The Enhancing Effect of Stable Oxygen Functional Groups on Porous-Carbon-Supported Pt Catalysts for Alkaline Hydrogen Evolution.

The oxygen functionalization of carbon materials has widely been employed to improve the catalytic performance of carbon-supported Pt (Pt/C) catalysts. Hydrochloric acid (HCl) has often been employed to clean carbons during the preparation of carbon materials. However, the effect of oxygen functionalization through a HCl treatment of porous carbon (PC) supports on the performance of the alkaline hydrogen evolution reaction (HER) has rarely been investigated. Herein, the impact of HCl combined with the heat treatment of PC supports on the HER performance of Pt/C catalysts has been comprehensively investigated. The structural characterizations revealed similar structures of pristine and modified PC. Nevertheless, the HCl treatment resulted in abundant hydroxyl and carboxyl groups and the further heat treatment formed thermally stable carbonyl and ether groups. Among the catalysts, Pt loading on the HCl-treated PC followed by a heat treatment at 700 °C (Pt/PC-H-700) exhibited elevated HER activity with a lower overpotential of 50 mV at 10 mA cm-2 when compared to the unmodified Pt/PC (89 mV). Pt/PC-H-700 also exhibited better durability than the Pt/PC. Overall, novel insights into the impact of the surface chemistry properties of porous carbon supports on the HER performance of Pt/C catalysts were provided, which were useful for highlighting the feasible improvement of HER performances by regulating the surface oxygen species of porous carbon supports.

Relieving the Reaction Heterogeneity at the Subparticle Scale in Ni-Rich Cathode Materials with Boosted Cyclability.

Ni-rich layered LiNi0.8Co0.1Mn0.1O2 (NCM811), as a highly suitable candidate for commercialized cathode materials, inevitably suffers from reaction inhomogeneity during electrochemical processes owing to the polycrystalline aggregate particle morphology, especially at high voltages. With the cycles proceeding, intergranular microcracks induced by an anisotropic volume change emerge and accumulate, leading to contact loss of the internal grains. Subsequently, a decrease in accelerated diffusion kinetics and internal Li+ deactivation take place, which further deteriorate the reaction heterogeneity between the surface and bulk phases within polycrystalline subparticles, ultimately leading to rapid capacity failure. To deal with these issues, a microstructural tailored NCM811 with a suitable subparticle size and ordered primary grain arrangement is employed as an alternative cathode. Owing to the optimized microstructure, reaction homogeneity has been significantly promoted, which causes enhanced electrochemical properties with long-term cycling. It is revealed that the mechanically strengthened microstructure contributes to maintaining contact between the surface and bulk phases, resulting in a reversible H2-H3 phase transition and superior Li+ kinetics upon cycling. This microstructural engineering route based on the rational electrode architecture can boost reaction homogeneity and provide guidance for the design of advanced cathode materials.

[Expression of survivin and caspase-3 during the development process in rat cochlea].

OBJECTIVE: To explore the role of some apoptosis regulators during the development in rat cochlea. METHODS: The morphological development process of cochlea was observed in Wistar rat aged between embryo day 13 to postnatal day 14 in this experiment. Survivin and caspase-3 were respectively detected at protein and mRNA levels by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR). RESULTS: The expression of survivin and caspase-3 located in the bottom wall of the cochlear duct. Not only they widespread in the cell proliferation, but also they gradually enhanced in the cell differentiation. Both of them had a crest-time, and survivin was prior to caspase-3. In organ of corti during adult time, caspase-3 was not present and survivin was only expressed. CONCLUSIONS: During the development of the rat cochlea, both of them had similar location and trend. But they were derangement. This showed that both of them participated in the cochlear morphological development. It was suggested that the interaction between survivin and caspase-3 regulated the apoptosis, promoted the cochlear morphological development.

[Construction of recombinant adenoviral vector to coexpress human neurotrophin3 and EGFP gene and its conduction efficiency to rat cochlea in vitro].

OBJECTIVE: To construct an adenoviral vector that codes for both human NT3 and EGFP, to confirm the transduction efficiency in rat cochlear cultures and to assess the protection of NT3 on SGNs survival. METHOD: PAdeasy-1 and pAdTrack CMV were used to constructed Ad/NT3 adenovirus and then to transfer postnatal day 3 rat cochlear cultures. The transduction efficiency was determined by microscope observation. The amounts of SGNs were counted to evaluated protection of Ad/NT3 on SGNs survival. RESULT: EGFP positive cells were observed in all cochlear turns. There was approximately 49% in outer sulcus cells and 27% in the interdental cells; less than 2% of the hair cells and SGN. The amounts of SGN of treated Ad/NT3 adenovirus are more than cochlea SGN only Ad/EGFP adenovirus after cultured for 15 days. CONCLUSION: Ad/NT3 adenovirus could transduce EGFP and NT3 in large number of supporting cells, but few hair cells or SGNs. The putative release of NT3 from these supporting cells could enhance cell survival and promote neurite outgrowth from SGNs.

[Effect of the spiral ganglion cell and nerve fiber of rat cochlea in vitro to hypoxia].

OBJECTIVE: To establish a practical model for Wistar rat cochlea organ culturing in vitro, and to observe the growing status in hypoxia of the spiral ganglion cell and nerve fiber. METHOD: We used an in vitro hypoxia model and dissociated cultures of the basal membrane from the cochlea of 3-day-old Wistar rats. And put them in incubator (37 degrees C, 90% N2, 5% CO2, 5% O2) to hypoxia culture for different times. The culture were Immunofluorescence dyed and count the number of the spiral ganglion cell and the cell density in unit area (24 mm x 36 mm), and observe the morph of nerve fiber under the confocal microscope, the results were compared with controls. RESULT: Hypoxia early (6 h) nerve fiber appear edema, spiral ganglion cell didn't change compared with controls; nerve fiber appear break and disintegration and the spiral ganglion cell decrease in 12 hours culturing, and the cell density in unit area had remarkable difference compared with control (P < 0.01). Hypoxia leads to the cell density decrease in a time-dependent manner, the longer of cultures times in hypoxia, the heavier of damage in spiral ganglion cell and nerve fiber. Twelve hours culturing, and the cell density in unit area had remarkable difference compared with control (P < 0.01). Hypoxia leads to the cell density decrease in a time-dependent manner, the longer of cultures times in hypoxia, the heavier of damage in spiral ganglion cell and nerve fiber. CONCLUSION: The study findings suggest that hypoxia makes the spiral ganglion cell and nerve fiber damage of culturing in vitro, and nerve fiber more susceptible than spiral ganglion cell for hypoxia.

[Expressions of neurotrophin factor receptor in spiral ganglion cell of cisplatin-induced ototoxicity].

OBJECTIVE: To investigate the effects of high-affinity tyrosine kinase receptors TrkB, TrkC and the low-affinity neurotrophin receptor p75 in spiral ganglion cell (SGC) of cisplatin-induced ototoxicity. METHODS: The 50 adult Wistar rats were divided randomly into 5 groups received intraperitoneal injection of cisplatin with vary dose. Control group was received equivalent volumes of saline. The group received 1 day intraperitoneal injection was cisplatin treated at a dose of 5 mg/kg and killed at next day. The group received 3 days was cisplatin treated for 3 days at same dose daily and then killed at next day. The group A received 5 days was cisplatin treated for 5 days and killed at next day. The group B received 5 days was cisplatin treated for 5 days and then were sacrificed after 7 days. The change of mRNA level of neurotrophin receptors in cochlear tissue were examined by RT-PCR. The expressing pattern of TrkB, TrkC, P75 in damaged cochlea were study by immunochemistry using antibodies against TrkB, TrkC, P75 protein. RESULTS: The research data showed the expression of Trk B, Trk C, p75 exhibited in SGC was dynamic along with the administration lasting. The mRNA and protein level of Trk B (x(-) +/- s) at day 1 and 3 after cisplatin treatment were 0.76 +/- 0.06, 88.78 +/- 4.28, 0.82 +/- 0.09 and 91.64 +/- 4.06, with significant difference among those and other groups (P < 0.05). The mRNA and protein level of TrkC at day 1 after cisplatin treatment were 0.80 +/- 0.06 and 89.66 +/- 2.76, with significant difference among that and other groups (P < 0.05). The mRNA and protein level of p75 at the control group and cisplatin treated groups were 0.64 +/- 0.04, 55.16 +/- 3.10, 0.77 +/- 0.04, 78.46 +/- 3.86, 1.01 +/- 0.09, 105.02 +/- 6.61, 1.18 +/- 0.09, 111.10 +/- 6.08, 0.51 +/- 0.04 and 42.74 +/- 5.20, with significant difference among the control group and cisplatin treated groups (P < 0.05). CONCLUSIONS: The expression of Trk B increased to peak at day 1 - 3 after cisplatin treatment and decreased at day 5 early and following weeks. The expression of Trk C went up to peak at day 1 after cisplatin treatment and went down during subsequently time. P75 kept a trend of continuance increased during the drug treatment and decrease at drug stopped. The expression of Trk B, Trk C and P75 may be involved in cochlear insult with cisplatin-induced. Trk B and Trk C may play an important role in the reparative process of cochlear, especially at early stage of the damage. P75 could promote SGC apoptosis in cisplatin-induced neurotoxicity.

[Expression of BDNF and trk B in the cochleas of the aged rats].

OBJECTIVE: To explore the correlation between the expression of brain derived neurotrophic factor (BDNF) and presbycusis in the cochleae of the aged rats. METHOD: The mRNA expression of BDNF and presbycusis in the cochleas of the aged rats was quantitated by real time PCR. RESULT: The expression of BDNF in the cochleas of the aged rats with presbycusis was obviously less than that in the control group. And the difference was statistically significant. CONCLUSION: The expression of BDNF is closely correlated to presbycusis in the aged rats.

[The protection of Tiron to the injury of organ of Corti cultured in vitro caused by exogenous H2O2 in mouse].

OBJECTIVE: In order to observe the action of H2O2 on inner and outer hair cells of organ of Corti in mouse, and discuss whether Tiron can effectively resistant the injury of free radicals in cultured cochlea in vitro or not. METHOD: Using the culture technology of organ of Corti in newborn mouse in vitro, established the model of the injury of inner and outer hair cells caused by exogenous H2O2. And observed the protection to the damage by H2O2 at different concentration of Tiron. RESULT: When the concentration of H2O2 is higher than 1.0 mmol/L, the loss of hair cells in the bottom, middle, and parietal turn of basilar membrane vary, the injury of bottom turn is more severe. In lower than 0.5 mmol/L group, the injury of hair cells is no relationship with the location. Adding Tiron (10 mmol/L) in culture can apparently decrease the injury of hair cells caused by H2O2. When the concentration of H2O2 is 0.01-1.0 mmol/L, Tiron can almost inhibit the loss of hair cells completely. CONCLUSION: There is apparently preventive effection of Tiron on organ of Corti cultured in vitro, and the mechanism of inhibiting injury caused by H2O2 is probably by clearing O2- and combining irony ion.

[Effects of mtDNA deletion associated with abnormal expression in rat cochlear with presbycusis].

OBJECTIVE: To investigate the effects of the common deletion (4834-bp) of mitochondrial DNA (mtDNA) in rat cochlear with presbycusis. METHODS: The mtDNA 4834-bp deletion was analyzed by PCR. The mitochondrial-encoded cytochrome c oxidase subunit I (COXI) transcript level and cytochrome c oxidase (COX) activity were measured by RT-PCR and histochemical methods respectively. RESULTS: The 4834-bp deletion occurred in all the senescent rat cochlear. The COXI transcript level was decreased associated with the decline of COX activity. CONCLUSION: The mtDNA 4834-bp deletion presented in the rat cochlear with presbycusis, which lead to the decrease of COXI transcript level and COX activity, may play an important role in the pathogens of presbycusis.

[Research into the human leucocyte antigen I deletion and local lymphocytes infiltration in laryngeal carcinoma].

OBJECTIVE: To detect the deletion of human leucotyte antigen (HLA) class I antigen expression in laryngeal carcinoma tissue and discuss the relationship between its expression and tumor infiltrating lymphocyte (TIL) cell infiltration or/and malignancy of tumor cell. METHODS: From Feb 2001 to May 2001 specific mouse antihuman HLA class I monoclonal antibody was combined to examined tissue, 64 samples of laryngeal carcinoma were detected by streptavidin-peroxidase (SP) method immunohistochemistry. RESULTS: All of 64 cases, 57 were positive HLA class I antigen and 7 were negative, the negative expression rate was 10.9% (7/64). CD3+ and CD8+ T cell infiltrated in HLA class I positive tumor mass were significantely more than those in negative tissue. the malignant degree elevated along with the declination of HLA class I antigen expression. By 3 years follow up, the mortalitywas not statistically significant in both HLA- group and HLA+ group (P > 0.05). CONCLUSION: There is deletion of HLA class I antigen in laryngeal tissue, which favours penetration of cytotoxic lymphoid cells into tumor mass; alteration in HLA class I expression may be used by cancer cells to avoid immune surveillance.

[E-cadherin gene mutation in recurrent and metastatic carcinoma of larynx].

OBJECTIVE: To evaluate the role of E-cadherin gene in the process of recurrent and metastasis of laryngeal cancer and to investigate the metastatic mechanism of laryngeal cancer. METHOD: Exploration of exon 5 and exon 7 of the E-cadherin gene by polymerase chain reaction (PCR), SSCP in the laryngeal cancer. RESULT: In normal laryngeal tissues, there was no E-cadherin gene mutation. E-cadherin gene mutation occured only in the primary carcinoma with cervical metastasis and recurrent laryngeal carcinoma. The mutation rate were 67.71% and 28.57% respectively. E-cadherin gene mutation occured more frequently in advanced carcinomas than that in early ones. CONCLUSION: E-cadherin gene mutation with its functional suppression was one of the molecular mechanisms of the laryngeal metastasis. It is suggested that E-cadherin may be a valuable prognostic marker for the carcinoma of larynx.