Experimental and Theoretical Research on Photocatalytic Nitrogen Reduction Using MoS2 Nanosheets with Polysulfide Vacancies.

MoS2 nanosheets with different concentrations of S vacancies (VS-MoS2) were synthesized and used for photocatalytic nitrogen reduction reactions (pNRR), and the mechanism of S vacancies enhancing the activity of MoS2 was explored through DFT calculation. The material characterization confirmed the successful construction of S vacancies at different concentrations on the spherical cluster structure of MoS2. The experimental results show that the introduction of S vacancies significantly improves the activity of pNRR, and it increases significantly with the increase of vacancy number, consistent with the trend of photoelectric performance. VS-MoS2-3 exhibits the highest pNRR efficiency, which is 3.5 times higher than that of pristine MoS2, and after being reused three times, the activity only decreased by about 11%. DFT calculation results indicate that the exposed Mo atoms generated by S vacancies alter the charge layout on the MoS2 surface while providing abundant Mo active sites. Meanwhile, the band gap structure will narrow with the increase of S vacancies, which is beneficial for the transfer of surface charges. In addition, the increase of S vacancies, on the one hand, strengthens the adsorption of MoS2 on N2, weakens the adsorption of H, improves the selectivity of nitrogen, and is conducive to the progress of NRR. On the other hand, more electrons can be transferred from MoS2 to the adsorbed N2 molecules, enhancing the hybridization between them and better activating N2.

Construction dual vacancies to regulate the energy band structure of ZnIn2S4 for enhanced visible light-driven photodegradation of 4-NP.

Most of the intrinsic photocatalysts with visible light response can only generate one active radical due to the limitation of their band structures, which is immediate cause limiting their photocatalytic degradation performance. In this work, ZnIn2S4 with Zn vacancy and S vacancy (VZn+S-ZnIn2S4) was prepared for the first time. As expected, the VZn+S-ZnIn2S4 exhibits remarkable photocatalytic performance for 4-Nitrophenol (4-NP) degradation under visible light and the apparent rate constant is about 11 times that of pristine ZnIn2S4. The construction of dual vacancies can regulate the energy band structure of the ZnIn2S4, enabling it to generate •OH and •O2- simultaneously. Meanwhile, dual vacancies system can also extremely improve the separation efficiency of carriers. It is worth noting that Zn vacancy and S vacancy can capture photogenerated holes and photogenerated electrons, respectively, which is beneficial for photogenerated carriers to participate in radical generation reactions. In addition, a possible 4-NP degradation pathway was proposed based on HPLC-MS analysis. This work provides a new way to construct photocatalysts for photodegradation of pollutants in wastewater.

PD-1/PD-L1 inhibitor monotherapy in recurrent or metastatic squamous cell carcinoma of the head and neck: a meta-analysis.

PURPOSE: To evaluate the efficacy and safety of programmed cell death-1/programmed cell death-ligand 1 inhibitor monotherapy compared to the standard of care in the first-line setting for recurrent or metastatic head and neck squamous cell carcinoma. MATERIALS AND METHODS: The PubMed, Embase, and Cochrane Library databases were searched for relevant randomized controlled trials. The clinical outcomes of overall survival, progression-free survival, objective response rates, and grade 3 or higher adverse events were analyzed using Stata SE 15 software with a significance level set to 0.05. RESULTS: We identified four randomized controlled trials (1 nivolumab, 2 pembrolizumab, and 1 durvalumab), including a total of 2474 patients. The results of the meta-analysis showed pooled hazard ratios of overall and progression-free survival for programmed cell death-1/programmed cell death-ligand 1 inhibitor monotherapy of 0.82 (95% CI: 0.73-0.91, p < 0.001) and 0.96 (95%CI: 0.84-1.07, p < 0.001) and pooled odds ratios of objective response rates and grade 3 or higher adverse events of 1.04 (95%CI: 0.46-2.37; p = 0.926) and 0.28 (95%CI: 0.22-0.35, p < 0.001), respectively. Subgroup analysis showed that inhibitors for both programmed cell death-1 (nivolumab and pembrolizumab) and programmed cell death-ligand 1 (durvalumab) were associated with significantly longer overall survival (HR = 0.80, 95% CI: 0.70-0.90, p < 0.001 and HR = 0.88, 95%CI: 0.70-1.06, p < 0.001, respectively). CONCLUSIONS: Programmed cell death-1/programmed cell death-ligand 1 inhibitor monotherapy showed more clinical benefit versus the standard of care in patients with recurrent or metastatic head and neck squamous cell carcinoma, with an acceptable safety profile.

The study of microtubule dynamics and stability at the postsynaptic density in a rat pilocarpine model of temporal lobe epilepsy.

BACKGROUND: The recurrence and drug resistance of temporal lobe epilepsy (TLE) has been ceaselessly challenging scientists and epilepsy experts. There has been an accumulation of evidence linking the dysregulation of postsynaptic proteins etiology and the pathology of epilepsy. For example, NMDA receptors, AMPA receptors, and metabotropic glutamate receptors (mGluRs). Furthermore, our earlier proteomic analysis proved there to be differential expressions of cytoskeletons like microtubules among rat groups. These differential expressions were shown in TLE-spontaneous recurrent seizures (TLE-SRS), TLE without SRS (TLE-NSRS) and control groups. Therefore, we aimed to understand how the microtubule system of the hippocampal postsynaptic density (PSD) regulates the development of TLE. METHODS: In this study, a pilocarpine-induced Sprague-Dawley rat TLE model were used, and Western blot, Nissl staining, and the immunoelectron microscopic method were utilized to determine the dynamic change of microtubules (α- and ß-tubulin) in PSD and the extent of hippocampal neuron loss respectively in acute SE, and latent and chronic (spontaneous seizures) periods. Animal models were then stereotactically treated using colchicine, a microtubule depolymerizer, and paclitaxel, a microtubule polymerization agent, after each animal's acute SE period so as to further explore the function of PSD microtubules. RESULTS: Our study revealed 3 principal findings. One, both α- and ß-tubulin were decreased from the 3rd to the 30th day (lowest at the 7th day) in the seizure group compared with the controls. Two, both α- and ß-tubulin were found to be more downregulated in the TLE-SRS and the TLE-NSRS group than in the control group (especially in the TLE-SRS group). The same trend was also noticed for hippocampal neuron loss. Three, the paclitaxel lowered the chronic SRS rate and increased the expression of PSD ß-tubulin in the hippocampus. CONCLUSIONS: Altogether, these results indicate that the microtubule system of PSD may play an essential role in the development and recurrence of epilepsy, and it may be used as a new target for the prevention and treatment of this refractory disease.

Effect of metals on zooplankton abundance and distribution in the coast of southwestern Taiwan.

Three transects were established along the southwestern coast of Taiwan; transects from north to south were respectively extended from the Kaohsiung Harbor, Kaoping River estuary, and Fangshan River estuary. Six metals including Pb, Cd, Cr, Cu, Zn, and Ni were analyzed in the zooplankton and seawater samples. A total of 24 groups of zooplankton were identified. Calanoid was the frequently collected group and accounted for greater than 40% of the relative abundance of zooplankton. Results showed that metal concentrations in seawater close to coast were higher than those in the outside of transect. The mean of metal concentrations in zooplankton followed the hierarchy: Zn > Cu > Pb > Ni > Cr > Cd. On the whole, metal concentrations in zooplankton from sampling sites in the coastal region were observed to be higher than those in the offshore region. The bioconcentration factor of zooplankton ranged within 103-105 for all studied metals and indicated that zooplankton in the seawater of southwestern Taiwan can accumulate metal even at background concentrations of metals. The value of diversity indices exhibited an increase in the distance to the coast, whereas the abundance showed no significant correlation with that. Consequently, the lowest mean abundance of zooplankton and the highest average metal bioaccumulation were found in transect outside Kaohsiung Harbor, representing that Kaohsiung Harbor has the contamination of anthropogenic metals that results in the impact on zooplankton.

Spatial variability of soil organic carbon in Three Gorges Reservoir area, China.

Soil organic carbon (SOC) is an important component of the global carbon pool. It is a critical indicator of soil quality. We studied SOC content (SOCC) and SOC density (SOCD) of the Three Gorges Reservoir (TGR) area in China. Soil samples from 306 sites across the study area were assessed for SOCC, SOCD and bulk density. Total SOC stocks in the TGR area were estimated at 5.82×10-1Pg. We examined relationships between SOCC and SOCD, and the environmental and land-use/land-cover (LULC) variables. The plow layer (0-0.3m) had a significantly higher mean SOCC (20.6gkg-1) than the subsoil layer (16.5gkg-1); elevation, LULC, soil type and soil thickness were the most influential factors affecting SOCC in the plow layer. In the subsoil layer, elevation and soil thickness were dominant in determining SOCC and SOCD. To study the spatial variability of SOC, we used statistical modeling and GIS-based techniques to map the distribution of SOCC and SOCD of the study area. Both SOCC and SOCD in the plow layer showed patchy distribution and were positively correlated with elevation and vegetation coverage. Spatial variability of SOCD in the subsoil layer showed a gradual transition between LULC categories. The lower SOCC of farmland appeared to be related to the repeated removal of agricultural produce from the land. Preservation of permanent vegetation cover and changing of the traditional farming practices will help to improve SOC stock and increase soil productivity in the TGR area.

Computational simulation study on the anion recognition properties of functionalized tetraphenyl porphyrins.

The anion recognitions of tetra-(2-formamido) phenyl porphyrin (APP), tetra-(2-ureido) phenyl porphyrin (UPP), and their zinc derivatives (ZnAPP and ZnUPP) to three anions (Cl(-), H2PO4 (-), CH3COO(-)) were studied using quantum mechanical calculations (QM) and molecular dynamics (MD) simulations. The density functional theory (DFT) calculations at M06-2X/6-31G (d, p) level indicated that the anion recognition ability of ZnAPP was better than that of APP, and the anion selectivity was in the order Cl(-) < H2PO4 (-) < CH3COO(-). The selectivity trends for ZnUPP and UPP were found to be H2PO4 (-) < Cl(-) < CH3COO(-). The structures, thermodynamic properties, and recognition mechanisms were discussed in detail. The 2 ns MD simulations were then carried out for anion@ZnAPP and anion@ZnUPP complexes in mixed solvent DMSO/water. The MD simulation results showed that anion@ZnUPP complexes exhibited higher stability than anion@ZnAPP, which was in good agreement with QM results. H-bonds formed between the anions and the side-chains of receptors, and zinc coordination bonds with anions contributed significantly to the stability of complexes. The anion selectivity of ZnAPP and ZnUPP in the solvent phase were also discussed and compared with those in the gas phase.

Ameliorative effects of physcion 8-O-ß-glucopyranoside isolated from Polygonum cuspidatum on learning and memory in dementia rats induced by Aß1-40.

CONTEXT: Polygonum cuspidatum Sieb. Et Zucc. (Polygonaceae) has been traditionally used in folk medicine to treat various diseases. OBJECTIVE: This study investigates the ameliorative effects of physcion 8-O-ß-glucopyranoside (PSG) isolated from P. cuspidatum on learning and memory in dementia rats induced by Aß1-40. MATERIALS AND METHODS: Dementia rats were prepared by intracerebroventricular injection of Aß1-40. PSG (5, 10, 20, and 40 mg/kg/d, for 5 d) was administered orally. Ameliorative activity of PSG in dementia rats was evaluated by the Morris water maze (MWM) test, and its mechanisms were explored by evaluating AchE activity, levels of DA, NE, and 5-HT in hippocampus, and drebrin protein expressions in hippocampus. RESULTS: Our results indicated that PSG (5, 10, 20, and 40 mg/kg/d) significantly inhibited the prolonged latency in dementia rats (p < 0.05), and inhibitory rates were 16.5, 22.7, 33.0, and 44.8% after 5 d of learning, indicating that PSG improves learning and memory of dementia rats. Furthermore, PSG significantly decreased AchE activity (10, 20, and 40 mg/kg/d; p < 0.05), increased 5-HT (20 and 40 mg/kg/d, p < 0.05), NE (10, 20, and 40 mg/kg/d; p < 0.05), and DA levels (5, 10, 20, and 40 mg/kg; p < 0.05) in the hippocampus. Additionally, PSG obviously decreased the Aß contents in hippocampus (10, 20, and 40 mg/kg/d; p < 0.05), and up-regulated drebrin protein expressions (5, 10, 20, and 40 mg/kg/d; p < 0.05). CONCLUSIONS: PSG can significantly enhance learning and memory in Aß1-40-induced dementia rats, and the mechanisms may be related to increase levels of Ach, 5-HT, NE, and DA, decrease Aß contents, and up-regulation of drebrin proteins in hippocampus.

Induction of GADD34 Regulates the Neurotoxicity of Amyloid ß.

The possible roles played by growth arrest and DNA damage-inducible gene 34 (GADD34) in Alzheimer's disease (AD) are so far less understood. In this study, we found that GADD34 was increased in the brains of AD transgenic J20 mice. The deposition of ß-amyloid (Aß) peptide is the main component of neurotic plaques in AD brain. Thus, we examined the effect of Aß in the expression of GADD34 in human SH-SY5Y cells in vitro. Amyloid ß (Aß1-42) treatment led to increased expression of GADD34. Pretreatment with 50 nmol/L of c-Jun N-terminal kinases (JNK) inhibitor SP600125 abolished the upregulation of GADD34. c-Jun silencing by transfection with c-Jun small-interfering RNA abolished the effects of Aß1-42 on the expression of GADD34. Importantly, chromatin immunoprecipitation studies verified the ability of c-Jun to bind to the GADD34 promoter, and this ability was increased more than 3-fold by Aß1-42. These data suggest that the induction of GADD34 by Aß is mediated by JNK/c-Jun pathway. Finally, depletion of GADD34 significantly rescued Aß-induced cell apoptosis as evidenced by a marked decrease in the number of terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells. Consistently, knockdown of GADD34 attenuated caspase 3 activation induced by Aß1-42.

The Pael-R gene does not mediate the changes in rotenone-induced Parkinson's disease model cells.

In this study, we established cell models for Parkinson's disease using rotenone. An RNA interference vector targeting Parkin-associated endothelin receptor-like receptor (Pael-R) was transfected into the model cells. The results of reverse-transcription polymerase chain reaction and western blot analysis showed that Pael-R expression was decreased after RNA interference compared with the control group (no treatment) and the model group (rotenone treatment), while the rate of apoptosis and survival of dopaminergic cells did not differ significantly between groups, as detected by flow cytometry and an MTT assay. These experimental findings indicate that the Pael-R gene has no role in the changes in rotenone-induced Parkinson's disease model cells.

Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome.

Patients with generalized epilepsy exhibit cerebral cortical disinhibition. Likewise, mutations in the inhibitory ligand-gated ion channels, GABAA receptors (GABAARs), cause generalized epilepsy syndromes in humans. Recently, we demonstrated that heterozygous knock-out (Hetα1KO) of the human epilepsy gene, the GABAAR α1 subunit, produced absence epilepsy in mice. Here, we determined the effects of Hetα1KO on the expression and physiology of GABAARs in the mouse cortex. We found that Hetα1KO caused modest reductions in the total and surface expression of the ß2 subunit but did not alter ß1 or ß3 subunit expression, results consistent with a small reduction of GABAARs. Cortices partially compensated for Hetα1KO by increasing the fraction of residual α1 subunit on the cell surface and by increasing total and surface expression of α3, but not α2, subunits. Co-immunoprecipitation experiments revealed that Hetα1KO increased the fraction of α1 subunits, and decreased the fraction of α3 subunits, that associated in hybrid α1α3ßγ receptors. Patch clamp electrophysiology studies showed that Hetα1KO layer VI cortical neurons exhibited reduced inhibitory postsynaptic current peak amplitudes, prolonged current rise and decay times, and altered responses to benzodiazepine agonists. Finally, application of inhibitors of dynamin-mediated endocytosis revealed that Hetα1KO reduced base-line GABAAR endocytosis, an effect that probably contributes to the observed changes in GABAAR expression. These findings demonstrate that Hetα1KO exerts two principle disinhibitory effects on cortical GABAAR-mediated inhibitory neurotransmission: 1) a modest reduction of GABAAR number and 2) a partial compensation with GABAAR isoforms that possess physiological properties different from those of the otherwise predominant α1ßγ GABAARs.

[Expression of HSP27 in CA1 area of hippocampus in temporal lobe epilepsy model].

OBJECTIVE: To explore the expression of heat shock protein 27 (HSP27) in the CA1 area of hippocampus in temporal lobe epilepsy (TLE) so as to elucidate the relationship between HSP27 and epileptogenesis of TLE. METHODS: The model of TLE was induced by lithium-pilocarpine in the experiment group. And the rats were further divided into the STLE and non-STLE groups based upon the absence or presence of recurrent spontaneous seizure in the next 30 days. Total protein fractions from CA1 area of hippocampus were successively obtained through tissue homogenates abstraction. The HSP27 expression in the CA1 area of hippocamp from three groups was semi-quantitatively analyzed by Western blot. And the expression of HSP27 in CA1 area was detected by pre-embedding immunogold electron microscopy. RESULTS: Expression of HSP27 in the hippocampus CA1 area as detected by Western blot was in accord with that by immunogold electron microscopy. Relative optical density values were 0.912 ± 0.011, 0.431 ± 0.011 and 0.428 ± 0.010 respectively. And gold particles were 50.0 ± 4.2, 23.0 ± 2.8 and 20.0 ± 2.3 respectively. The expression of HSP27 was the highest in the hippocampus CA1 area of the STLE group. There was statistical significance as compared with the non-STLE and normal groups (P = 0.0001). The non-STLE group was higher than the normal group. But there was no significant difference as compared with the normal group (P = 0.63). CONCLUSIONS: HSP27 in the hippocampus CA1 area may participate in the epileptogenesis of TLE.

The cavity dispersion noncoaxiality effects on broadband few-cycle pulse generation in Ti:sapphire laser.

The cavity dispersion noncoaxiality (CDN) effects on broadband few-cycle pulse generation of a Kerr-lens mode-locked Ti:sapphire laser is investigated theoretically and experimentally. It is found that the influence of CDN is comparable with that of self-focusing and self-phase-modulation in the frequency-dependent mode size (FDMS) effects. Spectra extending from 680 nm to 1020 nm with pulse duration shorter than three optical cycles are favorably generated under the minimum CDN in the vicinity of the coaxial point of the sub-cavity.

[Proteomic screening of postsynaptic density proteins related with temporal lobe epilepsy].

OBJECTIVE: To explore the postsynaptic density (PSD) proteins related with the development of temporal lobe epilepsy (TLE). METHODS: Five SD rats were injected intra-peritoneally with lithium chloride and then pilocarpine twice to establish epilepsy models. At last 24 rats developed TLE, and 12 developed non-TLE. Then rats underwent intraperitoneal injection of normal saline (Norm group). Thirty days after the appearance of epilepticus the rats were decapitated with their brains taken out. The PSD proteins were extracted and purified by using sucrose gradient centrifugation and membrane sequence extraction, isolated by using two-dimensional gel electrophoresis. PDQuest software was used to screen the specifically and differentially expressed protein spots. Partial differentially expressed PSD protein spots were selected and identified by MALDI-TOF-MS. Several identified proteins were detected in the PSD fraction by Western blotting. RESULTS: Compared with the non-TLE and Norm groups, there were 40 differential protein spots in the TLE group. The expression levels of heat shock protein-27 (HSP-27), fructose-bisphosphate aldolase A (FBA), creatine kinase (CK), thyroid receptor-interacting protein 6 (TRIP6), myelin basic protein S (MBP), and LIM domain were up-regulated, but the expression levels of tubulin, actin, internexin-alpha, peptidyl-prolyl cis-trans isomerase (PPIase), sorting nexin 3 (SNX3), aconitate hydratase (ACO), glyceradehydea-3-phosphate dehydrogenase (GADPH), and succinate-coenzyme A ligase (SCOAL) were down-regulated in the TLE group. The HSP27, tubulin-alpha, and SNX3 were in the PSD gels were immunostaining positive in the 3 groups. CONCLUSION: The differential expression of PSD proteins in TLE may be due to injury induced neural plasticity. But the degree thereof may contribute to the development of TLE. These identified proteins can be regarded as important candidates for or against the development of TLE.

The study of Golgi apparatus in Alzheimer's disease.

Alzheimer's disease is an irreversible, progressive neurodegenerative disorder leading invariably to death, usually within 7-10 years after diagnosis and is the leading cause of dementia in the elderly. Not only is Alzheimer's disease a tragic disease in which people suffer from neurodegeneration in the years to come, it also becomes an incredible burden on the public health system. However, there is currently no effective treatment to halt the progression or prevent the onset of Alzheimer's disease. This is partly due to the fact that the complex pathophysiology of Alzheimer's disease is not yet completely understood. Recently, Golgi apparatus is found to play an important role in Alzheimer's disease. In this review, we discuss the changes of Golgi apparatus during clinical progression and pathological development of Alzheimer's disease. First, changes of Golgi apparatus size in Alzheimer's disease are summarized. We then address the role of Golgi apparatus in the neuropathology of Alzheimer's disease. Finally, the role of Golgi apparatus in the pathogenesis of Alzheimer's disease is discussed. Understanding the contribution of Golgi apparatus dysfunction to Alzheimer's disease and its pathophysiological basis will significantly impact our ability to develop more effective therapies for Alzheimer's disease.

Aetiology of epilepsy in surgically treated patients in China.

The aim of this retrospective, multicenter clinical study was to evaluate the aetiology of epilepsy in surgically treated patients in China. The detailed clinical records of all intractable partial epilepsy (IPE) were reviewed in five tertiary referral centres from June 1991 to June 2000. 1650 patients (927 males, 723 females) were recruited. 41.4% had aetiological factors, including the histories of major brain trauma (20.9%), febrile seizure (6.5%), meningitis (5.4%), encephalitis (5.0%), prenatal distress (2.1%), birth trauma (0.8%) and family history of seizure (0.7%). The pathological lesions were divided into eight groups according to the nature of the lesion: scar (19.2%), vascular malformations (VM) (17.7%), hippocampal sclerosis (HS) (16.2%), tumours (15.0%), gliosis (12.1%), neuronal migration disorders (NMDs) (7.4%), intracranial infection (4.5%), and other lesions (7.9%). In conclusion, effective management of these aetiological factors and pathological lesions may be essential to deal with IPE. Scar, HS, VM, NMDs are the most likely consequences of antecedent morbid events.

Betel nut indulgence as a cause of epilepsy.

We report a 29-year-old man with secondarily generalised seizure and cardiac impairment. He was an indulger in betel nuts without other aetiological or precipitating factors, and no abnormality on neuroradiologic investigation. The occurrence of his seizures related to an overdose of betel nuts. It is clinically important to know that epilepsy may be induced by betel nut chewing.

Surgical treatment of thoracic esophageal carcinoma: report of 326 cases.

OBJECTIVE: To review our experience in surgical treatment of 326 cases of thoracic esophageal carcinoma. METHODS: The clinical data of 326 patients with thoracic esophageal carcinoma from January 1990 to January 2001 were analyzed retrospectively. Among the 326 patients, the lesions of 32 patients were identified in the upper thoracic segment of the esophagus, and were found in the middle segment in 213 cases with the left 81 cases having lesions in the lower segment. Left cervical esophagogastrostomy was performed through triple incision (left cervical, right thoracic and abdominal) in 79 cases. Esophagocolostomy through triple incision was performed in 5 cases. Another 156 patients received left cervical esophagogastrostomy through two incisions (left cervical and left thoracic). Supra-aorticarch esophagogastrostomy through left posterola- teral thoracotomy was performed in 53 cases, and sub-arch esophagogastrostomy through left posterolateral thoracotomy in 33 cases. RESULTS: The post-operative mortality was 1.23% (4/326), with a five-year survival rate of 35.3%. CONCLUSION: Subtotal esophagectomy combined with thorough lymph node dissection can be the first choice for thoracic esophageal carcinoma to improve the postoperative survival rate and the quality-of life-of the patients.