The aim of this paper is to consider the relationship between the regulation of state property and the rule of law, and for this purpose the authors analyze the Decision of the Constitutional Court of BiH No. U-4/21 which declared certain provisions of the Law on Forests of Republika Srpska unconstitutional. The paper discusses not only the issues of the relationship between state property and the rule of law, but also the issues of judicial activism and the rule of law. In particular, the authors analyze the extent to which the courts, and in this particular case the Constitutional Court of BiH, in order to protect the rule of law, may interfere in the competences of the legislature. In this context, the authors consider the justification of judicial activism of the Constitutional Court of BiH in case U-4/21, considering whether the Constitutional Court of BiH has the right to protect the principle of the rule of law in such a way. Finally, the authors explain why judicial activism is necessary when it comes to the relationship between constitutional and legislative power and why judicial activism of the BiH Constitutional Court was necessary in the case U-4/21.

The rule of law is one of the key concepts in the 21st century. The idea of the rule of law exists to the extent that there are reflections on the state and law, and a relationship between these two concepts. The aim of this paper is to show in one place the development of the idea of the rule of law through history. In this sense, the authors look at the thoughts of philosophers who have largely determined the direction of development of the idea of the rule of law. Of course, not all philosophers who have contemplated the rule of law are listed in the paper, but it nevertheless attempts to show in chronological order how the rule of law as an idea developed from Plato to its modern theorists.

Zika virus (ZIKV) is an enveloped, positive-sense, single-stranded RNA virus that belongs to the genus Flavivirus, family Flaviviridae, which includes many human and animal pathogens, such as dengue virus (DENV), West Nile virus, and Japanese encephalitis virus. In the original as well as subsequent experimental and clinical reports, ZIKV seems to have moderate neurotropism (in animal models) and neurovirulence (in human fetuses), but no neuroinvasiveness (in human adults). Intrauterine ZIKV infection (viral pathology) has been linked to an increased incidence of microcephaly, while increased Guillain-Barré syndrome (GBS) following ZIKV infection is likely immune-mediated (immunopathology). Clinically, in ZIKV infection, antibodies against other flaviviruses, such as DENV, have been detected; these antibodies can cross-react with ZIKV without ZIKV neutralization. In theory, such non-neutralizing antibodies are generated at the expense of decreased production of neutralizing antibodies (“antigenic sin”), leading to poor viral clearance, while the non-neutralizing antibodies can also enhance viral replication in Fc receptor (FcR)-bearing cells via antibody-dependent enhancement (ADE). Here, we propose three potential roles of the antibody-mediated pathogenesis of ZIKV infection: 1) cross-reactive antibodies that recognize ZIKV and neural antigens cause GBS; 2) ZIKV-antibody complex is transported transplacentally via neonatal FcR (FcRn), resulting in fetal infection; and 3) ZIKV-antibody complex is taken up at peripheral nerve endings and transported to neurons in the central nervous system (CNS), by which the virus can enter the CNS without crossing the blood-brain barrier.

Multiple sclerosis (MS) has been suggested to be an autoimmune demyelinating disease of the central nervous system (CNS), whose primary target is either myelin itself, or myelin-forming cells, the oligodendrocytes. Although axonal damage occurs in MS, it is regarded as a secondary event to the myelin damage. Here, the lesion develops from the myelin (outside) to the axons (inside) “Outside-In model”. The Outside-In model has been supported by an autoimmune model for MS, experimental autoimmune (allergic) encephalomyelitis (EAE). However, recently, 1) EAE-like disease has also been shown to be induced by immune responses against axons, and 2) immune responses against axons and neurons as well as neurodegeneration independent of inflammatory demyelination have been reported in MS, which can not be explained by the Outside-In model. Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD) is a viral model for MS. In TMEV infection, axonal injury precedes demyelination, where the lesion develops from the axons (inside) to the myelin (outside) “Inside-Out model”. The initial axonal damage could result in the release of neuroantigens, inducing autoimmune responses against myelin antigens, which potentially attack the myelin from outside the nerve fiber. Thus, the Inside-Out and Outside-In models can make a “vicious” immunological cycle or initiate an immune cascade.