Phosphate limitation intensifies negative effects of ocean acidification on globally important nitrogen fixing cyanobacterium.

Growth of the prominent nitrogen-fixing cyanobacterium Trichodesmium is often limited by phosphorus availability in the ocean. How nitrogen fixation by phosphorus-limited Trichodesmium may respond to ocean acidification remains poorly understood. Here, we use phosphate-limited chemostat experiments to show that acidification enhanced phosphorus demands and decreased phosphorus-specific nitrogen fixation rates in Trichodesmium. The increased phosphorus requirements were attributed primarily to elevated cellular polyphosphate contents, likely for maintaining cytosolic pH homeostasis in response to acidification. Alongside the accumulation of polyphosphate, decreased NADP(H):NAD(H) ratios and impaired chlorophyll synthesis and energy production were observed under acidified conditions. Consequently, the negative effects of acidification were amplified compared to those demonstrated previously under phosphorus sufficiency. Estimating the potential implications of this finding, using outputs from the Community Earth System Model, predicts that acidification and dissolved inorganic and organic phosphorus stress could synergistically cause an appreciable decrease in global Trichodesmium nitrogen fixation by 2100.

Lipid metabolism-related genes as biomarkers and therapeutic targets reveal endometrial receptivity and immune microenvironment in women with reproductive dysfunction.

BACKGROUND: In recent years, alterations in lipid metabolism are currently considered a hallmark feature of many diseases. However, the role in women with reproductive dysfunction (WRD) remains to be fully elucidated. Here, this study aimed to explore the effect of lipid metabolism-related genes (LMRGs) on endometrial receptivity of WRD. METHODS: This study retrospectively analyzed endometrial receptivity array (ERA) in GEO database. The differential expression genes (DEGs) were obtained by limma differential analysis, and the core genes and corresponding predicted microRNA were obtained through protein-protein interaction (PPI) analysis and TargetScan database, so as to predict the chemical targets of drug therapy. Through the intersection of DEGs and LMRGs, the target gene expression profile was obtained for subsequent consensus clustering analysis and immune analysis. In addition, the immune cell infiltration was assessed by applying the ESTIMATE and MCPcounter algorithm and potential drug targets were obtained from the HERB website. RESULTS: 1473 genes showed differential expression between the groups of WRD and fertile women, and then a large number of lipid metabolism-related pathways and immune-related pathways were enriched. Twelve core genes and corresponding predicted miR-134-3p were obtained; most importantly, we found that these 12 genes were all LMRGs. Through drug target prediction, we obtained three drugs that regulate lipid metabolism and improve blood circulation, namely lovastatin, estrogen, and quercetin. EHHADH (AUC = 0.85) and PTEN (AUC = 0.82) have the best diagnostic performance. UMAP and heatmap revealed large differences between three clusters. LMRGs revealed specific manifestations of WRD in endometrial receptivity and immune microenvironment. CONCLUSIONS: Our study explored the expression pattern of LMRGs in endometrium of WRD, screened the corresponding biomarkers, and proposed the combination of traditional Chinese and Western medicine to improve the endometrial receptivity.

A novel 1p33p32.2 deletion involving SCP2, ORC1, and DAB1 genes in a patient with craniofacial dysplasia, short stature, developmental delay, and leukoencephalopathy: A case report.

INTRODUCTION: Microdeletion syndromes occur from deletion of 5Mb of a chromosome in approximately 5% of patients with unexplained intellectual disability. Interstitial microdeletions at bands 1p33 and 1p32.2 of the short arm of chromosome 1 are rare and have not been previously reported in relation to disease. PATIENT CONCERNS: We present a case of a 39-month boy with Pierre Robin sequence, development delay/intellectual disability, growth retardation, short stature, leukoencephalopathy, craniofacial dysplasia, and speech delay. The child was referred to the Child health care department in October 2014 for his delayed language development and aggravated aggression. DIAGNOSIS: Molecular diagnostic testing with G-band karyotyping was normal but clinical microarray analysis detected a 10 Mb microdeletion at 1p33p32.2. INTERVENTIONS: The patient received rehabilitation. OUTCOMES: Three candidate genes were pinpointed to the deleted area, including ORC1, SCP2, and DAB1. Phenotype-genotype analysis suggested that these three genes are likely to be responsible for the main phenotypes observed in the patient, such as microcephaly, growth retardation, short stature, leukoencephalopathy, and development delay/intellectual disability. CONCLUSIONS: The spectrum of phenotypes this case presented with are likely to be caused by 1p33p32.2 deletion which could represent a new microdeletion syndrome.

[Effect of sphingosine-1-phosphate on chemotherapy-induced ovarian damage and on the efficacy of chemotherapy in mice bearing S180 tumor].

OBJECTIVE: To investigate the effects of sphingosine-1-phosphate (S1P) on cyclophosphamid (CTX) and cisplatin (DDP)-induced ovarian damage and on the efficacy of chemotherapy in mice bearing S180 murine sarcoma. METHODS: Fifty-two female C57BL/6 mice were randomized into normal control group (n=10), tumor-bearing model group (n=14), CTX+DDP group (n=14), and S1P+CTX+DDP group (n=14). Before medication and on day 11 of medication during diestrus stage, the mice were sacrificed to measure the ovarian weight, numbers of primordial follicles and growing follicles, tumor weight, and serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol ( E2). RESULTS: At day 11 of medication, the levels of serum FSH and E2, but not LH, showed significant differences in CTX+DDP group from those in the other groups (P<0.01). FSH, E2, and LH levels were comparable between S1P+CTX+DDP group and the control group (P>0.05). The number of primodial follicles and weight of ovaries in CTX+DDP group decreased significantly compared to those in the other groups (P<0.01). The number of growing follicles in CTX+DDP group was significantly lower than that in the control and model groups(P<0.01), but similar to that in S1P group (P>0.05). The number of primodial follicles and growing follicles and ovarian weight in S1P+CTX+DDP group were close to those in the control and model groups (P>0.05). In CTX+DDP and S1P+CTX+DDP groups, the tumor weight were significantly lower than that in the other two groups (P<0.01), and the tumor inhibition rates were both higher than 60%. CONCLUSION: S1P can ameliorate chemotherapy-induced ovarian damage in mice without affecting the efficacy of chemotherapy.