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Microalgae is an easy-to-obtain natural biological material with many varieties and abundant natural reserves. Microalgae are rich in natural fluorescein, which can be used as a contrast agent for fluorescence imaging and photoacoustic imaging for medical imaging. With its active surface, microalgae can effectively adsorb functional molecules, metal elements, etc., and have good application prospects in the field of drug delivery. Microalgae can generate oxygen through photosynthesis to increase local oxygen concentration, reverse local hypoxia to enhance the efficacy of hypoxic tumors and promote wound healing. In addition, microalgae have good biocompatibility, and different administration methods have no obvious toxicity. This paper reviews the research progress on the biomedical application of microalgae in bioimaging, drug delivery, hypoxic tumor treatment, wound healing.
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Humans , Drug Delivery Systems , Hypoxia , Microalgae , Oxygen , Wound HealingABSTRACT
The uridine diphosphate_glucuronosyl transferase 1A1(UGT1A1)gene mutation can affect the ex_pression of UGT1A1 gene and enzyme activity,and then reduce bilirubin metabolism leading to unconjugated hyperbi_lirubinemia. With the development of molecular biotechnology,more and more studies are trying to identify the patho_genesis of these polymorphisms by analyzing the expression and enzyme activity of UGT1A1 gene polymorphisms. Now, the progresses in the study of the expression of UGT1A1 gene polymorphism were reviewed.
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Objective To investigate the influence of newborns born to mother with systemic lupus erythematosus (SLE).Method The clinical data of SLE mothers and their infants bern in the obstetric and were admitted to the neonatal ward ward of the First Affiliated Hospital of Guangxi Medical University from July 2012 to March 2015 were studied retrospectively.The infants were divided into active SLEactivity group and stable SLE group.The incidence of preterm birth,small for gestational age (SGA),cardiac conduction block,anemia,and thrombocytopenia were compared between the two groups of SLE mothers.Result A total of 66 infants were included in SLE mothers,including 14 cases (21.2％) of preterm infants and 18 cases of SGA (27.3％).14 cases belonged to the active SLE group while 52 cases belonged to the SLE stable group.When comparing the 2 groups,there were no differences found on the rates of preterm infant and small for gestational age (P ＞ 0.05).The cardiac conduction block,anemia and thrombocytopenia happened separately in three cases of the active group,which had not seen in the SLE stable group.There was no statistically significant difference between the two groups (P ＞ 0.05).Of the 66 cases,2 were diagnosed with neonatal lupus erythematosus (NLE) with an incidence of 3％.Conclusion SLE mothers with an active disease 10 days before delivery did not significantly increase the incidence of preterm infants and SGA,but were at risk of NLE.
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Objective To test the mutation locus of uridine diphospho-glucuronosyltransferase gene (UGT1A1) in a Chinese patient with Crigler-Najjar syndrome type Ⅰ and her family members,analyzing the genetic characteristics of the pedigree.Methods Genomic DNA was extracted from the patient and her family members and other 50 full-term infants with normal serum bilirubin as a healthy control group.Fifty cases of full-term newborn whose serum bilirubin level were nomal were study as controls.The promoter and all exons of UGT1A1 gene were amplified by the method of polymerase chain reactions (PCR),and mutations were identified by direct sequencing.Results The propositus and her miscarriage sister were homozygous for a nonsense mutation at nucleotide number 715 (715C ＞ T) in exon 1 of gene UGT1A1,substituting of stop codon (TAG) for glutamine (CAG) at position 239 (Q239X).The other 5 members were heterozygous in the same mutation locus.A TA insertion mutation and a G71R mutation in exon 1 were observed in the family members.The patient and her sister were homozygous of A(TA)7TAA mutation while other four were heterozygous.Propositus,grandmother,mother and her younger brother were heterozygous of G71 R mutation.No mutation was found in exons 2-5.No mutation was found in other fifty healthy cases in the healthy control group.Conclusions Q239X homozygous mutations is considered to be the lethal gene in this Crigler-Najjar syndrome family.Collaborative G71 R and A(TA)7TAA mutations may further reduce the enzyme activity of UGT1A1,causing varying degrees of bilirubin disorder.