Treatment of Severe Destructive Foot and Ankle Injury in a Young Child with a Skin Regeneration Technique.

Null.

Treating aplasia cutis congenita in a newborn with the combination of ionic silver dressing and moist exposed burn ointment: A case report.

BACKGROUND: Aplasia cutis congenita (ACC) in newborns is a condition in which congenital defects or hypoplasia is present in part of the epidermis, dermis and even subcutaneous tissue (including muscle and bones). First reported by Cordon in 1767, ACC is a rare disease with a low incidence of 1/100000 to 3/10000. Currently, there are 500 cases reported worldwide. ACC can be accompanied by other malformations. The onset mechanism of the disease remains unknown but is thought to be correlated to factors such as genetics, narrow uterus, foetal skin and amniotic membrane adhesion, use of teratogenic drugs in early pregnancy and viral infection. CASE SUMMARY: In August 2018, we treated a newborn with ACC on the left lower limbs using a combination of ionic silver dressing and moist exposed burn ointment (MEBO) and achieved a satisfactory treatment outcome. The skin defects were observed on the external genitals and on areas from the left foot to 3/4 of the upper left side. Subcutaneous tissue and blood vessels were observed in the regions with skin defects. The following treatments were provided. First, the wound was rinsed with 0.9% sodium chloride solution followed by disinfection with povidone-iodine twice. And then MEBO was applied to the wound at a thickness of approximately 1 mm. After applying ionic silver dressing, the wound was covered with sterile gauze. The wound dressing was replaced every 2-3 d. At the 4-mo follow-up, the treatment outcome was satisfactory. There was minimal scar tissue formation, and limb function was not impaired. CONCLUSION: The combination of ionic silver dressing and MEBO to ACC is helpful.

Expression and biochemical characterization of α-ketoglutarate decarboxylase from cyanobacterium Synechococcus sp. PCC7002.

α-Ketoglutarate decarboxylase (α-KGD), one member of α-keto acid decarboxylases, catalyzing non-oxidative decarboxylation of α-ketoglutarate to form succinic semialdehyde, was proposed to play critical role in completing tricarboxylic acid (TCA) cycle of cyanobacteria. Although the catalytic function of α-KGD from Synechococcus sp. PCC7002 was demonstrated previously, there was no detailed biochemical characterization of α-KGD from Synechococcus sp. PCC7002 yet. In this study, the gene encoding α-KGD from Synechococcus sp. PCC7002 was amplified and soluble expression of recombinant α-KGD was achieved by coexpressing with pTf16 chaperone plasmid in E. coli BL21 (DE3). Kinetic analysis showed that the activity of α-KGD was dependent on cofactors of thiamine pyrophosphate and divalent cation. Meanwhile this α-KGD was specific for α-ketoglutarate with respect to the decarboxylation activity despite of the pretty low activity of acetolactate synthase. The catalytic efficiency of α-KGD (the values of kcat and kcat/Km for α-ketoglutarate were 1.2s-1 and 6.3×103M-1s-1, respectively) might provide evidence for its physiological role in TCA cycle of Synechococcus sp. PCC7002.

Kinetic characterization and structural modeling of an NADP+-dependent succinic semialdehyde dehydrogenase from Anabaena sp. PCC7120.

Succinic semialdehyde dehydrogenases (SSADH) of cyanobacteria played a pivotal role in completing the cyanobacterial tricarboxylic acid cycle. The structural information of cofactor preference and catalysis for SSADH from cyanobacteria is currently available. However, the detailed kinetics of SSADH from cyanobacteria were not characterized yet. In this study, an all3556 gene encoding SSADH from Anabaena sp. PCC7120 (ApSSADH) was amplified and the recombinant ApSSADH was purified homogenously. Kinetic analysis showed that ApSSADH was an NADP+-dependent SSADH, which utilized NADP+ and succinic semialdehyde (SSA) as its preferred substrates and the activity of ApSSADH was inhibited by its substrate of SSA. At the same time, the Ser157 residue was found to function as the determinant of cofactor preference. Further study demonstrated that activity and substrate inhibition of ApSSADH would be greatly reduced by the mutation of the residues at the active site. Bioinformatic analysis indicated that those residues were highly conserved throughout the SSADHs. To our knowledge this is the first report exploring the detailed kinetics of SSADH from cyanobacteria.

Expression, purification and characterization of sll1981 protein from cyanobacterium Synechocystis sp. PCC6803.

The sll1981 protein from cyanobacterium Synechocystis sp. PCC6803 had been reported to exhibit acetolactate synthase (ALS) and L-myo-inositol-1-phosphate synthase (MIPS) activities previously. Based on amino acids sequences alignment, sll1981 protein was postulated to function as α-ketoglutarate decarboxylase (α-KGD), which played important role in completing cyanobacterial tricarboxylic acid (TCA) cycle. However the detailed enzymatic kinetics of sll1981 as ALS, MIPS and α-KGD were not determined yet. In this study, the recombinant sll1981 protein was purified from supernatant of E. coli cell and the substrate specificity of sll1981 towards pyruvate, d-glucose-6-phosphate and α-ketoglutarate was examined using homogenous recombinant sll1981. Steady-state kinetics results showed that sll1981 was a dual functional enzyme, which displayed much higher activity as α-KGD than as ALS. At the same time the MIPS activity of sll1981 was not detectable, although it was reported to be as MIPS previously. These findings not only confirmed the previous statement of the function of sll1981 as ALS and disputed the claimed function of sll1981 as MIPS, but also affirmed the new function of sll1981 as α-KGD. Therefore sll1981 was probably a key enzyme in completing the TCA cycle of Synechocystis sp. PCC6803.

Plasma D-lactate Levels in Necrotizing Enterocolitis in Premature Infants.

BACKGROUND: D-Lactate is normally present in the blood of humans at nanomolar concentrations due to methylglyoxal metabolism; millimolar D-lactate concentrations can arise due to excess gastrointestinal microbial production. OBJECTIVES: To examine the levels of plasma D-lactate in the necrotizing enterocolitis in premature infants. PATIENTS AND METHODS: 128 premature infants were divided into control (group I, n = 69), feeding intolerance (group II, n = 42) and NEC (group III, n = 27) groups. Plasma D-lactate levels were measured at the onset of feeding intolerance or NEC and at weeks 2-3 in control infants (group I) by ELISA. Data were analyzed using descriptive statistics, non-parametric tests and Student's t-test. RESULTS: In groups I, II, III, median birth weights were 1845.7 ± 267.5 g, 1913.1 ± 306.5 g, and 1898.4 ± 285.3 g, median gestational ages were 34.3 ± 1.7 weeks, 33.9 ± 2.2 weeks and 35.1 ± 2.6 weeks, ages of sampling were 12.3 ± 2.9 days, 14.6 ± 3.7 days and 15.1 ± 1.8 days, respectively. The differences of median birth weights, median gestational ages and ages of sampling were not statistically significant (P > 0.05). The plasma D-lactate levels in groups I, II, III were 3.6 ± 1.9 µg/mL, 12.7 ± 8.3 µg/mL, and 35.4 ± 29.1 µg/mL, respectively, group III had higher plasma D-lactate level than groups I, II, and the difference among these groups was significant (x(2) = 21.6, P < 0.01). CONCLUSIONS: Plasma D-lactate significantly increased early in NEC. Plasma D-lactate levels were associated with extensive disease in NEC infants. Therefore, it could be used as a diagnosis indicator in the early stage of NEC.

[Value of serum cytosolic ß-glucosidase in diagnosis of neonatal necrotizing enterocolitis].

OBJECTIVE: This study was conducted to compare serum cytosolic ß-glucosidase (CBG) levels of age-matched control patients with those of infants with necrotizing enterocolitis (NEC) thereby to determine the eventual association between serum CBG levels with extensive disease in infants with NEC. METHOD: A total of 96 premature infants were divided into the early NEC group (n = 25), confirmed NEC group (n = 23) and the control group (n = 48). Serum CBG concentration, C-reactive protein (CRP) and peripheral blood white blood cells (WBC) were measured at the onset of the disease in patients in early NEC or confirmed NEC groups and at weeks 2-3 in control infants. Data were analyzed using descriptive statistics, non-parametric tests, Student's t-test, linear correlation, Spearman correlation analysis, receiver operating characteristic (ROC) curve were used for statistical analysis. RESULTS: The median birth weights (mean ± SE) in the three groups were not statistically significant (P > 0.05). Serum CBG concentration in the 3 groups were (112.369 ± 108.539) nmol/L, (693.013 ± 211.614) nmol/L and (36.478 ± 28.31) nmol/L, respectively. The infants in the confirmed NEC group had highest CBG levels, compared with the other 2 groups (P < 0.05). When the levels of CBG ≥ 65 ng/ml, CRP ≥ 2 mg/L and WBC < 5 × 10(9)/L within 3 days after birth or > 20 × 10(9)/L 3 days after birth were considered as positive parameters, the sensitivity of CBG and CRP was higher than that of WBC (P < 0.05). Among these indices, CBG had the highest specificity (87.4%), positive predictive (95.6%) and Youden's index (81.3%). CBG is correlated with CRP (the Spearman correlation coefficient was 0.379, P < 0.01). CONCLUSION: Serum CBG concentration increases early in NEC. Serum CBG level was associated with extensive disease in infants with NEC. Therefore CBG can be used as a marker in the early diagnosis of NEC.