The promotion of publishing company`s products in international market

Bakalaura darbā autors analizē izdevniecības uzņēmuma produktu virzīšanas iespējas starptautiskajā tirgū. Darba mērķis, ir pamatojoties uz teorijā un analīzē gūtajām atziņām par produktu virzīšanas tirgū metodēm, analizējot Latvijas lielāko nacionālo izdevniecību „Žurnāls Santa” un Eiropas lielākās izdevniecības, analizējot starptautisko izdevniecības produktu tirgu, un produktu konkurētspēju starptautiskajā tirgū, noteikt, ka izdevniecībai SIA „Žurnāls Santa” ir konkurētspējīgi produkti, kurus ir iespējams virzīt starptautiskajā tirgū. Bakalaura darbs sastāv no ievada, trim nodaļām, secinājumu un priekšlikumu daļas, kā arī pielikumiem. Darbs sastāv no 80 lappusēm, tabulām un 3 pielikumiem. Atslēgvārdi: izdevniecības produktu virzīšana tirgū, tirgus struktūras analīze, starptautiskais tirgus, konkurentu analīze.Author of the bachelor analyze opportunities of the publishing company product promotion in international market. The goal of bachelor is based on the theoretical part and analysis about product promotion methods in the market, by analysis of Latvia`s largest publishing companies "Žurnāls Santa" and Europes largest publishing companies, analysis of the international market for printed output and product competitiveness in the international market, provide that the publishing company "Žurnāls Santa" has competitive products, which can be promoted in international market. Bachelor consists of introduction, three chapters, par of conclusions and suggestions, and attachments. Bachelor consists of 80 pages, tables and three attachments. Keywords: product promotion, market structure analysis, international market, competitor analysis

Cognitive abilities of Alzheimer's disease transgenic mice are modulated by social context and circadian rhythm

In the present study, we used a new training paradigm in the intelliCage automatic behavioral assessment system to investigate cognitive functions of the transgenic mice harboring London mutation of the human amyloid precursor protein (APP.V717I). Three groups of animals: 5-, 12- and 18-24-month old were subjected to both Water Maze training and the IntelliCage-based appetitive conditioning. The spatial memory deficit was observed in all three groups of transgenic mice in both behavioral paradigms. However, the APP mice were capable to learn normally when co-housed with the wild-type (WT) littermates, in contrast to clearly impaired learning observed when the transgenic mice were housed alone. Furthermore, in the transgenic mice kept in the Intellicage alone, the cognitive deficit of the young animals was modulated by the circadian rhythm, namely was prominent only during the active phase of the day. The novel approach to study the transgenic mice cognitive abilities presented in this paper offers new insight into cognitive dysfunctions of the Alzheimer's disease mouse model

Cognitive abilities of Alzheimer's disease transgenic mice are modulated by social context and circadian rhythm

In the present study, we used a new training paradigm in the intelliCage automatic behavioral assessment system to investigate cognitive functions of the transgenic mice harboring London mutation of the human amyloid precursor protein (APP.V717I). Three groups of animals: 5-, 12- and 18-24-month old were subjected to both Water Maze training and the IntelliCage-based appetitive conditioning. The spatial memory deficit was observed in all three groups of transgenic mice in both behavioral paradigms. However, the APP mice were capable to learn normally when co-housed with the wild-type (WT) littermates, in contrast to clearly impaired learning observed when the transgenic mice were housed alone. Furthermore, in the transgenic mice kept in the Intellicage alone, the cognitive deficit of the young animals was modulated by the circadian rhythm, namely was prominent only during the active phase of the day. The novel approach to study the transgenic mice cognitive abilities presented in this paper offers new insight into cognitive dysfunctions of the Alzheimers disease mouse model.This work was supported by MemStick grant (7 Frame-work Program of EU), the NCCR “Neural Plasticity and Re-pair” and Swiss National Science Foundation