Risk factors of temperature increase after cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy.

Background: Cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy (CRS-HIPEC) is the standard treatment for patients with peritoneal cancer (PC). Following CRS-HIPEC, patients may also face risks caused by whole body hyperthermia. This study analyzed the incidence of temperature increases following CRS-HIPEC and identified the attendant risk factors. Methods: A retrospective analysis was carried out among 458 patients who received CRS-HIPEC at the Fourth Hospital of Hebei Medical University between August 2018 and January 2021. The patients were divided into two groups according to post-HIPEC axillary temperature (≥38°C), with the demographics and the laboratory test results subsequently analyzed and compared, and the risk factors pertaining to temperature increases analyzed using univariate and multivariate logistic regression. Results: During CRS-HIPEC, 32.5% (149/458) of the patients with a temperature increase had an axillary temperature of not lower than 38°C, and 8.5% (39/458) of the patients with hyperpyrexia had an axillary temperature of not lower than 39°C. Female gender, gynecological malignancies, type of chemotherapy drug, increased postoperative neutrophil percentage, and a sharp drop in postoperative prealbumin were associated with the incidence of a temperature increase and axillary temperatures of >38°C. Among these factors, the type of chemotherapy drug was identified as an independent risk factor for a temperature increase during CRS-HIPEC. Conclusion: By determining the risk factors pertaining to temperature increases during CRS-HIPEC, medical staff can identify the attendant risks among the patients and thus take preventive measures in a timely manner to maintain the patient's body temperature at a stable level. This suggests that further clinical research should be conducted to build a risk-prediction model for temperature increases following CRS-HIPEC.

Preservation of Autologous Brachiocephalic Vessels with Assistance of Three-Dimensional Printing Based on Convolutional Neural Networks.

Background: Preservation of autologous brachiocephalic vessels in Stanford type A aortic dissection has good short-time outcomes. However, getting access to the details is not easy by conventional examination methods. This study is aimed at reconstructing the aortic arch model by three-dimensional (3D) printing based on convolutional neural networks (CNN) to understand the details for performing surgery. Methods: Three patients with type A aortic dissection from October 2017 to June 2018 were indicated for simplified Sun's procedure. Convolutional neural network (CNN) is used as a deep learning model, and the model was preset by transfer learning. The genetic algorithm (GA) was used to optimize the parameters. The aortic arch models were reconstructed using the segmented image. Results: The predicted damage area (mean 0.021 mm2) of the model optimized by deep learning was consistent with the experimental results (mean 0.023 mm2). Among the three patients, one patient died due to multiple organ failure and septic shock on the 11th day after surgery. The other two patients were cured, no reoperation was reported, and their cardiac functions were defined as class I during the 13 and 20 months of follow-up. Conclusion: It is feasible to use CNN to optimize the manufacturing of the aortic arch models.

Stem cells in the treatment of renal fibrosis: a review of preclinical and clinical studies of renal fibrosis pathogenesis.

Renal fibrosis commonly leads to glomerulosclerosis and renal interstitial fibrosis and the main pathological basis involves tubular atrophy and the abnormal increase and excessive deposition of extracellular matrix (ECM). Renal fibrosis can progress to chronic kidney disease. Stem cells have multilineage differentiation potential under appropriate conditions and are easy to obtain. At present, there have been some studies showing that stem cells can alleviate the accumulation of ECM and renal fibrosis. However, the sources of stem cells and the types of renal fibrosis or renal fibrosis models used in these studies have differed. In this review, we summarize the pathogenesis (including signaling pathways) of renal fibrosis, and the effect of stem cell therapy on renal fibrosis as described in preclinical and clinical studies. We found that stem cells from various sources have certain effects on improving renal function and alleviating renal fibrosis. However, additional clinical studies should be conducted to confirm this conclusion in the future.

Astragaloside IV attenuates high glucose-induced EMT by inhibiting the TGF-ß/Smad pathway in renal proximal tubular epithelial cells.

In the present study, we examined the molecular mechanism of astragaloside IV (AS-IV) in high glucose (HG)-induced epithelial-to-mesenchymal transition (EMT) in renal proximal tubular epithelial cells (PTCs). NRK-52E cell viability and apoptosis were determined by the cell counting kit-8 (CCK-8) assay and flow cytometric analysis, respectively. Expressions of E-cadherin, N-cadherin, vimentin, and occludin were measured by Western blot, and those of E-cadherin and N-cadherin were additionally measured by immunofluorescence analysis. Transforming growth factor-ß1 (TGF-ß1) and α-smooth muscle actin (α-SMA) expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The expressions of Smad2, Smad3, phosphorylated-Smad2 (p-Smad2), and p-Smad3 were measured using Western blot. We found that AS-IV could recover NRK-52E cell viability and inhibit HG-induced cell apoptosis. TGF-ß1, α-SMA, Smad2, Smad3, p-Smad2, and p-Smad3 expressions were decreased in the AS-IV-treated groups compared with the HG group. Moreover, the expressions of E-cadherin and occludin were remarkably up-regulated and those of N-cadherin and vimentin were down-regulated in the AS-IV-treated groups compared with the HG group. Interestingly, the TGF-ß1 activator SRI-011381 hydrochloride had an antagonistic effect to AS-IV on HG-induced EMT behavior. In conclusion, AS-IV attenuates HG-induced EMT by inhibiting the TGF-ß/Smad pathway in renal PTCs.

Soil carbon and nitrogen fraction dynamics affected by tillage erosion.

Understanding the impact of tillage erosion on soil organic carbon (SOC) and nitrogen (N) fractions is essential for targeted soil conservation in mountainous and hilly areas. However, little is known about this issue. In this study, we selected a tillage erosion-dominated hillslope from the Sichuan Basin, China, to determine the effect of tillage erosion on particulate OC (POC), dissolved OC (DOC), light fraction OC (LFOC), ammonium N (NH4+-N), nitrate N (NO3--N) and alkali-hydrolysable N (AN). Additionally, we investigated the microbial activities in relation to soil C and N dynamics, including soil microbial biomass, ß-glucosidase and urease activities. Tillage erosion induced serious soil loss in upper slope positions and soil deposition in lower slope positions. The observations of the various labile OC fraction distributions across the hillslope suggest that tillage erosion exerts less impact on DOC and LFOC dynamics but a notable effect on POC. The distribution pattern in total organic carbon under tillage erosion mainly depends on POC redistribution. The POC redistribution is a major factor affecting microbial activities. The AN is more prone to the tillage erosion impact than NH4+-N and NO3--N. Effective soil conservation measures should be taken to weaken the adverse impacts of tillage erosion on POC and AN redistribution in sloping farmlands.

[Rapid identification of Cordyceps and its products using DNA barcoding method].

Cordyceps is one of the most valuable traditional Chinese medicines. There are various counterfeits in markets because of high price and limited output. In this study,116 Cordyceps,146 hosts and 29 related products were collected and detected by using normal DNA barcoding technology and specific PCR method. The results indicated that Cordyceps and its adulterants could be distinguished from each other through DNA barcoding technology based on ITS and COⅠsequences. Two pairs specific primers ITSSF1/ITSSR1 and ITSSF2/ITSSR2 were developed to amplify 297 bp and 136 bp ITS regions of Cordyceps sinensis,respectively. It could be used to identify C. sinensis specifically and rapidly. Furthermore,specific primers ITSSF1/ITSSR1 and ITSSF2/ITSSR2 combined with ITS and COⅠsequences could differentiate powder Cordyceps from fermentation mycelia and could identify related products. Therefore,the method developed from this study could be applied to identify the powder of Cordyceps from fermentation mycelia and related products efficiently.

Abnormality of intestinal cholesterol absorption in ApcMin/+ mice with colon cancer cachexia.

Colorectal cancer syndrome has been one of the greatest concerns in the world, particularly in developed countries. Several epidemiological studies have shown that dyslipidemia may be associated with the progression of intestinal cachexia, but there is little research on the function of the small intestine, which is involved in blood lipid metabolism, in dyslipidemia. In the present study, we aimed to explore the function of intestinal cholesterol absorption in the ApcMin/+ mouse model using an intestinal lipid absorption test. We found that both triglyceride (TG) and total cholesterol (TC) uptake were inhibited in the intestine of ApcMin/+ mice with age and the intestinal peroxisome proliferator-activated receptor α (PPARα) downregulated the processes of ß-oxidation, oxidative stress response, and cholesterol absorption in APC-deficient mice. In addition, reduced expression levels of farnesoid X receptor (FXR) and apical sodium-dependent bile acid transporter (ASBT) indicated that bile acid metabolism might be associated with intestinal cholesterol absorption in ApcMin/+ mice. Thus, our data suggested that the intestine plays an essential role in cholesterol uptake and that bile acid metabolism seems to cause a decrease in intestinal cholesterol uptake in ApcMin/+ mice.

[Rapid identification of Gekko gecko by loop-mediated isothermal amplification based on 12S rRNA sequence].

Gekko gecko (Tokay Gecko) is a valuable traditional Chinese medicine. In this study, the loop-mediated isothermal amplification (LAMP) technique was introduced for visual rapid identification of G. gecko from adulterants. A total of sixty-five 12S rRNA sequences of fourteen species of G. gecko and its adulterants were obtained. The results showed that G. gecko could be identified from its adulterants through BLAST analysis based on 12S rRNA regions. The 12S rRNA sequences of ten batches of G. gecko were conserved. There were only two haplotypes and three variation sites in the available regions for primers design. Six specific LAMP primers were successfully designed online based on 12S rRNA sequences. The visual rapid detection of G. gecko could be achieved with the optimized conditions (64 °C for 1 h and 80 °C for 5 min). And the required minimal template concentration was 5 µg·L⁻¹ while conventional PCR with 0.5 mg·L⁻¹. Consequently, the LAMP method established from this study was rapid, specific, highly sensitive, and simple. It could be applied to detect G. gecko from its adulterants efficiently.

PPAR­Î³ agonist rosiglitazone protects rat peritoneal mesothelial cells against peritoneal dialysis solution­induced damage.

Long-term peritoneal dialysis (PD) leads to ultrafiltration failure (UFF). Peritoneal mesothelial cells, which form the innermost monolayer of the peritoneal cavity, have been shown to regulate various responses, including inflammation, in UFF. The present study was designed to investigate the effect of the peroxisome proliferator­activated receptor­Î³ (PPAR­Î³) agonist, rosiglitazone, on peritoneal dialysis solution (PDS)­induced injuries in rat peritoneal mesothelial cells (RPMCs). RPMCs were cultured for different durations and with different concentrations of PDS. The gene expression levels of aquaporin­1 (AQP­1) and zonula occluden­1 (ZO­1) were determined using reverse transcription­quantitative polymerase chain reaction analysis. The protein levels of AQP­1, ZO­1 and PPAR­Î³ were measured using western blot analysis. Interleukin (IL)­6 and IL­8 were detected using ELISA. The RPMCs were damaged by stimulation with 4.25% PDS for 72 h. The expression levels of AQP­1 and ZO­1 were increased, and the secretion of IL­6 and IL­8 were decreased by rosiglitazone. The use of the PPAR­Î³ inhibitor, GW­9662, completely prevented the effects of rosiglitazone. These results indicated that PDS exposure stimulated an inflammatory response in the RPMCs. The PPAR­Î³ activator, rosiglitazone, appeared to relieve the injury by inhibiting inflammation, and regulating the expression of AQP­1 and ZO­1, however further investigations are required to elucidate the potential underlying mechanism.

Atorvastatin alleviates renal ischemia-reperfusion injury in rats by promoting M1-M2 transition.

Acute kidney injury (AKI) often occurs as a result of ischemia-reperfusion (IR). Previous studies have demonstrated that inflammation is an important contributor to AKI. Atorvastatin (ATO) possesses anti­inflammatory properties and has been demonstrated to exert protective effects against renal IR injury (IRI). However, the underlying mechanism requires further study. In the present study, a rat model of renal IRI was successfully established. Consistent with the results of a previous study, ATO significantly attenuated IRI, which was supported by a decrease in serum creatinine and an increase in creatinine clearance rate, as well as alleviated pathological alterations in renal tubular cells. There are two types of activated macrophages: Proinflammatory M1 and anti­inflammatory M2 macrophages, which have been demonstrated to exert contributory and protective effects on IRI, respectively. The present study demonstrated that treatment with ATO significantly decreased M1 macrophage density and increased M2 macrophage density, as compared with the IR group. In addition, it is well known that M1 macrophages can be induced by T helper 1 cytokines, including tumor necrosis factor (TNF)­α and interferon (IFN)­Î³, whereas M2 macrophages can be induced by peroxisome proliferator-activated receptor (PPAR)­Î³. The present study indicated that ATO treatment significantly decreased the expression levels of TNF­α and IFN­Î³, and increased PPAR­Î³ expression. In conclusion, ATO may ameliorate renal IRI by promoting M1­M2 transition. Furthermore, ATO­mediated macrophage polarization in rats with renal IRI may be associated with the downregulation of TNF­α and IFN­Î³, and the upregulation of PPAR-γ.

Potassium supplementation and long-term outcomes in chronic peritoneal dialysis patients with end-stage renal disease: a propensity score matching study.

OBJECTIVE: In this retrospective matched-cohort study, the association between potassium supplementation and long-term outcomes was determined. METHODS: Chronic peritoneal dialysis (PD) patients, aged ≥ 16 years, being referred to four PD centers in China, with serum potassium levels ≤ 3.5 mEq/L on three consecutive monthly in Q4 2008 and without receiving oral potassium supplementation in the prior three months were included in this study. Patients were divided into two groups, either to receive (test group) or not (control group) oral potassium supplementation in both Q4 2008 and the subsequent follow-up period, until 31 December 2014. The patients from the test group were matched to those from the control group using a propensity score. The clinical outcomes for all-cause and cardiovascular mortality were estimated by Matched Cox regression models during 61.5 months of median follow-up. All patients were also categorized according to serum potassium correction levels (<3.0, 3.0 to <4.0, 4.0 to <5.0 and ≥5.0 mEq/L) after the whole follow-up. The hazard ratios (HRs) were used to assess the relationship between corrected potassium levels and all-cause and cardiovascular mortality in PD patients. Subgroup analysis was used to determine the homogeneity of the associations between potassium supplementation and all-cause mortality. RESULTS: All-cause mortality occurred in 108 patients (605/10,000 person-years) in the test group and 114 patients (677/10,000 person-years) in the control group during 1786- and 1685-year follow-up, respectively [hazard ratio (HR), 0.89; 95% confidence interval (CI), 0.68-1.16; p = 0.38]. Cardiovascular mortality occurred in 97 patients (542/10,000 person-years) in the test group and 101 patients (598/10,000 person-years) in the control group (HR, 0.89; 95% CI, 0.67-1.18; p = 0.43). There were no significant interactions between potassium supplementation and any of the subgroups, except for diabetes mellitus and volume overload. During a median follow-up of 61.5 months, adjusted all-cause mortality hazard ratio (HR) and 95% confidence interval (CI) for corrected serum potassium of <3.0, 3.0 to < 4.0, and ≥5.0 mEq/L, compared with 4.0 to < 5.0 mEq/L (reference), were 2.23 (1.17-3.72), 1.35 (0.89-1.81), and 1.74 (1.05-3.72), respectively. CONCLUSION: The use of potassium supplementation in chronic PD patients is not associated with mortality. While it may be necessary for the correction of hypokalemia or the maintenance of normokalemia, and the consequent reduction of hypokalemia-associated mortality. Additionally, use of aldosterone antagonists may be preferable for the handling of hypokalemia in PD patients.

Involvement of peroxisome proliferator activated receptor-γ in the anti-inflammatory effects of atorvastatin in oxygen-glucose deprivation/reperfusion-stimulated RAW264.7 murine macrophages.

Ischemia­reperfusion (I/R) injury is important in the pathogenesis and/or progression of various diseases, including stroke, cardiovascular disease and acute renal injury. Increasing evidence indicates that atorvastatin exerts protective effects in I/R injury­associated diseases; however, the underlying mechanisms remain to be fully elucidated. In the present study, oxygen­glucose deprivation (OGD)/reperfusion­stimulated. RAW264.7 murine macrophages served as a model of I/R injury. The knockdown of peroxisome proliferator activated receptor­Î³ (PPARγ) expression in these cells increased OGD/reperfusion­induced expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor­α (TNF­α) and interferon­Î³ (IFN­Î³), and enhanced OGD/reperfusion­induced downregulation of the expression of cluster of differentiation (CD) 206, at the mRNA and protein levels. Conversely, overexpression of PPARγ significantly attenuated OGD/reperfusion­induced alterations in the expression of iNOS, TNF­α, IFN­Î³ and CD206 at the mRNA and protein levels. Notably, atorvastatin inhibited OGD/reperfusion­induced iNOS expression and reversed OGD/reperfusion­induced downregulation of the expression of CD206 and PPARγ at the mRNA and protein levels. The results of the present study indicate that atorvastatin exhibits significant anti­inflammatory effects in OGD/reperfusion­stimulated RAW264.7 cells, possibly via PPARγ regulation. The findings of the present study may reveal a novel mechanism underlying the protective effects of atorvastatin in I/R injury­associated diseases.

Levels of vitamin D receptor and CYP24A1 in patients with end-stage renal disease.

OBJECTIVE: This study was performed to detect the expression of vitamin D receptor (VDR) and cytochrome P450, family 24, subfamily A, polypeptide 1 (CYP24A1) in 24 end stage renal disease (ESRD) patients and 24 healthy controls. METHOD: In this study, 24 ESRD patients and 24 healthy controls were included. RESULTS: In our study, the levels of VDR in patients with ESRD were reduced when compared with those from healthy controls (5.20±0.32 vs 8.59±1.03; P<0.01). However, the levels of CYP24A1 in ESRD patients were increased than those from healthy controls (50.18±21 vs 7.78±1.31; P<0.01). Correlation analysis showed that VDR levels were negatively correlated with CYP24A1 (r=-0.723; P<0.01). CONCLUSION: VDR levels were reduced and CYP24A1 levels were increased in patients with ESRD, and VDR levels were negatively correlated with CYP24A1.

Sodium salicylate suppresses GABAergic inhibitory activity in neurons of rodent dorsal raphe nucleus.

Sodium salicylate (NaSal), a tinnitus inducing agent, can activate serotonergic (5-HTergic) neurons in the dorsal raphe nucleus (DRN) and can increase serotonin (5-HT) level in the inferior colliculus and the auditory cortex in rodents. To explore the underlying neural mechanisms, we first examined effects of NaSal on neuronal intrinsic properties and the inhibitory synaptic transmissions in DRN slices of rats by using whole-cell patch-clamp technique. We found that NaSal hyperpolarized the resting membrane potential, decreased the input resistance, and suppressed spontaneous and current-evoked firing in GABAergic neurons, but not in 5-HTergic neurons. In addition, NaSal reduced GABAergic spontaneous and miniature inhibitory postsynaptic currents in 5-HTergic neurons. We next examined whether the observed depression of GABAergic activity would cause an increase in the excitability of 5-HTergic neurons using optogenetic technique in DRN slices of the transgenic mouse with channelrhodopsin-2 expressed in GABAergic neurons. When the GABAergic inhibition was enhanced by optical stimulation to GABAergic neurons in mouse DRN, NaSal significantly depolarized the resting membrane potential, increased the input resistance and increased current-evoked firing of 5-HTergic neurons. However, NaSal would fail to increase the excitability of 5-HTergic neurons when the GABAergic synaptic transmission was blocked by picrotoxin, a GABA receptor antagonist. Our results indicate that NaSal suppresses the GABAergic activities to raise the excitability of local 5-HTergic neural circuits in the DRN, which may contribute to the elevated 5-HT level by NaSal in the brain.

Frequencies of apolipoprotein E alleles in depressed patients undergoing hemodialysis--a case-control study.

OBJECTIVE: To explore the relation between the frequencies of apolipoprotein E (ApoE) alleles and the occurrence of depression in patients undergoing hemodialysis in a Chinese population. METHODS: We examined the ApoE alleles in a sample of 288 subjects: 72 patients with depression under hemodialysis, 74 patients without depression under hemodialysis, 75 patients with depression under nondialytic treatment and 67 patients without depression under nondialytic treatment. The depression state was assessed using the Center for Epidemiological Studies Depression (CES-D) scale. Associations between the occurrence of depression and the frequencies of ApoE alleles were examined using multinomial logistic regression models with adjustment of relevant covariates. Information about sociodemographics, clinical data, vascular risk factors and cognitive function was also collected and evaluated. RESULTS: The frequencies of ApoE-ɛ2 were significantly different between depressed and non-depressed patients irrespective of dialysis (p < 0.05), but no significant difference was found in the frequencies of ApoE-ɛ4 (p > 0.05). Serum ApoE levels were significantly different between depressed and non-depressed patients in the whole sample (p < 0.05). Multinomial logistic regression models showed significant association between the frequency of ApoE-ɛ2 and the occurrence of depression in the Chinese population after control of relevant covariates, including age, sex, educational level, history of smoking and drinking, vascular risk factors and cognitive function. CONCLUSIONS: No association between the frequency of ApoE-ɛ4 and the occurrence of depression was found in patients undergoing hemodialysis. Further research is needed to find out if ApoE-ɛ2 acts as a protective factor in Chinese dialysis population since it might decrease the prevalence of depression and delay the onset age.

Altered neuronal intrinsic properties and reduced synaptic transmission of the rat's medial geniculate body in salicylate-induced tinnitus.

Sodium salicylate (NaSal), an aspirin metabolite, can cause tinnitus in animals and human subjects. To explore neural mechanisms underlying salicylate-induced tinnitus, we examined effects of NaSal on neural activities of the medial geniculate body (MGB), an auditory thalamic nucleus that provides the primary and immediate inputs to the auditory cortex, by using the whole-cell patch-clamp recording technique in MGB slices. Rats treated with NaSal (350 mg/kg) showed tinnitus-like behavior as revealed by the gap prepulse inhibition of acoustic startle (GPIAS) paradigm. NaSal (1.4 mM) decreased the membrane input resistance, hyperpolarized the resting membrane potential, suppressed current-evoked firing, changed the action potential, and depressed rebound depolarization in MGB neurons. NaSal also reduced the excitatory and inhibitory postsynaptic response in the MGB evoked by stimulating the brachium of the inferior colliculus. Our results demonstrate that NaSal alters neuronal intrinsic properties and reduces the synaptic transmission of the MGB, which may cause abnormal thalamic outputs to the auditory cortex and contribute to NaSal-induced tinnitus.

Activation of presynaptic GABAB receptors modulates GABAergic and glutamatergic inputs to the medial geniculate body.

The medial geniculate body (MGB) receives ascending inputs from the inferior colliculus and descending inputs from the auditory cortex. In the present study, we intended to determine whether activation of presynaptic GABA(B) receptors modulates GABAergic and glutamatergic inputs to the MGB with whole-cell patch-clamp recordings in brain slices of the rat. To evoke a synaptic response, we electrically stimulated the ascending and descending inputs to MGB neurons with bipolar electrodes placed on the brachium of the inferior colliculus and the superior thalamic radiation. To isolate presynaptic mechanisms, we blocked the effects of postsynaptic GABA(B) receptors by filling recording electrodes with the internal solution containing cesium and QX-314. The activation of presynaptic GABA(B) receptors by exogenous agonist was shown to modulate synaptic inputs to the MGB as demonstrated by that (1) baclofen, a GABA(B) receptor agonist, reversibly suppressed both inhibitory postsynaptic currents (IPSCs) and excitatory postsynaptic currents (EPSCs) and this suppressive effect could be blocked by CGP35348, a GABA(B) receptor antagonist, (2) baclofen significantly increased the ratio of IPSCs or EPSCs elicited by paired-pulse stimulation, and (3) baclofen depressed EPSCs and IPSCs in response to repetitive stimulation. The activation of presynaptic GABA(B) receptors by endogenously released GABA was shown to modulate the synaptic transmission as demonstrated by that CGP55845, another GABA(B) receptor antagonist, increased the ratio of IPSCs to paired-pulse stimulation in young (P8-10) rats, although not in juvenile (P15-18) rats. Our study provides electrophysiological evidence for the presence of functional presynaptic GABA(B) receptors in the MGB and suggests an age-dependent role of these receptors in the synaptic transmission in this central auditory region.

Differential effects of sodium salicylate on current-evoked firing of pyramidal neurons and fast-spiking interneurons in slices of rat auditory cortex.

Sodium salicylate (SS) can penetrate the blood-brain barrier to target neurons in the central auditory system. Understanding how SS alters functional behaviors of different types of central auditory neurons will provide insights into the neural mechanisms of SS-induced tinnitus. Here, we report the differential effects of SS on current-evoked firing of pyramidal neurons and fast-spiking interneurons in layer II/III of auditory cortex slices in young rats (P12-P19). The two neuronal types were identified according to their characteristic patterns of current-evoked firing as recorded with whole-cell patch-clamp techniques and by their morphological features. Following perfusion of the brain slice with 1.4mM SS, the threshold current needed to evoke an action potential remained unchanged for pyramidal neurons (68.96+/-10.68 pA vs 70.39+/-12.14 pA, n=7, P>0.05), but significantly increased for fast-spiking interneurons (56.9+/-13.69 pA vs 74.04+/-15.73 pA, n=7, P<0.05). The drug perfusion caused no significant change in current-evoked firing rates in pyramidal neurons (-2.43+/-7.07%, n=14, P>0.05); however, it drastically and reversibly depressed those in fast-spiking interneurons by up to -49.88+/-10.39% (n=14, P<0.05). Our results suggest that functionally impairing fast-spiking interneurons, which are GABAergic and inhibitory, is probably one of the pathways through which SS raises excitability in the central auditory system and consequently produces tinnitus.

[Enhanced biodecolourization of azo dyes by the catalysis of anthraquinone dyes intermediators].

Enhanced biodecolourization of azo dyes by suspended and immobilized quinone-reducing community using kinds of anthraquinone dyes intermediators as redox mediators was investigated. The suspended bacterium community could enhance the biodecolourization of many kinds of azo dyes using bromoamine acid (BAA) as a redox mediator, the optimum conditions for Acid Red 3R were as follows: pH 6-9, glucose, BAA and initial dye concentrations 400-600 mg/L, 19-34.2 mg/L and < or = 900 mg/L, respectively. Under these conditions, the maximal decolourization rate was about 95%, which is reached within 7 h for suspended cells and 14 h for immobilized cells. However, the latter needed 38-57 mg/L BAA as a redox mediator. In addition, after 7 cycles without BAA addition, the decolourization rate of Acid Red 3R by immobilized cells retained over 85%.