[Prospective study on the effects of resistance training with elastic band at home on muscle function and walking ability of severely burned children].

Objective: To explore the effects of resistance training with elastic band at home on muscle function and walking ability of severely burned children. Methods: A prospective non-randomized controlled study was conducted. From January 2022 to April 2023, 40 children with severe burns who met the inclusion criteria were admitted to Tongren Hospital of Wuhan University & Wuhan Third Hospital. According to the willingness of the children or their families, the children were assigned to conventional rehabilitation group and combined rehabilitation group. During the study, 8 children dropped out of the study, 17 children were finally included in the conventional rehabilitation group with 6 males and 11 females, aged (8.5±2.4) years, and 15 children were included in the combined rehabilitation group with 5 males and 10 females, aged (9.6±2.5) years. The children in the 2 groups received conventional burn rehabilitation treatment in the hospital, including active and passive activity training, scar massage, and pressure therapy. The children in combined rehabilitation group received resistance training with elastic band of 3 to 5 times per week after discharge, and the children in conventional rehabilitation group received daily activity ability training after discharge. Before home rehabilitation training (1 week before discharge) and 12 weeks after home rehabilitation training, the grip strength was measured using a handheld grip dynamometer, the muscle strengths of the upper and lower limbs were measured using a portable dynamometer for muscle strength, lean body mass was measured by bioelectrical impedance measuring instrument, and the 6-min walking distance was measured. Data were statistically analyzed with independent sample t test, paired sample t test, Mann-Whitney U test, or Fisher's exact probability test. Results: After 12 weeks of home rehabilitation training, the grip strengths of children in combined rehabilitation group and conventional rehabilitation group were (15±4) and (11±4) kg, respectively, which were significantly higher than (10±4) and (9±4) kg before home rehabilitation training (with t values of -9.99 and -11.89, respectively, P values all <0.05); the grip strength of children in combined rehabilitation group was significantly higher than that in conventional rehabilitation group (t=3.24, P<0.05). After 12 weeks of home rehabilitation training, the muscle strengths of upper and lower limbs of children in combined rehabilitation group (with t values of -11.39 and -3.40, respectively, P<0.05) and the muscle strengths of upper and lower limbs of children in conventional rehabilitation group (with t values of -7.59 and -6.69, respectively, P<0.05) were significantly higher than those before home rehabilitation training, and the muscle strengths of upper and lower limbs of children in combined rehabilitation group were significantly higher than those in conventional rehabilitation group (with t values of 3.80 and 7.87, respectively, P<0.05). After 12 weeks of home rehabilitation training, the lean body mass of children in combined rehabilitation group was significantly higher than that before home rehabilitation training (t=0.21, P<0.05). After 12 weeks of home rehabilitation training, the 6-min walking distances of children in conventional rehabilitation group and combined rehabilitation group were significantly longer than those before home rehabilitation training (with t values of -5.33 and -3.40, respectively, P<0.05), and the 6-min walking distance of children in combined rehabilitation group was significantly longer than that in conventional rehabilitation group (t=3.81, P<0.05). Conclusions: Conventional burn rehabilitation treatment in hospital and home resistance training with elastic band for 12 weeks after discharge can significantly improve the muscle function and walking ability of severely burned children.

[Research advances on the application of rehabilitation exercise training in pediatric burn rehabilitation].

The sequelae of pediatric burn seriously affect the physical function and quality of life of children with burns. Rehabilitation exercise training mainly based on aerobic and resistance exercise can effectively alleviate the negative effects. This article reviews the effects of rehabilitation exercise training on cardiopulmonary function, muscle function, and quality of life of children with burns, and introduces the latest rehabilitation exercise training prescription for children with burns based on type, mode, intensity, frequency, and time of exercise, so as to improve the level of rehabilitation treatment for children with burns.

Associations of IL-1ß and IL-6 gene polymorphisms with Parkinson's disease.

OBJECTIVE: The aim of this study was to explore the associations of interleukin-1ß (IL-1ß) and IL-6 gene polymorphisms with the pathogenesis of Parkinson's disease. PATIENTS AND METHODS: A total of 200 patients with Parkinson's disease in our hospital were collected as the disease group. Meanwhile, 200 healthy subjects were taken as the control group. Peripheral blood samples were drawn from all research subjects. The polymorphic regions of IL-1ß and IL-6 were amplified via polymerase chain reaction (PCR). Moreover, the polymorphisms were detected and analyzed, followed by further analysis based on the changes in gene expressions and Hoehn-Yahr grade of patients. RESULTS: The allele distributions at IL-1ß rs571556428 (p=0.015) and IL-6 rs543214973 (p=0.012) were statistically different between control group and disease group. In disease group, the G allele frequency at IL-1ß rs571556428 and T allele frequency at IL-6 rs543214973 were significantly higher (p<0.05). Genotype distributions at IL-1ß rs572292175 (p=0.017) and rs571556428 (p=0.000), and IL-6 rs543214973 (p=0.002) in disease group were also different from those in control group. In addition, the frequencies of CT genotype at IL-1ß rs572292175, AA genotype at IL-1ß rs571556428 and AA genotype at IL-6 rs543214973 in disease group were significantly lower (p<0.05). After modeling and analysis, it was found that the distribution of recessive model at IL-1ß rs571556428 (p=0.012) and IL-6 rs543214973 (p=0.014) in disease group exhibited significant differences from those in control group. The frequencies of TA haplotype at IL-1ß rs572292175 and rs571556428 (p=0.038) and GA haplotype at IL-6 rs1474348 and rs543214973 (p=0.047) in disease group were lower than those in control group (p<0.05). The polymorphisms at IL-1ß rs571556428 and IL-6 rs1474348 were significantly associated with gene expression (p<0.05). Moreover, the expressions of IL-1ß and IL-6 rose significantly in patients with GG genotype at rs571556428 and CG genotype at rs1474348, respectively (p<0.05). Furthermore, the polymorphism at IL-1ß rs571556428 was significantly correlated with the grade of Parkinson's disease (p=0.000). Parkinson's disease was in a higher grade (grade 4-5) in patients with AA genotype, whereas in a lower grade (grade 1-2) in patients with GG and AG genotypes. CONCLUSIONS: IL-1ß and IL-6 gene polymorphisms are significantly associated with the pathogenesis of Parkinson's disease.

MiR-20a lowers chemosensitivity of liver cancer Huh-7 cells via regulating NF-кB expression.

OBJECTIVE: The aim of this study was to explore the regulatory effect of micro ribonucleic acid (miR)-20a on nuclear factor-κB (NF-кB) in liver cancer Huh-7 cells, and to elucidate its influence on the chemosensitivity of Huh-7 cells. MATERIALS AND METHODS: Huh-7 cells with overexpression of miR-20a or knockout of miR-20a were first constructed. Quantitative polymerase chain reaction (qPCR) was adopted to detect the expression level of miR-20a in each group of cells. The sensitivity of cells to cisplatin and doxorubicin in each group was measured using methyl thiazolyl tetrazolium (MTT) assay, and the 50% inhibitory concentration (IC50) was calculated. Hoechst 33258 staining was performed to detect the apoptosis of cells in each group. Furthermore, the expression levels of apoptosis-associated proteins and the NF-кB signaling pathway-related proteins in each group of cells were determined via Western blotting. RESULTS: The expression level of miR-20a in blank control group was considerably higher than that in knockout group (p<0.01). Meanwhile, cells in overexpression group exhibited a notably higher expression level of miR-20a than blank control group (p<0.01). Cells in knockout group had dramatically enhanced sensitivity to doxorubicin and cisplatin (p<0.01), with a prominently decreased IC50 value (p<0.01). However, cells in overexpression group exhibited remarkably weakened sensitivity (p<0.01) and increased IC50 value (p<0.01). After treatment with doxorubicin and cisplatin, the apoptosis level of cells rose substantially in knockout group (p<0.01), whereas declined significantly in overexpression group (p<0.01). Moreover, knockout group exhibited a notably elevated expression level of Caspase-3 (p<0.01), and a considerably decreased ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein (Bax) (p<0.01). The expression level of Caspase-3 declined remarkably (p<0.01), however, the ratio of Bcl2/Bax increased substantially (p<0.01) in overexpression group. The expression level of NF-кB inhibitor beta (NF-кBIB) was markedly up-regulated (p<0.01), while the expression levels of Livin and Survivin declined remarkably (p<0.01) in knockout group. Furthermore, overexpression group had a considerably decreased expression level of NF-кBIB (p<0.01), but notably increased expression levels of Livin and Survivin (p<0.01). CONCLUSIONS: MiR-20a up-regulates the expressions of the downstream proteins Livin and Survivin, decreases the expressions of apoptosis-associated proteins, weakens the sensitivity of cells to chemotherapy drugs and lowers the apoptosis level of cells by activating the NF-кB signaling pathway in liver cancer Huh-7 cells.

Taq1a polymorphism (rs1800497) is associated with obesity-related outcomes and dietary intake in a multi-ethnic sample of children.

BACKGROUND: In adults, the Taq1a polymorphism (rs1800497) near the D2 receptor (DRD2) gene is associated with body mass index and binge eating and is more prevalent among non-Hispanic Blacks (NHB) and Hispanic-Americans (HA) relative to non-Hispanic Whites (NHW). We hypothesize Taq1a polymorphism (rs1800497) risk alleles contribute to paediatric racial/ethnic differences in obesity phenotypes. OBJECTIVES: This study aims to characterize the relationship between the Taq1a polymorphism (rs1800497), diet and adiposity in a multi-ethnic cohort of 286 children (98 NHB, 76 HA and 112 NHW), ages 7-12. METHODS: Dual-energy X-ray absorptiometry, computed tomography scans and two 24-h dietary recalls assessed body composition, fat distribution and dietary intakes, respectively. RESULTS: Children with two Taq1a risk alleles (NHB = 50.0%, HA = 43.3%, NHW = 6.7%) reported a 20% increase in total energy intake (P = 0.0034) and per cent of calories from sugar consumed (P = 0.0077) than did children with less than two risk alleles. Children with two Taq1a risk alleles demonstrated significantly higher total body fat (P = 0.0145), body fat percentage (P = 0.0377), intra-abdominal adiposity (P = 0.0459), subcutaneous abdominal adiposity (P = 0.0213) and total abdominal adiposity (P = 0.0209) than did children with one or no Taq1a risk alleles. CONCLUSIONS: Our results suggest that having two Taq1a risk alleles is associated with an increase in reported calorie and sugar consumption and is a potential risk factor for early development of excess adiposity in multi-ethnic children. These results need to be confirmed in a larger sample.

The effects of experimentally manipulated social status on acute eating behavior: A randomized, crossover pilot study.

Both subjective and objectively measured social status has been associated with multiple health outcomes, including weight status, but the mechanism for this relationship remains unclear. Experimental studies may help identify the causal mechanisms underlying low social standing as a pathway for obesity. Our objective was to investigate the effects of experimentally manipulated social status on ad libitum acute dietary intakes and stress-related outcomes as potential mechanisms relating social status and weight. This was a pilot feasibility, randomized, crossover study in Hispanic young adults (n=9; age 19-25; 67% female; BMI ≥18.5 and ≤30kg/m(2)). At visit 1, participants consumed a standardized breakfast and were randomized to a high social status position (HIGH) or low social status position (LOW) in a rigged game of Monopoly™. The rules for the game differed substantially in terms of degree of 'privilege' depending on randomization to HIGH or LOW. Following Monopoly™, participants were given an ad libitum buffet meal and energy intakes (kcal) were estimated by pre- and post-weighing foods consumed. Stress-related markers were measured at baseline, after the game of Monopoly™, and after lunch. Visit 2 used the same standardized protocol; however, participants were exposed to the opposite social status condition. When compared to HIGH, participants in LOW consumed 130 more calories (p=0.07) and a significantly higher proportion of their daily calorie needs in the ad libitum buffet meal (39% in LOW versus 31% in HIGH; p=0.04). In LOW, participants reported decreased feelings of pride and powerfulness following Monopoly™ (p=0.05) and after their lunch meal (p=0.08). Relative to HIGH, participants in LOW demonstrated higher heart rates following Monopoly™ (p=0.06), but this relationship was not significant once lunch was consumed (p=0.31). Our pilot data suggest a possible causal relationship between experimentally manipulated low social status and increased acute energy intakes in Hispanic young adults, potentially influenced by decreased feelings of pride and powerfulness. Increased energy intake over time, resulting in positive energy balance, could contribute to increased risk for obesity, which could partially explain the observed relationship between low social standing and higher weight. Larger and longitudinal studies in a diverse sample need to be conducted to confirm findings, increase generalizability, and assess whether this relationship persists over time.

3-hydroxy-3-methyl glutaryl coenzyme A reductase: an essential actor in the biosynthesis of cantharidin in the blister beetle Epicauta chinensis Laporte.

Cantharidin (C(10)H(12)O(4)) is a monoterpene defensive toxin in insects involved in chemical defence as well as in courtship and mating behaviours. It is relatively well known in the medical literature because of its high anticancer activity and as an effective therapy for molluscum contagiosum. However, little is known about its biosynthesis pathway in vivo, and no enzyme involved in cantharidin biosynthesis has been identified. The purpose of this study was to identify the crucial enzyme that is involved in the biosynthesis of cantharidin. Using the homology cloning method, a 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGR) gene, the rate-limiting enzyme in the mevalonate pathway, was cloned from the blister beetle Epicauta chinensis. Quantitative reverse transcription PCR and gas chromatography methods revealed that the HMGR transcripts had a positive correlation with cantharidin production in the beetles (R = 0.891). RNA interference (RNAi) knockdown of HMGR mRNA expression was achieved by microinjection of a specific double-stranded RNA with more than 90% RNAi efficiency, and an apparent decrease of cantharidin production was observed. Furthermore, the HMGR mRNA was greatly upregulated by exogenous juvenile hormone III (JH III), and cantharidin production was also raised in males; however, when injecting the JH III with RNAi of HMGR mRNA at the same time, cantharidin production did not rise. These results demonstrate that HMGR is an essential enzyme in cantharidin biosynthesis in the blister beetle E. chinensis, which further verifies previous research results demonstrating that cantharidin is synthesized de novo by the mevalonate pathway in blister beetles.

Serum immunoglobulin E level and its impact on the pregnancy outcome associated with fetal growth restriction: a prospective cohort study.

We evaluated the relationship between total serum immunoglobulin E (IgE) levels and pregnancy outcome in a prospective cohort study focusing on fetal growth restriction (FGR). Sixty women with FGR and twenty with normal singleton pregnancy were enrolled during their third trimester. Infants were followed up for 6 months. Blood samples were obtained from pregnant women during the third trimester; cord blood samples were also taken. Six months after birth, blood samples were obtained from infants. Demographic and baseline characteristics were compared between groups. Birth weight, length and head circumference of neonates in the FGR group were lower than those in the control group. Total serum IgE level was significantly increased in third-trimester pregnant women with FGR compared with normal group (P < 0.05). However, this trend was not observed in the cord blood at birth or peripheral blood of 6-month-old infants. The prevalence of atopic eczema between the 2 groups was similar. Linear regression analysis revealed that the IgE level in the third trimester was negatively correlated with birth weight (P < 0.05). Higher serum IgE level in the cord blood was significantly associated with an increased risk of being small for gestational age (P < 0.05). In conclusion, IgE levels in the third trimester of pregnancy and cord blood are strongly related to birth outcomes of FGR.

Epidemiological investigation of physique situation for birth high-risk children aged 9-15 years in Chengdu, Southwest China.

BACKGROUND: As the intrauterine environment can effect children's growth and development, this study aimed to explore the relationship between birth high-risk and physique situation of 9 to 15-year-old children by cross-sectional investigation, and to provide clues for the monitoring, prevention, and treatment of growth deviation in children. MATERIALS AND METHODS: This study recruited 7,194 students aged 9 to 15 years in primary and junior schools. Their parents were asked to complete the birth situation questionnaire. Measurements included height, weight, and body mass index (BMI). Birth high-risk infant was defined according to the gestational age and birth weight. Growth deviation was classified as underweight, short stature, overweight, and obesity. RESULTS: The prevalence of all kinds of growth deviations in preterm, full-term, and post-term birth groups were similar, the same as the physique situation at school age among both sexes. The incidence of small for gestational age (SGA) was 6.23%, when at school age, part of SGA had catch-up growth. However, the prevalence of underweight and short stature for SGA was highest in three groups. The weight and height at school age in SGA group was less than that in appropriate for gestational age (AGA) and large for gestational age (LGA) groups. The prevalence of overweight and obesity for LGA and macrosomia were highest in three groups. At school age, the weight in macrosomia and LGA groups was higher than that in the other groups. CONCLUSIONS: Longitudinal height and weight development and growth of children with birth high-risk are different from normal children. In order to improve healthy situation, more attention should be paid to height and weight development of those children with birth high-risk at school age, even in pre-school age. Prevention may already begin during pregnancy.

Globular adiponectin elicits neuroprotection by inhibiting NADPH oxidase-mediated oxidative damage in ischemic stroke.

Recent studies indicate that adiponectin can attenuate cerebral ischemic lesions via its functional area located in the C-terminal globular domain, which is called globular adiponectin (gAD). However, the mechanisms underlying this action remain unclear. In this study, we investigated the antioxidant properties of gAD during cerebral ischemia. Adult male C57BL/6 mice received an intracerebral injection of gAD with or without tetrabromocinnamic acid (TBCA, a NADPH oxidase activator). Mice were subjected to middle cerebral artery occlusion (MCAO) after gAD injection. Infarct volume, neurological function, the activity of antioxidant enzymes (superoxide dismutase [SOD], catalase), the content of malondialdehyde (MDA), and the expression of Bax, Bcl-2, cleaved caspase-3 and NADPH oxidase 2 (NOX2) were examined at 24h after MCAO. Infarct volume was attenuated in gAD-transduced mice when compared with mice in the MCAO group, with significant improvement in neurological function. In addition, neuronal apoptosis was attenuated, along with the expression of Bax/Bcl-2 and cleaved caspase 3. Furthermore, the activities of SOD and catalase increased, and the content of MDA reduced. However, TBCA blocked the effect of gAD on cerebral protection and its antioxidant abilities. Taken together, these results demonstrate that the neuroprotective action of gAD may result from the promotion of antioxidant capacity by inhibiting the NOX2 signaling system.

A prognostic model for patients with hepatocellular carcinoma within the Milan criteria undergoing non-transplant therapies, based on 1106 patients.

BACKGROUND: The Milan criteria are used to select candidates with small hepatocellular carcinoma (HCC) for liver transplantation. Due to severe shortage of donors, majority of patients within the Milan criteria need to seek alternative treatments. AIM: To propose a prognostic model for these patients undergoing non-transplant therapies. METHODS: A total of 1106 HCC patients, who were within the Milan criteria and received non-transplant therapies were retrospectively analysed. Patients were randomly assigned to the derivation and validation set according to treatments. A prognostic model was constructed from independent predictors of survival identified in the multivariate Cox model of the derivation set and was confirmed in the validation set. RESULTS: In the Cox model, serum bilirubin ≥1.5 mg/dL [risk ratio (RR): 1.525, P = 0.016], α-fetoprotein (AFP) ≥100 ng/mL (RR: 1.728, P < 0.001), mild ascites (RR: 1.705, P = 0.025) and moderate/severe ascites (RR: 4.163, P < 0.001) were independent predictors of poor survival in the derivation set (n = 553). A prognostic model with a total of 0-4 points was derived with the sum of three variables: 1 point each for bilirubin ≥1.5 mg/dL, AFP ≥100 ng/mL and mild ascites, and 2 points for moderate/severe ascites. This scoring system accurately predicted the survival in the validation set (n = 553; P < 0.001). The model consistently discriminated the survival in patients stratified by curative and noncurative treatments (both P values <0.001). CONCLUSION: The newly proposed prognostic scoring model, based on serum bilirubin and AFP level, and severity of ascites, is informative to predict the survival in non-transplant HCC patients within the Milan criteria.

Serum alpha-fetoprotein response can predict prognosis in hepatocellular carcinoma patients undergoing radiofrequency ablation therapy.

AIMS: To evaluate the clinical inference of serum alpha-fetoprotein (AFP) response in hepatocellular carcinoma (HCC) patients undergoing percutaneous radiofrequency ablation (RFA). MATERIALS AND METHODS: Three hundred and thirteen previously untreated HCC patients were enrolled in the study. The optimal AFP response was defined as >20% decrease from baseline after 1 month of RFA for those with a baseline AFP level of ≥100 ng/ml. The impact of AFP response on prognosis was analysed and prognostic factors were assessed. RESULTS: After a median follow-up of 26.7 ± 19.1 months, 49 patients died and 264 patients were alive. The cumulative 5 year survival rates were 75.3 and 57.4% in patients with an initial AFP of <100 ng/ml and ≥100 ng/ml, respectively (p = 0.003). In the 58 patients with a baseline AFP of ≥100 ng/ml and initial completed tumour necrosis after RFA, the cumulative 5 year survival rates were 62.4 and 25.7% in optimal and non-optimal AFP responders, respectively (p = 0.001). By multivariate analysis, the prothrombin time international normalized ratio >1.1 (p = 0.009), non-optimal AFP response (p = 0.023), and creatinine >1.5 mg/dl (p = 0.021) were independent risk factors predictive of poor overall survival. Besides, the cumulative 5 year recurrence rates were 83.4 and 100% in optimal and non-optimal AFP responders, respectively (p < 0.001). Multivariate analysis demonstrated platelet count ≤10(5)/mm(3) (p = 0.048), tumour size >2 cm (p = 0.027), and non-optimal AFP response (p < 0.001) were independent risk factors associated with tumour recurrence after RFA. CONCLUSIONS: Serum AFP response may be a useful marker for predicting prognosis in HCC patients undergoing RFA.

Comparison of the model for end-stage liver disease (MELD), MELD-Na and MELDNa for outcome prediction in patients with acute decompensated hepatitis.

BACKGROUND AND AIM: The model for end-stage liver disease (MELD) is used to predict the outcome of patients with cirrhosis. Incorporation of serum sodium (Na) into MELD may further increase its prognostic ability. Two Na-containing MELD models, MELD-Na and MELDNa, were proposed to enhance the prognostic ability. This study compared the predictive accuracy of these models for acute decompensated hepatitis. METHODS: We investigated the outcome of 182 patients with acute decompensated hepatitis. RESULTS: Twenty (11%) patients died at 3 months. The MELD-Na and MELDNa both had significantly higher area under the receiver operating characteristic curve (AUC) in comparison to MELD (MELD-Na: 0.908, MELDNa: 0.895, MELD: 0.823, p=0.004 and 0.001, respectively). Among 96 patients without specific antiviral treatment, the MELD-Na and MELDNa consistently had significantly higher AUC than the MELD (MELD-Na: 0.901, MELDNa: 0.882, MELD: 0.810, p=0.008 and 0.004, respectively). Three independent indicators, pre-existing cirrhosis (odds ratio [OR]: 5.67, 95% confidence interval [CI]: 1.72-18.7), serum albumin<3.7 g/dL (OR: 5.68, 95% CI: 1.18-27.03) and serum sodium (Na)<138 mequiv./L (OR: 10.0, 95% CI: 2.08-47.62), were associated with 3-month mortality. CONCLUSION: MELD-Na and MELDNa provide better prognostic accuracy than the MELD for patients with acute decompensated hepatitis. The adequacy of liver reserve determines the outcome of these patients.

The MELD-Na is an independent short- and long-term prognostic predictor for hepatocellular carcinoma: a prospective survey.

BACKGROUND AND AIM: Serum sodium has been suggested to incorporate into the model for end-stage liver disease to enhance its prognostic ability for cirrhosis. A mathematical equation based on model for end-stage liver disease and sodium, known as "MELD-Na", was developed for outcome prediction for cirrhosis. The severity of liver cirrhosis is a key component to predict survival in patients with hepatocellular carcinoma. This study investigated the prognostic role of MELD-Na for hepatocellular carcinoma. PATIENTS AND METHODS: A total of 535 unselected hepatocellular carcinoma patients were prospectively enrolled to evaluate the performance of MELD-Na. RESULTS: The MELD-Na was better than model for end-stage liver disease in predicting 6-month mortality by comparing the area under receiver operating characteristic curve (0.782 vs. 0.761, p=0.101). MELD-Na, but not model for end-stage liver disease, was an independent predictor associated with 6-month mortality in multivariate logistic regression analysis (odds ratio: 1.14, p=0.001). In the survival analysis, MELD-Na also independently predicted mortality, with an additional risk of 4.3% per unit increment of the score (p<0.001). Patients with MELD-Na scores between 10 and 20 and scores >20 had 2.1-fold (p<0.001) and 7.5-fold (p<0.001) risk of mortality, respectively, compared to patients with a score <10 in the Cox proportional hazard model. CONCLUSION: The MELD-Na score is a feasible and independent prognostic predictor for both short- and long-term outcome predictions in patients with hepatocellular carcinoma.

Evaluation of interleukin-6, interleukin-10 and human hepatocyte growth factor as tumor markers for hepatocellular carcinoma.

AIM: Serum alpha-fetoprotein (AFP) is the most important tumor marker for hepatocellular carcinoma (HCC). Previous reports indicated that HCC was also associated with increased levels of interleukin (IL)-6, IL-10 and hepatocyte growth factor (HGF). This study investigated the role of these cytokines as tumor markers for HCC. METHOD: A total of 128 adults were prospectively enrolled and categorized into four groups: normal subjects (n=29), chronic hepatitis B or C (n=50), non-HCC tumors (n=23) and HCC (n=26). Serum AFP, IL-6, IL-10 and HGF levels were determined in all subjects. RESULTS: The expression of IL-6 or IL-10 (> or =3 pg/ml), or high level of HGF (>1000 pg/ml) or AFP (>20 ng/ml) was observed in only 0-3% of normal subjects. Patients with HCC more frequently had higher IL-6 and IL-10 levels (p<0.05), whereas HGF levels in HCC patients were not significantly elevated compared to patients with chronic hepatitis or non-HCC tumors. Among patients with low (<20 ng/ml) AFP level, IL-6 or IL-10 expression was significantly associated with the existence of HCC (p<0.05). Patients with large (>5 cm) HCC more often had increased IL-6, IL-10 or AFP levels (p values all <0.05). CONCLUSIONS: Serum levels of IL-6 and IL-10 are frequently elevated in patients with HCC but not in benign liver disease or non-HCC tumors. IL-6 and IL-10 may help identify a subset of HCC patients with low AFP level, and may serve as complementary tumor markers in these patients.

Association of core promoter/precore mutations and viral load in e antigen-negative chronic hepatitis B patients.

Apart from core promoter A1762T/G1764A and precore G1896A mutations, other hepatitis B virus (HBV) mutants are detected in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB). The aim of this study was to determine the effects of those mutants on clinical manifestation and viral loads of genotypes B and C HBV. Seventy-nine HBeAg-negative CHB patients with hepatitis flare were enrolled in this study and their HBV precore/core region were sequenced. Serial biochemical profiles and viral loads were assessed and compared. Fifty-three patients (67%) were infected by genotype B HBV and 26 (33%) were infected by genotype C HBV. The clinical manifestation and HBV viral loads were comparable between the two groups. However, genotype B was significantly associated with precore G1896A mutation (92.5%), and more mutations within nucleotide 1809-1817 were detected in patients infected by genotype B as compared with those infected by genotype C (18.9%vs 3.8%). Most of the cases had mutations at the -2, -3 or -5 position from the precore AUG initiation codon. Triple core promoter mutations T1753C/A1762T/G1764A [corrected] appeared to be linked to genotype C rather than genotype B HBV (19.2%vs 1.9%; P = 0.013). In multivariate analysis, the presence of either triple core promoter 1753/1762/1764 mutation or nucleotide 1809-1817 mutation was the only factor associated with lower HBV viral load (<70 Meq/mL) (odds ratio = 9.01; 95% CI 1.11-71.43; P = 0.04). In conclusion, minor HBV variants with mutations in the core promoter and precore region were detectable in genotypes B and C. Such HBV variants are genotype specific and related to viraemia levels.