Rupture process of the 2021 M7.4 Maduo earthquake and implication for deformation mode of the Songpan-Ganzi terrane in Tibetan Plateau.

The deformation mode of the Tibetan Plateau is of crucial importance for understanding its construction and extrusion processes, as well as for the assessment of regional earthquake potential. Block motion and viscous flow models have been proposed to describe the deformation field but are not fully supported by modern geophysical observations. The 2021 Mw 7.4 Maduo earthquake, which occurred inside the Songpan-Ganzi terrane (SGT) in central-east Tibet, provides a chance to evaluate the associated deformation mode of the region. We conduct a joint inversion for this earthquake and resolve a bilateral rupture process, which is characterized by super- and subshear rupture velocities, respectively. We interpret this distinct rupture behavior to be the result of the respective slip concentration depths of the two ruptured segments. We analyze geological, seismic, and geodetic evidence and find that the SGT upper crust shows distributed shear deformation and distinct transverse anisotropy, which are associated with folded structures originating from compression of the paleo-Tethys ocean accretional prism realigned by following shear deformation. The SGT receives lateral shear loading from its NS boundary and accommodates a right-step sinistral motion across the terrane boundary faults. The unique tectonic setting of the SGT defines locations and behaviors of internal faulting and strong earthquakes such as the 2021 Maduo earthquake, with the latter occurring on slow-moving faults at intervals of several thousands of years.

The evolution of preexisting primary immune thrombocytopenia after COVID-19 onset: A nationally representative, prospective, multicentre, observational study.

The symptoms in patients with primary immune thrombocytopenia (ITP) after COVID-19 onset remain largely unclear. The aim of this study was to describe the platelet count fluctuations in ITP patients following the diagnosis of COVID-19. A prospective multicentre observational study was conducted from December 15th, 2022, to January 31st, 2023 in 39 general hospitals across China. Patients with preexisting primary ITP who were newly diagnosed with COVID-19 were enrolled. A total of 1216 ITP patients with newly-diagnosed COVID-19 were enrolled. 375 (30.8%) patients experienced ITP exacerbation within eight weeks after the diagnosis of COVID-19, and most exacerbation (266/375, 70.9%) developed in the first two weeks. Immunosuppressive therapy for ITP and severe/critical COVID-19 infection were independent variables associated with ITP exacerbation. Overall the platelet count had a transient increasing trend, and the platelet peak value occurred at two weeks after COVID-19 infection. Then, the platelet count decreased to the baseline level in the following weeks. The platelet count had a transient increasing trend in ITP patients following the diagnosis of COVID-19. ITP exacerbation only occurred in less than one-third of ITP patients. Nonimmunosuppressive therapy may have an advantage to prevent ITP exacerbation during COVID-19.

Astaxanthin Ameliorates Skeletal Muscle Atrophy in Mice With Cancer Cachexia.

Astaxanthin (AST) is a natural marine carotenoid with a variety of biological activities. This study aimed to demonstrate the possible mechanisms by which AST improves skeletal muscle atrophy in cancer cachexia. In this study, the effects of different doses of AST (30 mg/kg b.w., 60 mg/kg b.w. and 120 mg/kg b.w.) on skeletal muscle functions were explored in mice with cancer cachexia. The results showed that AST (30, 60 and 120 mg/kg b.w.) could effectively protect cachexia mice from body weight and skeletal muscle loss. AST dose-dependently ameliorated the decrease in myofibres cross-sectional area and increased the expression of myosin heavy chain (MHC). AST treatment decreased both the serum and muscle level of IL-6 but not TNF-α in C26 tumor-bearing cachexia mice. Moreover, AST alleviated skeletal muscle atrophy by decreasing the expression of two muscle-specific E3 ligases MAFBx and MuRF-1. AST improved mitochondrial function by downregulating the levels of muscle Fis1, LC3B and Bax, upregulating the levels of muscle Mfn2 and Bcl-2. In conclusion, our study show that AST might be expected to be a nutritional supplement for cancer cachexia patients.

Pioglitazone reduces serum ketone bodies in sodium-glucose cotransporter-2 inhibitor-treated non-obese type 2 diabetes: A single-centre, randomized, crossover trial.

AIM: To examine the effects of the thiazolidinedione (TZD) pioglitazone on reducing ketone bodies in non-obese patients with T2DM treated with the sodium-glucose cotransporter-2 (SGLT2) inhibitor canagliflozin. METHODS: Crossover trials with two periods, each treatment period lasting 4 weeks, with a 4-week washout period, were conducted. Participants were randomly assigned in a 1:1 ratio to receive pioglitazone combined with canagliflozin (PIOG + CANA group) versus canagliflozin monotherapy (CANA group). The primary outcome was change (Δ) in ß-hydroxybutyric acid (ß-HBA) before and after the CANA or PIOG + CANA treatments. The secondary outcomes were Δchanges in serum acetoacetate and acetone, the rate of conversion into urinary ketones, and Δchanges in factors related to SGLT2 inhibitor-induced ketone body production including non-esterified fatty acids (NEFAs), glucagon, glucagon to insulin ratio, and noradrenaline (NA). Analyses were performed in accordance with the intention-to-treat principle. RESULTS: Twenty-five patients with a mean age of 49 ± 7.97 years and a body mass index of 25.35 ± 2.22 kg/m2 were included. One patient discontinued the study during the washout period. Analyses revealed a significant increase in the levels of serum ketone bodies and an elevation in the rate of conversion into urinary ketones after both interventions. However, differernces in levels of ketone bodies (except for acetoacetate) in the PIOG + CANA group were significantly smaller than in the CANA group (219.84 ± 80.21 µmol/L vs. 317.69 ± 83.07 µmol/L, p < 0.001 in ß-HBA; 8.98 ± 4.17 µmol/L vs. 12.29 ± 5.27 µmol/L, p = 0.018 in acetone). NEFA, glucagon, glucagon to insulin ratio, and NA were also significantly increased after both CANA and PIOG + CANA treatments; while only NEFAs demonstrated a significant difference between the two groups. Correlation analyses revealed a significant association between the difference in Δchanges in serum NEFA levels with the differences in Δchanges in ketones of ß-HBA and acetoacetate. CONCLUSION: Supplementation of pioglitazone could alleviate canagliflozin-induced ketone bodies. This benefit may be closely associated with decreased substrate NEFAs rather than other factors including glucagon, fasting insulin and NA.

A novel mutation in hERG gene associated with azithromycin-induced acquired long QT syndrome.

BACKGROUND: Mutations in human ether-à-go-go-related gene (hERG) potassium channels are closely associated with long QT syndrome (LQTS). Previous studies have demonstrated that macrolide antibiotics increase the risk of cardiovascular diseases. To date, the mechanisms underlying acquired LQTS remain elusive. METHODS: A novel hERG mutation I1025N was identified in an azithromycin-treated patient with acquired long QT syndrome via Sanger sequencing. The mutant I1025N plasmid was transfected into HEK-293 cells, which were subsequently incubated with azithromycin. The effect of azithromycin and mutant I1025N on the hERG channel was evaluated via western blot, immunofluorescence, and electrophysiology techniques. RESULTS: The protein expression of the mature hERG protein was down-regulated, whereas that of the immature hERG protein was up-regulated in mutant I1025N HEK-293 cells. Azithromycin administration resulted in a negative effect on the maturation of the hERG protein. Additionally, the I1025N mutation exerted an inhibitory effect on hERG channel current. Moreover, azithromycin inhibited hERG channel current in a concentration-dependent manner. The I1025N mutation and azithromycin synergistically decreased hERG channel expression and hERG current. However, the I1025N mutation and azithromycin did not alter channel gating dynamics. CONCLUSIONS: These findings suggest that hERG gene mutations might be involved in the genetic susceptibility mechanism underlying acquired LQTS induced by azithromycin.

Isorhamnetin ameliorates cisplatin-induced acute kidney injury in mice by activating SLPI-mediated anti-inflammatory effect in macrophage.

OBJECTIVE: Isorhamnetin (IH) has been reported to have significant anti-inflammatory effects in various diseases, but its role and mechanism in AKI remain unclear. This study aimed to explore the potential role and mechanism of isorhamnetin in inhibiting macrophage related inflammation and improving AKI injury. METHODS: We established an AKI mouse model by intraperitoneal injection of cisplatin in vivo, and constructed an inflammatory cell model by stimulating RAW264.7 cells with LPS. Creatinine and urea nitrogen were measured to evaluate the changes of renal function in AKI mice. The changes of renal pathological structure were observed by H&E staining. The inflammatory factor-related proteins and RNA expression levels were detected by Western blot and real time PCR. RESULTS: Isorhamnetin protected the kidney from cisplatin induced AKI and significantly inhibited the mRNA and protein levels of inflammatory cytokines (IL-1ß, IL-6, and TNF-α) both in AKI kidney and LPS-stimulated RAW264.7 cells. Interestingly, the data also demonstrated that isorhamnetin significantly upregulated the expression of secretory leukocyte peptidase inhibitor (SLPI), an anti-inflammatory factor, in AKI kidney and LPS-stimulated macrophages, as well as inhibited the M1 macrophage and activated M2 macrophage in vitro. Blocking of SLPI by siRNA activated Mincle-associated inflammatory signaling in macrophages, and the inhibitory effect of isorhamnetin on inflammation was significantly attenuated. CONCLUSION: Isorhamnetin inhibits macrophage inflammation and protects kidney in AKI may be related to downregulating Mincle/Syk/NF-κB-maintained macrophage phenotype by activating SLPI.

Deubiquitination module is critical for oxidative stress response and biofilm formation in Candida glabrata.

Candidiasis is one of the most important fungal diseases and generally refers to diseases of the skin or mucosal tissues caused by Candida species. Candida glabrata is an opportunistic human fungal pathogen. Infection with C. glabrata has significantly increased due to innate antifungal drug tolerance and the ability to adhere to mucocutaneous surfaces. Spt-Ada-Gcn5 acetyltransferase complex contains two different post-translational modifications, histone acetylation (HAT) module and deubiquitination (DUB) module, which are decisive in gene regulation and highly conserved in eukaryotes. Previous research in our laboratory found that the HAT module ADA2 could regulate C. glabrata oxidative stress tolerance, drug tolerance, cell wall integrity, and virulence. However, the roles of the DUB module that is comprised of UBP8, SGF11, SGF73, and SUS1 genes in those phenotypes are not yet understood. In this study, we found that DUB module genes UBP8, SGF11, and SUS1, but not SGF73 positively regulate histone H2B DUB. Furthermore, ubp8, sgf11, and sus1 mutants exhibited decreased biofilm formation and sensitivity to cell wall-perturbing agent sodium dodecyl sulfate and antifungal drug amphotericin B. In addition, the sgf73 mutant showed increased biofilm formation but was susceptible to oxidative stresses, antifungal drugs, and cell wall perturbing agents. The ubp8, sgf11, and sus1 mutants showed marginal hypovirulence, whereas the sgf73 mutant exhibited virulence similar to the wild type in a murine systemic infection model. In conclusion, the C. glabrata DUB module plays distinct roles in H2B ubiquitination, oxidative stress response, biofilm formation, cell wall integrity, and drug tolerance, but exhibits minor roles in virulence.

In this study, we found that the deubiquitination (DUB) module of the Spt-Ada-Gcn5 acetyltransferase complex is involved in H2B DUB, oxidative stress response, biofilm formation, cell wall integrity, and drug tolerance in the human fungal pathogen Candida glabrata. The multiple functions controlled by the DUB module exhibit conserved and divergent functions between Saccharomyces cerevisiae, C. albicans, and C. glabrata.

Deciphering biochar compost co-application impact on microbial communities mediating carbon and nitrogen transformation across different stages of corn development.

Under current climatic conditions, developing eco-friendly and climate-smart fertilizers has become increasingly important.The co-application of biochar and compost on agricultural soils has received considerable attention recently.Unfortunately, little is known about its effects on specific microbial taxa involved in carbon and nitrogen transformation in the soil.Herein, we report the efficacy of applying biochar-based amendments on soil physicochemical indices, enzymatic activity, functional genes, bacterial community, and their network patterns in corn rhizosphere at seedling (SS), flowering (FS), and maturity (MS) stages.The applied treatments were: compost alone (COM), biochar alone (BIOC), composted biochar (CMB), fortified compost (CMWB), and the control (no fertilizer (CNTRL).The non-metric multidimensional scaling (NMDS) indicated total nitrogen (TN), pH, NO3--N, urease, protease, and microbial biomass C (MBC) as the dominant environmental factors driving soil bacteria in this study.The dominant N mediating genes belonged to nitrate reductase (narG) and nitronate monooxygenase (amo), while beta-galactosidase, catalase, and alpha-amylase were the dominant genes observed relating to C cycling.Interestingly, the abundance of these genes was higher in COM, CMWB, and CMB compared with the CNTRL and BIOC treatments.The bacteria network properties of CWMB and CMB indicated robust niche overlap associated with high cross-feeding between bacterial communities compared to other treatments.Path and stepwise regression analyses revealed norank_Reyranellaceae and Sphingopyxis in CMWB as the major bacterial genera and the major predictive indices mediating soil organic C (SOC), NH4+-N, NO3--N, and TN transformation.Overall, biochar with compost amendments improved soil nutrient conditions, regulated the composition of the bacterial community, and benefited C/N cycling in the soil ecosystem.

Efficacy of omega-3 fatty acids for hospitalized COVID-19 patients: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND AND OBJECTIVES: Emerging expert consensuses and guidelines recommend that omega-3 fatty acids may have anti-inflammatory effects in hospitalized patients with coronavirus disease (COVID-19). However, these recommendations are based on pathophysiological studies of inflammation rather than direct clinical evidence. We conducted this systematic review and meta-analysis to evaluate the efficacy of omega-3 fatty acid supplementation in hospitalized patients with COVID-19. METHODS AND STUDY DESIGN: We retrieved literature from PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), WANFANG, Chinese Biomedical Literature Database, and Cochrane Library databases up to May 1, 2023. Data from studies comparing omega-3 fatty acids with a placebo or other pharmaceutical nutrients were analyzed. RESULTS: Of 3032 records, 42 full-text articles were reviewed, five eligible studies were identified, and one study was found in the references. In total of six studies involving 273 patients were included, pooled, and analyzed. Compared to the control group, omega-3 fatty acid intervention reduced the overall mortality of hospitalized patients with COVID-19 (RR=0.76; 95% CI, [0.61, 0.93]; p=0.010). No serious or unexpected drug-related adverse events were observed. No statistical significance was observed in inflammatory markers such as CRP (MD=-9.69; 95% CI, [-22.52, 3.15]; p=0.14; I2=97%) and IL-6; however, the neutrophil/lymphocyte ratio was significantly lower in the omega-3 FAs group on day 7 of intervention (p < 0.001). CONCLUSIONS: Omega-3 fatty acid administration may be associated with reduced mortality in hospitalized patients with COVID-19. Given the small sample size of enrolled studies, more rigorous and large-scale trials are urgently needed in the future to verify its efficacy.

Enteral glutamine supplements for patients with severe burns: A systematic review and meta-analysis.

PURPOSE: Our previous study in 2009 concluded that glutamine may shorten the length of hospital stay (LOS) in patients with severe burns. Recent large-scale studies have suggested a decline in the effectiveness of glutamine in treating patients with severe burns over the last decade. Therefore, we conducted this systematic review and meta-analysis to update the status of glutamine uses in patients with severe burns. METHODS: We retrieved related literature prior to December 2022 from the PubMed, Web of Science, Cochrane Library, Embase, SinoMed, Wanfang, and CNKI databases. Terms such as glutamine, enteral and burn were linked for searching. Adults patients with severe burns were included and non-randomized controlled trials were excluded. Data from studies that compared enteral glutamine for severe burns with a control group were extracted. The primary outcomes of mortality and infectious morbidities were pooled and analyzed. The modified Jadad scale and Cochrane collaboration's tool were used to assess the risk of bias in RCTs, and the Review Manager 5.4 was used to pool and analyze the data. RESULTS: Six randomized controlled trials involving 1398 patients were included in the analysis. There were no significant differences in overall mortality (risk ratio (RR) = 0.37; 95% confidence interval (CI): 0.06 - 2.37; p = 0.300) or infectious morbidities (RR = 0.73; 95% CI: 0.41 - 1.31; p = 0.290). The incidence of multiple organ dysfunction syndrome was similar between the 2 groups (RR = 0.27; 95% CI: 0.03 - 2.24; p = 0.220). The LOS (mean difference (MD) = -8.97; 95% CI: -15.22 to -2.71; p = 0.005) and LOS/total burn surface area (MD = -0.27; 95% CI: -0.54 to 0.00; p = 0.050) decreased in the enteral glutamine group. The incidence of wound infection was significantly reduced (RR = 0.42; 95% CI: 0.16 - 1.06; p = 0.070). CONCLUSION: Compared to the control group, enteral glutamine administration may not improve the mortality, although it may be associated with a shorter LOS, a lower LOS/total burn surface area ratio, and may reduce the risk of wound infection in patients with severe burns.

SUMOylation regulates Rb hyperphosphorylation and inactivation in uveal melanoma.

Small ubiquitin-like modifier (SUMO)ylation is one of the posttranslational modifications and is implicated in many tumor types. Modulation of SUMOylation can affect tumor progression, but the underlying mechanisms remain unclear. Here, we show that, for the first time, in uveal melanoma (UM), the most common intraocular malignancy in adults, global SUMOylation is upregulated and participates in tumor growth. Inhibition of SUMOylation in UM is sufficient to reduce tumor growth both in vitro and in vivo. Furthermore, we found that retinoblastoma protein (Rb) is a target protein and a critical downstream effector of the upregulated SUMOylation activity in UM. Increased SUMOylation of the Rb protein leads to its hyperphosphorylation and inactivation in UM cells, promoting UM cell proliferation. In summary, our results provide novel insight into the mechanism underlying SUMOylation-regulated tumor growth in UM.

Emerging Function of Ecotype-Specific Splicing in the Recruitment of Commensal Microbiome.

In recent years, host-microbiome interactions in both animals and plants has emerged as a novel research area for studying the relationship between host organisms and their commensal microbial communities. The fitness advantages of this mutualistic interaction can be found in both plant hosts and their associated microbiome, however, the driving forces mediating this beneficial interaction are poorly understood. Alternative splicing (AS), a pivotal post-transcriptional mechanism, has been demonstrated to play a crucial role in plant development and stress responses among diverse plant ecotypes. This natural variation of plants also has an impact on their commensal microbiome. In this article, we review the current progress of plant natural variation on their microbiome community, and discuss knowledge gaps between AS regulation of plants in response to their intimately related microbiota. Through the impact of this article, an avenue could be established to study the biological mechanism of naturally varied splicing isoforms on plant-associated microbiome assembly.

Sodium alginate/collagen hydrogel loaded with human umbilical cord mesenchymal stem cells promotes wound healing and skin remodeling.

Stem cell transplantation is a promising therapy for wound healing, but the low retention and survival of transplanted stem cells limit their application. Injectable hydrogels exert beneficial effects in skin tissue engineering. In this study, an injectable hydrogel composed of sodium alginate (SA) and collagen type I (Col) was synthesized as a tissue scaffold to improve the efficacy of stem cells in a full-thickness excision wound model. Our results showed that SA/Col hydrogel was injectable, biodegradable, and exhibited low immunogenicity, which could promote the retention and survival of hUC-MSCs in vivo. SA/Col loaded with hUC-MSCs showed reduced wound size (p < 0.05). Histological and immunofluorescence results confirmed that SA/Col loaded with hUC-MSCs significantly promoted the formation of granulation, enhanced collagen deposition and angiogenesis, increased VEGF and TGF-ß1 expression (p < 0.05), and mitigated inflammation evidenced by lower production of TNF-α and IL-1ß and higher release of IL-4 and IL-10 (p < 0.05). Furthermore, SA/Col loaded with hUC-MSCs significantly lowered the expression of NLRP3 inflammasome-related proteins (p < 0.05). Taken together, our results suggest that SA/Col loaded with hUC-MSCs promotes skin wound healing via partly inhibiting NLRP3 pathway, which has potential to the treatment of skin wounds.

Aging and age-related diseases: from mechanisms to therapeutic strategies.

Aging is a physiological process mediated by numerous biological and genetic pathways, which are directly linked to lifespan and are a driving force for all age-related diseases. Human life expectancy has greatly increased in the past few decades, but this has not been accompanied by a similar increase in their healthspan. At present, research on aging biology has focused on elucidating the biochemical and genetic pathways that contribute to aging over time. Several aging mechanisms have been identified, primarily including genomic instability, telomere shortening, and cellular senescence. Aging is a driving factor of various age-related diseases, including neurodegenerative diseases, cardiovascular diseases, cancer, immune system disorders, and musculoskeletal disorders. Efforts to find drugs that improve the healthspan by targeting the pathogenesis of aging have now become a hot topic in this field. In the present review, the status of aging research and the development of potential drugs for aging-related diseases, such as metformin, rapamycin, resveratrol, senolytics, as well as caloric restriction, are summarized. The feasibility, side effects, and future potential of these treatments are also discussed, which will provide a basis to develop novel anti-aging therapeutics for improving the healthspan and preventing aging-related diseases.

Comparison of the biological characteristics of umbilical cord mesenchymal stem cells derived from the human heterosexual twins.

Mesenchymal stromal/stem cells (MSCs) are attracting more and more attention due to their tissue regenerative properties and immunomodulatory functions. MSCs may be the most acceptable, safe, and effective source for allogeneic cell therapy, and have been used in medical treatment. However, the similarities and differences between umbilical cord-derived MSCs (UC-MSCs) of heterosexual twins remain poorly understood. In this study, we compared the biological characteristics of UC-MSCs of heterosexual twins in vitro. We found that male fetal UC-MSCs and female fetal UC-MSCs share a similar phenotype and multi-lineage differentiation potential, and male fetal UC-MSCs show a significantly higher proliferation and adipogenic ability than female fetal UC-MSCs. UC-MSCs from heterosexual twins showed significant differences in the expression levels of NANOG, OCT4, TERT, and SOX2. In addition, male MSCs are more potent in the expression of inflammatory cytokines to lipopolysaccharide (LPS)-induced inflammation. In future clinical applications using MSCs for inflammation-related diseases, these biological characteristics differences with different genders will guide our clinical methods.

EGFRvIII epigenetically regulates ARHI to promote glioma cell proliferation and migration.

Epidermal growth factor receptor variant III (EGFRvIII) is a tumor-specific mutation widely expressed in glioma. However, its role and molecular mechanism in glioma have not been completely elucidated. Immunohistochemistry analyses of EGFRvIII, enhancer of zeste homolog 2 (EZH2) and aplysia ras homolog I (ARHI) were performed in tumor tissues from patients with glioma. Regulatory mechanisms among EGFRvIII, EZH2 and ARHI were examined by western blot and chromatin immunoprecipitation (ChIP). Cell proliferation and migration of glioma cells were examined. EGFRvIII and EZH2 expression were upregulated, while ARHI was downregulated in glioma tissues. EZH2 knockdown increased ARHI expression in glioma cell lines. ChIP assay suggested that EZH2 was enriched in the ARHI promoter. Furthermore, ectopic expression of EGFRvIII upregulated EZH2, suppressed ARHI expression, and promoted glioma cell proliferation. Additionally, treatment with 3-deazaneplanocin A (DZNep, an inhibitor of EZH2) inhibited expression of EZH2, increased protein level of ARHI, and partially abrogated the promoting effects of ARHI knockdown on glioma cell proliferation and migration. In summary, EGFRvIII-mediated epigenetic suppression of ARHI promoted glioma cell proliferation and migration via upregulating EZH2.

Hard Palate Mucoperiosteal Transplantation for Defects of the Upper Eyelid: A Pilot Study and Evaluation.

PURPOSE: To use hard palate mucoperiosteum to reconstruct the upper eyelid wisely and to evaluate its function and outcome. METHODS: In this case series, medial or lateral defects of the upper eyelid were reconstructed with a hard palate mucoperiosteum graft and a bandage contact lens to protect the cornea. Slit-lamp examinations, in vivo confocal microscopy, patient surveys, and pathologic examinations were performed as evaluations. RESULTS: Seven patients were included in this study. The average follow-up time was 21.9 months. Postoperatively, all patients maintained their preoperative corneal transparency, and the best-corrected visual acuities remained stable. Postoperative corneal examination by in vivo confocal microscopy was similar to the normal contralateral eye in all cases. All hard palate mucoperiosteal grafts merged smoothly with the normal tarsoconjunctiva. The mean ratio of the graft length to the upper eyelid decreased from 48.6% during the operation to 32.2% during the follow-up; the average shrinkage rate was 16.3% ± 7.1%. Both in vivo confocal microscopy and the pathologic examinations showed that stratified squamous epithelium comprised the main part of the hard palate graft. All patients could blink normally and had a relatively normal appearance. All patients were satisfied with the overall outcome of this therapy. Main complications included loss of eyelashes (100%), abnormal curvature of the eyelid (28.5%), mild lagophthalmos (14.3%), trichiasis (14.3%), and slight exfoliation of the corneal epithelium (42.8%). CONCLUSIONS: not only effectively reconstructs the upper eyelid but also provides protection for the cornea.

En échelon and orthogonal fault ruptures of the 11 April 2012 great intraplate earthquakes.

The Indo-Australian plate is undergoing distributed internal deformation caused by the lateral transition along its northern boundary--from an environment of continental collision to an island arc subduction zone. On 11 April 2012, one of the largest strike-slip earthquakes ever recorded (seismic moment magnitude M(w) 8.7) occurred about 100-200 kilometres southwest of the Sumatra subduction zone. Occurrence of great intraplate strike-slip faulting located seaward of a subduction zone is unusual. It results from northwest-southeast compression within the plate caused by the India-Eurasia continental collision to the northwest, together with northeast-southwest extension associated with slab pull stresses as the plate underthrusts Sumatra to the northeast. Here we use seismic wave analyses to reveal that the 11 April 2012 event had an extraordinarily complex four-fault rupture lasting about 160 seconds, and was followed approximately two hours later by a great (M(w) 8.2) aftershock. The mainshock rupture initially expanded bilaterally with large slip (20-30 metres) on a right-lateral strike-slip fault trending west-northwest to east-southeast (WNW-ESE), and then bilateral rupture was triggered on an orthogonal left-lateral strike-slip fault trending north-northeast to south-southwest (NNE-SSW) that crosses the first fault. This was followed by westward rupture on a second WNW-ESE strike-slip fault offset about 150 kilometres towards the southwest from the first fault. Finally, rupture was triggered on another en échelon WNW-ESE fault about 330 kilometres west of the epicentre crossing the Ninetyeast ridge. The great aftershock, with an epicentre located 185 kilometres to the SSW of the mainshock epicentre, ruptured bilaterally on a NNE-SSW fault. The complex faulting limits our resolution of the slip distribution. These great ruptures on a lattice of strike-slip faults that extend through the crust and a further 30-40 kilometres into the upper mantle represent large lithospheric deformation that may eventually lead to a localized boundary between the Indian and Australian plates.

The prescriptions from Shenghui soup enhanced neurite growth and GAP-43 expression level in PC12 cells.

BACKGROUND: Shenghui soup is a traditional Chinese herbal medicine used in clinic for the treatment of forgetfulness. In order to understanding the prescription principle, the effects of "tonifying qi and strengthening spleen" group (TQSS) including Poria cocos (Schw.) Wolf. and Panax ginseng C.A.Mey and "eliminating phlegm and strengthening intelligence" group (EPSI) composed of Polygala tenuifolia Willd., Acorus calamus L. and Sinapis alba L from the herb complex on neurite growth in PC12 cells, two disassembled prescriptions derived from Shenghui soup and their molecular mechanisms were investigated. METHODS: Firstly, CCK-8 kit was used to detect the impact of the two prescriptions on PC12 cell viability; and Flow cytometry was performed to measure the cell apoptosis when PC12 cells were treated with these drugs. Secondly, the effect of the two prescriptions on the differentiation of PC12 cells was observed. Finally, the mRNA and protein expression levels of GAP-43 were analyzed by RT-PCR and western blot, respectively. RESULTS: "Tonifying qi and strengthening spleen" prescription decreased cell viability in a dose-dependent manner, but had no significant effect on cell apoptosis. Meanwhile, it could improve neurite growth and elevate the mRNA and protein expression level of GAP-43. "Eliminating phlegm and strengthening intelligence" prescription also exerted the similar effects on cell viability and apoptosis. Furthermore, it could also enhance cell neurite growth, with a higher expression level of GAP-43 mRNA and protein. CONCLUSION: "Tonifying qi and strengthening spleen" and "eliminating phlegm and strengthening intelligence" prescriptions from Shenghui soup have a positive effect on neurite growth. Their effects are related to the up-regulating expression of GAP-43.