Strafvorderlijke gegevensverwerking

As a result of society’s increasing digitisation, the police have ever more opportunities to collect, investigate and combine huge amounts of personal data using advanced technology. Examples are provided from recent cases where police have gained access to millions of encrypted messages from various servers, including Ennetcom, EncroChat and Sky Global. However, the current legal framework is, as yet, ill-equipped to deal with this new reality. Partly for this reason, legislators are facing new questions about how the (further) processing of data in detection should be regulated by law. Commissioned by the WODC, this study examines the legal safeguards in criminal justice data collection in relation to the legal safeguards governing the processing of these data. The Code of Criminal Procedure mainly focuses on the collection of data and to a much lesser extent on its further use, but this may involve a (fresh) invasion of citizens’ privacy. The Police Data Act contains some provisions to data processing, but the relationship with the Dutch Code of Criminal Procedure is not entirely clear. This study identifies the requirements and safeguards under European law for the processing of data for criminal justice purposes. Further inspiration is drawn from experience with the Intelligence and Security Services Act 2017 in which powers of collection and (further) processing are regulated in a single law. Finally, it explores how, in several countries (Germany, Belgium and Norway), the requirements arising from European law have been translated into legal regulations and how these regulations are designed. This study provides tools that legislators can use to reconsider the methods of standardisation and legal regulation design to better protect citizens' privacy. The recommendations thus focus on strengthening the legal framework on data processing and its supervision by creating an explicit legal framework in the Code of Criminal Procedure and establishing an independent supervisor focused on the processing of personal data by investigative authorities

Strafvorderlijke gegevensverwerking

As a result of society’s increasing digitisation, the police have ever more opportunities to collect, investigate and combine huge amounts of personal data using advanced technology. Examples are provided from recent cases where police have gained access to millions of encrypted messages from various servers, including Ennetcom, EncroChat and Sky Global. However, the current legal framework is, as yet, ill-equipped to deal with this new reality. Partly for this reason, legislators are facing new questions about how the (further) processing of data in detection should be regulated by law. Commissioned by the WODC, this study examines the legal safeguards in criminal justice data collection in relation to the legal safeguards governing the processing of these data. The Code of Criminal Procedure mainly focuses on the collection of data and to a much lesser extent on its further use, but this may involve a (fresh) invasion of citizens’ privacy. The Police Data Act contains some provisions to data processing, but the relationship with the Dutch Code of Criminal Procedure is not entirely clear. This study identifies the requirements and safeguards under European law for the processing of data for criminal justice purposes. Further inspiration is drawn from experience with the Intelligence and Security Services Act 2017 in which powers of collection and (further) processing are regulated in a single law. Finally, it explores how, in several countries (Germany, Belgium and Norway), the requirements arising from European law have been translated into legal regulations and how these regulations are designed. This study provides tools that legislators can use to reconsider the methods of standardisation and legal regulation design to better protect citizens' privacy. The recommendations thus focus on strengthening the legal framework on data processing and its supervision by creating an explicit legal framework in the Code of Criminal Procedure and establishing an independent supervisor focused on the processing of personal data by investigative authorities

The Inertia Contributions due to Floodwater Mass

The Stability in Waves committee of the 27th ITTC investigated ow to deal with the ship inertia contributions due to floodwater mass from three points of view: (1) floodwater domain, (2) loodwater inertia itself, (3) floodwater entering the ship. The committee suggested three criteria indicating the concept of how to deal with floodwater and providing clues on what to onsider as floodwater when examining damaged ships: (1) whether the water is moving with the ship and the mass of that volume of water, (2) whether there is a significant pressure jump across the compartment boundary, and (3) whether the dynamics of water can be solved separately. For floodwater inertia, the committee divided this into the partially flooded case and fully flooded case, and investigated the properties and showed how to deal with floodwater inertia for each case. For the case of the floodwater entering the ship, the treatment of the inertia change due to floodwater was derived using the momentum change principle. The related ITTC procedure was updated reflecting this work

Air Pressure Scale Effects during Damage Model Tests

The Stability in Waves committee of the 27th ITTC has nvestigated the significance of scale effects in air pressure on flooding model tests under atmospheric conditions. For this purpose, the committee classified the flooding cases into the trapped air case and vented air cases, and investigated the flooding process for a simple geometry using the state equation of air and the orifice equation. As a result, the committee concluded that the scale effect is large for the case of trapped air and small vent area. For the other cases, the effect is small and can therefore be neglected in the model test of a damaged ship. The committee further proposed some guidelines that can be used to reduce the scale effect of air pressure

Bi-allelic variants in DNA mismatch repair proteins MutS Homolog MSH4 and MSH5 cause infertility in both sexes

STUDY QUESTION: Do bi-allelic variants in the genes encoding the MSH4/MSH5 heterodimer cause male infertility? SUMMARY ANSWER: We detected biallelic, (likely) pathogenic variants in MSH5 (4 men) and MSH4 (3 men) in six azoospermic men, demonstrating that genetic variants in these genes are a relevant cause of male infertility. WHAT IS KNOWN ALREADY: MSH4 and MSH5 form a heterodimer, which is required for prophase of meiosis I. One variant in MSH5 and two variants in MSH4 have been described as causal for premature ovarian insufficiency (POI) in a total of five women, resulting in infertility. Recently, pathogenic variants in MSH4 have been reported in infertile men. So far, no pathogenic variants in MSH5 had been described in males. STUDY DESIGN, SIZE, DURATION: We utilized exome data from 1305 men included in the Male Reproductive Genomics (MERGE) study, including 90 males with meiotic arrest (MeiA). Independently, exome sequencing was performed in a man with MeiA from a large consanguineous family. PARTICIPANTS/MATERIALS, SETTING, METHODS: Assuming an autosomal-recessive mode of inheritance, we screened the exome data for rare, biallelic coding variants in MSH4 and MSH5. If possible, segregation analysis in the patients' families was performed. The functional consequences of identified loss-of-function (LoF) variants in MSH5 were studied using heterologous expression of the MSH5 protein in HEK293T cells. The point of arrest during meiosis was determined by γH2AX staining. MAIN RESULTS AND THE ROLE OF CHANCE: We report for the first time (likely) pathogenic, homozygous variants in MSH5 causing infertility in 2 out of 90 men with MeiA and overall in 4 out of 902 azoospermic men. Additionally, we detected biallelic variants in MSH4 in two men with MeiA and in the sister of one proband with POI. γH2AX staining revealed an arrest in early prophase of meiosis I in individuals with pathogenic MSH4 or MSH5 variants. Heterologous in vitro expression of the detected LoF variants in MSH5 showed that the variant p.(Ala620GlnTer9) resulted in MSH5 protein truncation and the variant p.(Ser26GlnfsTer42) resulted in a complete loss of MSH5. LARGE SCALE DATA: All variants have been submitted to ClinVar (SCV001468891-SCV001468896 and SCV001591030) and can also be accessed in the Male Fertility Gene Atlas (MFGA). LIMITATIONS, REASONS FOR CAUTION: By selecting for variants in MSH4 and MSH5, we were able to determine the cause of infertility in six men and one woman, leaving most of the examined individuals without a causal diagnosis. WIDER IMPLICATIONS OF THE FINDINGS: Our findings have diagnostic value by increasing the number of genes associated with non-obstructive azoospermia with high clinical validity. The analysis of such genes has prognostic consequences for assessing whether men with azoospermia would benefit from a testicular biopsy. We also provide further evidence that MeiA in men and POI in women share the same genetic causes. STUDY FUNDING/COMPETING INTEREST(S): This study was carried out within the frame of the German Research Foundation sponsored Clinical Research Unit 'Male Germ Cells: from Genes to Function' (DFG, CRU326), and supported by institutional funding of the Research Institute Amsterdam Reproduction and Development and funds from the LucaBella Foundation. The authors declare no conflict of interest

Bi-allelic variants in DNA mismatch repair proteins MutS Homolog MSH4 and MSH5 cause infertility in both sexes

STUDY QUESTION: Do bi-allelic variants in the genes encoding the MSH4/MSH5 heterodimer cause male infertility? SUMMARY ANSWER: We detected biallelic, (likely) pathogenic variants in MSH5 (4 men) and MSH4 (3 men) in six azoospermic men, demonstrating that genetic variants in these genes are a relevant cause of male infertility. WHAT IS KNOWN ALREADY: MSH4 and MSH5 form a heterodimer, which is required for prophase of meiosis I. One variant in MSH5 and two variants in MSH4 have been described as causal for premature ovarian insufficiency (POI) in a total of five women, resulting in infertility. Recently, pathogenic variants in MSH4 have been reported in infertile men. So far, no pathogenic variants in MSH5 had been described in males. STUDY DESIGN, SIZE, DURATION: We utilized exome data from 1305 men included in the Male Reproductive Genomics (MERGE) study, including 90 males with meiotic arrest (MeiA). Independently, exome sequencing was performed in a man with MeiA from a large consanguineous family. PARTICIPANTS/MATERIALS, SETTING, METHODS: Assuming an autosomal-recessive mode of inheritance, we screened the exome data for rare, biallelic coding variants in MSH4 and MSH5. If possible, segregation analysis in the patients' families was performed. The functional consequences of identified loss-of-function (LoF) variants in MSH5 were studied using heterologous expression of the MSH5 protein in HEK293T cells. The point of arrest during meiosis was determined by γH2AX staining. MAIN RESULTS AND THE ROLE OF CHANCE: We report for the first time (likely) pathogenic, homozygous variants in MSH5 causing infertility in 2 out of 90 men with MeiA and overall in 4 out of 902 azoospermic men. Additionally, we detected biallelic variants in MSH4 in two men with MeiA and in the sister of one proband with POI. γH2AX staining revealed an arrest in early prophase of meiosis I in individuals with pathogenic MSH4 or MSH5 variants. Heterologous in vitro expression of the detected LoF variants in MSH5 showed that the variant p.(Ala620GlnTer9) resulted in MSH5 protein truncation and the variant p.(Ser26GlnfsTer42) resulted in a complete loss of MSH5. LARGE SCALE DATA: All variants have been submitted to ClinVar (SCV001468891-SCV001468896 and SCV001591030) and can also be accessed in the Male Fertility Gene Atlas (MFGA). LIMITATIONS, REASONS FOR CAUTION: By selecting for variants in MSH4 and MSH5, we were able to determine the cause of infertility in six men and one woman, leaving most of the examined individuals without a causal diagnosis. WIDER IMPLICATIONS OF THE FINDINGS: Our findings have diagnostic value by increasing the number of genes associated with non-obstructive azoospermia with high clinical validity. The analysis of such genes has prognostic consequences for assessing whether men with azoospermia would benefit from a testicular biopsy. We also provide further evidence that MeiA in men and POI in women share the same genetic causes. STUDY FUNDING/COMPETING INTEREST(S): This study was carried out within the frame of the German Research Foundation sponsored Clinical Research Unit 'Male Germ Cells: from Genes to Function' (DFG, CRU326), and supported by institutional funding of the Research Institute Amsterdam Reproduction and Development and funds from the LucaBella Foundation. The authors declare no conflict of interest