Early prosthodontic intervention on two three-year-old twin girls with ectodermal dysplasia.

AIM: Early prosthodontic treatment for cases of ectodermal dysplasia (ED) is usually difficult because of oligodontia, undeveloped alveolar ridges, and the young age of the patients. Although some cases of prosthetic management of ED patients have been reported in the literature, there have been few cases about prosthetic treatment in children younger than 5 years of age. CASE REPORT: This case report presents early prosthetic oral rehabilitation of 2 twin sisters with ectodermal dysplasia and severe hypodontia in the primary dentition. Fixed partial dentures with bands retained on deciduous molars were fabricated when the girls were 3 years old. New flexible removable partial dentures were made when the girls turned 6 years to accommodate the ongoing alveolar development. After the dental treatment, the two girls' aesthetics, phonetics, and chewing functions all improved significantly, which in turn raised the girls' self-esteem and increased their overall quality of life. CONCLUSION: These two cases demonstrated that properly timed and managed early prosthodontic intervention can improve the overall life quality of young patients with ectodermal dysplasia.

Circulating miR-31-5p may be a potential diagnostic biomarker in nasopharyngeal carcinoma.

Aberrant expression of miR-31-5p has been detected in various cancers and plays a significant role in tumorigenesis. Low miR-31-5p expression was present in nasopharyngeal carcinoma (NPC) tissues and cell lines and acted as a tumor suppressive miRNA. Currently, circulating miRNAs are emerging as novel biomarkers for the early diagnosis of cancers using a non-invasive method. However, circulating miR-31-5p has rarely been reported in NPC. Therefore, the aim of this study was to explore peripheral blood miR-31-5p levels as a noninvasive biomarker and evaluate its clinical value for the early diagnosis of patients with NPC. A total of 110 participants were recruited, including 55 NPC patients and 55 healthy controls. Peripheral blood samples were collected from these participants, and total RNA was extracted to quantify the relative expression of miR-31-5p by RT-qPCR. We found a significantly lower expression of miR-31-5p in the NPC patients than in the healthy controls. Furthermore, low expression of miR-31-5p was highly correlated with tumor-node-metastasis (TNM) stage (I+II vs III+IV, p=0.001), T classification (T1 vs T2+T3+T4, p=0.036) and local lymph node metastasis (N1-N3 vs N0, p=0.002), but not distant metastasis (p=0.288). Moreover, miR-31-5p showed a moderate diagnostic performance (AUC=0.866, sensitivity = 0.782, specificity = 0.818). Thus, we concluded that circulating miR-31-5p can be a potentially novel and non-invasive biomarker for the early diagnosis of NPC and an attractive therapeutic target in NPC patients.

Bone marrow mesenchymal stem cells overexpressing human basic fibroblast growth factor increase vasculogenesis in ischemic rats

Administration or expression of growth factors, as well as implantation of autologous bone marrow cells, promote in vivo angiogenesis. This study investigated the angiogenic potential of combining both approaches through the allogenic transplantation of bone marrow-derived mesenchymal stem cells (MSCs) expressing human basic fibroblast growth factor (hbFGF). After establishing a hind limb ischemia model in Sprague Dawley rats, the animals were randomly divided into four treatment groups: MSCs expressing green fluorescent protein (GFP-MSC), MSCs expressing hbFGF (hbFGF-MSC), MSC controls, and phosphate-buffered saline (PBS) controls. After 2 weeks, MSC survival and differentiation, hbFGF and vascular endothelial growth factor (VEGF) expression, and microvessel density of ischemic muscles were determined. Stable hbFGF expression was observed in the hbFGF-MSC group after 2 weeks. More hbFGF-MSCs than GFP-MSCs survived and differentiated into vascular endothelial cells (P<0.001); however, their differentiation rates were similar. Moreover, allogenic transplantation of hbFGF-MSCs increased VEGF expression (P=0.008) and microvessel density (P<0.001). Transplantation of hbFGF-expressing MSCs promoted angiogenesis in an in vivo hind limb ischemia model by increasing the survival of transplanted cells that subsequently differentiated into vascular endothelial cells. This study showed the therapeutic potential of combining cell-based therapy with gene therapy to treat ischemic disease.

Bone marrow mesenchymal stem cells overexpressing human basic fibroblast growth factor increase vasculogenesis in ischemic rats.

Administration or expression of growth factors, as well as implantation of autologous bone marrow cells, promote in vivo angiogenesis. This study investigated the angiogenic potential of combining both approaches through the allogenic transplantation of bone marrow-derived mesenchymal stem cells (MSCs) expressing human basic fibroblast growth factor (hbFGF). After establishing a hind limb ischemia model in Sprague Dawley rats, the animals were randomly divided into four treatment groups: MSCs expressing green fluorescent protein (GFP-MSC), MSCs expressing hbFGF (hbFGF-MSC), MSC controls, and phosphate-buffered saline (PBS) controls. After 2 weeks, MSC survival and differentiation, hbFGF and vascular endothelial growth factor (VEGF) expression, and microvessel density of ischemic muscles were determined. Stable hbFGF expression was observed in the hbFGF-MSC group after 2 weeks. More hbFGF-MSCs than GFP-MSCs survived and differentiated into vascular endothelial cells (P<0.001); however, their differentiation rates were similar. Moreover, allogenic transplantation of hbFGF-MSCs increased VEGF expression (P=0.008) and microvessel density (P<0.001). Transplantation of hbFGF-expressing MSCs promoted angiogenesis in an in vivo hind limb ischemia model by increasing the survival of transplanted cells that subsequently differentiated into vascular endothelial cells. This study showed the therapeutic potential of combining cell-based therapy with gene therapy to treat ischemic disease.

[Detection of anti-HIV-1/2 and HIV nucleic acid in population of non-remunerated blood donors in Shenzhen].

OBJECTIVE: To study the prevalent status of HIV-1 in population of non-remunerated blood donors in Shenzhen. METHODS: 46,095 non-remunerated blood donors were tested for anti-HIV-1/2 by ELISA. The donors of anti-HIV positive were further detected for HIV DNA from peripheral blood mononuclear cells (PMBCs) by nested-PCR and HIV RNA from plasma by RT-PCR. The partial genome of env of 2 blood donors were sequenced. RESULTS: The anti-HIV-1 was tested positive in 7 of 46 095 voluntary blood donors and the positive rate was 0.015%. In these 7 non-remunerated blood donors of anti-HIV-1 positive,7 were positive for HIV DNA in PMBCs and 5 positive for HIV RNA in plasma. The sequence analysis showed that 2 donors were infected by HIV-1 subtype E strains. CONCLUSIONS: There exists HIV-1 subtype E infection in population of non-remunerated blood donors in Shenzhen. It is essential to detect and monitor strictly the population of non-remunerated blood donors.

Diversity of cDNAs encoding phospholipase A2 from Agkistrodon halys pallas venom, and its expression in E. coli.

As a step toward understanding the structure and function of phospholipase A2(PLA2), we isolated several novel cDNAs encoding Agkistrodon halys Pallas PLA2 isoenzymes including B-PLA2, Asn49-PLA2, A-PLA2, A'-PLA2 and BA1-PLA2 by polymerase chain reaction with oligonucleotide primers corresponding to the N- and C-terminus of these enzymes. The amino acid sequences of A-PLA2 deduced from cDNA are consistent with that isolated from venom except for four residues. Asn49-PLA2 and B-PLA2 are highly similar (> 95%), but the critical residue Asp49 in the active centre of B-PLA2 is replaced by Asn49 in Asn49-PLA2. The N-terminal residues (1-24) of BA1-PLA2 shows high similarity to that of B-PLA2 which has strong ability to hemolyze erythrocytes, while its C-terminal residues (72-125) are the same as that of A-PLA2 which can inhibit platelet aggregation. The successful cloning of these isoenzymes not only provide excellent native material to study the structure-function relationship of PLA2s, but also to disclose the genesis of structural diversity of PLA2s, namely DNA modification and gene rearrangement. The cloned cDNA for A-PLA2 has been expressed in E. coli. By Q-Sepharose column chromatography, denaturation-renaturation and FPLC, we obtained the active recombinant protein with the initiator Met. This is the first report of the production of an active recombinant PLA2 with the initiator Met.

Specificity and regulation of the dicarboxylate carrier on the peribacteroid membrane of soybean nodules.

Malate and succinate were taken up rapidly by isolated, intact peribacteroid units (PBUs) from soybean (Glycine max (L.) Merr.) root nodules and inhibited each other in a competitive manner. Malonate uptake was slower and was severely inhibited by equimolar malate in the reaction medium. The apparent Km for malonate uptake was higher than that for malate and succinate uptake. Malate uptake by PBUs was inhibited by (in diminishing order of severity) oxaloacetate, fumarate, succinate, phthalonate and oxoglutarate. Malonate and butylmalonate inhibited only slightly and pyruvate,isocitrate and glutamate not at all. Of these compounds, only oxaloacetate, fumarate and succinate inhibited malate uptake by free bacteroids. Malate uptake by PBUs was inhibited severely by the uncoupler carbonylcyanidem-chlorophenyl hydrazone and the respiratory poison KCN, and was stimulated by ATP. We conclude that the peribacteroid membrane contains a dicarboxylate transport system which is distinct from that on the bacteroid membrane and other plant membranes. This system can catalyse the rapid uptake of a range of dicarboxylates into PBUs, with malate and succinate preferred substrates, and is likely to play an important role in symbiotic nitrogen fixation. Energization of both the bacteroid and peribacteroid membranes controls the rate of dicarboxylate transport into peribacteroid units.