Analysis of Contemporary Judicial Practices on Prostitution Delicts in Slovenia

POVZETEK ANALIZA NOVEJŠE SLOVENSKE SODNE PRAKSE NA PODROČJU PROSTITUCIJSKIH DELIKTOV Leta 2004 je začela veljati novela kazenskega zakonika, ki je na področju prostitucijskih deliktov prinesla veliko spremembo. Zakonodajalec je z namenom združitve takratnih kaznivih dejanj zvodništva in posredovanja pri prostituciji določil novo kaznivo dejanje: zloraba prostitucije. Sodelovanje pri tuji prostituciji je od takrat kaznivo, če je izvršeno »zaradi izkoriščanja«. Gre za nov zakonski znak, ki je zožil polje kaznivosti. Ker je pojem nekoliko nejasen in nedoločen, je in bo naloga sodne prakse, da ga napolni. Proces razlage se je že začel, pri čemer se sodišča sklicujejo na določene elemente, ki naj bi potrjevali obstoj izkoriščanja. V storilčevem ravnanju se na primer išče namen koristoljubnosti. Ni sporno, da storilec pridobiva finančno korist na račun prostitucije, prav tako naj ne bi bila problematična višina premoženjske koristi, ki nastane pri prostituciji, pač pa problem predstavlja način razdelitve zaslužka. Namen koristoljubnosti, ki vodi v ekonomsko izkoriščanje, se po mnenju sodne prakse kaže tudi v nadzoru prostitutkinih zaslužkov. Prostitutka je tudi sicer pod strogim nadzorom osebe, ki sodeluje pri njeni prostituciji z namenom izkoriščanja. Nadzor storilec vrši tako, da sam sprejema klice strank, se z njimi dogovarja o kraju, času in ceni spolnih storitev. Pri kontroli gre lahko še dlje in omejuje prostost in gibanje prostitutke, nadzoruje njeno komunikacijo in podobno. Cilj je vzdrževati stanje podrejenosti prostitutk, pri čemer se poslužuje tudi sile ali groženj. Storilec v odnosu do prostitutke vzpostavlja jasno hierarhijo, svojo dominanco pa potrjuje z zaničevalnimi in nespoštljivimi ravnanji ali komunikacijo. S prostitutko, ki jo izkorišča, ravna kot s »sredstvom za pridobivanje koristi«. Izkoriščanje slabega ekonomskega položaja, v katerem se znajdejo prostitutke, po mnenju sodišč prav tako potrjuje zlorabo prostitucije. Sodna praksa pa kot element izkoriščanja upošteva tudi sodelovanje pri prostituciji, ki predstavlja dalj časa trajajočo in utečeno dejavnost. Sodišča bolj ali manj uspešno opredeljujejo pomen zakonskega znaka »zaradi izkoriščanja«, nikakor pa se razlaga še ni ustalila. Dobro je, da vse bolj presojajo celotno situacijo in okoliščine, v katerih so se znašle prostitutke, in se ne osredotočajo več zgolj na storilčev namen koristoljubnosti. Ključne besede: zloraba prostitucije, izkoriščanje, prostitucija, namen koristoljubnosti, trgovina z ljudmi, seksualno deloSUMMARY ANALYSIS OF CONTEMPORARY JUDICIAL PRACTICES ON PROSTITUTION DELICTS IN SLOVENIA In 2004 the amending law on the Criminal Code became effective, which introduced a great change in the field of prostitution delicts. The legislator, in order to combine the previous criminal offences of trading in prostitution (»pimping«) and mediation in prostitution, declared a new criminal offence: abuse of prostitution. Cooperation in prostitution of others has been punishable since then if it happens “due to exploitation”. This is a new legal marker which narrowed the field of punishable acts. Since the term is slightly unclear and undefined, it isand will be the role of case law to fill it. The interpretation process has already begun with the courts referring to certain elements which should confirm the existence of exploitation. For example, evidence of self-serving interest is being sought in the offender’s actions. Financial gain from prostitution for the offender is indisputable, as well as the amount of financial gain, while the problem arises with the distribution of said gain. According to case law, the purpose of self-serving interest which leads to economic exploitation is seen in the control of the prostitute’s profits. The prostitute is also controlled in other ways by the person who deals with the prostitution for the purpose of exploitation. Control is enforced by the offender taking the customers’ calls and negotiating with them about the place, time and price of sexual services. Control can extend beyond this to limiting freedom and movement of the prostitute, supervision of communication by the prostitute and so on. The goal is to maintain the state of subordination of prostitutes by using force and/or threats. The offender establishes a clear hierarchy in regard to the prostitute and confirms dominance with contempt and disrespectful actions or communication. The prostitute who is being exploited is being treated as a “means to gain benefits”. The abuse of the poor economic state in which the prostitutes find themselves is also confirmed by courts as abuse of prostitution. Case law also counts cooperation in prostitution as a long-lasting and well established activity as an element of exploitation. The courts are more or less successful in filling up the meaning of the legal marker “due to exploitation”nevertheless, the explanation has not yet been settled. It is good that the entire situation and circumstances of the prostitutes are being taken into consideration and not only the offender’s purpose of self-serving interest. Key words: abuse of prostitution, exploitation, prostitution, purpose of self-serving interest, human trafficking, sexual labo

Effects of <i>Pkd1</i> or/and <i>Kif3a</i> deficiency on osteoblastic differentiation and maturation <i>ex vivo</i>.

<p>(A) ALP activity. Single <i>Pkd1</i>^+/Δ osteoblasts displayed time-dependent increments in ALP activities, but the ALP activity was significantly lower at different time points during 14 days of culture compared with wild-type control. In contrast, single <i>Kif3a</i>^+/Δ osteoblasts exhibited normal time-dependent increments in ALP activity and had no difference at the time-matched points with control. However, <i>Kif3a</i> deficiency predominated over the effects of <i>Pkd1</i> deficiency on ALP activity in compound <i>Pkd1</i>^+/Δ;<i>Kif3a</i>^+/Δ osteoblasts. (B) Quantification of mineralization. Single <i>Pkd1</i>^+/Δ osteoblasts had time-dependent increments in calcified nodule formation as measured by Alizarin Red-S staining, but the calcified nodules was significantly lower at 21 days of culture compared with wild-type control. In contrast, single <i>Kif3a</i>^+/Δ osteoblasts exhibited normal time-dependent increments in calcified nodule formation and <i>Kif3a</i> deficiency predominated over the effects of <i>Pkd1</i> deficiency on calcified nodule formation in compound <i>Pkd1</i>^+/Δ and <i>Kif3a</i>^+/Δ osteoblasts. (C–D) Osteogenic and adipogenic gene expression profiles by real-time RT-PCR. Single <i>Pkd1</i>^+/Δ osteoblasts in osteogenic medium showed a significant attenuation in osteogenesis, evidenced by a significant reduction in osteoblastic markers such as <i>Runx2</i> and <i>Osteocalcin</i> expressions (C), whereas a markedly increase of adipocyte markers such as <i>PPARγ</i> and <i>aP2</i> (D) was observed when compared with wild-type control. In contrast, there was no obvious difference in osteoblast-lineage markers between single <i>Kif3a</i>^+/Δ and wild-type osteoblast cultures, but a significant decrease in adipocyte markers was observed in single <i>Kif3a</i>^+/Δ osteoblast cultures compared with wild-type control. <i>Kif3a</i> deficiency predominated over the effects of <i>Pkd1</i> deficiency on osteogenic differentiation but retained less adipogenesis potentials in compound <i>Pkd1</i>^+/Δ and <i>Kif3a</i>^+/Δ osteoblast cultures. (E) Western blot analysis. Phosphorylated Akt at Ser473 (panel 1), total Akt (panel 2), and β-actin (panel 3) levels in the cytoplasm from cultured osteoblasts were detected by Western blot. Single heterozygous <i>Pkd1</i>^+/Δ cells displayed the decreased phosphorylation of the Akt compared with wild-type control, whereas single heterozygous <i>Kif3a</i>^+/Δ had no changes, and compound heterozygous <i>Pkd1</i>^+/Δ;<i>Kif3a</i>^+/Δ cells become normal. Data are expressed as the mean±SD from triple three independent experiments. Values sharing the same superscript are not significantly different at <i>P</i><0.05. * indicates significant difference from wild type, single heterozygous <i>Kif3a</i>^+/Δ, and compound heterozygous <i>Pkd1</i>^+/Δ;<i>Kif3a</i>^+/Δ mice at <i>p<</i>0.05.</p

Effects of <i>Pkd1</i> or/and <i>Kif3a</i> deficiency on adipocytic differentiation in BMSC cultures.

<p>(A) Representative cells were stained with Oil Red O in 10-days cultured <i>Pkd1</i>^+/Δ or/and <i>Kif3a</i>^+/Δ BMSCs as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0015240#s4" target="_blank">Materials and Methods</a>. (B) Relative Oil Red O absorbance from above indicated cultures. Stained lipid was extracted and the absorbance at 510 nm was measured. Clearly, there was a significant increase of adipogenesis potential in single <i>Pkd1</i>^+/Δ BMSC cultures, <i>Kif3a</i> deficiency entirely reversed the effects of <i>Pkd1</i> deficiency on adipogenesis potentials in compound <i>Pkd1</i>^+/Δ;<i>Kif3a</i>^+/Δ BMSC cultures. There was no significant difference in adipocytic differentiation between single <i>Kif3a</i>^+/Δ and wild-type BMSC cultures. Data are expressed as the mean±SD from triple three independent experiments. Values sharing the same superscript are not significantly different at <i>P</i><0.05.</p

Biochemistry analysis of serum in 6-week-old mice.

<p>Data are mean ± S.D. from 6–8 individual mice. * and # indicates significant difference from control <i>Pkd1</i>^flox/flox and <i>Col1a1(3.6)</i>-Cre;<i>Pkd1</i>^flox/+ mice at <i>p<</i>0.05, respectively. Osteocalcin is produced by osteoblasts, and TRAP is produced by osteoclasts.</p

Confirmation of <i>Pkd1</i> and <i>Kif3a</i> deficiency and <i>in vivo</i> and <i>in vitro</i>.

<p>(A) Schematic illustration of wild-type (<i>Pkd1</i>⁺) and deleted (<i>Pkd1</i>^Δ) <i>Pkd1</i> allele which has been removed the lox P cassette containing Exon 2–4 via Cre-mediated recombination (upper two panels), as well as wild-type (<i>Kif3a</i>⁺) and deleted (<i>Kif3a</i>^Δ) <i>Kif3a</i> allele which has been excised the lox P cassette containing Exon 2 via Cre-mediated recombination (lower two panels). (B) Genotype PCR analysis of tail genomic DNA harvested from different individual mice. Four genotypes were generated in this breeding strategy. (C–D) Real-time RT-PCR analysis of total <i>Pkd1</i> and <i>Kif3a</i> transcripts from the tibias of 6-week-old mice (C) and the cultured primary osteoblasts (D) by real-time RT-PCR. The level of <i>Pkd1</i> or <i>Kif3a</i> transcripts exhibited almost ∼50% decreases in long bone samples and primary cultured osteoblasts from single <i>Pkd1</i>^+/Δ or <i>Kif3a</i>^+/Δ mice, and both <i>Pkd1</i> and <i>Kif3a</i> transcripts retained the same reductions in compound <i>Pkd1</i>^+/Δ;<i>Kif3a</i>^+/Δ mice compared with wild-type control mice. The value of <i>Pkd1</i> or <i>Kif3a</i> vs. cyclophilin A from the indicated genotype was a fold difference over wild-type. Data are expressed as the mean±SD from 5 to 6 individual mice. Values sharing the same superscript are not significantly different at <i>P</i><0.05. (E-F) Immunofluorescence of primary cilia in cultured primary osteoblasts. Immunostaining of primary cilia (Red) was performed with acetylated α-tubulin antibody as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0015240#s4" target="_blank">Materials and Methods</a>. Counterstaining with a nuclear marker (DAPI blue) was used to calculate the percentage presence of primary cilia in cultured primary osteoblasts. There were no obvious number differences in the primary cilia among these four genotype osteoblasts.</p

<i>Col1a1(3.6)</i>-Cre-mediated conditional deletion of <i>Pkd1</i> leads to severe osteopenia in <i>Col1a1(3.6)</i>-Cre;<i>Pkd1</i>^flox/flox adult mice.

<p>(A) Bone mineral density (BMD), (B) Bone structure of femurs, (C) Bone mineral apposition rate (MAR), and (D) Femur length at 6 weeks of age. There was a <i>Pkd1</i> gene dose-dependent reduction in BMD in both male and female heterozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/+ and homozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice compared with age-matched control mice (<i>Pkd1</i>^flox/flox). µCT analysis revealed that the lower bone mass in male <i>Col1a1(3.6)</i>-Cre-mediated mice with conditional deletion of <i>Pkd1</i> resulted from reductions in both trabecular BV/TV and cortical CtTh that were proportionate to the reduction of <i>Pkd1</i> gene dose. These reductions in bone mass and structure were associated with a 19% and 41% reduction in mineral apposition rate (MAR) in male heterozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/+ and homozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice compared with age-matched control mice, respectively. In addition, the femurs of homozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice were 17% shorter in length, indicating a postnatal bone growth retardation. Data represent the mean ± S.D. from five to six individual mice. *Significant difference from control (<i>Pkd1</i>^flox/flox) and ^#significant difference from <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/+ mice at <i>P<</i>0.05, respectively.</p

<i>Col1a1(3.6)</i>-Cre-mediated conditional deletion of <i>Pkd1</i> causes polycystic pancreas and kidney.

<p>(A) Gross appearance of liver, kidney, and pancreas. There was no cyst formation in the liver, kidney, and pancreas in heterozygous <i>Col1a1(3.6)</i>-Cre;<i>Pkd1</i>^flox/+ mice, whereas age-matched homozygous <i>Col1a1(3.6)</i>-Cre;<i>Pkd1</i>^flox/flox mice developed severe renal and pancreatic cysts at 6 weeks of age. (B–D) Hematoxylin-eosin-stained sections (5X) of liver, pancreas, and kidney from 6-week-old mice. Cysts were not observed in the livers from heterozygous and homozygous mice, and renal and pancreatic cysts were also not found in kidney and pancreas tissues from heterozygous <i>Col1a1(3.6)</i>-Cre;<i>Pkd1</i>^flox/+ mice. However, homozygous <i>Col1a1(3.6)</i>-Cre;<i>Pkd1</i>^flox/flox mice exhibited massive cyst formation in both the pancreas and kidney. Interestingly, glomeruli formation in the kidney and endocrine islet formation in pancreas appeared to be unaffected. In addition, expansion of pancreatic ducts formed large pancreatic cysts that led to massive acinar cell loss, formation of abnormal tubular structures, and appearance of endocrine cells in ducts.</p

Effects of <i>Col1a1(3.6)</i>-Cre-mediated conditional deletion of <i>Pkd1</i> on osteoblastic proliferation and maturation, as well as gene expression profiles <i>ex vivo</i>.

<p>(A) Total <i>Pkd1</i> transcripts by real-time RT-PCR. All <i>Pkd1</i> transcripts were dose-dependently reduced in primary osteoblast cultures from heterozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/+ and homozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice. (B) BrdU incorporation. A gene dose-dependent increase of BrdU incorporation was observed during 6 h of primary osteoblast culture from heterozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/+ and homozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice. (C) ALP activity. Osteoblasts from control, heterozygous, and homozygous mice displayed time-dependent increments in ALP activity during 21 days of culture, but ALP activity was gene dose- and time-dependently decreased in heterozygous and homozygous osteoblasts compared to control osteoblasts. (D) Quantification of mineralization. Alizarin Red-S was extracted with 10% cetylpyridinium chloride and quantified as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0046038#s4" target="_blank">Materials and Methods</a>. A time-dependent increment of Alizarin Red-S accumulation was observed in control, heterozygous, and homozygous osteoblasts during 21 days of culture, but the accumulation was gene dose-dependently decreased in heterozygous and homozygous osteoblasts cultures compared to control osteoblasts at day 21 of culture. (<i>E–I</i>) Gene expression profiles by real-time RT-PCR. Osteoblastic markers such as <i>Runx2</i>, <i>Akp2</i>, and <i>FGF23</i> were gene dose-dependently reduced during 18 days of osteogenic culture from heterozygous and homozygous osteoblasts. In contrast, a marked increase of adipocyte markers such as <i>PPARγ2</i> and <i>aP2</i> was observed from heterozygous and homozygous osteoblasts under the same osteogenic media when compared with control osteoblasts. Data are expressed as the mean ± SD from three independent experiments. *Significant difference from control (<i>Pkd1</i>^flox/flox); ^#significant difference from heterozygous <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/+ mice at <i>P<</i>0.05, respectively.</p

<i>Col1a1(3.6)</i>-Cre-mediated conditional deletion of <i>Pkd1</i> results in enhanced adipogenesis in bone marrow and in bone stromal cell cultures.

<p>(A) Histology of adipocytes in decalcified tibias. Oil Red O staining (upper panel) showed that the numbers of adipocytes and fat droplets in tibia bone marrow were greater in 6-week-old <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice compared with age-matched control <i>Pkd1</i>^flox/flox mice. Osmium tetroxide (OsO4) staining by μCT analyses (lower panel) showed that adipocyte volume/marrow volume (Ad.V/Ma.V, %) and adipocyte number (Ad.N, mm⁻³) were much higher in the proximal tibia from 6-week-old <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox mice compared with age-matched control <i>Pkd1</i>^flox/flox mice. (B) Adipocytic differentiation in BMSC cultures. An increase of adipogenesis potential was observed in 6-week-old <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox BMSC cultures, evidenced by a significant increase of Oil Red O staining in adipogenic cultures. (C and D) Expression of adipogenic markers by real-time RT-PCR. Significantly increased levels of <i>PPARγ</i> and <i>aP2</i> mRNAs were observed in 6-week-old <i>Col1a1(3.6)</i>-Cre; <i>Pkd1</i>^flox/flox BMSC cultures compared with control (<i>Pkd1</i>^flox/flox) cultures. Data are expressed as the mean ± SD from three independent experiments. ^# Significant difference from control (<i>Pkd1</i>^flox/flox) at <i>P<</i>0.05.</p

The potential role of hedgehog/Gli2 signaling in <i>Pkd1</i> or/and <i>Kif3a</i> deficient mice.

<p>(A–B) Expression of total <i>Gli2</i> transcripts in the tibias (A) and 10 days osteoblast cultures (B) by real-time RT-PCR. A significant reduction of <i>Gli2</i> expression was observed in tibias and osteoblasts from single heterozygous <i>Pkd1</i>^+/Δ mice when compared with other three groups. In contrast, a markedly increase of <i>Gli2</i> expression was found in single heterozygous <i>Kif3a</i>^+/Δ mice compared to control and other groups. (C) Effects of <i>Gli2</i> on <i>Runx2</i>-P1 and <i>PPARγ</i>2 promoter activity. Overexpression of Gli2 results in up-regulation of <i>Runx2</i>-P1 promoter activity but down-regulation of <i>PPARγ</i>2 promoter activity in C3H10T1/2 cells. (D) Effects of Shh on <i>Runx2</i>-P1 and <i>PPARγ</i>2 promoter activity. Consistent with the effects of Gli2, administration of Shh (1 µg/ml) results in up-regulation of <i>Runx2</i>-P1 promoter activity but down-regulation of <i>PPARγ</i>2 promoter activity in C3H10T1/2 cells. (E–F) Effects of Shh on <i>Gli2</i>, <i>Gli3</i>, <i>Runx2</i>-II, and <i>PPARγ</i>2 expressions in C3H10T1/2 cells. Consistent with promoter activity data, administration of Shh (1 µg/ml) increases <i>Gli2</i> and <i>Runx2</i>-II transcripts, have no changes in <i>Gli3 mRNA</i> message, but decreases <i>PPARγ</i>2 gene expression in C3H10T1/2 cell cultures. (G–H) Effects of PC1 C-tail construct on <i>Gli2</i>, <i>Runx2</i>-II, and <i>PPARγ</i>2 expressions in C3H10T1/2 cells. Gain of function PC1 C-tail construct (PC1-AT) stimulated <i>Runx2</i>-P1 promoter activity but inhibited <i>PPARγ</i>2 promoter activity. Consistent with tibias and primary osteoblasts data, <i>Gli2</i> and <i>Runx2</i>-II transcripts were significantly increased in C3H10T1/2 cells, which were transiently transfected with PC1-AT for 48 hours. The slgØ construct was served as vector control. Data are expressed as the mean±SD from triple three independent experiments. Values sharing the same superscript are not significantly different at <i>P</i><0.05.</p