Recurrent hematuria involving urinary system with Klippel-Trenaunay syndrome: A case report.

RATIONALE: Klippel-Trenaunay syndrome (KTS) is a rare congenital venous malformation, it had been found to be caused by mutations of the phosphatidylinositol 4, 5-diphosphate 3-kinase catalytic subunit alpha (PIK3CA) gene. Currently KTS is defined as a triad of skin wine pigmented spots, varicose veins and malformations of the lower extremities, and hypertrophy of bone and soft tissue, involving urinary system up to 6% to 30%. When the urinary system is involved, KTS is often presented as painless massive gross hematuria. PATIENT CONCERNS: This article describes a woman who was hospitalized with painless massive gross hematuria. Physical examination revealed significant hypertrophy of the right lower limb with varicose veins, port-wine stains in the skin, and right perineal hemangiomatous changes with swelling. The patient was admitted to hospital 4 times for repeated hematuria and infection. DIAGNOSES: By physical examination, CT urography, ureteroscopy and cystoscopy, the patient was diagnosed to have Klippel-Trenaunay syndrome, involving the urinary system. INTERVENTIONS: The patient hematuria improved after multiple indwelling D-J tubes and anti-inflammatory treatment. OUTCOMES: The final symptoms of hematuria improved significantly, follow-up so far has not recurred. LESSONS: This case presents the possibility of painless gross hematuria with KTS. Most of patients can be improved by conservative treatment. Cystoscopic laser therapy is the preferred treatment for poor bleeding control. Cystectomy and nephrectomy should be considered when life-threatening.

Quercetin improves cerebral ischemia/reperfusion injury by promoting microglia/macrophages M2 polarization via regulating PI3K/Akt/NF-κB signaling pathway.

The modulation of microglial polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype shows promise as a therapeutic strategy for ischemic stroke. Quercetin, a natural flavonoid abundant in various plants, possesses anti-inflammatory, anti-apoptotic, and antioxidant properties. Nevertheless, its effect and underlying mechanism on microglia/macrophages M1/M2 polarization in the treatment of cerebral ischemia/reperfusion injury (CI/RI) remain poorly explored. In the current study, we observed that quercetin ameliorated neurological deficits, reduced infarct volume, decreased the number of M1 microglia/macrophages (CD16/32+/Iba1+), and enhanced the number of M2 microglia/macrophages (CD206+/Iba1+) after establishing the CI/RI model in rats. Subsequent in vivo and in vitro experiments indicated that quercetin downregulated M1 markers (CD86, iNOS, TNF-α, IL-1ß, and IL-6) and upregulated M2 markers (CD206, Arg-1, IL-10, and TGF-ß). Network pharmacology analysis and molecular docking revealed that the PI3K/Akt/NF-κB signaling pathway emerged as the core pathway. Western blot confirmed that quercetin upregulated the phosphorylation of PI3K and Akt, while alleviating the phosphorylation of IκBα and NF-κB both in vivo and in vitro. However, the PI3K inhibitor LY294002 reversed the effects of quercetin on M2 polarization and the expression of key proteins in the PI3K/Akt/NF-κB pathway in primary microglia after oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. Collectively, our findings demonstrate that quercetin facilitates microglia/macrophages M2 polarization by modulating the PI3K/Akt/NF-κB signaling pathway in the treatment of CI/RI. These findings provide novel insights into the therapeutic mechanisms of quercetin in ischemic stroke.

Buyang Huanwu decoction promotes angiogenesis of rat brain microvascular endothelial cells after oxygen-glucose deprivation reperfusion injury via activation of PI3K-AKT signaling pathway.

OBJECTIVE: To investigate the effect and mechanism of Buyang Huanwu decoction (BYHWD) on angiogenesis of rat brain microvascular endothelial cells (RBMECs) after oxygen-glucose deprivation reperfusion (OGD/R) injury. METHODS: RBMECs were pretreated with BYHWD containing serum 24 h before OGD/R injury was induced. Cells were randomly divided into blank control group, model control group, BYHWD group (provided BYHWD containing serum) and LY294002 group [treated with phosphoinositide 3-kinase (PI3K) inhibitor LY294002 for 1 h before provided BYHWD containing serum]. The cell viability, migration and tube formation abilities of RBMECs were detected by CCK-8, scratch wound healing, Transwell migration and tube formation assays, respectively. The protein expression levels of PI3K, p-PI3K, protein kinase B (AKT), p-AKT, hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) were determined by Western blotting. RESULTS: Compared with model control group, cell viability, migration and tube formation abilities of RBMECs were significantly improved in BYHWD group (all P<0.01), the protein expression levels of p-PI3K, p-AKT, HIF-1α and VEGF were up-regulated (all P<0.05); while above effects were blocked by LY294002. CONCLUSION: BYHWD can promote angiogenesis of RBMECs after OGD/R injury, which may be related to the increased protein expression of HIF-1α and VEGF through activation of PI3K-AKT signaling pathway.

Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Promote Angiogenesis in Ischemic Stroke Mice via Upregulation of MiR-21-5p.

Exosomes derived from bone mesenchymal stem cells (BMSC-Exos) are one of the main factors responsible for the therapeutic effects of BMSCs. The study aimed to investigate whether BMSC-Exos could promote angiogenesis in ischemic stroke mice via miR-21-5p. In ischemic stroke mice, the therapeutic effects of BMSC-Exos were evaluated by neurological functions and infarct volume. Microvessel density was detected by BrdU/vWF immunofluorescence staining. In in vitro experiments, the proangiogenic effects of BMSC-Exos were assessed via proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs). The miR-21-5p inhibitor was transfected into BMSCs using Lipofectamine 2000. miR-21-5p expression was detected by qRT-PCR. The expression levels of VEGF, VEGFR2, Ang-1, and Tie-2 were determined by Western blot. BMSC-Exos significantly improved neurological functions and reduced infarct volume, upregulated microvessel density, and miR-21-5p expression after cerebral ischemia. In vitro assays revealed that BMSC-Exos enhanced HUVECs functions including proliferation, migration, and tube formation. BMSC-Exos increased the expression levels of VEGF, VEGFR2, Ang-1, and Tie-2. However, the proangiogenic effects of BMSC-Exos on HUVECs were reversed by the miR-21-5p inhibitor. These results suggest that BMSC-Exos could promote angiogenesis via miR-21-5p upregulation, making them an attractive treatment strategy for stroke recovery.

Metagenomic analysis of microbial community structure and function in a improved biofilter with odorous gases.

Biofilters have been broadly applied to degrade the odorous gases from industrial emissions. A industrial scale biofilter was set up to treat the odorous gases. To explore biofilter potentials, the microbial community structure and function must be well defined. Using of improved biofilter, the differences in microbial community structures and functions in biofilters before and after treatment were investigated by metagenomic analysis. Odorous gases have the potential to alter the microbial community structure in the sludge of biofilter. A total of 90,016 genes assigned into various functional metabolic pathways were identified. In the improved biofilter, the dominant phyla were Proteobacteria, Planctomycetes, and Chloroflexi, and the dominant genera were Thioalkalivibrio, Thauera, and Pseudomonas. Several xenobiotic biodegradation-related pathways showed significant changes during the treatment process. Compared with the original biofilter, Thermotogae and Crenarchaeota phyla were significantly enriched in the improved biofilter, suggesting their important role in nitrogen-fixing. Furthermore, several nitrogen metabolic pathway-related genes, such as nirA and nifA, and sulfur metabolic pathway-related genes, such as fccB and phsA, were considered to be efficient genes that were involved in removing odorous gases. Our findings can be used for improving the efficiency of biofilter and helping the industrial enterprises to reduce the emission of waste gases.

ACT001 inhibits pituitary tumor growth by inducing autophagic cell death via MEK4/MAPK pathway.

ACT001, derived from traditional herbal medicine, is a novel compound with effective anticancer activity in clinical trials. However, little is known regarding its role in pituitary adenomas. Here, we demonstrated that ACT001 suppressed cell proliferation and induced cell death of pituitary tumor cells in vitro and in vivo. ACT001 was also effective in suppressing the growth of different subtypes of human pituitary adenomas. The cytotoxic mechanism ACT001 employed was mainly related to autophagic cell death (ACD), indicated by autophagosome formation and LC3-II accumulation. In addition, ACT001-mediated inhibitory effect decreased when either ATG7 was downregulated or cells were cotreated with autophagy inhibitor 3-methyladenine (3-MA). RNA-seq analysis showed that mitogen-activated protein kinase (MAPK) pathway was a putative target of ACT001. Specifically, ACT001 treatment promoted the phosphorylation of JNK and P38 by binding to mitogen-activated protein kinase kinase 4 (MEK4). Our study indicated that ACT001-induced ACD of pituitary tumor cells via activating JNK and P38 phosphorylation by binding with MEK4, and it might be a novel and effective anticancer drug for pituitary adenomas.

Radiomic features as a risk factor for early postoperative seizure in patients with meningioma.

PURPOSE: This study aim to identify the clinical risk factors of and to develop a radiomics-based predictive model for early postoperative seizure. METHODS: We retrospectively assessed 322 operative patients with meningioma who met the inclusion criteria from January 2014 to December 2016 at The First Affiliated Hospital of Wenzhou Medical University. Univariate and multivariate analyses were performed to determine the predictive value of clinical variables. Magnetic resonance imaging (MRI) was performed to obtain the radiomic score (Rscore) for early postoperative seizure. Radiological features were evaluated using the AK software. The minimal redundancy (mRMR) and least absolute shrinkage and selection operator (LASSO) methods were used to assess for radiomic features, and the Rscore was obtained based on radiomic characteristics using a specific formula. RESULTS: In total, 260 patients who met the inclusion criteria were finally enrolled in this study. Among them, 20 experienced early postoperative seizure. Logistic regression analysis showed that Rscore was associated with a significantly high risk of seizure (p<0.000). Receiver operating characteristic (ROC) curve analysis revealed that the area under the ROC curve of the Rscore was 0.92 (95% confidence interval: 0.853-0.987). The model had a high accuracy for predicting early postoperative seizure. CONCLUSIONS: The Rscore was found to be associated with a high risk of early postoperative seizures. Thus, a higher Rscore (>-1.644) can identify high-risk patients requiring intensive care.

Surgery and Medical Treatment in Microprolactinoma: A Systematic Review and Meta-Analysis.

OBJECTIVE: Dopamine agonists (DAs) are recommended as the first-line treatment for prolactinomas; however, tumour recurrence after drug withdrawal remains a clinical problem. Recent studies have reported high remission rates via surgery in microprolactinomas. The aim of this systematic review and meta-analysis was to compare the clinical result of DA treatment with surgery as initial therapy in patients with treatment-naive microprolactinoma. METHODS: A comprehensive literature search for studies and reports regarding microprolactinoma patients treated with DAs and/or surgery published between January 1970 and November 2020 was conducted using four electronic databases (PubMed, Embase, Google Scholar, and the Cochrane Library). Clinical treatment outcome was evaluated by the biochemical remission of serum prolactin level to normal after treatment. The I 2 statistic was used to quantify heterogeneity. Pooled data were analysed according to a random effect model. RESULTS: Eighteen studies with 661 patients were included for analysis. The DA treatment group achieved a higher remission rate at ≥12 months follow-up (96% vs. 86%; P=0.019). Surgery showed a higher remission rate than the DA treatment group after the treatment withdrawal (78% vs. 44%; P=0.003). Patients with preoperative prolactin level of ≤200 ng/mL had a higher remission rate than patients with preoperative prolactin level of >200 ng/mL (92% vs. 40%; P=0.029). CONCLUSION: Surgery showed a high remission rate in treatment-naive microprolactinoma patients after treatment withdrawal and may be an alternative first-line treatment strategy in addition to DAs, particularly in patients with a preoperative prolactin level of ≤200 ng/mL.

GATA3 maintains the quiescent state of cochlear supporting cells by regulating p27kip1.

Haplo-insufficiency of the GATA3 gene causes hypoparathyroidism, sensorineural hearing loss, and renal disease (HDR) syndrome. Previous studies have shown that Gata3 is required for the development of the prosensory domain and spiral ganglion neurons (SGNs) of the mouse cochlea during embryogenesis. However, its role in supporting cells (SCs) after cell fate specification is largely unknown. In this study, we used tamoxifen-inducible Sox2CreERT2 mice to delete Gata3 in SCs of the neonatal mouse cochlea and showed that loss of Gata3 resulted in the proliferation of SCs, including the inner pillar cells (IPCs), inner border cells (IBCs), and lateral greater epithelium ridge (GER). In addition, loss of Gata3 resulted in the down-regulation of p27kip1, a cell cycle inhibitor, in the SCs of Gata3-CKO neonatal cochleae. Chromatin immunoprecipitation analysis revealed that GATA3 directly binds to p27kip1 promoter and could maintain the quiescent state of cochlear SCs by regulating p27kip1 expression. Furthermore, RNA-seq analysis revealed that loss of Gata3 function resulted in the change in the expression of genes essential for the development and function of cochlear SCs, including Tectb, Cyp26b1, Slitrk6, Ano1, and Aqp4.

Brusatol Inhibits Tumor Growth and Increases the Efficacy of Cabergoline against Pituitary Adenomas.

Cabergoline (CAB) is the first choice for treatment of prolactinoma and the most common subtype of pituitary adenoma. However, drug resistance and lack of effectiveness in other pituitary tumor types remain clinical challenges to this treatment. Brusatol (BT) is known to inhibit cell growth and promote apoptosis in a variety of cancer cells. In our present studies, we investigate the effects of BT on pituitary tumor cell proliferation in vitro and in vivo. BT treatment resulted in an increase in Annexin V-expressing cells and promoted the expression of apoptosis-related proteins in rat and human pituitary tumor cells. Investigation of the mechanism underlying this effect revealed that BT increased the production of reactive oxygen species (ROS) and inhibited the phosphorylation of 4EBP1 and S6K1. Furthermore, treatment with a combination of BT and CAB resulted in greater antitumor effects than either treatment alone in nude mice and pituitary tumor cells. Collectively, our results suggest that the BT-induced ROS accumulation and inhibition of mTORC1 signaling pathway leads to inhibition of tumor growth. Combined use of CAB and BT may increase the clinical effectiveness of treatment for human pituitary adenomas.

A Quantified Risk-Scoring System for the Recurrence of Meningiomas: Results From a Retrospective Study of 392 Patients.

Aim: This study aimed to identify the independent risk factors of recurrence in patients undergoing primary resection of meningioma and construct a scoring system for the prediction of the risk of postoperative recurrence. Materials and Methods: The clinical data of 591 patients who underwent primary surgical resection for meningioma at the First Affiliated Hospital of Wenzhou Medical University between November 2010 and December 2016 were retrospectively reviewed. The clinical, radiological, and pathological characteristics were evaluated, and the independent risk factors for recurrence were identified via receiver operating characteristic (ROC) curve and logistic analyses. A scoring system that included these independent risk factors was used to construct a risk-predicting model that was evaluated via a ROC curve analysis. The recurrences of different subgroups were observed by Kaplan-Meier's curves. Results: The clinical data of 392 patients with meningioma were used to construct the scoring system. The logistic analysis showed that sex (OR = 2.793, 95% CI = 1.076-7.249, P = 0.035), heterogeneous tumor enhancement (OR = 4.452, 95% CI = 1.714-11.559, P = 0.002), brain invasion (OR = 2.650, 95% CI = 1.043-6.733, P = 0.041), Simpson's removal grade (OR = 5.139, 95% CI = 1.355-19.489, P = 0.016), and pathological grade (OR = 3.282, 95% CI = 1.123-9.595, P = 0.030) were independent risk factors for recurrence. A scoring system was developed and used to divide the patients into the following four subgroups: subgroup 1 with scores of 0-75 (n = 249), subgroup 2 with scores of 76-154 (n = 88), subgroup 3 with scores of 155-215 (n = 46), and subgroup 4 with scores of 216-275 (n = 9). The incidences of recurrence in each subgroup were as follows: subgroup 1, 1.2%; subgroup 2, 5.7%; subgroup 3, 26.1%; and subgroup 4, 66.7% (P < 0.001). The scoring system reliably predicted the postoperative recurrence of meningioma with a high area under the ROC curve. Conclusions: Our scoring system is a simple and reliable instrument for identifying meningioma patients at risk of postoperative recurrence and could help in optimizing individualized clinical treatment.

Generation and characterization of Lhx4tdT reporter knock-in and Lhx4loxP conditional knockout mice.

LHX4 is a LIM-homeodomain transcription factor essential for the development of spinal cord and pituitary gland. Mice with homozygous Lhx4-null mutation suffer early postnatal death from lung defect. In this study, to facilitate the research on Lhx4 function, we designed a targeting construct to generate two novel Lhx4 mouse lines: Lhx4 loxP conditional knockout and Lhx4 tdT reporter knock-in mice. Lhx4 tdT/+ , Lhx4 loxP/+ , and Lhx4 loxP/loxP were viable, fertile, and did not display any gross abnormalities. By breeding Lhx4 loxP line with Cre-expressing mice, the Exon 3 of Lhx4 was efficiently removed, resulting in a shift in the reading frame and the inactivation of Lhx4. The expression of tdTomato knock-in reporter recapitulated the endogenous LHX4 expression and was detected in the retina, spinal cord, pituitary gland, and hindbrain of Lhx4 tdT mice. Thus, Lhx4 tdT and Lhx4 loxP mouse lines provide valuable tools for unraveling the tissue-specific role of Lhx4 at postnatal stages in mice.

Gfi1-GCE inducible Cre line for hair cell-specific gene manipulation in mouse inner ear.

Tissue-specific inducible Cre recombinase mouse lines allow precise genetic manipulations in spatiotemporal manners and are pivotal for functional studies of genes during development and in adults. Growth factor independence 1 (GFI1) is an essential transcription factor expressed in the hair cells of mouse inner ear and Gfi1 locus serves as an excellent anchor site to drive the expression of inducible Cre recombinase in mouse inner hair cells. In this study, we have generated Gfi1-P2A-GFP-CreERT2 (Gfi1-GCE) knock-in mouse line by in-frame fusion of a self-cleaving GCE to the C-terminus of GFI1. We have shown that as predicted, the expression of GCE and GFI1 was detected specifically in the cytosol and nuclei of hair cells, respectively, of uninduced Gfi1-GCE mice, suggesting the successful cleavage and simultaneous expression of GFI1 and GCE. In addition, the in-frame fusion of the self-cleaving GCE does not interrupt the function of Gfi1 in the inner ear. Administration of tamoxifen leads to nuclear translocation of GCE and results in an efficient activation of tdTomato reporter gene expression specifically in most hair cells throughout development and in adults. Thus, this inducible Gfi1-GCE mouse line is a highly efficient Cre deleter and is suitable for gene manipulation in developing and adult inner ear hair cells.

CTRP9 ameliorates cellular senescence via PGC­1α/AMPK signaling in mesenchymal stem cells.

Stroke is the second most common cause of death worldwide, and thus, it imposes great financial burdens on both individuals and society. Mesenchymal stem cell (MSC) therapy is a promising approach for ischemic brain injury. However, MSC treatment potential is progressively reduced with age, limiting their therapeutic efficacy for brain repair post­stroke. C1q and tumor necrosis factor­related protein 9 (CTRP9) is a novel cytoprotective cytokine with antioxidant effects, which is highly expressed in brain tissue. The present study tested the hypothesis that CTRP9 might act as an antisenescence factor to promote the rejuvenation of aged MSCs. MSCs were isolated from the bone marrow of young (8­weeks­old) and aged (18­months­old) male C57BL/6 mice. Cell proliferation was measured by Cell Counting Kit­8 assay and cell viability was determined by MTT assay. Gene expression levels of interleukin (IL)­6 and IL­10 were evaluated with reverse transcription­quantitative polymerase chain reaction, and secretion of vascular endothelial growth factor, basic fibroblast growth factor, hepatocyte growth factor, and insulin­like growth factor were measured by ELISA. The expression levels of proteins in the peroxisome proliferator­activated receptor γcoactivator (PGC)­1α/AMP­activated protein kinase (AMPK) signaling pathway were investigated with western blotting. Oxidative stress was evaluated by detecting mitochondrial membrane potential, reactive oxygen species, superoxide dismutase activity and malondialdehyde. MSCs isolated from aged mice exhibited reduced proliferation and viability, and impaired immunoregulatory and paracrine abilities, compared with MSCs from younger mice. CTRP9 had a significant antisenescence effect in aged MSCs by activating PGC­1α/AMPK signaling and decreasing the oxidative response. Silencing either PGC­1α or AMPK abolished the above effects of CTRP9. These results suggest that CTRP9 may have a critical role in cellular senescence by facilitating stem cell rejuvenation, and may therefore have the potential to enhance the efficacy of stem cell therapy.

A metabolic profiling analysis of the nephrotoxicity of acyclovir in rats using ultra performance liquid chromatography/mass spectrometry.

Acyclovir (ACV) exposure is a common cause of acute kidney injury (AKI). The toxicity mechanism of ACV has always been a matter of debate. The present study investigated into the time-effect relationship and dose-effect relationship of ACV-induced nephrotoxicity in rats using metabonomics. Twenty-four rats were randomly divided into four groups: a 0.9% NaCl solution group, and 100, 300, and 600mg/kg ACV-treated groups; the ACV or vehicle solution was administered with a single intravenous injection. Urine was collected at different time periods (12h before administration, and 0-6h, 7-12h, and 13-24h after administration). Routine urinalysis was conducted by a urine automatic analyzer. Renal markers, including urine urea nitrogen, urine creatinine, and urinary N-acetyl-ß-d-glucosaminidase (NAG) activity, were determined using established protocols. Urinary metabolites were evaluated using ultra performance liquid chromatography/mass spectrometry (UPLC/MS). In the ACV-treated rats, increased levels of protein (PRO), occult blood (BLD), white blood cell (WBC), and NAG activity in urine were observed, while the urine creatinine and urea nitrogen levels showed a decrease compared with the control. Moreover, urine metabolites significantly changed after the treatment with ACV, and all the effects induced by ACV were dose-time dependent. Finally, 4 metabolites (guanine, 4-guanidinobutyric acid, creatinine, and urea) were identified, which can be used for further research on the mechanism of ACV-induced nephrotoxicity.

Andrographolide-induced apoptosis in human renal tubular epithelial cells: Roles of endoplasmic reticulum stress and inflammatory response.

Andrographolide sodium bisulfate as a kind of soluble derivative of andrographolide (AD), is obviously known to be nephrotoxicity, but AD has not been reported clearly. Our study aimed to investigate the induction of apoptosis in human renal tubular epithelial (HK-2) cells by AD and its possible mechanism. Our results demonstrated that AD (0-250µmol/L) inhibited Hk-2 cells proliferation in a dose- and time-dependent manner and induced apoptosis, accompanied by decreased of superoxide dismutase (SOD) activity and increased of malondialdehvde (MDA) content. Simultaneously, AD regulated the expression of endoplasmic reticulum (ER) molecular chaperone glucose-regulated protein 78 (GRP78/Bip) protein, elevated the expressions of C/EBP homologous protein (CHOP) and Caspase-4, indicating activation of ER stress signaling, and induced the alterative expression of kidney injury molecule-1 (KIM-1), tumor necrosis factor-α (TNF-α) and Interleukin-6 (IL-6) proteins. It provided evidence that ER stress and inflammation would be significant mechanisms responsible for AD-induced apoptosis in addition to oxidative stress.

Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model.

Acyclovir (ACV) is an effective and widely used antiviral agent. However, its clinical application is limited by severe nephrotoxicity. We assessed ACV-induced nephrotoxicity and identified the differentially expressed proteins using mass spectrometry-based proteomic analysis. In total, 30 ICR mice were intraperitoneally administrated ACV (150 or 600 mg/kg per day) for 9 days. After administration of ACV, levels of serum creatinine and urea nitrogen increased significantly. In addition, mouse kidneys exhibited histopathological changes and reduced expression levels of vascular endothelial growth factor (VEGF) and its receptor VEGFR2. In the proteomic analysis, more than 1,000 proteins were separated by two-dimensional polyacrylamide gel electrophoresis, and a total of 20 proteins were up- or down-regulated in the ACV group compared with the saline group. Among these, six proteins (MHC class II antigen, glyoxalase 1, peroxiredoxin 1, αB-crystallin, fibroblast growth factor receptor 1-IIIb, and cytochrome c oxidase subunit Vb) were identified in association with ACV-induced nephrotoxicity. These findings were confirmed by Western blotting analysis. The differential expression levels of α-BC, Prx1, Glo I and CcO Vb suggest that oxidative damage and mitochondrial injury may be involved in ACV-induced nephrotoxicity. Furthermore, VEGF and FGF may play a role in tissue repair and the restoration process following ACV nephrotoxicity.

Antifungal activities of metabolites produced by a termite-associated Streptomyces canus BYB02.

Two main antifungal metabolites resistomycin and tetracenomycin D were isolated and purified from a termite-associated Streptomyces canus BYB02 by column chromatography. The structures of isolated compounds were determined on the basis of extensive spectroscopic analysis. Resistomycin possessed strong activities against mycelial growth of Valsa mali (IC(50) = 1.1 µg/mL) and Magnaporthe grisea (IC(50) = 3.8 µg/mL), which were comparable to those of referenced cycloheximide, with IC(50) values of 2.3 and 0.3 µg/mL, respectively. A further spore germination test showed that resistomycin exhibited potent reduction in spore germination for M. grisea , with an IC(50) value of 5.55 µg/mL. Finally, the in vivo antifungal activity experiment showed that resistomycin possessed significant preventive efficacy against rice blast, which was more potent than that of referenced carbendazim, with control efficacies of 66.8 and 58.7%, respectively. The present results suggest that resistomycin has potential to be used as a fungicide.

[A probability wave theory on the ion movement across cell membrane].

The ionic quantity across the channel of the cell membrane decides the cell in a certain life state. The theory analysis that existed on the bio-effects of the electro-magnetic field (EMF) does not unveil the relationship between the EMF exerted on the cell and the ionic quantity across the cell membrane. Based on the cell construction, the existed theory analysis and the experimental results, an ionic probability wave theory is proposed in this paper to explain the biological window-effects of the electromagnetic wave. The theory regards the membrane channel as the periodic potential barrier and gives the physical view of the ion movement across cell-membrane. The theory revises the relationship between ion's energy in cell channel and the frequency exerted EMF. After the application of the concept of the wave function, the ionic probability across the cell membrane is given by the method of the quantum mechanics. The numerical results analyze the physical factors that influences the ion's movement across the cell membrane. These results show that the theory can explain the phenomenon of the biological window-effects.