Privacy-Preserving Credit Scoring via Functional Encryption

The majority of financial organizations managing confidential data are aware of security threats and leverage widely accepted solutions (e.g., storage encryption, transport-level encryption, intrusion detection systems) to prevent or detect attacks. Yet these hardening measures do little to face even worse threats posed on data-in-use. Solutions such as Homomorphic Encryption (HE) and hardware-assisted Trusted Execution Environment (TEE) are nowadays among the preferred approaches for mitigating this type of threats. However, given the high-performance overhead of HE, financial institutions —whose processing rate requirements are stringent— are more oriented towards TEE-based solutions. The X-Margin Inc. company, for example, offers secure financial computations by combining the Intel SGX TEE technology and HE-based Zero-Knowledge Proofs, which shield customers’ data-in-use even against malicious insiders, i.e., users having privileged access to the system. Despite such a solution offers strong security guarantees, it is constrained by having to trust Intel and by the SGX hardware extension availability. In this paper, we evaluate a new frontier for X-Margin, i.e., performing privacy-preserving credit risk scoring via an emerging cryptographic scheme: Functional Encryption (FE), which allows a user to only learn a function of the encrypted data. We describe how the X-Margin application can benefit from this innovative approach and —most importantly— evaluate its performance impact

Gall-bladder dysmotility - A risk factor for gall-stone formation in hypertriglyceridaemia and reversal on triglyceride-lowering therapy with bezafibrate and fish oil

Doel: Onderzoeken van de pathofysiologische mechanismen die de kans op galstenen verhogen bij hypertriglyceridemie (HTG) en het vergelijken van de effecten van triglycerideverlagende therapie met bezafibraat en visolie op determinanten van cholelithiasis (biliaire lipidesamenstelling en galblaasmotoriek) bij HTG-patiënten.Opzet: Gekruiste opzet met ‘random’-volgorde.Patiënten en methoden: De galblaasmotoriek werd postprandiaal en tijdens cholecystokinine(CCK)-infusie echografisch onderzocht. De determinanten van cholelithiasis en de serumlipiden werden vergeleken tussen 9 HTG-patiënten en 10 normolipidemische controlepersonen van hetzelfde geslacht, dezelfde leeftijd en ‘body mass’-index. Bij de HTG-patiënten werden de effecten van bezafibraat en gezuiverde omega-3-olie (‘visolie’) bepaald.Resultaten: De serumtriglyceride(TG)-spiegel van de HTG-patiënten was 14-voudig verhoogd, vergeleken met de controlepersonen. De lipidesamenstelling van de gal, de nuchtere galblaasvolumen en de serum-CCK-spiegels verschilden niet tussen HTG-patiënten en controlepersonen. De galblaaslediging was verminderd bij HTG-patiënten versus controlepersonen tijdens CCK-infusie (–22) en ook na een maaltijd (–37; beide p &lt; 0,001). De postprandiale serum-CCK-spiegels waren significant hoger bij HTG-patiënten. Zowel bezafibraat als visolie verlaagde de serum-TG-spiegel (–68 en –51 ten opzichte van de uitgangswaarde; beide: p &lt; 0,01). Nuchtere CCK-spiegels verschilden niet, terwijl de CCK-geïnduceerde galblaaslediging onder bezafibraat toenam met 29 (p &lt; 0,001) en met visolie met 13 (p = 0,07). De postprandiale galblaasmotoriek verbeterde tijdens zowel bezafibraat- (+47) als visoliebehandeling (+25; beide: p &lt; 0,02), waarschijnlijk gedeeltelijk door een toegenomen gevoeligheid van de galblaas voor CCK (voor beide: p &lt; 0,05 vergeleken met de uitgangsfase). Bezafibraat, in tegenstelling tot visolie, verhoogde de molaire cholesterol-galzuurratio (+40; p ≤ 0,05), terwijl beide behandelingen geen effect hadden op de cholesterolsaturatie-index.Conclusies: De verminderde galblaasmotoriek bij HTG-patiënten lijkt het gevolg te zijn van verminderde gevoeligheid voor CCK, wat kan bijdragen aan het verhoogde risico op galsteenvorming. Bij HTG-patiënten verbetert triglycerideverlagende therapie met visolie of bezafibraat de verminderde galblaasmotoriek zonder nadelig effect op de biliaire cholesterolverzadiging.Objective. To unravel the mechanisms responsible for the increased risk of gall-stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride-lowering therapy with bezafibrate and fish oil on determinants of cholelithiasis (biliary-lipid composition and gall-bladder motility) in HTG patients. Design. Randomised cross over. Patients and methods. Gall-bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between 9 HTG patients and 10 age, sex and body-mass index matched normolipidaemic controls. The effects of bezafibrate and purified omega-3-oil ('fish oil') in HTG patients were studied. Results. HTG patients showed 14-fold higher serum-triglyceride (TG) levels than controls. Biliary-lipid composition, fasting gall-bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall-bladder emptying was reduced in HTG patients compared with controls during CCK infusion (-22%) as well as in response to a meal (-37%; both p &lt; 0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (-68 and -51% versus baseline, respectively; both p &lt; 0.01). Fasting CCK levels were not affected whereas CCK-induced gall-bladder emptying increased during bezafibrate (+29%; p &lt; 0.001) and tended to increase upon fish-oil therapy (+13%; p = 0.07). Postprandial gall-bladder motility improved at least partly with bezafibrate and fish oil (+47 and +25% versus baseline, respectively; both p &lt; 0.02) due to increased gallbladder sensitivity to CCK (both p &lt; 0.05 versus baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p ≤ 0.05), but no effects on the cholesterol-saturation index were seen with either treatment. Conclusions. We suggest that impaired gall-bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall-stone disease in HTG patients. Triglyceride-lowering therapy by both fish oil and bezafibrate improves gall-bladder dysmotility without adversely affecting biliary-cholesterol saturation.</p

Gall-bladder dysmotility - A risk factor for gall-stone formation in hypertriglyceridaemia and reversal on triglyceride-lowering therapy with bezafibrate and fish oil

Doel: Onderzoeken van de pathofysiologische mechanismen die de kans op galstenen verhogen bij hypertriglyceridemie (HTG) en het vergelijken van de effecten van triglycerideverlagende therapie met bezafibraat en visolie op determinanten van cholelithiasis (biliaire lipidesamenstelling en galblaasmotoriek) bij HTG-patiënten.Opzet: Gekruiste opzet met ‘random’-volgorde.Patiënten en methoden: De galblaasmotoriek werd postprandiaal en tijdens cholecystokinine(CCK)-infusie echografisch onderzocht. De determinanten van cholelithiasis en de serumlipiden werden vergeleken tussen 9 HTG-patiënten en 10 normolipidemische controlepersonen van hetzelfde geslacht, dezelfde leeftijd en ‘body mass’-index. Bij de HTG-patiënten werden de effecten van bezafibraat en gezuiverde omega-3-olie (‘visolie’) bepaald.Resultaten: De serumtriglyceride(TG)-spiegel van de HTG-patiënten was 14-voudig verhoogd, vergeleken met de controlepersonen. De lipidesamenstelling van de gal, de nuchtere galblaasvolumen en de serum-CCK-spiegels verschilden niet tussen HTG-patiënten en controlepersonen. De galblaaslediging was verminderd bij HTG-patiënten versus controlepersonen tijdens CCK-infusie (–22) en ook na een maaltijd (–37; beide p &lt; 0,001). De postprandiale serum-CCK-spiegels waren significant hoger bij HTG-patiënten. Zowel bezafibraat als visolie verlaagde de serum-TG-spiegel (–68 en –51 ten opzichte van de uitgangswaarde; beide: p &lt; 0,01). Nuchtere CCK-spiegels verschilden niet, terwijl de CCK-geïnduceerde galblaaslediging onder bezafibraat toenam met 29 (p &lt; 0,001) en met visolie met 13 (p = 0,07). De postprandiale galblaasmotoriek verbeterde tijdens zowel bezafibraat- (+47) als visoliebehandeling (+25; beide: p &lt; 0,02), waarschijnlijk gedeeltelijk door een toegenomen gevoeligheid van de galblaas voor CCK (voor beide: p &lt; 0,05 vergeleken met de uitgangsfase). Bezafibraat, in tegenstelling tot visolie, verhoogde de molaire cholesterol-galzuurratio (+40; p ≤ 0,05), terwijl beide behandelingen geen effect hadden op de cholesterolsaturatie-index.Conclusies: De verminderde galblaasmotoriek bij HTG-patiënten lijkt het gevolg te zijn van verminderde gevoeligheid voor CCK, wat kan bijdragen aan het verhoogde risico op galsteenvorming. Bij HTG-patiënten verbetert triglycerideverlagende therapie met visolie of bezafibraat de verminderde galblaasmotoriek zonder nadelig effect op de biliaire cholesterolverzadiging.Objective. To unravel the mechanisms responsible for the increased risk of gall-stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride-lowering therapy with bezafibrate and fish oil on determinants of cholelithiasis (biliary-lipid composition and gall-bladder motility) in HTG patients. Design. Randomised cross over. Patients and methods. Gall-bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between 9 HTG patients and 10 age, sex and body-mass index matched normolipidaemic controls. The effects of bezafibrate and purified omega-3-oil ('fish oil') in HTG patients were studied. Results. HTG patients showed 14-fold higher serum-triglyceride (TG) levels than controls. Biliary-lipid composition, fasting gall-bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall-bladder emptying was reduced in HTG patients compared with controls during CCK infusion (-22%) as well as in response to a meal (-37%; both p &lt; 0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (-68 and -51% versus baseline, respectively; both p &lt; 0.01). Fasting CCK levels were not affected whereas CCK-induced gall-bladder emptying increased during bezafibrate (+29%; p &lt; 0.001) and tended to increase upon fish-oil therapy (+13%; p = 0.07). Postprandial gall-bladder motility improved at least partly with bezafibrate and fish oil (+47 and +25% versus baseline, respectively; both p &lt; 0.02) due to increased gallbladder sensitivity to CCK (both p &lt; 0.05 versus baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p ≤ 0.05), but no effects on the cholesterol-saturation index were seen with either treatment. Conclusions. We suggest that impaired gall-bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall-stone disease in HTG patients. Triglyceride-lowering therapy by both fish oil and bezafibrate improves gall-bladder dysmotility without adversely affecting biliary-cholesterol saturation.</p

Gall-bladder dysmotility - A risk factor for gall-stone formation in hypertriglyceridaemia and reversal on triglyceride-lowering therapy with bezafibrate and fish oil

Doel: Onderzoeken van de pathofysiologische mechanismen die de kans op galstenen verhogen bij hypertriglyceridemie (HTG) en het vergelijken van de effecten van triglycerideverlagende therapie met bezafibraat en visolie op determinanten van cholelithiasis (biliaire lipidesamenstelling en galblaasmotoriek) bij HTG-patiënten.Opzet: Gekruiste opzet met ‘random’-volgorde.Patiënten en methoden: De galblaasmotoriek werd postprandiaal en tijdens cholecystokinine(CCK)-infusie echografisch onderzocht. De determinanten van cholelithiasis en de serumlipiden werden vergeleken tussen 9 HTG-patiënten en 10 normolipidemische controlepersonen van hetzelfde geslacht, dezelfde leeftijd en ‘body mass’-index. Bij de HTG-patiënten werden de effecten van bezafibraat en gezuiverde omega-3-olie (‘visolie’) bepaald.Resultaten: De serumtriglyceride(TG)-spiegel van de HTG-patiënten was 14-voudig verhoogd, vergeleken met de controlepersonen. De lipidesamenstelling van de gal, de nuchtere galblaasvolumen en de serum-CCK-spiegels verschilden niet tussen HTG-patiënten en controlepersonen. De galblaaslediging was verminderd bij HTG-patiënten versus controlepersonen tijdens CCK-infusie (–22) en ook na een maaltijd (–37; beide p &lt; 0,001). De postprandiale serum-CCK-spiegels waren significant hoger bij HTG-patiënten. Zowel bezafibraat als visolie verlaagde de serum-TG-spiegel (–68 en –51 ten opzichte van de uitgangswaarde; beide: p &lt; 0,01). Nuchtere CCK-spiegels verschilden niet, terwijl de CCK-geïnduceerde galblaaslediging onder bezafibraat toenam met 29 (p &lt; 0,001) en met visolie met 13 (p = 0,07). De postprandiale galblaasmotoriek verbeterde tijdens zowel bezafibraat- (+47) als visoliebehandeling (+25; beide: p &lt; 0,02), waarschijnlijk gedeeltelijk door een toegenomen gevoeligheid van de galblaas voor CCK (voor beide: p &lt; 0,05 vergeleken met de uitgangsfase). Bezafibraat, in tegenstelling tot visolie, verhoogde de molaire cholesterol-galzuurratio (+40; p ≤ 0,05), terwijl beide behandelingen geen effect hadden op de cholesterolsaturatie-index.Conclusies: De verminderde galblaasmotoriek bij HTG-patiënten lijkt het gevolg te zijn van verminderde gevoeligheid voor CCK, wat kan bijdragen aan het verhoogde risico op galsteenvorming. Bij HTG-patiënten verbetert triglycerideverlagende therapie met visolie of bezafibraat de verminderde galblaasmotoriek zonder nadelig effect op de biliaire cholesterolverzadiging.Objective. To unravel the mechanisms responsible for the increased risk of gall-stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride-lowering therapy with bezafibrate and fish oil on determinants of cholelithiasis (biliary-lipid composition and gall-bladder motility) in HTG patients. Design. Randomised cross over. Patients and methods. Gall-bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between 9 HTG patients and 10 age, sex and body-mass index matched normolipidaemic controls. The effects of bezafibrate and purified omega-3-oil ('fish oil') in HTG patients were studied. Results. HTG patients showed 14-fold higher serum-triglyceride (TG) levels than controls. Biliary-lipid composition, fasting gall-bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall-bladder emptying was reduced in HTG patients compared with controls during CCK infusion (-22%) as well as in response to a meal (-37%; both p &lt; 0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (-68 and -51% versus baseline, respectively; both p &lt; 0.01). Fasting CCK levels were not affected whereas CCK-induced gall-bladder emptying increased during bezafibrate (+29%; p &lt; 0.001) and tended to increase upon fish-oil therapy (+13%; p = 0.07). Postprandial gall-bladder motility improved at least partly with bezafibrate and fish oil (+47 and +25% versus baseline, respectively; both p &lt; 0.02) due to increased gallbladder sensitivity to CCK (both p &lt; 0.05 versus baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p ≤ 0.05), but no effects on the cholesterol-saturation index were seen with either treatment. Conclusions. We suggest that impaired gall-bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall-stone disease in HTG patients. Triglyceride-lowering therapy by both fish oil and bezafibrate improves gall-bladder dysmotility without adversely affecting biliary-cholesterol saturation.</p

Gall bladder dysmotility: a risk factor for gall stone formation in hypertriglyceridaemia and reversal on triglyceride lowering therapy by bezafibrate and fish oil

Background and aim: The aim of this study was to unravel the mechanisms responsible for the increased risk of gall stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride lowering therapy by bezafibrate and fish oil on determinants of cholelithiasis (biliary lipid composition and gall bladder motility) in HTG patients. Patients and methods: Gall bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between nine HTG patients and 10 age, sex, and body mass index matched normolipidaemic controls. The effects of bezafibrate and fish oil in HTG patients were studied in a randomised cross over trial. Results: HTG patients showed 14-fold higher serum triglyceride (TG) levels than controls. Biliary lipid composition, fasting gall bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall bladder emptying was reduced in HTG patients compared with controls during CCK infusion (−22%) as well as in response to a meal (−37%; both p<0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (−68% and −51% v baseline, respectively; both p<0.01). Fasting CCK levels were not affected whereas CCK induced gall bladder emptying increased during bezafibrate (+29%; p<0.001) and tended to increase on fish oil therapy (+13%; p=0.07). Postprandial gall bladder motility improved on bezafibrate and fish oil (+47 and +25% v baseline, respectively; both p<0.02) at least partly due to increased gall bladder sensitivity to CCK (both p<0.05 v baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p≤0.05) but no effects on cholesterol saturation index were seen with either treatment. Conclusions: We suggest that impaired gall bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall stone disease in HTG patients. Triglyceride lowering therapy by both fish oil and bezafibrate improve gall bladder dysmotility without adversely affecting biliary cholesterol saturation