concern more complete. Biological warfare threat, in past, just only text on textbook and field manual. But after 911 anthrax envelope events, people realized that the biological warfare threat have come to the real world and what dangerous world we live with. Biological science and technology have improved people's quality of life and prolonged our length of life, in the other hand, it also threaten human being's survival. Biological warfare can be use in many different ways and can be the best weapon to make terror. The target or strategic goal can be used to assassin, cause mass casualty, bloke or disturb food supply, destroy economics and social order, influence political choose and make chaos. It is not easy to find the difference between distribution of disease and biological warfare. Moreover, that made counter insurgence more difficult. We have counter insurgence mechanism to deal with biological warfare attack and disease distribution, when face kinds of biological threat, it shows insufficient. We need to improve our anti-bioterrorism capability continuously. Analysis possible threat and get counter insurgence plan, build national bio-shied framework and all-out defense system to protect national security. Keyword: biological warfare, insurgence mechanism, national bio-shied framework, all-out defense system

A diabetes é um distúrbio endócrino do metabolismo dos carboidratos, clinicamente caracterizada por hiperglicemia, resultante da incapacidade do organismo em secretar insulina, defeitos na sua ação ou ambos. Na última década, houve um crescente aumento no número de trabalhos sobre a múltipla hereditariedade de um tipo de diabetes rara e não imunológica diagnosticada antes dos 6 meses de vida, a diabetes neonatal (DN). A maioria dos estudos, existentes na literatura referentes à DN, foi realizada em pacientes e aborda principalmente aspectos clínicos, etiológicos e terapêuticos. No entanto, existe uma deficiência de estudos realizados em modelos animais, a fim de avaliar danos moleculares em tecidos submetidos à hiperglicemia neonatal. Recentemente, as consequências da diabetes no sistema nervoso central (SNC) têm recebido maior atenção, uma vez que os recentes estudos mostram que a hiperglicemia é capaz de promover a ruptura da homeostase redox no cérebro de ratos. Neste sentido, o estresse oxidativo (EO) parece representar um dos mecanismos pelos quais a hiperglicemia danifica o tecido cerebral em um período crucial de desenvolvimento. Diante disso, o presente trabalho objetivou estudar não só a relação do EO com a hiperglicemia neonatal em cérebro de ratos, mas também avaliar se os danos oxidativos promovidos pelas espécies reativas de oxigênio (ERO) na condição hiperglicêmica podem estar envolvidos no processo de morte celular neuronal. Para isso, foram utilizados ratos Wistar de 5 dias de vida, divididos em dois grupos: controle e diabético. O modelo de diabetes foi induzido pela administração intraperitoneal de estreptozotocina (STZ) em uma única dose de 100 mg/Kg peso corporal, sendo que foram considerados diabéticos os ratos com glicemia >200mg/dL. Os animais foram sacrificados com 10 dias de vida, ou seja, 5 dias após a administração de STZ. O cérebro total dos animais foi homogeneizado, centrifugado e o homogeneizado utilizado para as medidas de parâmetros de EO e expressão proteica. Além disso, o cérebro total foi utilizado em cortes histológicos para análise do parâmetro de morte celular neuronal, avaliada pela técnica FluoroJade C. Os parâmetros de EO analisados foram o metabolismo da glutationa, que engloba a atividade das enzimas glutationa S-transferase (GST), glutationa redutase (GR), glutamato-cisteína ligase (GCL) e a 8 determinação da concentração de glutationa total e reduzida (GSH/GSSG). A medida do peróxido de hidrogênio (H2O2) também foi avaliada, juntamente com a quantificação proteica por “Western Blot” do fator nuclear eritroide relacionado ao fator 2 (Nrf2), da superóxido dismutase (SOD), da catalase (CAT), da glutationa peroxidase (GPx), da heme oxigenase 1 (HO-1) e da tiorredoxina (TRX). Os parâmetros relativos à sobrevivência e morte celular avaliados foram a quantificação proteica por “Western Blot” da proteína cinase B (AKT), da proteína cinase B fosforilada (p-AKT), da glicogênio sintase cinase 3 β (GSK3β), da p38 proteína cinase ativada por mitógenos (p38), proteína cinase c-Jun N-terminal (JNK), da célula-B de linfoma 2 (Bcl2) e da proteína X associada a Bcl2 (Bax). Os ratos submetidos ao modelo de hiperglicemia neonatal não apresentaram diferenças significativas nos parâmetros relacionados ao metabolismo da glutationa (GST, GR, GCL e GSH/GSSG), tampouco nas concentrações de H2O2 quando comparados ao grupo controle. A expressão proteica do Nrf2 foi diminuída no grupo diabético, enquanto que a expressão da CAT, HO-1 e TRX se apresentaram aumentadas no grupo diabético quando comparado ao grupo controle. Não foram encontradas diferenças significativas nas expressões proteicas da SOD e GPx. As expressões proteicas das proteínas p38 e Bcl2 foram aumentadas, enquanto a expressão da p-AKT se mostrou reduzida no grupo diabético. Já com relação à expressão das proteínas JNK, GSK3β e Bax não houve diferença significativa nos grupos analisados. Finalmente, com relação à técnica que avaliou morte celular neuronal, o grupo diabético apresentou três vezes mais marcações de neurônios fluorescentes, ou seja, com morte celular quando comparado com o grupo controle. Portanto, esses resultados sugerem que o EO pode representar um mecanismo envolvido nos efeitos da hiperglicemia no SNC de ratos neonatos. Além disso, as alterações na expressão de proteínas envolvidas em vias de sobrevivência/morte celular colaboram para o resultado de morte celular verificado no cérebro de animais com hiperglicemia neonatal e mostram os efeitos nocivos da DN em um período crucial de desenvolvimento cerebral. / Diabetes is an endocrine disorder of the carbohydrates metabolism clinically characterized by hyperglycemia, resulting from the inability of the body to secrete insulin, defeats in its action and both. In the last decade, there has been an increasing number of studies about neonatal diabetes (DN), a type of diabetes non-immunological diagnosed before 6 months of life. The most studies related to DN was developed in patients and mainly deal with clinical, etiological and therapeutic aspects. However, there is a few of studies in animal models in order to assess molecular damage in tissues submitted to neonatal hyperglycemia. Recently, the consequences of diabetes in the central nervous system (CNS) have received increased attention, as recent studies show that hyperglycemia is capable of promoting the rupture of redox homeostasis in the rat brain. Wherefore, the present work aimed to study not only the relationship between EO and neonatal hyperglycemia in rat brain, but also evaluate if the oxidative damage promoted by reactive oxygen species (ROS) in the hyperglycemic condition may be involved in the neuronal cell death process. For this, 5-day-old Wistar rats were used to promote the induction of diabetes, which was done with a single intraperitoneal streptozotocin (STZ) administration (100 mg/kg body weight). Rats with glycemia> 200 mg/dL were considered diabetic. The rats were sacrificed in 10 days of life, wherefore five days after STZ adiminstration. The whole brain of the rats was homogenized, centrifuged and homogenized used for EO techniques and protein expression measurements. In addition, total brain was used in histological sections for analysis of the neuronal cell death. The EO parameters evaluated were the activity of the glutathione S-transferase (GST), glutathione reductase (GR), glutamate-cystein ligase (GCL) and the determination of total and reduced glutathione concentration (GSH/GSSG). Hydrogen peroxide (H2O2) was evaluated along with Western Blot protein quantification of catalase (CAT), glutathione peroxidase (GPx), heme oxygenase (HO-1) and thioredoxin (TRX). Relative to cell survival and death were evaluated protein kinase B (Akt), phosphorylated protein kinase B (p-Akt), glycogen synthase kinase 3β (GSK3β), p38 mitogen-activated protein kinase (p38), c-Jun amino-terminal kinases (JNK), phosphorylated c-Jun amino-terminal kinases (p-JNK), B-cell 10 lymphoma 2 (Bcl2) and Bcl2-associated protein X (Bax) by western blot. The neonatal hyperglycemia was not able to promote significant differences in the glutathione metabolism (GST, GR, GCL and GSH / GSSG) nor in the H2O2 measurement when compared to the control group. Nrf2 protein expression was decreased whereas CAT, HO-1 and TRX protein expression were increased in the diabetic group when compared to the control group. No significant differences were found in the protein expression of SOD and GPx. Also, p38 and Bcl2 protein expression was increased, whereas p-Akt was decreased in the diabetic group, already regarding the expression of JNK, p-JNK, Jsk3β and Bax proteins there were no significant difference in the analyzed groups. Finally, relative to neuronal cell death technique, the diabetic group presented three fold more neuronal cell death with fluorescent marking characteristic, when compared to the control group. Therefore, these results suggest that OE may represent a mechanism involved in the effects of hyperglycemia in the central nervous system of neonatal rats. In addition, changes in the expression of proteins involved in survival/death cell pathways contribute to the outcome of cell death, result found in the brain of animals with neonatal hyperglycemia and finally show the harmful effects of neonatal diabetes in a crucial period of brain development.

A diabetes é um distúrbio endócrino do metabolismo dos carboidratos, clinicamente caracterizada por hiperglicemia, resultante da incapacidade do organismo em secretar insulina, defeitos na sua ação ou ambos. Na última década, houve um crescente aumento no número de trabalhos sobre a múltipla hereditariedade de um tipo de diabetes rara e não imunológica diagnosticada antes dos 6 meses de vida, a diabetes neonatal (DN). A maioria dos estudos, existentes na literatura referentes à DN, foi realizada em pacientes e aborda principalmente aspectos clínicos, etiológicos e terapêuticos. No entanto, existe uma deficiência de estudos realizados em modelos animais, a fim de avaliar danos moleculares em tecidos submetidos à hiperglicemia neonatal. Recentemente, as consequências da diabetes no sistema nervoso central (SNC) têm recebido maior atenção, uma vez que os recentes estudos mostram que a hiperglicemia é capaz de promover a ruptura da homeostase redox no cérebro de ratos. Neste sentido, o estresse oxidativo (EO) parece representar um dos mecanismos pelos quais a hiperglicemia danifica o tecido cerebral em um período crucial de desenvolvimento. Diante disso, o presente trabalho objetivou estudar não só a relação do EO com a hiperglicemia neonatal em cérebro de ratos, mas também avaliar se os danos oxidativos promovidos pelas espécies reativas de oxigênio (ERO) na condição hiperglicêmica podem estar envolvidos no processo de morte celular neuronal. Para isso, foram utilizados ratos Wistar de 5 dias de vida, divididos em dois grupos: controle e diabético. O modelo de diabetes foi induzido pela administração intraperitoneal de estreptozotocina (STZ) em uma única dose de 100 mg/Kg peso corporal, sendo que foram considerados diabéticos os ratos com glicemia >200mg/dL. Os animais foram sacrificados com 10 dias de vida, ou seja, 5 dias após a administração de STZ. O cérebro total dos animais foi homogeneizado, centrifugado e o homogeneizado utilizado para as medidas de parâmetros de EO e expressão proteica. Além disso, o cérebro total foi utilizado em cortes histológicos para análise do parâmetro de morte celular neuronal, avaliada pela técnica FluoroJade C. Os parâmetros de EO analisados foram o metabolismo da glutationa, que engloba a atividade das enzimas glutationa S-transferase (GST), glutationa redutase (GR), glutamato-cisteína ligase (GCL) e a 8 determinação da concentração de glutationa total e reduzida (GSH/GSSG). A medida do peróxido de hidrogênio (H2O2) também foi avaliada, juntamente com a quantificação proteica por “Western Blot” do fator nuclear eritroide relacionado ao fator 2 (Nrf2), da superóxido dismutase (SOD), da catalase (CAT), da glutationa peroxidase (GPx), da heme oxigenase 1 (HO-1) e da tiorredoxina (TRX). Os parâmetros relativos à sobrevivência e morte celular avaliados foram a quantificação proteica por “Western Blot” da proteína cinase B (AKT), da proteína cinase B fosforilada (p-AKT), da glicogênio sintase cinase 3 β (GSK3β), da p38 proteína cinase ativada por mitógenos (p38), proteína cinase c-Jun N-terminal (JNK), da célula-B de linfoma 2 (Bcl2) e da proteína X associada a Bcl2 (Bax). Os ratos submetidos ao modelo de hiperglicemia neonatal não apresentaram diferenças significativas nos parâmetros relacionados ao metabolismo da glutationa (GST, GR, GCL e GSH/GSSG), tampouco nas concentrações de H2O2 quando comparados ao grupo controle. A expressão proteica do Nrf2 foi diminuída no grupo diabético, enquanto que a expressão da CAT, HO-1 e TRX se apresentaram aumentadas no grupo diabético quando comparado ao grupo controle. Não foram encontradas diferenças significativas nas expressões proteicas da SOD e GPx. As expressões proteicas das proteínas p38 e Bcl2 foram aumentadas, enquanto a expressão da p-AKT se mostrou reduzida no grupo diabético. Já com relação à expressão das proteínas JNK, GSK3β e Bax não houve diferença significativa nos grupos analisados. Finalmente, com relação à técnica que avaliou morte celular neuronal, o grupo diabético apresentou três vezes mais marcações de neurônios fluorescentes, ou seja, com morte celular quando comparado com o grupo controle. Portanto, esses resultados sugerem que o EO pode representar um mecanismo envolvido nos efeitos da hiperglicemia no SNC de ratos neonatos. Além disso, as alterações na expressão de proteínas envolvidas em vias de sobrevivência/morte celular colaboram para o resultado de morte celular verificado no cérebro de animais com hiperglicemia neonatal e mostram os efeitos nocivos da DN em um período crucial de desenvolvimento cerebral. / Diabetes is an endocrine disorder of the carbohydrates metabolism clinically characterized by hyperglycemia, resulting from the inability of the body to secrete insulin, defeats in its action and both. In the last decade, there has been an increasing number of studies about neonatal diabetes (DN), a type of diabetes non-immunological diagnosed before 6 months of life. The most studies related to DN was developed in patients and mainly deal with clinical, etiological and therapeutic aspects. However, there is a few of studies in animal models in order to assess molecular damage in tissues submitted to neonatal hyperglycemia. Recently, the consequences of diabetes in the central nervous system (CNS) have received increased attention, as recent studies show that hyperglycemia is capable of promoting the rupture of redox homeostasis in the rat brain. Wherefore, the present work aimed to study not only the relationship between EO and neonatal hyperglycemia in rat brain, but also evaluate if the oxidative damage promoted by reactive oxygen species (ROS) in the hyperglycemic condition may be involved in the neuronal cell death process. For this, 5-day-old Wistar rats were used to promote the induction of diabetes, which was done with a single intraperitoneal streptozotocin (STZ) administration (100 mg/kg body weight). Rats with glycemia> 200 mg/dL were considered diabetic. The rats were sacrificed in 10 days of life, wherefore five days after STZ adiminstration. The whole brain of the rats was homogenized, centrifuged and homogenized used for EO techniques and protein expression measurements. In addition, total brain was used in histological sections for analysis of the neuronal cell death. The EO parameters evaluated were the activity of the glutathione S-transferase (GST), glutathione reductase (GR), glutamate-cystein ligase (GCL) and the determination of total and reduced glutathione concentration (GSH/GSSG). Hydrogen peroxide (H2O2) was evaluated along with Western Blot protein quantification of catalase (CAT), glutathione peroxidase (GPx), heme oxygenase (HO-1) and thioredoxin (TRX). Relative to cell survival and death were evaluated protein kinase B (Akt), phosphorylated protein kinase B (p-Akt), glycogen synthase kinase 3β (GSK3β), p38 mitogen-activated protein kinase (p38), c-Jun amino-terminal kinases (JNK), phosphorylated c-Jun amino-terminal kinases (p-JNK), B-cell 10 lymphoma 2 (Bcl2) and Bcl2-associated protein X (Bax) by western blot. The neonatal hyperglycemia was not able to promote significant differences in the glutathione metabolism (GST, GR, GCL and GSH / GSSG) nor in the H2O2 measurement when compared to the control group. Nrf2 protein expression was decreased whereas CAT, HO-1 and TRX protein expression were increased in the diabetic group when compared to the control group. No significant differences were found in the protein expression of SOD and GPx. Also, p38 and Bcl2 protein expression was increased, whereas p-Akt was decreased in the diabetic group, already regarding the expression of JNK, p-JNK, Jsk3β and Bax proteins there were no significant difference in the analyzed groups. Finally, relative to neuronal cell death technique, the diabetic group presented three fold more neuronal cell death with fluorescent marking characteristic, when compared to the control group. Therefore, these results suggest that OE may represent a mechanism involved in the effects of hyperglycemia in the central nervous system of neonatal rats. In addition, changes in the expression of proteins involved in survival/death cell pathways contribute to the outcome of cell death, result found in the brain of animals with neonatal hyperglycemia and finally show the harmful effects of neonatal diabetes in a crucial period of brain development.

Issues related to research methodology increasingly occupy a central role in the field of International Positioning Process. It is becoming clear that greater attention to methodological issues is essential for the development of this field into a management discipline. Many efforts have been made to distinguish the disciplines/practices in international business. However, the field is still criticized for lack of theories and absence of paradigm. A recent survey of literature noted that the field has made more progress in finding research questions than in answering them, one of them being Identifying Dimensions for the International Positioning Process (IPP) for defence goods. This is largely because of lack of a theoretical foundation continued to plague international business research. Research in International Business is at critical crossroad today, with increased emphasis on developing theoretical concepts and testing empirical relationships rooted in such concepts. Such a transformation critically depends on conceptualizing and operationalizing the derivative constructs in an international business environment. This is motivated by management’s desire to gain profits and competitive advantage through appropriate market selection, right market entry mode decision and competitive positioning techniques. The combination of these three aspects of international business, leads to the development of the concept, called International positioning process (IPP). While researchers have made significant efforts on new techniques and approaches of international positioning processes, certain important issues remain largely unexplored. First, it is not challenging to find methodologies and approaches for market selection, entry mode choice and global competitive advantage, but in understanding how to blend them together for tailoring IPP. There is a need for developing holistic model for customized IPP that aims on translating positioning process into global competitive advantage. Another observable omission in the past literature is the missing link among three components of positioning process: market selection, entry mode choice and competitive positioning. To address this neglect, the present study attempts to develop a model for global positioning process. Development of a significant bond among three components of global positioning process, not only creates harmony among them, but aims to make IPP more effective. The study aims to develop set of dimensions for the construct, international positioning process (IPP). Specifically the objectives of this study are as under, • To conceptualize a multi- variable construct IPP. • To develop information framework for IPP. • To evaluate/analyze the dimensions developed for IPP, such that they satisfactorily fulfill reliability properties. • To differentiate IPP across industries and develop generic and industry- specific model. • To operationalise the model for defence industry. • To evolve comprehensive set of conclusions for IPP. In an attempt to achieve these objectives, this study attempts to integrate three aspects of international business: market selection, entry mode decision and competitive positioning of goods/services, and evolved the concept of International Positioning Process. The study identifies 91 variables for IPP through exhaustive literature review and develops an information framework that comprises four cardinal dimensions, twelve adjuvant dimensions and 35 decision variables. The information mentioned in the framework, is evaluated using statistical tool package – R, and refined using factor analysis. The primary data was collected using structured questionnaire by eliciting response from 329 International Business Companies (IBCs) which are involved in international business. The data of 329 IBCs explored that all the four cardinal dimensions, mentioned in the framework, are the reliable steps for IPP. The outcome of analysis develops the generic model for IPP that comprises 19 highly influencing decision variables in contrast to 91 variables available in the literature, which are finally summarized into 4 statistically significant steps for effective IPP. To tailor the customised and industry specific model for IPP, it was imperative to study how IPP differs across the industries. The difference in international positioning paradigm across the industries, analysed with multivariate discriminant analysis, one way ANOVA and factor analysis, indicates defence industry as most sensitive for making international business decisions. It evolves that defence industry seeks more safe, focused and efficient international positioning strategy for the international positioning of its products. This study attempts to customize the IPP model for defence goods which has not been addressed in the literature yet. The study explores set of highly influencing decision variables for international positioning of defence products, which are finally summarized into 4 statistically significant steps. The model is operationalised for Defence Research and Development Organization (DRDO) of India. It assesses international marketing capability of DRDO, identifies suitable markets, and makes decision for appropriate market entry modes and competitive positioning of selected defence goods. The study evolved five most suitable international markets for selected DRDO systems. Risk analysis is performed for all the identified markets to evaluate suitability of the market and to decide entry modes. The IPP model for defence industry is successfully implemented in one of the identified markets i.e. Malaysia, for the target DRDO systems. The study evolves that defence organizations attain more effectiveness in international positioning process through holistic mode as compared to extended & traditional modes. However, like any other study this does provide scope for further research and IPP can be a candidate for further extensions and refinements.