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1

Cohen, D. E., L. S. Leighton, and M. C. Carey. "Bile salt hydrophobicity controls vesicle secretion rates and transformations in native bile." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 3 (September 1, 1992): G386—G395. http://dx.doi.org/10.1152/ajpgi.1992.263.3.g386.

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After drainage of the bile salt pool, we infused unanesthetized bile fistula prairie dogs (Cynomys ludovicianus) intravenously with taurine-conjugated chenodeoxycholate (TCDC), cholate (TC), ursodeoxycholate (TUDC), and ursocholate (TUC) in concentrations that attained greater than 94% enrichment of biliary bile salts. With decreases in bile salt hydrophobicity, maximum steady state lecithin and to a lesser extent cholesterol secretion rates decreased in the rank order, TCDC greater than TC greater than TUDC greater than TUC. By phase analysis, TCDC-rich and TC-rich biles plotted inside their respective micellar zones, whereas TUDC-rich and TUC-rich biles plotted outside and were so-called "supersaturated" with cholesterol. Quasi-elastic light scattering and electron microscopy, when performed within 30 min of collection, revealed unilamellar vesicles in all biles. By 24 h, vesicles in TCDC-rich and TC-rich biles had dissolved into mixed micelles, whereas vesicles in TUDC-rich biles formed mixed micelles plus multilamellar liquid crystals, and vesicles in TUC-rich biles formed multilamellar liquid crystals exclusively. Because cholesterol/phospholipid molar ratios of multilamellar liquid crystals were less than or equal to 1, cholesterol monohydrate crystals did not form in these biles. We conclude that, despite drastic alterations in bile salt detergency, unilamellar vesicles are the final common pathway for lecithin and cholesterol secretion into bile. During equilibration of bile, the fate of unilamellar vesicles may be micellar, micellar plus liquid crystalline, or liquid crystalline only depending on the detergency (i.e., hydrophobic-hydrophilic balance) of the secreted bile salt.
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2

Thewles, A., R. A. Parslow, and R. Coleman. "Effect of diosgenin on biliary cholesterol transport in the rat." Biochemical Journal 291, no. 3 (May 1, 1993): 793–98. http://dx.doi.org/10.1042/bj2910793.

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Biliary cholesterol output in rats was stimulated over 3-fold by feeding diosgenin for 5 days, whereas biliary outputs of phospholipid and bile salts were not changed by diosgenin feeding. Isolating and perfusing the liver without bile salts resulted in a rapid and substantial decrease in biliary bile salt output; bile salt depletion abolished the diosgenin-induced increment in biliary cholesterol output, showing that the diosgenin-elevated biliary cholesterol output was bile-salt-dependent. Diosgenin treatment also produced a significant decrease in biliary alkaline phosphodiesterase I. Fresh bile obtained from control and diosgenin-fed rats was subjected to gel-permeation chromatography in order to separate different-sized biliary cholesterol carriers. Two major peaks of cholesterol were eluted, with cholesterol also being eluted between the peaks. The cholesterol peak eluted at the lower molecular mass (20-30 kDa) was observed in all bile samples. The higher-molecular-mass peak, which was eluted at the void volume, was not observed in all biles; control biles contained very little high-molecular-mass form of cholesterol, whereas biles from the diosgenin group contained up to 47% of cholesterol in the high-molecular-mass fraction. Diosgenin treatment produced a range of elevated biliary cholesterol values which positively correlated with the proportion of cholesterol contained in the high-molecular-mass fraction (r = 0.98). The results show that diosgenin induced a marked bile-salt-dependent increase in biliary cholesterol output and a shift in biliary cholesterol transport to higher-molecular-mass structures.
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3

Cohen, D. E., M. Angelico, and M. C. Carey. "Quasielastic light scattering evidence for vesicular secretion of biliary lipids." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (July 1, 1989): G1—G8. http://dx.doi.org/10.1152/ajpgi.1989.257.1.g1.

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We employed quasielastic light scattering, negative-stain, and freeze-fracture electron microscopy to study the time-dependent physicochemical behavior of biliary lipids in fresh rat bile. Three to five minutes after bile collection, the earliest light scattering measurements and electron microscopy revealed unilamellar vesicles (mean hydrodynamic radius, Rh = 430-740 A) coexisting with mixed micelles (Rh = 20-120 A) in all biles. Both percent biliary vesicles (1 to greater than 70%) and micellar sizes varied inversely with bile salt concentration (range 1.6-72 mM) both during endogenous pool drainage and sodium taurocholate infusion. With bile salt concentrations in the vicinity of or below the estimated critical micellar concentration, biliary vesicle concentrations remained constant or increased slightly with passage of time. However, with micellar bile salt concentrations, complete conversion of vesicles to micelles occurred at rates that were directly proportional to bile salt concentration. Back-extrapolation of weighted Rh averages of micelles plus vesicles as functions of time gave sizes of approximately 470 A at 1 min, suggesting the predominance of homogeneously sized unilamellar vesicles at the earliest stages of bile formation. After micellization of lipids, mixed protein aggregates of vesicle size were demonstrated in all biles. These experiments elucidate the dynamic coexistence of lipid vesicles and mixed micelles in cholesterol unsaturated biles and demonstrate that vesicle-to-micelle interconversions of biliary lipid aggregates are normal physiological phenomena within the biliary tree.(ABSTRACT TRUNCATED AT 250 WORDS)
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4

Spivak, W., and M. C. Carey. "Reverse-phase h.p.l.c. separation, quantification and preparation of bilirubin and its conjugates from native bile. Quantitative analysis of the intact tetrapyrroles based on h.p.l.c. of their ethyl anthranilate azo derivatives." Biochemical Journal 225, no. 3 (February 1, 1985): 787–805. http://dx.doi.org/10.1042/bj2250787.

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We describe a facile and sensitive reverse-phase h.p.l.c. method for analytical separation of biliary bile pigments and direct quantification of unconjugated bilirubin (UCB) and its monoglucuronide (BMG) and diglucuronide (BDG) conjugates in bile. The method can be ‘scaled up’ for preparative isolation of pure BDG and BMG from pigment-enriched biles. We employed an Altex ultrasphere ODS column in the preparative steps and a Waters mu-Bondapak C18 column in the separatory and analytical procedures. Bile pigments were eluted with ammonium acetate buffer, pH 4.5, and a 20 min linear gradient of 60-100% (v/v) methanol at a flow rate of 2.0 ml/min for the preparative separations and 1.0 ml/min for the analytical separations. Bile pigments were eluted in order of decreasing polarity (glucuronide greater than glucose greater than xylose conjugates greater than UCB) and were chemically identified by t.l.c. of their respective ethyl anthranilate azo derivatives. Quantification of UCB was carried out by using a standard curve relating a range of h.p.l.c. integrated peak areas to concentrations of pure crystalline UCB. A pure crystalline ethyl anthranilate azo derivative of UCB (AZO . UCB) was employed as a single h.p.l.c. reference standard for quantification of BMG and BDG. We demonstrate that: separation and quantification of biliary bile pigments are rapid (approximately 25 min); bile pigment concentrations ranging from 1-500 microM can be determined ‘on line’ by using 5 microliters of bile without sample pretreatment; bilirubin conjugates can be obtained preparatively in milligram quantities without degradation or contamination by other components of bile. H.p.l.c. analyses of a series of mammalian biles show that biliary UCB concentrations generally range from 1 to 17 microM. These values are considerably lower than those estimated previously by t.l.c. BMG is the predominant, if not exclusive, bilirubin conjugate in the biles of a number of rodents (guinea pig, hamster, mouse, prairie dog) that are experimental models of both pigment and cholesterol gallstone formation. Conjugated bilirubins in the biles of other animals (human, monkey, pony, cat, rat and dog) are chemically more diverse and include mono-, di- and mixed disconjugates of glucuronic acid, xylose and glucose in proportions that give distinct patterns for each species.
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5

Rahman, K., and R. Coleman. "Selective biliary lipid secretion at low bile-salt-output rates in the isolated perfused rat liver. Effects of phalloidin." Biochemical Journal 237, no. 1 (July 1, 1986): 301–4. http://dx.doi.org/10.1042/bj2370301.

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At high bile-salt-secretion rates the biliary secretion of phospholipids and cholesterol is dependent on that of the bile salts. However, at low bile-salt outputs some secretion remains. Isolated perfused rat livers were used in these experiments in order to study the bile-salt-independent secretion of biliary lipids. The livers were isolated and saline (0.9% NaCl), or phalloidin dissolved in saline, was added to the perfusion fluid after 1 h of liver isolation. The concentration and output of cholesterol was significantly decreased in phalloidin-treated livers compared with the controls, whereas there was no significant decrease in phospholipids; the secretion of cholesterol and phospholipids can thus be uncoupled from each other by the action of phalloidin. These experiments suggest that a proportion of cholesterol gets into bile independently of bile salts and phospholipids. These findings are discussed in relation to the supersaturation of some biles with cholesterol and its relationship to the bile-salt-independent fraction of cholesterol.
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6

Vitetta, Luis, and Avni Sali. "Primary Bile Duct Stones and Bacterial Activity." HPB Surgery 6, no. 1 (January 1, 1992): 23–33. http://dx.doi.org/10.1155/1992/81017.

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The results of this study suggest that infection with beta-glucuronidase active bacteria is the initial event in the nucleation of primary bile duct stones (PBDS).PBDS from five patients were morphologically fragile and “earthy” with alternating light and dark brown pigment layers with no evidence of a distinct central nucleus that may have been reminiscent of a different structure. Chemically, calcium bilirubinate and calcium palmitate were prominent throughout their structure. All bile duct biles had a positive culture and were always associated with at least one bacterial species which was beta-glucuronidase active. Moreover, fragments of PBDS nuclear areas had positive cultures that were comparable with those present in their individual bile duct bile. Microscopic examination of bile showed abundant precipitation of calcium bilirubinate granules in all samples.Thus, bile duct bile infection with beta-glucuronidase active bacteria (e.g. E. coli, C. perfringens) appears to be a key factor in PBDS pathogenesis, having a precursor role, rather than being a consequence. Bile stasis is likely to be a co-factor which must have a supportive role in subsequent stone growth.
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7

Berman, Marvin D., and Martin C. Carey. "Metastable and equilibrium phase diagrams of unconjugated bilirubin IXα as functions of pH in model bile systems: Implications for pigment gallstone formation." American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 1 (January 1, 2015): G42—G55. http://dx.doi.org/10.1152/ajpgi.00277.2014.

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Metastable and equilibrium phase diagrams for unconjugated bilirubin IXα (UCB) in bile are yet to be determined for understanding the physical chemistry of pigment gallstone formation. Also, UCB is a molecule of considerable biomedical importance because it is a potent antioxidant and an inhibitor of atherogenesis. We employed principally a titrimetric approach to obtain metastable and equilibrium UCB solubilities in model bile systems composed of taurine-conjugated bile salts, egg yolk lecithin (mixed long-chain phosphatidylcholines), and cholesterol as functions of total lipid concentration, biliary pH values, and CaCl2 plus NaCl concentrations. Metastable and equilibrium precipitation pH values were obtained, and average pKa values of the two carboxyl groups of UCB were calculated. Added lecithin and increased temperature decreased UCB solubility markedly, whereas increases in bile salt concentrations and molar levels of urea augmented solubility. A wide range of NaCl and cholesterol concentrations resulted in no specific effects, whereas added CaCl2 produced large decreases in UCB solubilities at alkaline pH values only. UV-visible absorption spectra were consistent with both hydrophobic and hydrophilic interactions between UCB and bile salts that were strongly influenced by pH. Reliable literature values for UCB compositions of native gallbladder biles revealed that biles from hemolytic mice and humans with black pigment gallstones are markedly supersaturated with UCB and exhibit more acidic pH values, whereas biles from nonstone control animals and patients with cholesterol gallstone are unsaturated with UCB.
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8

Whiting, M. J., and J. McK Watts. "Cholesterol gallstone pathogenesis: a study of potential nucleating agents for cholesterol crystal formation in bile." Clinical Science 68, no. 5 (May 1, 1985): 589–96. http://dx.doi.org/10.1042/cs0680589.

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1. Cholesterol monohydrate crystal formation was measured quantitatively in model bile solutions, which were supersaturated with cholesterol, by a radiochemical method and qualitatively in human gallbladder bile by polarizing microscopy. 2. Various agents, which have been postulated to act as nucleating factors for cholesterol crystal and gallstone formation, were added to bile and their effect on the appearance of cholesterol crystals was determined. These agents included calcium salts found in gallstones (calcite, aragonite, apatite, bilirubinate), Escherichia coli bacteria, pigment residues from cholesterol gallstones, bilirubin and several mucin preparations. 3. Human gallbladder bile, which was collected from patients with and without cholesterol gallstones, was also mixed with model bile to examine whether nucleating or anti-nucleating factors were present. 4. None of the agents tested markedly and consistently promoted cholesterol monohydrate crystal formation in model or human bile, except seed crystals of cholesterol monohydrate which were used as a control. Human gallbladder bile from obese patients without gallstones delayed the appearance of cholesterol crystals in model bile solutions, whereas gallbladder bile from gallstone patients did not. 5. These results do not provide experimental support for the hypothesis that calcium salts and pigment material found in gallstones, or gallbladder mucin at concentrations less than 10 mg/ml, act as nucleating agents for cholesterol crystal and stone formation. The difference between gallbladder biles from patients with and without gallstones in their propensity to form cholesterol crystals may be due to the presence of an anti-nucleating factor in normal bile.
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9

Das, John B., Nicholas D. Poulos, and G. Ghaus Ansari. "Biliary Lipid Composition and Bile Acid Profiles During and After Enteral Fast of Total Parenteral Nutrition in the Rabbit." Journal of Pediatric Gastroenterology and Nutrition 22, no. 1 (January 1996): 85–91. http://dx.doi.org/10.1002/j.1536-4801.1996.tb01508.x.

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SummaryFeeding and fasting influence biliary lipid composition. With total parenteral nutrition (TPN), it is possible to study the effects of a long‐term “enteral fast” on biliary lipid composition without the metabolic illeffects on nutrient deprivation. We compared the lipid and bile acid (BA) contents of hepatic and gallbladder biles in rabbits on completion of a 14‐day regimen of TPN with those in rabbits returned to oral feeds for 6 weeks after a similar spell of TPN. Chow‐fed rabbits served as controls. With TPN, plasma phospholipid and cholesterol levels were elevated. Basal bile flow and the secretion of bile acids and phospholipids were decreased in the TPN and post‐TPN groups, while the cholesterol secretion rate was essentially unchanged. During TPN, the molar percent of cholesterol (relative to bile acids and phospholipid) in hepatic bile was increased. Biliary glycolithocholic acid (GLCA; as a percent of total conjugated BA) in hepatic bile increased from 1.7% (0.9% SEM) in the chow‐fed to 8.5% (1.5% SEM) during TPN. In TPN and post‐TPN groups, the gallbladder was enlarged to more than twice normal (chow‐fed) size, and contained a dark, mucoid bile (biliary sludge). In this bile, (a) there was a 2.5‐fold increase in bile acid concentration; and (b) the molar percent of cholesterol decreased while that of bile acids increased. TPN produced a state of functional cholestasis, which extended into the post‐TPN period. Gallbladder distension was the common denominator of the hepatobiliary dysfunction in the TPN and post‐TPN rabbits. With sequestration of bile acids in the gallbladder during and after TPN, the circulating bile acid pool was constricted, and the enterohepatic circulation impaired. As cholesterol secretion was low at all times, cholesterol supersaturation did not occur. The molar percent of cholesterol in gallbladder bile decreased, while that of bile acids increased; this suggests absorption of cholesterol by gallbladder mucosa. The increase in biliary GLCA probably resulted from bacterial biotransformation of glycochenodeoxycholic acid to lithocholic acid and its increased absorption from the cecum during TPN.
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10

Ackerman, Norman B., Leian F. Sillin, and Kalkunte Suresh. "Consequences of intraperitoneal bile: Bile ascites versus bile peritonitis." American Journal of Surgery 149, no. 2 (February 1985): 244–46. http://dx.doi.org/10.1016/s0002-9610(85)80078-7.

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11

Spivak, W., D. DiVenuto, and W. Yuey. "Non-enzymic hydrolysis of bilirubin mono- and diglucuronide to unconjugated bilirubin in model and native bile systems. Potential role in the formation of gallstones." Biochemical Journal 242, no. 2 (March 1, 1987): 323–29. http://dx.doi.org/10.1042/bj2420323.

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Pigment gallstones contain considerable amounts of unconjugated bilirubin (UCB) in the form of calcium bilirubinate and/or bilirubin polymers. Since more than 98% of bile pigments are excreted as conjugates of bilirubin, the source of this UCB needs to be identified. By using a rapid h.p.l.c. method, we compared the non-enzymic hydrolysis of bilirubin monoglucuronide (BMG) and bilirubin diglucuronide (BDG) to UCB in model bile and in native guinea-pig bile. Model biles containing 50 microM solutions of pure BMG and BDG were individually incubated in 25 mM-sodium taurocholate (NaTC) and 0.4 M-imidazole/5 mM-ascorbate buffer (TC-BUF) at 37 degrees C. Over an 8 h period, BMG hydrolysis produced 4-6 times more UCB than BDG hydrolysis. At pH 7.4, 25% of the BMG was converted into UCB, whereas only 4.5% of BDG was converted into UCB. Hydrolysis rates for both BMG and BDG followed the pH order 7.8 greater than 7.6 approximately equal to 7.4 greater than 7.1 Incubation with Ca2+ (6.2 mM) at pH 7.4 in TC-BUF resulted in precipitated bile pigment which, at 100 X magnification, appeared similar to precipitates seen in the bile of patients with pigment gallstones. At pH 7.4, lecithin (crude phosphatidylcholine) (4.2 mM) was a potent inhibitor of hydrolysis of BMG and BDG. The addition of a concentration of cholesterol equimolar with that of lecithin eliminated this inhibitory effect. Guinea-pig gallbladder bile incubated with glucaro-1,4-lactone (an inhibitor of beta-glucuronidase) underwent hydrolysis similar to the model bile systems. The non-enzymic hydrolysis of bile pigments, especially BMG, may be an important mechanism of bile-pigment precipitation and, ultimately, of gallstone formation.
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12

Busuladžić, Adnan. "Nalaz ulomaka keramičkih posuda sa prikazom zmije iz Japre kod Bosanskog Novog." Godišnjak Centra za balkanološka ispitivanja, no. 39 (January 30, 2024): 125–34. http://dx.doi.org/10.5644/godisnjak.cbi.anubih.39.7.

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U antičko doba bile su prisutne predstave zmija u mnogim mitovima i kultovima. Zmija je često bila simbol života i smrti. Kao kultna životinja javlja se u Mitraizmu, a kao simbol zla javlja se u hrišćanskoj tradiciji. Na području velikog rudarskog nalazišta Japra pronađena su dva ulomka keramike sa predstavama zmija koje su bile omotane oko drške. Prema analogijom sa sličnim slučajevima može se reći da su ove posude povezane sa kultom Mitre i korišteni u vjerske svrhe.
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13

KURAMOTO, Taiju, Junko MIYAMOTO, Masaki KONISHI, Takahiko HOSHITA, Takako MASUI, and Mizuho UNE. "Bile Acids in Porcine Fetal Bile." Biological & Pharmaceutical Bulletin 23, no. 10 (2000): 1143–46. http://dx.doi.org/10.1248/bpb.23.1143.

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14

Neoptolemos, J. P. "Bile ducts and bile duct stones." Gut 40, no. 5 (May 1, 1997): 696. http://dx.doi.org/10.1136/gut.40.5.696-a.

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15

Reaves, Bradley, Jasmine Bowers, Nolen Scaife, Adam Bates, Arnav Bhartiya, Patrick Traynor, and Kevin R. B. Butler. "Mo(bile) Money, Mo(bile) Problems." ACM Transactions on Privacy and Security 20, no. 3 (August 11, 2017): 1–31. http://dx.doi.org/10.1145/3092368.

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16

Ponsky, Jeffrey L. "Bile Ducts and Bile Duct Stones." Gastrointestinal Endoscopy 45, no. 3 (March 1997): 340. http://dx.doi.org/10.1016/s0016-5107(97)70294-3.

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17

Bi, Dan, Xing-Yun Chai, Yue-Lin Song, Yu Lei, and Peng-Fei Tu. "Novel Bile Acids from Bear Bile Powder and Bile of Geese." CHEMICAL & PHARMACEUTICAL BULLETIN 57, no. 5 (2009): 528–31. http://dx.doi.org/10.1248/cpb.57.528.

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18

Spivak, W., C. Morrison, D. Devinuto, and W. Yuey. "Spectrophotometric determination of the critical micellar concentration of bile salts using bilirubin monoglucuronide as a micellar probe. Utility of derivative spectroscopy." Biochemical Journal 252, no. 1 (May 15, 1988): 275–81. http://dx.doi.org/10.1042/bj2520275.

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We have developed a simple biologically non-invasive method for determining the critical micellar concentration (CMC) of bile salts using pure naturally occurring bilirubin IX alpha monoglucuronide (BMG), an important bile pigment present in virtually all mammalian biles. This methodology employs visible absorbance spectroscopy of BMG in bile salts over a range of bile salt concentrations that include the reported CMC. Using 100 microM-BMG in 0.4 M-imidazole buffer at pH 7.8, we calculated that the CMC for sodium taurochenodeoxycholate is between 2.5 and 3.0 mM based on: (1) an abrupt change in lambda max. in this concentration range, (2) a precipitous decrease in the amplitude of the absorbance shoulder at 450 nm, (3) a sudden decrease in the second derivative absorbance of BMG at 400 nm and an increase in absorbance at 470 nm, (4) a sharp change in the 4th derivative absorbance at 375 and 395 nm. In contrast, sodium taurocholate, a bile salt that reportedly does not have a CMC but continuously self-associates over a wide concentration range, exhibited none of these changes. The use of derivative spectroscopy enhances the ability to detect the CMC changes and also indicates the number of BMG species in solution and their relative energy states.
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19

Dusserre, J. P., A. M. Montet, and J. C. Montet. "Effect of hyocholic acid on the prevention and dissolution of biliary cholesterol crystals in mice." Canadian Journal of Physiology and Pharmacology 66, no. 8 (August 1, 1988): 1028–34. http://dx.doi.org/10.1139/y88-168.

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Gallstone prevention and dissolution were studied in a mouse model of cholesterol cholelithiasis using hyocholic acid (3α, 6α, 7α-trihydroxy-5β-cholanic acid). Addition of hyocholic acid, 0.1 or 0.3%, in the lithogenic diet (1% cholesterol + 0.5% cholic acid) prevented the formation of cholesterol monohydrate crystals in 70 and 90% of cases, respectively. On the other hand, chow diet supplemented with 0.1 or 0.3% hyocholic acid dissolved cholesterol crystals in lithiasic mice in, respectively, 80 and 100% of cases within 12 days. In both protocols, biles were largely supersaturated with cholesterol; lecithin–cholesterol lamellar liquid crystals were responsible for the transport of the excess cholesterol content. The percentage of hydrophilic bile salts (hyocholic acid, hyodeoxycholic acid, β-muricholic acid) in bile, although moderate (15–50% of total bile salts), appears to induce such liquid crystalline dispersion. This study demonstrates that the balance between hydrophilic and hydrophobic bile salts plays a major role in the prevention and dissolution of cholesterol crystals. It is also shown that the desaturation of biliary cholesterol is not a prerequisite for gallstone dissolution.
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20

Camogliano, L., and A. Casu. "Bile acids in bile after monensin treatment." Experimental pathology 36, no. 1 (January 1989): 37–41. http://dx.doi.org/10.1016/s0232-1513(89)80108-2.

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21

Kuroki, S., K. Shimazu, M. Kuwabara, M. Une, K. Kihira, T. Kuramoto, and T. Hoshita. "Identification of bile alcohols in human bile." Journal of Lipid Research 26, no. 2 (February 1985): 230–40. http://dx.doi.org/10.1016/s0022-2275(20)34393-5.

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22

Cotting, J., and J. Reichen. "Bile salts and hydrodynamics of bile formation." Journal of Hepatology 8, no. 1 (January 1989): 13–21. http://dx.doi.org/10.1016/0168-8278(89)90156-6.

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23

Hiraoka, T., T. Kohda, D. Kosaka, T. Yamauchi, K. Kihira, T. Kuramoto, T. Hoshita, and G. Kajiyama. "Identification of bile alcohols in rat bile." Journal of Lipid Research 30, no. 12 (December 1989): 1889–93. http://dx.doi.org/10.1016/s0022-2275(20)38201-8.

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24

Witz, Misha. "Bile Composition and Bile Acid Pool Size." Archives of Surgery 120, no. 11 (November 1, 1985): 1306. http://dx.doi.org/10.1001/archsurg.1985.01390350086018.

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25

IIDA, Takashi, Toshiaki MOMOSE, Frederic C. CHANG, Junichi GOTO, and Tosio NAMBARA. "Potential bile acid metabolites. XV. Synthesis of 4.BETA.-hydroxylated bile acids; unique bile acids in human fetal bile." CHEMICAL & PHARMACEUTICAL BULLETIN 37, no. 12 (1989): 3323–29. http://dx.doi.org/10.1248/cpb.37.3323.

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26

Mijač, Marina, Ognjen Brborović, and Hana Brborović. "Pregled uzroka nesposobnosti željezničkih izvršnih radnika." Sigurnost 64, no. 4 (December 27, 2022): 397–408. http://dx.doi.org/10.31306/s.64.4.6.

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Istraživanje je provedeno na 409 željezničkih radnika koji su u razdoblju od 5 godina pregledavani u Ustanovi za zdravstvenu skrb dr. Mijač. Cilj je bio analizirati tip i vrstu zdravstvenog pregleda, ocjenu radne sposobnosti te ustanoviti razloge zbog kojih su radnici bili privremeno ili trajno nesposobni. Analizirani su broj i vrsta pregleda te broj i vrsta ocjene radne sposobnosti. Žene je uključivalo 3,3 % pregleda, a 96,7 % muškarce, vjerojatno zbog specifičnosti željezničkog posla te je najveći broj pregledanih pripadalo dobnoj skupini 41-62. Obavljena su 62 prethodna, 672 periodična, 10 ciljanih i 28 kontrolnih pregleda. Ocjene radne sposobnosti bile su 772 (88,23 %) sposoban, 27 (3,09 %) nesposoban i 76 (8,68 %) privremeno nesposoban. Najviše je obavljeno periodičnih pregleda, na kojima je najčešća ocjena bila sposoban. Na izvanrednim i kontrolnim pregledima također je najčešća ocjena bila sposoban. Ocjene sposoban, privremeno nesposoban te nesposoban najčešće su bile donesene na periodičnim pregledima. Neki radnici bili su samo jednom privremeno nesposobni jer je njihova dijagnoza zahtijevala kratkotrajno liječenje, a neki više puta, sve dok je njihova bolest bila u fazi liječenja te su po završetku liječenja mogli biti sposobni ili trajno nesposobni, ovisno o ishodu liječenja. Trajno nesposobni radnici proglašeni su nakon što je liječenje završeno te zdravstveno stanje radnika nije ispunjavalo uvjete zdravstvene sposobnosti radnog mjesta a u nekim slučajevima i zbog dobi. Bolesti koje su najčešće bile razlog onesposobljavanja bile su širokog spektra, a najčešće se radilo o kardiovaskularnim bolestima, psihičkim, poremećajima, nereguliranim endokrinim poremećajima, bolnim sindromima, neurološkim poremećajima, bolestima oka i bolestima uha. Uzimajući u obzir psihičku i fizičku zahtjevnost željezničkog posla, važno je pravovremeno utvrditi bolesti i stanja željezničara, ograničavajućih za obavljanje posla na siguran način za njih same, ali i za okolinu. Za istaknuti je i važnost prethodnih pregleda koji bi odmah trebali eliminirati neadekvatne radnike u smislu zdravstvene sposobnosti, a naknadno i periodičnih, kontrolnih i izvanrednih pregleda, kojima se prate eventualne promjene u zdravstvenom statusu te na taj način smanjuje mogućnost incidenata, ozljeda na radu i profesionalnih bolesti.
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Poupon, R., and Y. Chrétien. "Bile secretion." Gastroentérologie Clinique et Biologique 34, no. 6-7 (August 2010): 410–12. http://dx.doi.org/10.1016/j.gcb.2010.04.016.

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Abbott, David A., David E. Schlarman, Ping H. Patrick, Daniel M. Tal, and William H. Elliott. "Bile acids." Analytical Biochemistry 146, no. 2 (May 1985): 437–41. http://dx.doi.org/10.1016/0003-2697(85)90566-4.

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Rowe, Raymond C. "Bile Beans." International Journal of Pharmaceutical Medicine 17, no. 3-4 (2003): 137–40. http://dx.doi.org/10.1097/00124363-200317030-00007.

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Mikov, Momir, and J. Paul Fawcett. "Bile acids." European Journal of Drug Metabolism and Pharmacokinetics 31, no. 3 (September 2006): 133–34. http://dx.doi.org/10.1007/bf03190709.

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Kuhls, Stephanie, Annika Osswald, and Soeren Ocvirk. "Bile acids, bile pigments and colorectal cancer risk." Current Opinion in Gastroenterology 38, no. 2 (January 15, 2022): 173–78. http://dx.doi.org/10.1097/mog.0000000000000820.

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Meshikhes, Abdul-Wahed N., Amin AbulRahi, Sami A. Al-momen, Zakaria Al-Safran, and Qassim H. Al-Daolah. "An Unusual Bile Collection After Postcholecystectomy Bile Leakage." Surgical Laparoscopy, Endoscopy & Percutaneous Techniques 17, no. 2 (April 2007): 138–40. http://dx.doi.org/10.1097/sle.0b013e318045a0ac.

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Hofmann, Alan F. "Bile Acid Replacement in Bile Acid Synthesis Defects." Journal of Pediatric Gastroenterology and Nutrition 65, no. 6 (December 2017): e134. http://dx.doi.org/10.1097/mpg.0000000000001709.

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STPIERRE, M. "Cyclic GMP modulates bile acid independent bile flow." Hepatology 18, no. 4 (October 1993): A135. http://dx.doi.org/10.1016/0270-9139(93)92067-a.

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Matoba, N., M. Une, and T. Hoshita. "Identification of unconjugated bile acids in human bile." Journal of Lipid Research 27, no. 11 (May 1990): 1154–62. http://dx.doi.org/10.1016/s0022-2275(20)38751-4.

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van den Heuvel, M. C., K. P. de Jong, M. Boot, M. J. H. Slooff, S. Poppema, and A. S. H. Gouw. "Preservation of Bile Ductules Mitigates Bile Duct Loss." American Journal of Transplantation 6, no. 11 (November 2006): 2660–71. http://dx.doi.org/10.1111/j.1600-6143.2006.01511.x.

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WATANABE. "F7-6 Bile canalicular contraction and bile formation." International Hepatology Communications 3 (July 1995): S21. http://dx.doi.org/10.1016/0928-4346(95)90242-y.

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