The relationship between acid-suppressing drugs and phytobezoar formation: a retrospective analysis and discussion of phytobezoar formation.

OBJECTIVES: Although phytobezoars are a rare cause of gastrointestinal obstruction, they are most commonly found in patients with previous gastric surgery. It is well known that predisposing factors of phytobezoar formation are ingestion of fruits containing soluble tannin, presence of dilute hydrochloric acid in the stomach, and gastric stasis or delayed emptying. We investigated whether intake of acid-suppressing drugs that neutralize gastric acidity or inhibit gastric acid secretion to constitute a hypo-acidic condition, increases the risk of phytobezoar formation. MATERIALS AND METHODS: Between September 1992 and October 2008, 32 patients (24 male and 8 female) with gastrointestinal phytobezoars were diagnosed either surgically or endoscopically at the Tri-Service General Hospital, Taipei, Republic of China. The data were collected from hospital records and analyzed retrospectively. RESULTS: Eighteen (56.25%) of all patients had previous gastric surgery and 6 (42.9%) of the 14 patients who had not undergone surgery had diabetes mellitus. The majority of admissions were during winter and spring (between October and March) (P < 0.01) and none of the patients had taken acid-suppressing drugs during the 6 months before detection of gastrointestinal phytobezoars. CONCLUSIONS: In our study, intake of acid-suppressing drugs did not increase the risk of phytobezoar formation in patients with normal gastric motility. Moreover, we believe that the major factor in phytobezoar formation is gastric stasis or delayed emptying, which sufficiently prolongs the retention period of materials in the stomach, while dilute hydrochloric acid is a minor factor.

Outbreak of Elizabethkingia meningoseptica sepsis with meningitis in a well-baby nursery.

Between March and May 2012, three neonates born at a regional maternity hospital developed Elizabethkingia meningoseptica (previously Chryseobacterium meningosepticum) sepsis with meningitis aged <10 days, and were treated successfully with intravenous ciprofloxacin plus vancomycin or piperacillin-tazobactam for three to six weeks. Four (16.6%) of 24 environmental specimens obtained from the nursery and delivery room were positive for this organism. All of the clinical isolates and two isolates from storage boxes for pacifiers and pacifier covers were genetically identical. After changing the storage boxes to stainless steel boxes that underwent regular autoclave sterilization, there were no further cases of infection with E. meningoseptica.

Pharmacokinetics and immune response of 131I-chimeric mouse/human B72.3 (human gamma 4) monoclonal antibody in humans.

Chimeric B72.3, composed of the V-regions of murine B72.3 and the constant regions of human immunoglobulin G4 heavy and kappa light chain, was administered as a 131I-labeled conjugate to 12 patients with metastatic colon cancer. Seven of these patients had an antibody response after initial infusion, and the immune response was primarily directed to the murine V-region, although a small proportion of the antibody response was directed to topographical epitopes requiring the presence of both murine V-region and human CH-1 and kappa constant regions (neo-epitopes). The pharmacokinetics included a plasma disappearance curve best fit by a two-compartmental model with an alpha t 1/2 of 18 +/- 7 h and a beta t 1/2 of 224 +/- 66 h. A second infusion of the same dose of 131I-chimeric B72.3 was administered to four of these patients 8 wk after the first infusion. Two patients who had a high antibody response to initial infusion had an anamnestic antibody response, and the infused ch-B72.3 rapidly disappeared from the circulation with associated immune complexes and free 131I in the plasma. One patient with no initial antibody response had no antibody response and identical pharmacokinetics on second infusion. One patient with a modest transient antibody response to initial infusion had no antibody response on second infusion and a modest shortening of plasma circulation. Thus, the human immunoglobulin G4 isotype chimeric B72.3 monoclonal antibody has a plasma half-life 6 to 8 times as long as murine B72.3 and retains considerable immunogenicity in some patients which can adversely affect repetitive infusions.

Coexisting sharp ductal angulation with intrahepatic biliary strictures in right hepatolithiasis.

OBJECTIVE: To investigate the clinical characteristics of a coexisting sharp ductal angulation (< 90 degrees) with biliary stricture and to evaluate the difficulties it imposes in the management of retained or recurrent hepatolithiasis. DESIGN: Case-controlled study. SETTING: A referral center. PATIENTS: Eighteen consecutive patients having right-sided hepatolithiasis and a coexisting sharp ductal angulation associated with biliary stricture (group 1) were compared with 84 patients matched with sex, age, and conditions of hepatolithiasis and intrahepatic biliary stricture(s) but no sharp angulated duct (group 2). INTERVENTION: Postoperative cholangioscopic management (electrohydraulic lithotripsy or other lithotripsy, lithotomy, balloon dilation, biopsy, etc, via T-tube tract or percutaneous transhepatic route). MAIN OUTCOME MEASURES: Sessions of manipulations, incidence of complications associated with interventions or disease, and mortality were compared. RESULTS: Patients of group 1 needed more sessions of postoperative manipulation of stones and strictures (13.7 +/- 4.2 vs 8.0 +/- 2.3; P < .001). During management, there was a significantly increased vulnerability of severe and/or recurrent cholangitis (66.7% vs 9.5%; P < .001), septic shock (77.8% vs 11.9%; P < .001), liver abscess (55.6% vs 7.1%; P < .001), or massive hemobilia (33.3% vs 7.4%) in group 1 than in group 2. Their risks of coexisting secondary biliary cirrhosis (55.6% vs 9.5%; P < .001) and/or cholangiocarcinoma (16.6% vs 2.4%; P < .04) and mortality (27.8% vs 4.8%; P < .01) were also significantly higher in group 1. CONCLUSION: Our results suggest that the coexisting sharp ductal angulation with biliary strictures in right-sided hepatolithiasis is a distinct difficult clinical entity in the field of biliary tract calculi.

Stimulatory effect of D-ephedrine on beta3-adrenoceptors in adipose tissue of rats.

The effect of ephedrine on beta3-adrenoceptos (beta3-AR) was studied in the isolated adipose tissue of Wistar rat. Incubation with D-ephedrine (0.1-10 microM) induced a concentration-dependent decrease of uptake of [14C]-deoxy-D-glucose into white adipose tissues (WAT). The inhibitory effect of D-ephedrine was potentiated by BRL 37344, the agonist of beta3-AR and concentration-dependently inhibited by SR 59230A, the selective antagonist of beta3-AR. The action of D-ephedrine on beta3-AR was further blocked by the antibodies for beta3-AR, but not the immunoglobulin. in a concentration-dependent manner. Moreover, D-ephedrine increased glycerol release from the isolated brown adipose tissues (BAT) and this action was also abolished by SR 59230A at concentration sufficient to block beta3-AR. Thus, these results suggest that D-ephedrine has the ability to activate beta3-AR both in WAT and BAT of Wistar rats in vitro.

Stimulatory effect of paeoniflorin on the release of noradrenaline from ileal synaptosomes of guinea-pig in-vitro.

The effect of paeoniflorin (an active principle of Paeoniae Radix, commonly used in traditional Chinese medicine) on the release of noradrenaline (norepineprhine) from nerve terminals was investigated using guinea-pig isolated ileal synaptosomes. Release was determined as the amount of noradrenaline, quantified by high-performance liquid chromatography-electrochemical detection, from samples incubated with paeoniflorin or vehicle. Paeoniflorin stimulated the release of noradrenaline in a concentration-dependent manner without an effect on the level of lactate dehydrogenase in the bathing medium. Tetrodotoxin abolished the action of paeoniflorin at concentrations sufficient to block sodium channels. The depolarizing effect of paeoniflorin on the membrane potential was also illustrated by a concentration-dependent increase in the fluorescence of bisoxonol. Moreover, the effect of paeoniflorin on bisoxonol fluorescence in ileal synaptosomes seems more potent than that of 4-aminopyridine. That paeoniflorin causes influx of calcium ions via the depolarization of nerve terminals could be considered. The noradrenaline-releasing action of paeoniflorin was abolished by removal of calcium chloride from the bathing medium. This action of paeoniflorin was also attenuated by Rp-cAMP atconcentrations sufficientto inhibitthe action of cyclicAMP. Therefore, paeoniflorin could induce a calcium-dependent and cyclic-AMP-related release of noradrenaline from sympathetic nerve terminals of guinea-pig ileum. Guanethidine inhibited the noradrenaline-releasing action of paeoniflorin in a concentration-dependent manner. The effect of paeoniflorin on the increase of bisoxonol fluorescence was not modified by atropine. Release of noradrenaline by paeoniflorin from noradrenergic nerve terminals was characterized. These findings suggest that paeoniflorin can stimulate tetrodotoxin-sensitive depolarization of membranes to result in a calcium-dependent and cyclic-AMP-related release of noradrenaline from noradrenergic nerve terminals.

Oöcytes degeneration in the queen honey bee after infection by Nosema apis.

Terminal oöcytes containing yolk in both healthy and nosema infected queen honey bees were studied. In the healthy queens the terminal oöcytes exhibited a layer of follicular cells which were covered by a smooth-surfaced ovariole sheath. In the oöplasm were numerous electron-dense yolk granules and lipid yolk droplets. The elecron-dense yolk granules exhibited a crystalline structure. Stacks of endoplasmic reticulum were observed in the yolk granules throughout the oöplasm. Numerous mitochondria possessing well defined cristae were also observed. Oöcytes in the ovary of queen honey bees appeared degenerated after 7 days of infection by Nosema apis. The ovariole sheath was wrinkled. In the oöplasm, yolk granules were broken down into small spheres and granular substances. Numerous ribosomes without stacks of endoplasmic reticulate were observed. Lysosomes were abundant and numerous electron-dense materials surrounded by a membrane were detected. The oöcytes appeared to be extensively autolysed. The significance of these observations is discussed.

Ultrastructural analysis of the freeze-etched spore envelope of the microsporidian, Nosema apis Zander.

The outer limiting layer of the spore coat of Nosema apis is relatively smooth. The inner limiting layer shows two fractured faces, the concave face carrying many stud-like projections, 120 nm long and 50 nm high, while the convex face carries numerous depressions which are complementary to the projections. In addition, the convex face bears 7 nm particles. In between the outer and inner limiting layers lies the thick homogeneous portion of spore coat which is comprised of numerous microfibres, each 9 nm in diameter. These microfibres resemble those in the freeze-etched host endocuticle. Next to the inner limiting layer of the spore coat are double spore membranes. The convex faces of these spore membranes have a dense population of particles, each 7 nm in diameter.

Ultrastructure of mitochondria in the corpora allata of honeybees infected by Nosema apis before and after treatment with anti-Nosema drugs.

Ultrastructural differences were observed among mitochondria from the corpora allata of healthy, Nosema-infected, and anti-Nosema drug treated honeybees. Mitochondria in the corpora allata of the healthy honeybees were large in size, possessed well defined membrane, numerous mitochondrial granules and less electron-dense matrix. In the corpora allata of Nosema-infected honeybees, mitochondria were small in size and the mitochondrial matrix had a higher electron density. Mitochondria from the corpora allata of Nosema-infected honeybees after treatment with thimerosal, had a lower electron density in the mitochondrial matrix and a larger diameter than those from untreated honeybees. Mitochondria from fumagillin-treated honeybees had the smallest diameter and the highest electron density in the matrix among mitochondria observed in the present study. Image analysis also confirmed the differences in the electron density of the mitochondrial matrix among mitochondria in the corpora allata of four experimental groups of honey bees.

Ultrastructural differences of neurosecretion granules in the corpora cardiaca of the honeybee with and without infection by Nosema apis.

Axons of corpora cardiaca in the Nosema infected honeybees contained numerous tightly packed neurosecretion granules. These granules invariably possessed high electron densities. Neurosecretion granules of similar size were also observed in the axons of corpora cardiaca in the healthy honeybees. But these granules were shown to possess various electron densities. Image analysis revealed that some of these granules possessed an electron dense core, and the electron densities decreased gradually from the core, to the fringe of the granule. Some granules appeared to be completely broken down into fine granular substances, while others appeared to be completely broken down into finer particles. It is suggested that in the healthy honeybees, the releasing of neurosecretion from the corpora cardiaca had taken place normally, whereas in the diseased bee, the releasing mechanism had been blocked. The blockage is probably due to the infection.

Ultrastructural changes in the secretion granules of the hypopharyngeal glands of the honeybee infected by Nosema apis and after treatment with fumagillin.

Electron-dense secretion granules were numerous in the hypopharyngeal glands of healthy honeybees. In the hyopharyngeal glands of honeybees infected by Nosema apis, these granules appeared to have increased in size and lost their electron density, possessing a core area that consisted of numerous smaller granules, and a slightly electron dense fringe area, which in some cases possessed a crystalline structure. In the hypopharyngeal glands of infected honeybees after treatment with fumagillin, the secretion granules were also large and slightly electron dense, but the granular content was homogenous. Some of these granules were also partially crystallized. These ultrastructural changes in the secretion granules of diseased and fumagillin treated bees, is probably associated with a change in secretory activity of the glands.

Ultrastructural analysis on the gland secretion in the extracellular ducts of the hypopharyngeal glands of the honeybee infected by Nosema apis.

The hypopharyngeal glands of the honeybee secrete the larval food royal jelly, along with enzymes that are used in the production of honey from nectar. The composition of this secretion mixture varies with the physiological condition of the honeybee, and the final secretion mixture is conveyed through the extracellular ducts to the large excretory duct. The secretion products in the extracellular duct of both healthy and infected honeybees, was studied by transmission electron microscopy and image analysis. These products consisted of a densely packed, faintly visible granular substance. The granules were clearly defined by the computer enhanced image. The secretion products from the Nosema-infected honeybees exhibited the same granular structure, but were much less concentrated, thereby reducing the overall electron density of the secretion. These observations suggest that the composition of the secretion products from the hypopharyngeal glands in the Nosema-infected honeybees, was altered considerably.

[Effects of berberine on platelet aggregation and plasma levels of TXB2 and 6-keto-PGF1 alpha in rats with reversible middle cerebral artery occlusion].

Berberine (Ber) 20 mg.kg-1.d-1 for 1, 3, or 5 d inhibited platelet aggregation induced by ADP, arachidonic acid (AA) and collagen (Coll) in rats with 24 h reversible middle cerebral artery occlusion (MCAO), and the platelet adhesiveness was inhibited as well. Using radioimmunoassay method, the thromboxane B2(TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) contents in rat plasma were measured 24 h after MCAO. The results indicate that the TXB2 levels after drug treatment were lower than those in ischemia control rats, but the 6-keto-PGF1 alpha levels showed no obvious difference between the two groups. The same dose of Ber was also shown to inhibit thrombosis formation. This suggests that the decline of platelet aggregation and decrease of TXB2 content may be one of the important factors involved in the anti-cerebral ischemia effect of Ber.

[High performance liquid chromatographic method for the determination of ipriflavone in serum and its pharmacokinetic study in healthy volunteers].

A sensitive and rapid high performance liquid chromatographic method has been developed for the determination of ipriflavone in human serum. The average recovery of ipriflavone was 85% with relative standard deviation of 3.8%-5.4%. The calibration curve was linear in the range from 8 ng.ml-1 to 400 ng.ml-1 with gamma = 0.9981. The detection limit of the method was 3 ng.ml-1 (S/N > or = 3). The serum drug concentration-time curve exhibited a 2-compartment model and the mean T1/2 beta was 12.00 +/- 1.89 h (for ipriflavone made in Japan) and 9.05 +/- 0.80 h (for ipriflavone made in China). The AUC0-->infinity of the two kinds of ipriflavone were 804.99 ng.h.ml-1 and 807.40 ng.h.ml-1, respectively. The relative bioavailability of ipriflavone made in China vs that made in Japan was 1.003.

[Effect of berberine on intracellular free CA2+ concentration in cultured brain cells].

Intracellular free calcium concentration ([Ca2+]i) was measured with Ca(2+)-sensitive fluorescent indicator, Fura-2/AM, in cultured brain cells using AR-CM-MIC cation measurement system, and the effects of berberine (Ber) on the changes in [Ca2+]i induced by CaCl2, norepinephrine, KCl and H2O2 were studied. The results indicate that the resting [Ca2+]i was 35 +/- 8 nmol.L-1 in Ca(2+)-free Hank's solution. Ber showed no effect on the resting [Ca2+]i when the extracellular Ca2+ were 0.01-10 mmol.L-1. Ber 1-100 mumol.L-1 dose-dependently inhibited norepinephrine and H2O2 induced [Ca2+]i elevation. Ber at high concentration (10-100 mumol.L-1) inhibited K(+)-induced [Ca2+]i elevation. This suggests that the inhibitory effects of Ber on norepinephrine, K(+)-, and H2O2-induced [Ca2+]i elevation may be one of the mechanisms against cerebral ischemia.