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There was a trend toward lower proteolipid protein-1 levels in MPS I mice (p = 0.06). MPS I mice show subtle changes in white matter composition, with an unknown impact on pathogenesis in this model.Background Theileria orientalis infection causes a clinical syndrome in cattle characterised by weakness, reluctance to walk, anaemia, jaundice and death in peri-parturient cows and young calves, referred to as bovine anaemia caused by Theileria orientalis group (BATOG). Abortions in pregnant cows are also reported. Pallor, pyrexia and elevated heart and respiratory rates are typical findings on physical examination. Case report A syndrome of abortions, lethargy, inappetence, jaundice and deaths in beef cattle on two separate properties and a separate cluster of three properties within 15 km west of the town of Denmark in Western Australia was associated with the presence of severe regenerative anaemia and the presence of Theileria orientalis Ikeda genotype in blood samples taken from affected cattle and their cohorts. A diagnosis of bovine anaemia caused by the T. orientalis group was based on consistent clinical, haematological, biochemical and PCR findings. Conventional PCR testing detected only the T. orientalis Ikeda type. On the two properties where it was investigated, quantitative PCR testing for parasite load was suggestive of recent infections. Sequencing of T. orientalis major piroplasm surface protein gene PCR products demonstrated that they were identical to those from similar bovine cases in New South Wales. Conclusion The clinical history of affected cattle and the biochemical, haematological and PCR findings were consistent with bovine anaemia caused by the T. orientalis Ikeda genotype. This clinical syndrome had not been recognised in Western Australia before this series of cases.Background Autosomal recessive dystrophic epidermolysis bullosa (RDEB) is an incurable and severe inherited skin disorder characterized by recurrent blistering at the sublamina densa beneath the cutaneous basement membrane. It is caused by biallelic loss-of-function mutation in the gene encoding type VII collagen (COL7A1). This study aimed to identify the causative variants of a Chinese RDEB patient and further provide prenatal diagnosis for the ongoing risk pregnancy of the proband's mother. Methods Clinical exome sequencing (CES) has been performed and an in-house pipeline was used to conduct a phenotype-driven data analysis. A minigene assay was used to verify the pathogenicity of a novel splice site variant in the COL7A1. Results Here we report two compound heterozygous variants in COL7A1, c.3867delT (p.G1290Efs*35) and c.5532+4_5532+5delAG, identified in a RDEB patient by CES. The minigene assay confirmed that thec.5532+4_5532+5delAGchange was a noncanonic splice site variant leading to in an in-frame deletion of exon 64. Prenatal diagnosis indicated that the present pregnancy of the patient's mother was not affected. Conclusion Our study expands the mutation spectrum of COL7A1 and demonstrated that CES and minigene assays were efficient tools for RDEB molecular diagnoses.Background Long non-coding RNAs (lncRNAs) have been identified as crucial regulatory factors in the occurrence and progression of osteosarcoma. Methods Quantitative real-time polymerase chain reaction was used for detecting small nucleolar RNA host gene 4 (SNHG4) and miR-377-3p in osteosarcoma cells and tissues. Kaplan-Meier method was applied for evaluating the association between SNHG4 expression and the overall survival of osteosarcoma patients. CCK8, EdU, flow cytometry, and transwell assay were performed to examine the cell proliferation, apoptosis, cycle, and migration of osteosarcoma cells. Results In our study, we found that lncRNA SNHG4 was highly expressed in osteosarcoma tissues and cell lines. Additionally, the SNHG4 expression was related to distant metastasis, TNM stage, and survival of osteosarcoma patients. Through SNHG4 knockdown, the proliferation of osteosarcoma cells was considerably restrained and the cell apoptosis was induced in vivo and in vitro. Moreover, downregulated SNHG4 inhibited the cell migration and epithelial-mesenchymal transition in HOS and MG63 cells. In mechanism, we found that SNHG4 acts as a competing endogenous RNA to sponge miR-377-3p, which is downregulated in osteosarcoma. Our results showed that there is a negative correlation between SNHG4 and miR-377-3p expression in osteosarcoma patients. Conclusion Taken together, SNHG4 promotes cell proliferation and migration by sponging miR-377-3p in osteosarcoma.Belonging to the chalcogen group, the elements selenium (Se) and tellurium (Te) are located in Group VI-A of the periodic table. Zero-valent nanodimensioned Se (nano-Se) and Te (nano-Te) have displayed important biomedical applications in recent years. The past two decades have witnessed an explosion in novel cancer treatment strategies using nano-Se and nano-Te as aggressive weapons against tumors. Indeed, they are both inorganic nanomedicines that suppress tumor cell proliferation, diffusion, and metastasis. Abundant synthesis strategies for rational and precise surface decoration of nano-Se and nano-Te make them significant players in resisting cancers by means of powerful multi-modal treatment methods. This review focuses on the design and engineering of nano-Se- and nano-Te-based nanodelivery systems and their precise uses in cancer treatment. The corresponding anticancer molecular mechanisms of nano-Se and nano-Te are discussed in detail. Given their different photo-induced behaviors, the presence or absence of near infrared illumination is used as a defining characteristic when describing the anticancer applications of nano-Se and nano-Te. Finally, the challenges and future prospects of nano-Se and nano-Te are summarized and highlighted.Invited for this month's cover is the group of Gyorgy Szekely at King Abdullah University of Science and Technology (KAUST). The image shows the efficient TEMPO-based electrocatalytic transformation of biomass-based C6 -platform chemical HMF to DFF using non-precious-metal-based electrodes in green solvents with nanofiltration-enabled catalyst recovery. The Full Paper itself is available at 10.1002/cssc.202000453.G protein-coupled receptors (GPCRs), a superfamily of integral transmembrane proteins regulate a variety of physiological processes in insects. Juvenile hormone (JH) is known to stimulate Vitellogenin (Vg) synthesis in the fat body, secretion into the hemolymph and uptake by developing oocytes. However, the role of GPCRs in JH-dependent insect vitellogenesis and oocyte maturation remains elusive. In the present study, we performed transcriptomic analysis and RNAi screening in vitellogenic females of the migratory locust Locusta migratoria. Of 22 GPCRs identified in ovarian transcriptome, LGR4, OR-A1, OR-A2, Mthl1, Mthl5 and Smo were most abundant in the ovary. By comparison, mAChR-C expressed at higher levels in the fat body, whereas Oct/TyrR, OARβ, AdoR and ADGRA3 were at higher expression levels in the brain. Our RNAi screening demonstrated that knockdown of 6 GPCRs resulted in defective phenotypes of Vg accumulation in developing oocytes, accompanied by blocked ovarian development and impaired oocyte maturation. While LGR4 and Oct/TyrR appeared to control Vg synthesis in the fat body, OR-A1, OR-A2, mAChR-C and CirlL regulated Vg transportation and uptake. The findings provide fundamental evidences for deciphering the regulatory mechanisms of GPCRs in JH-stimulated insect reproduction.Objective Epidemiological evidence investigating serum uric acid and kidney cancer risk remains unclear. We conducted this study to examine the relationship between serum uric acid and the incidence and mortality of kidney cancer. Methods This is a prospective analysis of 444 462 participants without any cancer from the UK Biobank. Serum uric acid was measured at baseline and the incidence and mortality of kidney cancer was determined through contact with the cancer and death registry. Cox regression models were fitted to estimate the hazard ratio (HR) and 95% confidence interval (95%CI), adjusting for demography, lifestyle style, comorbidities, and medication use. Results We documented 638 incidence cases and 188 mortality cases of kidney cancer over a median of 6.5 years follow-up. People with the highest quartile had a 45% increased risk of kidney cancer compared to those with the lowest uric acid quartile (HR 1.45, 95%CI 1.08 to 1.93). Subgroup analyses showed that serum uric acid was associated with cancer risk among females but not among males (Q1 vs Q4 females HR1.47, 95%CI 1.01 to 2.16; males HR 1.19, 95%CI 0.91 to 1.56). Although we found serum uric acid was associated with an increased risk of kidney cancer mortality in age-stratified model (HR 2.49, 95% CI 1.61 to 3.84), this association disappeared after further adjustment for other confounders. Conclusions High uric acid is associated with a high incidence of kidney cancer, especially in women. More research is needed to confirm our findings.Fenton reaction-mediated chemodynamic therapy (CDT) can kill cancer cells via the conversion of H2 O2 to highly toxic HO•. However, problems such as insufficient H2 O2 levels in the tumor tissue and low Fenton reaction efficiency severely limit the performance of CDT. Here, the prodrug tirapazamine (TPZ)-loaded human serum albumin (HSA)-glucose oxidase (GOx) mixture is prepared and modified with a metal-polyphenol network composed of ferric ions (Fe3+ ) and tannic acid (TA), to obtain a self-amplified nanoreactor termed HSA-GOx-TPZ-Fe3+ -TA (HGTFT) for sustainable and cascade cancer therapy with exogenous H2 O2 production and TA-accelerated Fe3+ /Fe2+ conversion. The HGTFT nanoreactor can efficiently convert oxygen into HO• for CDT, consume glucose for starvation therapy, and provide a hypoxic environment for TPZ radical-mediated chemotherapy. Besides, it is revealed that the nanoreactor can significantly elevate the intracellular reactive oxygen species content and hypoxia level, decrease the intracellular glutathione content, and release metal ions in the tumors for metal ion interference therapy (also termed "ion-interference therapy" or "metal ion therapy"). Further, the nanoreactor can also increase the tumor's hypoxia level and efficiently inhibit tumor growth. It is believed that this tumor microenvironment-regulable nanoreactor with sustainable and cascade anticancer performance and excellent biosafety represents an advance in nanomedicine.Background The advanced lung cancer inflammation index (ALI) was first introduced for prognosis prediction in lung cancer patients and since then evaluated in several other malignancies. However, in pancreatic cancer (PC) the ALI and its prognostic utility were only investigated in a comparably small and specific cohort of locally advanced PC patients treated with chemoradiotherapy. Methods In our single-center cohort study, we included 429 patients with histologically verified PC who were treated between 2003 and 2015 at our academic institution. The ALI was defined as body mass index (BMI; kg/m2 ) × serum albumin levels (g/dL)/neutrophil-lymphocyte ratio (NLR) and we defined the optimal cutoff for biomarker dichotomization by ROC-analysis. Kaplan-Meier method as well as uni- and multivariate Cox regression Hazard proportional models were implemented to assess the prognostic potential of ALI in PC patients. We considered cancer-specific survival (CSS) as the primary endpoint of the study. Results The ALI showed a significant negative correlation with CA19-9 levels and C-reactive protein levels whereas we found an association with localized tumor stage and better performance status (P less then .