Effects of dietary supplementation with bioactive peptides derived from rapeseed protein on the growth performance, serum biochemistry and faecal micro-organism composition of weaned piglets.

The present study investigated the effects of supplementing bioactive peptides derived from rapeseed protein (rapeseed peptide, Rsp) on the growth performance, serum biochemistry and faecal micro-organism composition of weaned piglets. Sixty Duroc × Landrace × Yorkshire weaned piglets of similar weights were randomly divided into three groups. The control group (NC) was fed a basal diet, and the two treatment groups, Rsp-1 and Rsp-2, were fed a basal diet supplemented with 1% or 2% Rsp, respectively, for 28 days. Each treatment consisted of five replicates with four piglets per replicate. The results showed that Rsp treatment significantly improved the average daily gain and had a better feed-to-gain ratio (p < 0.05). The diarrhoea incidence and indices of Rsp-1 and Rsp-2 groups were significantly lower than the NC group (p < 0.05), and the effect of Rsp-2 on reducing the incidence of diarrhoea was significantly higher than that of Rsp-1 (p < 0.05). The serum albumin, serum immunoglobulin A and catalase levels of the Rsp-1 and Rsp-2 groups were significantly better than the NC group (p < 0.05). Additionally, Rsp treatment significantly gained the relative abundance of faecal Lactobacillaceae and decreased the relative abundance of faecal Eubacterium_coprostanoligenes_group, Treponema and Coprococcus (p < 0.05). In summary, Rsp supplementation improved the growth performance, ameliorated the diarrhoea, enhanced the immune and antioxidant functions and changed the composition of faecal micro-organisms in piglets. These findings indicate that Rsp positively affected the health of weaned piglets.

Inflammasome-targeting natural compounds in inflammatory bowel disease: Mechanisms and therapeutic potential.

Inflammatory bowel disease (IBD), mainly including Crohn's disease and ulcerative colitis, seriously affects human health and causes substantial social and economic burden. The pathogenesis of IBD is still not fully elucidated, whereas recent studies have demonstrated that its development is associated with the dysfunction of intestinal immune system. Accumulating evidence have proven that inflammasomes such as NLRP3 and NLRP6 play a prominent role in the pathogenesis of IBD. Thus, regulating the activation of inflammasomes have been considered to be a promising strategy in IBD treatment. A number of recent studies have provided evidence that blocking inflammasome related cytokine IL-1ß can benefit a group of IBD patients with overactivation of NLRP3 inflammasome. However, therapies for targeting inflammasomes with high efficacy and safety are rare. Traditional medical practice provides numerous medical compounds that may have a role in treatment of various human diseases including IBD. Recent studies demonstrated that numerous medicinal herb derived compounds can efficiently prevent colon inflammation in animal models by targeting inflammasomes. Herein, we summarize the main findings of these studies focusing on the effects of traditional medicine derived compounds on colitis treatment and the underlying mechanisms in regulating the inflammasomes. On this basis, we provide a perspective for future studies regarding strategies to improve the efficacy, specificity and safety of available herbal compounds, and to discover new compounds using the emerging new technologies, which will improve our understanding about the roles and mechanisms of herbal compounds in the regulation of inflammasomes and treatment of IBD.

Soil phosphorus accumulation in mountainous alpine grassland contributes to positive climate change feedback via nitrifier and denitrifier community.

Mountainous alpine ecosystems are sensitive to global change, where soil nutrient content would potentially vary under current climate change background, and thus possibly influence the activity of nitrifiers and denitrifiers, as well as N2O emissions. However, within mountainous alpine ecosystems, the potential variation of soil nutrients under current global change and the consequence to N2O emission from nitrification and denitrification are still unclarified, hampering a comprehensive understanding of the feedback mechanisms between the nitrogen cycle and climate change. In order to fill this knowledge gap, we selected alpine grasslands at three different elevations and investigated the distribution and environmental drivers of nitrifiers and denitrifiers. The results showed that the lowest elevation site tended to have higher total phosphorus (TP) accumulation within the topsoil. The abundance of functional groups, emission of CO2 and N2O, and the N2O/CO2 ratio showed a decreasing trend along elevation. TP was the greatest influence on denitrifier composition (nosZ/narG and nirS/nirK ratios) and considerably influenced nitrifier composition (AOA/AOB ratio), and was significantly correlated to the N2O/CO2 ratio. In microcosms of soils from the highest elevation site, TP addition decreased the ratios of nosZ/narG, nirS/nirK, and AOA/AOB, and increased N2O/CO2 ratio and N2O emission, thus contributing to positive climate change feedback. This study indicates the potential for change within the nitrifier and denitrifier communities under current climate change, and highlights the role TP plays in governing nitrification and denitrification in mountainous alpine ecosystems.

Wenyang Jieyu Decoction Alleviates Depressive Behavior in the Rat Model of Depression via Regulation of the Intestinal Microbiota.

BACKGROUND: Intestinal microbiota plays an important role in the occurrence and treatment of depression. This study investigated whether Wenyang Jieyu decoction (WYJYD) alleviates depressive behavior in the rat model via regulation of the intestinal microbiota. METHODS: Rat model of depression was established by stress stimulus. SD male rats were randomly allocated into normal control, model, model + low-dose WYJYD (1.89 g/kg/d), model + medium-dose WYJYD (3.08 g/kg/d), model + high-dose WYJYD (7.56 g/kg/d), and model + fluoxetine (3.33 mg/kg/d) groups. Behavioral changes were observed using forced swim test. Histopathological changes in hippocampal tissue were examined by HE staining. Indicators in serum were detected by ELISA. Indicators in hippocampal tissue were detected by qPCR and western blot. Microbiota distribution in feces was detected using high-throughput 16S rRNA gene sequencing. RESULTS: Compared with the model group, the immobility time in WYJYD and fluoxetine groups was significantly decreased (P < 0.05), and the cell structure was significantly improved. Compared with the model group, the 5-hydroxytryptamine (5-HT) and norepinephrine (NE) levels in medium- and high-dose WYJYD groups and the brain-derived neurotrophic factor (BDNF) level in the high-dose WYJYD group were significantly increased (P < 0.05, all), and the fibroblast growth factor-2 (FGF2), forkhead box protein G1 (FOXG1), and phospho-protein kinase B/protein kinase B (p-AKT/AKT) expressions were increased with WYJYD treatments. The Chao1 and ACE indices in high-dose WYJYD and the Simpson and Shannon indices in medium-dose WYJYD were significantly different than the model group. The similarity of the intestinal microbial community of each group after WYJYD treatment tended to be closer to the control group. Compared with the model group, as the dosage of WYJYD increased, the abundance of genera Coprococcus, Lachnospira, and rc4-4 was significantly increased, while the abundance of genera Desulfovibrio, Burkholderia, and Enterococcus was significantly decreased. CONCLUSION: WYJYD may alleviate the depressive behavior of the rat model by regulating the intestinal microbiota and neurotransmitters.

SYL3C aptamer-anchored microemulsion co-loading ß-elemene and PTX enhances the treatment of colorectal cancer.

The aim of this study is to construct a SYL3C aptamer-anchored microemulsion based on ß-elemene and PTX (SYL3C/EP-MEs) for enhancement on colorectal cancer therapy. Such microemulsion is consist of encapsulated drugs (ß-elemene and PTX), tumor targeting ligand (3'-end thiolated SYL3C aptamer), thiol conjugated site (maleimide-modified PEGylated 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine, mal-DOPE-PEG), pH-sensitive component (DOPE) and other necessary excipients. SYL3C/EP-MEs showed a spherical particle with an average particle size around 30 nm and a high encapsulation efficiency (>80%) for both drugs. ß-elemene and PTX could be released controllably from SYL3C/EP-MEs as pH values changed. SYL3C/EP-MEs displayed a selective affinity to HT-29 cells, leading to an obvious increase in cellular uptake, cell apoptosis and cytotoxicity. In the HT-29 tumor xenograft-bearing nude mice model studies, SYL3C/EP-MEs showed an overwhelming tumor growth inhibition, the longest survival time and the lowest systemic toxicity among all the treatments. The potential mechanism of enhanced anti-cancer ability was probably associated with the induction of M1 macrophage polarization, the downregulation of mutant p53 protein and the reduction of bcl-2 protein expression. Collectively, the microemulsion codelivery of ß-elemene and PTX using functionalization with SYL3C aptamer provides a novel approach for combinational colorectal cancer-targeted treatment.

YY1 binds to the E3' enhancer and inhibits the expression of the immunoglobulin κ gene via epigenetic modifications.

The rearrangement and expression of immunoglobulin genes are regulated by enhancers and their binding transcriptional factors that activate or suppress the activities of the enhancers. The immunoglobulin κ (Igκ) gene locus has three important enhancers: the intrinsic enhancer (Ei), 3' enhancer (E3'), and distal enhancer (Ed). Ei and E3' are both required for Igκ gene rearrangement during early stages of B-cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3' and Ed. The transcription factor YY1 affects the expression of many genes involved in B-cell development, probably by mediating interactions between their enhancers and promoters. Herein, we found that YY1 binds to the E3' enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer. Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3' enhancer. Moreover, in germinal centre B cells and plasma cells, YY1 expression was reversely associated with Igκ levels, implying that YY1 might facilitate antibody affinity maturation in germinal centre B cells through the transient attenuation of Igκ expression.

Quercetin Attenuates Vascular Calcification through Suppressed Oxidative Stress in Adenine-Induced Chronic Renal Failure Rats.

BACKGROUND: This study investigated whether quercetin could alleviate vascular calcification in experimental chronic renal failure rats induced by adenine. METHODS: 32 adult male Wistar rats were randomly divided into 4 groups fed normal diet, normal diet with quercetin supplementation (25 mg/kg·BW/d), 0.75% adenine diet, or adenine diet with quercetin supplementation. All rats were sacrificed after 6 weeks of intervention. Serum renal functions biomarkers and oxidative stress biomarkers were measured and status of vascular calcification in aorta was assessed. Furthermore, the induced nitric oxide synthase (iNOS)/p38 mitogen activated protein kinase (p38MAPK) pathway was determined to explore the potential mechanism. RESULTS: Adenine successfully induced renal failure and vascular calcification in rat model. Quercetin supplementation reversed unfavorable changes of phosphorous, uric acid (UA) and creatinine levels, malonaldehyde (MDA) content, and superoxide dismutase (SOD) activity in serum and the increases of calcium and alkaline phosphatase (ALP) activity in the aorta (P < 0.05) and attenuated calcification and calcium accumulation in the medial layer of vasculature in histopathology. Western blot analysis showed that iNOS/p38MAPK pathway was normalized by the quercetin supplementation. CONCLUSIONS: Quercetin exerted a protective effect on vascular calcification in adenine-induced chronic renal failure rats, possibly through the modulation of oxidative stress and iNOs/p38MAPK pathway.

Nutritive Value of Mulberry Leaf Meal and its Effect on the Performance of 35-70-Day-Old Geese.

Availability of feed crops for animal production is decreasing, creating a need to identify alternative food sources. With their high protein content, mulberry leaves are a likely candidate for feed supplementation and have been trialed on pigs and chickens, but little is known about their effect as a feed supplement on geese. Here, we determine the nutritive value of mulberry leaf meal (MLM), measure the digestibility of energy and amino acid of MLM in male Sichuan white geese, and evaluate the performance of these geese fed an MLM-supplemented diet. The composition of MLM was as follows: gross energy 4.94 Mcal/kg, crude protein 18.81%, ether extract 11.65%, crude fiber 12.45%, calcium 2.46%, phosphorous 0.24% and amino acids 0.26-1.92% (all % on a dry matter basis). Using the emptying then force-feeding method on 24 geese aged 194 days, we measured the apparent metabolizable energy of MLM as 1.58 Mcal/kg (on a dry matter basis), and the true total tract digestibility of the amino acids in MLM as 50.54-79.98%. We then randomly allocated a further 210 geese aged 35 days to one of five dietary treatments (control diet alone or supplemented with 4%, 8%, 12% or 16% MLM). Each treatment contained six replicate pens of seven birds per pen, and birds were maintained on their treatment until 70 days of age. Geese fed diets containing MLM exhibited lower weight gains, elevated feed consumption and an increased feed to gain ratio (P<0.05) compared with geese fed the control diet. Moreover, geese fed diets supplemented with MLM all experienced diarrhea, reduced amounts of subcutaneous fat and lower percentages of skin and abdominal fat (P<0.05) compared with control geese. In conclusion, MLM should be used with caution as a feed supplement for geese.

T-2 Toxin Alters the Levels of Collagen II and Its Regulatory Enzymes MMPs/TIMP-1 in a Low-Selenium Rat Model of Kashin-Beck Disease.

The objectives of this study are to assess T-2 toxin's involvement in low selenium (Se)-induced Kashin-Beck disease (KBD) in rats and unveil the mechanisms underlying this disease. Two hundred thirty rats were randomly divided into two groups after weaning and fed normal or low-Se diets (n = 115), respectively, for a month. After low-Se model confirmation, rats in each group were subdivided into five: two subgroups (n = 20) were fed their current diets (normal or low-Se diets, respectively) for 30 and 90 days, respectively; two other subgroups (n = 25) received their current diets + low T-2 toxin (100 ng/g BW/day) for 30 and 90 days, respectively; and 25 rats were fed their current diets + high T-2 toxin (200 ng/g BW/day) for 30 days. Articular cartilage samples were extracted for hematoxylin and eosin (H&E) staining and immunohistochemistry. Western blot and reverse transcription-polymerase chain reaction (RT-PCR) were used to assess protein and mRNA levels, respectively, of collagen II, matrix metalloproteinase (MMP-1), MMP -3, MMP-13, and tissue inhibitor of metalloproteinase-1 (TIMP-1). Low Se and T-2 toxin synergistically affected animal fitness. Interestingly, low Se + T-2 toxin groups showed KBD characteristics. MMP-1, -3, and -13 mRNA and protein levels generally increased in low-Se groups, while collagen II and TIMP-1 levels showed a downward trend, compared with normal diet fed animals for the same treatment (P < 0.05). T-2 toxin's effect was dose but not time dependent. Low Se and T-2 toxin synergistically alter the expression levels of collagen II as well as its regulatory enzymes MMP-1, MMP-3, MMP-13, and TIMP-1, inducing cartilage damage. Therefore, T-2 toxin may cause KBD in low-Se conditions.

Increased levels of IL-6, IL-1ß, and TNF-α in Kashin-Beck disease and rats induced by T-2 toxin and selenium deficiency.

The objective of this study is to investigate the possible role of inflammatory mediators such as IL-6, IL-1ß, and TNF-α in Kashin-Beck disease (KBD) children and rats fed with T-2 toxin under a selenium-deficient nutrition status in order to determine possible mechanism underlying KBD. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to their exposure to T-2 toxin for 4 weeks. The morphology of joint cartilages of KBD children and rats was examined by light microscopy, and the expression of proteoglycans was determined by histochemical staining. The serum levels of IL-6, IL-1ß, and TNF-α were determined by enzyme-linked immunosorbent assay. IL-6, IL-1ß and TNF-α were localized by immunohistochemistry, and their mRNA levels were detected by real-time RT-PCR. The serum levels of IL-6 were significantly elevated in rats fed with selenium-deficient, T-2 toxin, and T-2 toxin plus selenium-deficient diets compared to those in the normal diet, while the serum levels of IL-1ß and TNF-α were significantly increased only in the T-2 toxin plus selenium-deficient diet group. IL-6, IL-1ß and TNF-α protein and mRNA levels in cartilage were significantly higher in rats with diets of T-2 toxin and T-2 toxin plus selenium deficiency than in rats fed normal or selenium-deficient diet. While staining for the cytokines in cartilages of KBD children was significantly higher than that in controls. T-2 toxin under a selenium-deficient nutritional status induces increased levels of IL-6, IL-1ß, and TNF-α in serum and cartilages, which may account for the pathological mechanism underlying the cartilage damage in KBD.

Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin-Beck disease using T-2 toxin and selenium deficiency conditions.

The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. Our results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.

[Comparisons among three frequency-specific auditory evoked potentials in normal hearing adults].

OBJECTIVE: To provide supports for the application of auditory evoked potential (AEP) in the evaluation of behavioral threshold, by studying the difference and relevance between the pure tone audiometry (PTA) and three frequency-specific auditory evoked potentials, including 40 Hz auditory event related potentials (40 Hz AERP), tone burst auditory brainstem response (Tb-ABR) and auditory steady-state response (ASSR). METHODS: Three frequency-specific AEP and PTA thresholds were recorded at speech frequency (0.5, 1, 2, 4 kHz) from thirty-four adults with normal hearing (68 ears). Then, the relationship between the AEP thresholds and PTA thresholds were analyzed respectively. RESULTS: There were good correlations between three frequency-specific AEP thresholds and PTA thresholds at speech frequency. However, the difference of thresholds between each frequency-specific AEP and PTA was not same. The difference of thresholds were the smallest and the relevance were the best between 40 Hz AERP and PTA at 0.5 kHz, and between ASSR and PTA at 2, 4 kHz. At 1 kHz, there were not statistical difference between ASSR, 40 Hz AERP and PTA, while the relevance of 40 Hz AERP was better than ASSR. CONCLUSION: Different methods should be chosen to assess the objective behavioral thresholds at different frequency.

Oxidant damage in Kashin-Beck disease and a rat Kashin-Beck disease model by employing T-2 toxin treatment under selenium deficient conditions.

Kashin-Beck disease (KBD) is an endemic degenerative osteoarthropathy, but the mechanisms underlying its pathogenesis remains unclear. This study compares antioxidant capacity and lipid peroxidation using a novel model, in which rats were administered a selenium-deficient diet for 4 weeks prior to their exposure to T-2 toxin for 4 weeks. Changes in cell morphology and empty chondrocyte lacunae indicative of cell death, as well as cartilage proteoglycan loss in the deep zone of articular cartilage of knee joints were observed in rats with selenium-deficient diet plus T-2 toxin treatment. These changes were similar to those observed previously in KBD. The levels of thiobarbituric acid reactive substances (TBARS), indicative of lipid peroxidation in serum and cartilage, were significantly increased in all experimental groups compared to the normal diet group, while the levels of antioxidants, measured as total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidases (GPX), in serum and cartilage were significantly lower than that in the normal diet group. The mRNA expression of those antioxidants in cartilage tissue was significantly reduced by T-2 toxin alone or by selenium-deficient diet plus T-2 toxin treatment. These results indicate that increasing TBARS and decreasing antioxidants in serum and cartilage by T-2 toxin treatment with a selenium-deficient nutritional status may alter oxidative stress in joint tissues and contribute to the pathological process of cartilage damage in KBD.

[Forensic medical identification of 355 cases with hearing impairment].

OBJECTIVE: To analyze the difference of subjective hearing threshold and objective hearing threshold, and to discuss the importance of standard for hearing evaluation in forensic medicine. METHODS: Three hundred and fifty-five cases (387 ears) of forensic medical identification with hearing impairment were retrospectively analyzed including the items entrusted and hearing test results. All cases were collected from 2004 to 2012 in the forensic science center. RESULTS: In the 387 ears, 218 ears (56.3%) were evaluated the degree of disability and 106 ears (27.4%) were identified the degree of damage. In the disability degree evaluation, the subjective hearing threshold and the objective hearing threshold were significant different in 120 ears (55.0%), while in damage degree evaluation, the subjective hearing threshold and the objective hearing threshold were significant different in 69 ears (65.1%). CONCLUSION: Because of camouflaging or exaggerating the hearing impairment by the wounded, the subjective hearing threshold can't accurately assess the existence and the degree of hearing impairment. In the forensic identification, auditory brainstem response, 40 Hz auditory event related potential and auditory steady-state response should be combined in the application to evaluate the hearing impairment for the wounded in order to ensure the reliability of the evaluation of hearing impairment.

[Application of slow vertex response in auditory threshold prediction for subjects with hearing loss].

OBJECTIVE: To study the value of slow vertex response (SVR) in the evaluation of hearing loss by comparing the hearing thresholds acquired with SVR and pure tone audiometry (PTA). METHODS: Twenty-five subjects (40 ears) with sensorineural hearing loss were tested by PTA and SVR. According to the thresholds of PTA, these ears were subdivided into mild, moderate and severe hearing loss groups, and rank sum test was performed on the thresholds of SVR and PTA for all the hearing loss groups. Then, the correlation between PTA thresholds and SVR thresholds was analyzed and the mathematical models were established for predicting behavioral thresholds by the thresholds of SVR. RESULTS: At four test frequencies (0.5, 1, 2 and 4kHz), the thresholds of SVR had high correlations with thresholds of PTA. Four liner regression equations were established, and the correlation coefficient(r) were 0.971, 0.976, 0.957 and 0.928, respectively (P < 0.05). Back substitution test showed that the liner regression equations would be an easy method for estimating the behavior thresholds. CONCLUSION: The behavioral threshold can be well judged and evaluated by the liner regression equations established with SVR thresholds.

[The progress in the study on slow vertex response].

Slow vertex response (SVR) is one of long latency auditory evoked potentials. It is a biological and electric response originating from brain cortical neuron evoked by sound stimulus with the latency from 50 to 500 milliseconds. Of all the neuroelectric physiological audiometries, it is the earliest method applied in assessing the function of the auditory neural conduction pathway. The concept, neural generators of SVR have been introduced in this article. Influencing factors on SVR were discussed such as stimulus parameters, consciousness state, age, maturation of the subject. Applications of SVR in clinical and forensic medicine identification were also discussed.

Phenotypic alterations of dendritic cells are involved in suppressive activity of trichosanthin-induced CD8+CD28- regulatory T cells.

The nature and differentiation of regulatory CD8(+)CD28(-) T cells are poorly understood. In this study, we demonstrate that native Ag trichosanthin (Tk), a highly purified linear peptide isolated from a Chinese medicinal herb, is able to induce strong suppression of OVA-specific lymphoproliferation at low concentrations via activation of IL-4/IL-10-secreting CD8(+)CD28(-) regulatory T cells (Tregs). To elucidate the underlying mechanisms, we firstly identified two types of mouse inbred strains, high susceptible (HS) and low susceptible, for the Tk-related suppression. They are H-2(d) (or H-2(b)) and H-2(k), respectively. The suppression is evoked only if bone marrow-derived dendritic cells (BDCs) instead of purified T cells are treated with Tk in an OVA-specific T-BDC interaction. Moreover, a special pattern of cytokine/transcription factors (IL-4(+)IL-10(+)IFN-gamma(-)Gata3(+)T-bet(-)) during suppressed OVA-specific T cell proliferation was observed in HS C57BL/6 but not in low-susceptible C3H/He mice. Consistently, the percentage of CD8(+)CD28(-) Tregs preferentially expanded from 5.5 to 26.1% in the presence of Tk, an occurrence that was also detected only in HS C57BL/6 mice. These expanded Tregs were able to induce a strong inhibition of one-way MLCs, which indicated that the Tk-induced hyporeaction and the activation of CD8(+)CD28(-) Tregs might be under the influence of different genetic backgrounds. Additionally, obvious alterations of phenotypic parameters of BDCs after Tk stimulation were also identified, including enhanced production of IL-10, decreased secretion of IL-12, and detection of Jagged1, a Notch ligand on BDCs. Collectively, our data suggest that the changed APC-related factors are essential, at least in part, for the activation and differentiation of Tk-induced CD8(+)CD28(-) Tregs.

[Comparison of thresholds acquired with SVR and PTA in normal hearing subjects].

OBJECTIVE: To investigate the value of slow vertex response (SVR) for forensic appraisement of hearing dysfunction by comparing the thresholds acquired with SVR and pure tone audiometry (PTA). METHODS: Forty-six subjects with normal hearing were tested with PTA (0.125-8 kHz) and SVR (0.5-4 kHz). Paired t-test analysis was performed on the thresholds of SVR and PTA at each frequency (0.5, 1, 2 and 4 kHz), and analysis of variance was performed on the difference between the pure tone audiometry threshold and the evoked potential threshold among different frequency. RESULTS: At each frequency(0.5, 1, 2 kHz and 4 kHz), difference between the thresholds acquired with SVR and PTA was statistically significant(P < 0.05). The mean difference of the two thresholds were (5.98 +/- 6.72) dB HL at 0.5 kHz, (3.86 +/- 6.12) dB HL at 1 kHz, (7.12 +/- 6.56) dB HL at 2 kHz, (8.53 +/- 7.90) dB HL at 4kHz, and the mean difference at 1 kHz was the smallest. This variation between frequencies was also statistically significant. CONCLUSION: The thresholds acquired with SVR were higher than those acquired with PTA. The adjusted thresholds should be established at each frequency, when the SVR thresholds are used to evaluate the behavioural hearing thresholds.

[The correlativity between the threshold acquired with ASSR and PTA].

OBJECTIVE: To explore the correlativity between the thresholds acquired with auditory steady-state responses (ASSR) and pure tone audiometry (PTA). METHODS: Eighty-six subjects with normal and abnormal hearing (172 ears) were tested with ASSR and PTA at 500, 1000, 2000, 4000 Hz to get the thresholds of ASSR (single frequency) and PTA. Correlation analysis were done between the thresholds acquired with ASSR and PTA at different frequency (500, 1000, 2000, 4000 Hz) for each different hearing loss degree (< or = 20, 21-39, 40-59, 60-79, > or = 80 dB). RESULTS: At each frequency, there was a close correlativity between the thresholds acquired with ASSR and PTA. The rectified threshold of ASSR and PTA at different frequency and hearing loss degree had been obtained. CONCLUSION: The rectified ASSR threshold could be applied as an objective method for evaluating hearing loss to distinguish malingering deafness in the practice of forensic medicine.

[Comparison of thresholds acquired with ASSR and PTA in normal-hearing subjects].

OBJECTIVE: To provide new objective technology in evaluating hearing loss for forensic expert by comparing the thresholds acquired with auditory steady-state responses (ASSR) and pure tone audiometry (PTA) in our laboratory. METHODS: Twenty-seven subjects with normal hearing (54 ears, 18-28 years) were tested with PTA and ASSR at 500, 1000, 2000 and 4000 Hz. Paired t-test analysis was performed on threshold of ASSR and PTA at difference frequency (500, 1000, 2000 and 4000 Hz). RESULTS: At each frequency (500, 1000, 2000 and 4000 Hz), the thresholds acquired with ASSR were higher than those acquired with PTA (P<0.05). The mean difference of each frequency were (22.04+/-5.79) dB (500 Hz), (11.02+/-5.44) dB (1000 Hz), (12.59+/-5.89) dB (2000 Hz) and (17.78+/-7.25) dB (4000 Hz). The mean difference between the system automatically adjusted threshold of ASSR and PTA were (-3.96+/-5.79) dB at 500 Hz, (0.02+/-5.44) dB at 1000 Hz, (-0.41+/-5.89) dB at 2000 Hz, and(-1.25+/-7.25) dB at 4000 Hz. CONCLUSION: At each frequency (500, 1000, 2000 and 4000 Hz), the thresholds acquired with ASSR were higher than those acquired with PTA. The mean difference is 16.9 dB. As an objective and mature method, ASSR could be used in evaluation of hearing-loss degree for forensic expert. But adjusted threshold value should be established when ASSR is used to estimate hearing threshold in each laboratory.