Preparation of drug-loaded chitosan microspheres repair materials.

OBJECTIVE: With the development of society and the progress of science and technology, microspheres, as a new polymer material, have been applied to all aspects of human beings. Microspheres can play a huge role in food safety, electronic technology, sewage treatment, biomedicine, etc., and are non-toxic or harmless. There are three main types of substrates for the preparation of microspheres: natural polymers, semi-synthetic polymer materials, and synthetic polymer materials. MATERIALS AND METHODS: In this study, the inorganic material kaolin was modified by the emulsification-crosslinking method with chitosan and composite microspheres with large interlayer spacing were prepared, which were characterized by Fourier Transform Ioncyclotron Resonancel (FTIR) analysis and Scanning Electron Microscope (SEM). The prepared kaolin/chitosan microspheres were then placed in different amounts of aspirin and the optimal dose was investigated by encapsulation efficiency and drug loading rate. The drug release rate of 0.5 h, 1 h, 1.5 h, 2 h, 4 h, 6 h, and 12 h was then determined by simulating the human colon to determine the performance of the sustained-release drug. RESULTS: The experimental results showed that after the prepared composite microspheres were loaded with aspirin drug, we got the optimal dosage of 0.1 g by discussing the encapsulation efficiency and drug loading rate of the drug-loaded microspheres, and the encapsulation efficiency reached 80.80%, while the drug loading rate was 24.40%, the drug release capacity reached about 83% in about 12 hours. CONCLUSIONS: The research shows that the kaolin/chitosan drug-loaded microspheres prepared by the emulsification and cross-linking method are excellent drug-loading materials.

[Reconstruction of anal stenosis induced by scar contracture after repair of defect in perineal region with paraumbilical flap using random pattern flap].

Objective: To investigate the method and timing of reconstruction of anal stenosis induced by scar contracture after repair of defect in perineal region with paraumbilical flap using random pattern flap. Methods: Ten patients who suffered anal stenosis induced by scar contracture after the first phase repair of defect of perineal region with paraumbilical flap were hospitalized from July 2009 to September 2015. Eight patients were with central type scar contracture of perineal region after healing of burn wound, and two patients were with lesion of perineal region which had been excised. In 6 to 8 weeks after the first phase surgery, two or three random pattern flaps were designed around the narrow anus in the survived paraumbilical flap. After thorough release of the narrow anus, the random pattern flaps were transferred to enlarge the anus. The tip of the lifted triangular flap was transferred to insert into the anal canal. The skin of anal canal or rectal mucosa was pulled out to be crossly-stitched with the flap. Results: All the patients' narrow anuses were released and enlarged with one operation, and the diameters of the narrow anuses were enlarged to 2.0 to 3.0 cm. During follow-up of 6 to 36 months, the anal stenosis was totally released, and the symptom of difficult defecation was significantly improved; 7 patients were excellent and 3 patients were good with evaluation of clinical criteria of anus function; no symptom of anal stenosis or rectal mucosal prolapse was observed any more. Conclusions: In 6 to 8 weeks post repair of defect in perineal region with paraumbilical flap, designing of random pattern flap in the survived paraumbilical flap to enlarge and reconstruct the narrow anus has good therapeutic effects on anatomical narrow and difficult defecation.

Long-term exposure of K562 cells to benzene metabolites inhibited erythroid differentiation and elevated methylation in erythroid specific genes.

Benzene is a common occupational hazard and a widespread environmental pollutant. Previous studies have revealed that 72 h exposure to benzene metabolites inhibited hemin-induced erythroid differentiation of K562 cells accompanied with elevated methylation in erythroid specific genes. However, little is known about the effects of long-term and low-dose benzene metabolite exposure. In this study, to elucidate the effects of long-term benzene metabolite exposure on erythroid differentiation, K562 cells were treated with low-concentration phenol, hydroquinone and 1,2,4-benzenetriol for at least 3 weeks. After exposure of K562 cells to benzene metabolites, hemin-induced hemoglobin synthesis declined in a concentration- and time-dependent manner, and the hemin-induced expressions of α-, ß- and γ-globin genes and heme synthesis enzyme porphobilinogen deaminase were significantly suppressed. Furthermore, when K562 cells were continuously cultured without benzene metabolites for another 20 days after exposure to benzene metabolites for 4 weeks, the decreased erythroid differentiation capabilities still remained stable in hydroquinone- and 1,2,4-benzenetriol-exposed cells, but showed a slow increase in phenol-exposed K562 cells. In addition, methyltransferase inhibitor 5-aza-2'-deoxycytidine significantly blocked benzene metabolites inhibiting hemoglobin synthesis and expression of erythroid genes. Quantitative MassARRAY methylation analysis also confirmed that the exposure to benzene metabolites increased DNA methylation levels at several CpG sites in several erythroid-specific genes and their far-upstream regulatory elements. These results demonstrated that long-term and low-dose exposure to benzene metabolites inhibited the hemin-induced erythroid differentiation of K562 cells, in which DNA methylation played a role through the suppression of erythroid specific genes.

An intelligent tutoring system for trauma management (Trauma-Teach): a preliminary report.

Trauma-Teach is an interactive software for tutoring surgical trainees on medical trauma management procedures. Users of the system interact with a virtual patient suffering from trauma injuries. The task of the user is to stabilise the virtual patient, discover the underlying injuries and decide on an appropriate management plan. Artificial intelligence techniques are used to simulate the patient's pulmonary and cardiovascular systems in real time, determine the responses and results of treatments and diagnostics accordingly, model the patient deterioration if wrong actions are taken, and give a measure of reality to the system by selecting actual trauma cases from the hospital's database.

Effect of oleamide on Ca(2+) signaling in human bladder cancer cells.

The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca(2+) ([Ca(2+)](i)) in non-excitable and excitable cells was examined by using fura-2 as a fluorescent dye. [Ca(2+)](i) in pheochromocytoma cells, renal tubular cells, osteoblast-like cells, and bladder cancer cells were increased on stimulation of 50 microM oleamide. The response in human bladder cancer cells (T24) was the greatest and was further explored. Oleamide (10-100 microM) increased [Ca(2+)](i) in a concentration-dependent fashion with an EC(50) of 50 microM. The [Ca(2+)](i) signal comprised an initial rise and a sustained plateau and was reduced by removing extracellular Ca(2+) by 85 +/- 5%. After pre-treatment with 10-100 microM oleamide in Ca(2+)-free medium, addition of 3 mM Ca(2+) increased [Ca(2+)](i) in a manner dependent on the concentration of oleamide. The [Ca(2+)](i) increase induced by 50 microM oleamide was reduced by 100 microM La(3+) by 40%, but was not altered by 10 microM nifedipine, 10 microM verapamil, and 50 microM Ni(2+). In Ca(2+)-free medium, pre-treatment with thapsigargin (1 microM), an endoplasmic reticulum Ca(2+) pump inhibitor, abolished 50 microM oleamide-induced [Ca(2+)](i) increases; conversely, pretreatment with 50 microM oleamide reduced 1 microM thapsigargin-induced [Ca(2+)](i) increases by 50 +/- 3%. Suppression of the activity of phospholipase C with 2 microM U73122 failed to alter 50 microM oleamide-induced Ca(2+) release. Linoleamide (10-100 microM), another sleep-inducing lipid with a structure similar to that of oleamide, also induced an increase in [Ca(2+)](i). Together, it was shown that oleamide induced significant [Ca(2+)](i) increases in cells by a phospholipase C-independent release of Ca(2+) from thapsigargin-sensitive stores and by inducing Ca(2+) entry.

Fendiline, an anti-anginal drug, increases intracellular Ca2+ in PC3 human prostate cancer cells.

BACKGROUND: The effects of the anti-anginal drug fendiline on intracellular Ca2+ concentrations ([Ca2+]i) in human PC3 prostate cancer cells were examined. METHODS: [Ca2+]i was measured using the fluorescent dye fura-2. RESULTS: Fendiline (0.5-100 microM) increased [Ca2+]i in a concentration-dependent manner. Ca2+ removal partly inhibited the Ca2+ signals. In Ca2+-free medium, pretreatment with 100 microM fendiline inhibited most of the [Ca2+]i increase induced by 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), and pretreatment with thapsigargin abolished the fendiline-induced [Ca2+]i increases. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with 0.5-200 microM fendiline in Ca2+-free medium. Pretreatment with 1 microM U73122 to block the formation of inositol-1.4.5-trisphosphate (IP3) did not alter fendiline-induced internal Ca2+ release. CONCLUSIONS: The anti-anginal drug fendiline induced internal Ca2+ release and external Ca2+ entry. Because prolonged increases in [Ca2+]i may lead to cell injury and death, the long-term effect of fendiline on the function of prostate cancer cells should be investigated.

Effect of betulinic acid on intracellular-free Ca(2+) levels in Madin Darby canine kidney cells.

The effect of betulinic acid, an anti-tumor and apoptosis-inducing natural product, on intracellular-free levels of Ca(2+) ([Ca(2+)](i)) in Madin Darby canine kidney (MDCK) cells was examined by using fura-2 as a Ca(2+) dye. Betulinic acid caused significant increases in [Ca(2+)](i) concentration dependently between 25 and 500 nM with an EC(50) of 100 nM. The [Ca(2+)](i) signal was composed of an initial gradual rise and a plateau. The response was decreased by removal of extracellular Ca(2+) by 45+/-10%. In Ca(2+)-free medium, pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) abolished 250 microM betulinic acid-induced [Ca(2+)](i) increases. Conversely, pretreatment with betulinic acid only partly inhibited thapsigargin-induced [Ca(2+)](i) increases. Addition of 3 mM Ca(2+) induced a [Ca(2+)](i) increase after pretreatment with 250 nM betulinic acid in Ca(2+)-free medium for 5 min. This [Ca(2+)](i) increase was not altered by the addition of 20 microM SKF96365 and 10 microM econazole. Inhibiting inositol 1,4,5-trisphosphate formation with the phospholipase C inhibitor U73122 (2 microM) abolished 250 nM betulinic acid-induced Ca(2+) release. Pretreatment with 10 microM La(3+) inhibited 250 nM betulinic acid-induced [Ca(2+)](i) increases by 85+/-3%; whereas 10 microM of verapamil, nifedipine and diltiazem had no effect. In Ca(2+) medium, pretreatment with 2.5 nM betulinic aid for 260 s potentiated 10 microM ATP and 1 microM thapsigargin-induced [Ca(2+)](i) increases by 33+/-3% and 45+/-3%, respectively. Trypan blue exclusion revealed that acute exposure of 250 nM betulinic acid for 2-30 min decreased cell viability by 6+/-2%, which could be prevented by pretreatment with 2 microM U731222. Together, the results suggest that betulinic acid induced significant [Ca(2+)](i) increases in MDCK cells in a concentration-dependent manner, and also induced mild cell death. The [Ca(2+)](i) signal was contributed by an inositol 1,4, 5-trisphosphate-dependent release of intracellular Ca(2+) from thapsigargin-sensitive stores, and by inducing Ca(2+) entry from extracellular medium in a La(3+)-sensitive manner.

Fluoxetine-induced Ca2+ signals in Madin-Darby canine kidney cells.

The effect of fluoxetine on Ca2+ signaling in Madin-Darby canine kidney (MDCK) cells was investigated by using fura-2 as a Ca2+ probe. Fluoxetine increased [Ca2+]i concentration-dependently between 5 microM and 200 microM with an EC50 value of 40 microM. The response was reduced by external Ca2+ removal by 30%40%. In Ca2+-free medium pretreatment with 1 microM thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+ pump, abolished 100 microM fluoxetine-induced Ca2+ release. Addition of 3 mM Ca2+ to Ca2+-free medium increased [Ca2+]i when cells were pretreated with 100 microM fluoxetine. Suppression of 1,4,5-trisphosphate (IP3) formation by 2 microM U73122 (a phospholipase C inhibitor) did not affect 100 microM fluoxetine-induced Ca2+ release. Fluoxetine (5-100 microM) also increased [Ca2+]i in neutrophils, prostate cancer cells and bladder cancer cells from human and rat glioma cells.

Effect of diethylstilbestrol (DES) on intracellular Ca(2+) levels in renal tubular cells.

The effect of the estrogen diethylstilbestrol (DES) on intracellular Ca(2+) concentrations ([Ca(2+)](i)) in Madin Darby canine kidney (MDCK) cells was investigated, using the fluorescent dye fura-2 as a Ca(2+) indicator. DES (10-50 microM) evoked [Ca(2+)](i) increases in a concentration-dependent manner. Extracellular Ca(2+) removal inhibited 45 +/- 5% of the Ca(2+) response. In Ca(2+)-free medium, pretreatment with 50 microM DES abolished the [Ca(2+)](i) increases induced by 2 microM carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler) and 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor); and pretreatment with CCCP and thapsigargin partly inhibited DES-induced [Ca(2+)](i) signals. Adding 3 mM Ca(2+) increased [Ca(2+)](i) in cells pretreated with 50 microM DES in Ca(2+)-free medium, suggesting that DES may induce capacitative Ca(2+) entry. 17beta-Estradiol (2-20 microM) increased [Ca(2+)](i), but 100 microM diethylstilbestrol dipropionate had no effect. Pretreatment with the phospholipase C inhibitor U73122 (1 microM) to abolish inositol 1,4,5-trisphosphate formation inhibited 30% of DES-induced Ca(2+) release. DES (20 microM) also increased [Ca(2+)](i) in human normal hepatocytes and osteosarcoma cells. Cumulatively, this study shows that DES induced rapid and sustained [Ca(2+)](i) increases by releasing intracellular Ca(2+) and triggering extracellular Ca(2+) entry in renal tubular cells.

The willingness of families caring for victims of stroke to pay for in-home respite care--results of a pilot study in Taiwan.

This contingent survey was designed to investigate the willingness of family caregivers of stroke victims to pay for in-home respite care. Between September 1996 and December 1996, a designated family member from each family of 174 vascular accident patients hospitalized in the Taipei Metropolitan Area, including two medical centers, received the first interview during preparation and planning for discharge of the patient from the hospital, and follow up interview in their own homes at the end of the second month after the patient was discharged from the hospital. A willingness to pay for in-home respite care was measured as the percentage of monthly family income which would be sacrificed to receive the respite care. Logistic regressions were used to perform multivariate analysis. The willingness to pay for respite care ranged from US$ 363 to 2182, and 42.5% of the family caregivers interviewed indicated a willingness to pay at least 50% of monthly family income for respite care. Family income was strongly associated with the amount of money that family caregivers were willing to pay for respite care. After results were adjusted for the effect of variance in income level, the degree of dependence of patients on the caregiver was significantly associated with the percentage of monthly family income for respite care. The more severe the physical dysfunction of patient, the higher the willingness to pay for in-home respite care utilization. Initially, respite care could be provided to families caring for patients with severe dysfunction, and then the scope enlarged to include caregivers taking care of patients with mild dysfunction.

Therapeutic lamellar keratectomy in the management of experimental keratomycosis.

Keratomycosis, a vision-threatening corneal infection, is a challenge to the ophthalmologist because it is often refractory to medical treatment. Surgical keratectomy may not only debulk the major infectious source but potentiate the intracorneal penetration of the antifungal agents. To evaluate the efficacy of keratectomy in managing the fungal corneal ulcer, three common keratomycosis models, Candida, Fusarium, and Aspergillus keratitis, were established in 46 eyes of 23 rabbits (each group had 14, 16 and 16 eyes respectively). Within each keratitis group, the infected eyes were randomly divided into equally numbered experimental and control subgroups. The eyes of the experimental subgroups underwent therapeutic lamellar keratectomy once the typical fungal corneal infection had developed after inoculation. Following keratectomy, eyes of both the treated and control groups received natamycin eyedrops and were regularly examined biomicroscopically. Our results showed that therapeutic lamellar keratectomy is beneficial in chronic, indolent keratitis, such as Candida and Fusarium keratitis, where it promoted corneal healing and shortened the duration of treatment required. The procedure is a valuable adjunctive measure for antifungal agents in these two types of keratitis. However, acute keratitis of the Aspergillus group did not benefit from keratectomy; in these cases, surgery may actually increase the risk of corneal perforation.

Fendiline-Induced Ca2+ movement in A10 smooth muscle cells.

The effect of fendiline, an anti-anginal drug, on cytosolic free Ca2+ levels ([Ca2+]i) in A10 smooth muscle cells was explored by using fura-2 as a Ca2+ indicator. Fendiline at concentrations between 10-50 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 of 20 microM. External Ca2+ removal reduced the Ca2+ signal by 75%. Addition of 3 mM Ca2+ increased [Ca2+]i in cells pretreated with fendiline in Ca2+-free medium. The 50 microM fendiline-induced [Ca2+]i increase in Ca2+-containing medium was inhibited by 10 microM of La3+, nifedipine, or verapamil. In Ca2+-free medium, pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor) to deplete the endoplasmic reticulum Ca2+ store partly inhibited 50 microM fendiline-induced Ca2+ release; whereas pretreatment with 50 microM fendiline abolished 1 microM thapsigargin-induced Ca2+ release. Inhibition of phospholipase C activity with 2 microM U73122 did not alter 50 microM fendiline-induced Ca2+ release. Incubation with 50 microM fendiline for 10-30 min decreased cell viability by 10-20%. Together, the findings indicate that in smooth muscle cells fendiline induced [Ca2+]i increases. Fendiline acted by activating Ca2+ influx via L-type Ca2+ channels, and by releasing internal Ca2+ in a phospholipase C-independent manner. Prolonged exposure of cells to fendiline induced cell death.

Histamine-Induced increases in intracellular free Ca2+ levels in hepatoma cells.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+]i) in HA22/VGH human hepatoma cells were evaluated using fura-2 as a fluorescent Ca2+ dye. Histamine (0.2-5 microM) increased [Ca2+]i in a concentration-dependent manner with an EC50 value of about 1 microM. The [Ca2+]i response comprised an initial rise, a slow decay, and a sustained phase. Extracellular Ca2+ removal inhibited 50% of the [Ca2+]i signal. In Ca2+-free medium, after cells were treated with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), 5 microM histamine failed to increase [Ca2+]i. After pretreatment with 5 microM histamine in Ca2+-free medium for 4 min, addition of 3 mM Ca2+ induced a [Ca2+]i increase of a magnitude 7-fold greater than control. Histamine (5 microM)-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122), and by 5 microM pyrilamine but was not altered by 50 microM cimetidine. Together, this study shows that histamine induced [Ca2+]i increases in human hepatoma cells by stimulating H1, but not H2, histamine receptors. The [Ca2+]i signal was caused by Ca2+ release from thapsigargin-sensitive endoplasmic reticulum in an inositol 1,4,5-trisphosphate-dependent manner, accompanied by Ca2+ entry.

Influence of background exposure on detection and determination limits for a TL dosimetry system based on LiF:Mg,Cu,P(GR-200A).

Thermoluminescence dosemeters are widely used to monitor personal doses. For these low dose range applications, it is important to determine the detection limit L(D) and the determination limit L(Q) of the dosimetric system. The influence of background exposure on these limits for LiF:Mg,Cu,P(GR-200A) based TL dosimetry was investigated. Both the conventional analysis and the glow curve analysis methods were used to determinate these limits. The detection limit L(D) was compared with the recording level and the investigation level. A systematic error can occur in the occupational dose evaluation when the detection limit L(D) is more than the recording level. It was found that the L(D) of the dosimetric system-based LiF:Mg,Cu,P(GR-200A) was less than the recording level for exposure time tau > or = 10 days considering an annual dose limit of 1 mSv for the public recommended in ICRP Publication 60.

The application of computerised analysis of glow curves to personal dosimetry in LiF:Mg,Cu,P.

In personnel monitoring services, it is important to omit the high-temperature annealing process so that large numbers of TL detectors can be produced economically. There are two efficient ways of reducing the residual signal of LiF:Mg,Cu,P. One is by increasing the maximum readout temperature and the other is by improving the preparation procedure (increasing the Cu concentration and the sintering temperature) but both reduce the TL sensitivity. In personal dosimetry the real dosimetric signals are separated from the residual signals by computerised analysis of glow curves. The adverse influence of the high residual signals of LiF:Mg.Cu.P TL material has been effectively eliminated and the sensitivity remains stable. A good dosimetric result using only reader measurement without pre-irradiation oven annealing is attained in a dose range of 50-80,000 microGy.

Cotransplantation of hepatic stellate cells attenuates the severity of graft-versus-host disease.

Liver allografts seem to be immunologically privileged; they are the only solid transplant that can protect cotransplanted organs from rejection. The mechanisms of this "hepatic tolerance" are poorly understood. The aim of this study was to examine the immunomodulatory effect of hepatic stellate cells (HSCs) in mixed lymphocyte reactions in vitro and in graft-versus-host disease (GVHD) in vivo. Using a carboxyfluorescein diacetate succinimidyl ester-labeling method, we observed that the percentage of proliferative T cells was reduced when HSCs were present in a mixed lymphocyte culture. In addition, the degree of reduction was the same when HSCs were co-cultured in transwell inserts. Thus, soluble factors may participate in the immunomodulatory effect of HSCs. In GVHD experiments, irradiated BALB/c (H-2d) mice simultaneously received an intravenous mixture of bone marrow and splenic T cells from C57BL/6 (H-2b) mice. The HSCs prominently reduced symptoms and pathologic severity of GVHD in target organs. HSC cotransplanted mice survived for 57.5+/-30.6 days whereas the control hosts only survived for 15.3+/-5.2 days (P<.01). We concluded that HSCs may reduce T-cell proliferation against alloantigens and suppress acute GVHD to prolong recipient survival. Our study sheds some light on the immunosuppressive nature of the liver, suggesting a biological manipulation of alloreactivity for transplantation medicine.

Determination of molecular weight profile for a bioactive beta-(1-->3) polysaccharides (Curdlan).

This paper focuses on the development of methodology based on MALDI-TOF mass spectrometry for evaluation of molecular weight profile of the water-insoluble portion of an extracellular polysaccharide, i.e. Curdlan. As previously demonstrated, MALDI analysis of water-insoluble Curdlan fraction gave number-average (M(n)) and weight-average (M(w)) molecular weights of 8000 and 8700 Da, respectively [T.W.D. Chan, K.Y. Tang, Rapid Commun. Mass Spectrom. 17 (2003) 887]. To validate the MALDI determined molecular weight information, several additional analytical schemes were used to analysis the water-insoluble Curdlan fraction. In all cases, the water-insoluble Curdlan sample was fractionated by gel permeation chromatography (GPC) using Sephadex G-75 column. The M (n) of low-mass and narrow distributed polysaccharide fractions were obtained by MALDI-MS. Good linearity was found in the calibration plot constructed from the measured M (n)-values and the corresponding elution time/volume. The relative quantity of various fractionated samples was then measured using three different approaches. These include (a) direct refractometric analysis; (b) UV-vis absorption analysis of the Aniline Blue stained sample; and (c) GC-MS analysis of the hydrolyzed and TMS-derivatized sample. Using results obtained from theses quantification methods and the correlation function between the GPC retention time and M (n), the MW and MWD of water-insoluble Curdlan were obtained. Our results demonstrated that the previous use of MALDI methods for measuring M(n), M(w) and polydispersity (PD) of water-insoluble Curdlan (with and without GPC fractionation) were unreliable. However, by standardizing the narrow distributed polysaccharides using MALDI-MS method, reliable molecular weight information for dispersed polysaccharides could be obtained. The M (n),M (w) and PD of the water-insoluble Curdlan were found to be 22,000, 31,500 Da and 1.40, respectively.

Hepatitis B, 1997 and the Chinese community--an appraisal of their relationships.

In 1997, Hong Kong's sovereignty will go back to China. The United Kingdom has granted 50,000 families the right of abode to settle here. It is estimated that these 50,000 families will consist of approximately 225,000 people in all. Hepatitis B virus infection is extremely common in Hong Kong-50 per cent of the local population have been infected by the virus. Should the Department of Health consider implementing and introducing a screening and immunization programme? What is the current level of understanding about the virus among the Chinese community and health care professionals in the United Kingdom? Findings from a health promotion project have revealed that there is a gap in health care professionals' and patients' understanding of the issue. There is a need to raise awareness, to provide more information for health care professionals and patients, and to give serious consideration to a screening and vaccination programme.