Clinical Observation of Sequential Laser Therapy Combined with Tension Reducer for Postoperative Tension Incision Scar Growth.

Objective: To investigate the clinical effectiveness of laser and secure wound-closure system (Tension reducer) in the treatment of postoperative scarring after tension incision. Methods: A retrospectively observational study was conducted. Twenty-six patients who underwent surgical treatment in our department between June 2017 and December 2021 were selected, and those treated with laser and tension reducer were treated as a combined treatment group, and those treated with laser were treated as a conventional treatment group. Fifteen patients in the conventional group were treated with the pulsed dye laser and CO2 fractional laser at 1-2 month intervals. Eleven people in the combined treatment group were treated with the laser in addition to a tension reducer for 3-6 months. The scar width, scar thickness, scar hardness, pruritus score, modified Vancouver scar scale and complication rates between the two treatment modalities were compared between the two groups at 6 months postoperatively. Results: The scar thickness, scar hardness and modified Vancouver scar scale of 1.25 (0.14, 1.90) mm, 31.80 (21.00, 37.20) HA, (6.00 ± 2.17) in patients in the combined treatment group were less than those of patients in the conventional treatment group of 5.50 (4.00, 11.50) mm, 42.60 (32.50, 47.00) HA, (8.25±1.91), (Z=2.883, 2.718, t=2.904, p<0.05). The scar width and pruritus score in the combined treatment group, were 8.00 (5.00, 18.00) mm and 0 (0, 1) respectively, while the scar score and pruritus score in the conventional treatment group, were 5.50 (4.00, 11.50) mm respectively, with no statistically significant difference between the two groups. The complication rate was 55% in the combined treatment group and no adverse reactions occurred in the control group. Conclusion: Sequential laser combined with tension reducer treatment can effectively inhibit the proliferation of postoperative tension incision scar.

Potential protein-phenotype correlation in three lipopolysaccharide-responsive beige-like anchor protein-deficient patients.

BACKGROUND: Patients with lipopolysaccharide (LPS)-responsive beige-like anchor protein (LRBA) deficiency have a variety of clinical symptoms, but there is no apparent genotype-phenotype correlation, and patients carrying the same mutations may have different phenotypes. Therefore, it is not easy for doctors to make a decision regarding hematopoietic stem cell transplantation (HSCT) for LRBA-deficient patients. We hypothesized that there may be a protein-phenotype correlation to indicate HSCT for LRBA-deficient patients. AIM: To report on three Chinese LRBA-deficient patients and determine the correlation between residual protein expression and disease phenotypes. METHODS: Clinical data of three Chinese LRBA-deficient patients were collected, and protein levels were detected by Western blot analysis. In addition, LRBA mutation information of another 83 previously reported patients was summarized. RESULTS: All the major clinical findings indicated enteropathy, but patients 1 and 3 presented with more severe symptoms than patient 2. Endoscopy and histology indicated nonspecific colitis for patients 1 and 3 but Crohn's disease-like colitis for patient 2. Compound heterozygous mutations in LRBA were found in patient 1, and homozygous mutations in LRBA were found in patient 2 and patient 3. Only patient 2 responded well to traditional immunosuppressive treatment. Residual expression of the LRBA protein in patients 1 and 3 was very low, but in patient 2, a more than 0.5-fold in expression of the LRBA protein was found compared to that in the control. After HSCT, patient 1 had increased LRBA protein expression. We summarized the genetic information of 86 patients, and the mutations in patients 1 and 3 were novel mutations. CONCLUSION: We described three Chinese LRBA-deficient patients, two of whom carried novel mutations. These patients had no genotype-phenotype correlations, but their residual LRBA protein expression might be associated with disease outcome and could be an indicator for HSCT.

Intestinal dysbiosis in pediatric Crohn's disease patients with IL10RA mutations.

BACKGROUND: Several studies have employed animal models to explore the association between microbiota and interleukin (IL) 10 signaling; however, limited information is available about the human microbiome. AIM: To characterize the microbiome in patients with IL10RA mutations and to explore the association between gut dysbiosis and disease severity. METHODS: Fecal samples were collected from patients who were diagnosed with loss-of-function mutations in the IL10RA gene between January 2017 and July 2018 at the Children's Hospital of Fudan University. Age-matched volunteer children were recruited as healthy controls. Patients with Crohn's disease (CD) were used as disease controls to standardize the antibiotic exposure. Microbial DNA was extracted from the fecal samples. All analyses were based on the 16S rRNA gene sequencing data. RESULTS: Seventeen patients with IL10RA mutations (IL10RA group), 17 patients with pediatric CD, and 26 healthy children were included. Both patients with IL10RA mutations and those with CD exhibited a reduced diversity of gut microbiome with increased variability. The relative abundance of Firmicutes was substantially increased in the IL10RA group (P = 0.02). On further comparison of the relative abundance of taxa between patients with IL10RA mutations and healthy children, 13 taxa showed significant differences. The IL10RA-specific dysbiosis indices exhibited a significant positive correlation with weighted pediatric CD activity index and simple endoscopic score for CD. CONCLUSION: In patients with IL10RA mutations and early onset inflammatory bowel disease, gut dysbiosis shows a moderate association with disease severity.

Wenyang Huoxue Jiedu formula inhibits thin-cap fibroatheroma plaque formation via the VEGF/VEGFR signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: For many years, Guangzhou University of Chinese Medicine has been successfully using the empirical Wenyang Huoxue Jiedu formula (WHJF) to treat coronary heart disease. Modern theories of acute coronary syndrome mainly focus on rupture of thin-cap fibroatheromas (TCFAs), which is closely related to the release of vascular endothelial growth factor and its receptor (VEGF/VEGFR). AIM OF STUDY: We investigated the effects of WHJF on the formation of TCFA plaques and the potential mechanism (VEGF/VEGFR signaling pathway). MATERIALS AND METHODS: For the in vivo experiments, WHJF was administered to ApoE-/- mice, as a model of TCFA plaque formation. Aortic sections of the mice were obtained, and the vulnerability index and new vessel density of plaques were calculated by the Movat staining assay and immunohistochemistry kit, respectively. Protein and mRNA expression levels of VEGF/VEGFR in aortas were assayed by capillary electrophoresis immunoassay and quantitative real-time polymerase chain reaction analyses. In vitro, WHJF serum was produced in rats on the fourth day 2 h after the first administration of different concentrations of WHJF. Proliferation, migration, and lumen formation ability of human umbilical vein endothelial cells (HUVECs) treated with sera from these rats were assayed by the CKK-8 kit, Transwell plates, and Matrigel assay, respectively. Protein and mRNA expression levels of signaling molecules in the VEGF/VEGFR pathways were also examined. RESULTS: In vivo, the vulnerability index and new vessel density of plaques in the WHJF group were lower than those values in the blank control group (P < 0.05). No differences were found between the groups in the expression levels of VEGF/VEGFR (P > 0.05). In vitro, the proliferation, migration, and tube formation of HUVECs in the high-dose WHJF group were reduced compared to the control group (P < 0.05). This finding was in agreement with the downregulation of VEGFR-2 and pERK (P < 0.05). The mRNA expression of signaling molecules showed no difference between the groups (P > 0.05). CONCLUSIONS: WHJF inhibits TCFA formation by influencing the VEGF/VEGFR signaling pathway.

[Correlation between CYP2C19 Gene Polymorphism and Elderly Cerebral Infarction].

Objective To investigate the correlation between CYP2C19 gene polymorphism and elderly cerebral infarction.Methods Two polymorphisms including rs4244285 and rs4986893 of the CYP2C19 gene were detected by gene chip technology in 72 elderly patients with acute cerebral infarction (stroke group) and 77 otherwise healthy controls. The clinical data and the polymorphism distribution of CYP2C19 were compared,and the potential association between genetic polymorphism and cerebral infarction was analyzed by Logistic regression.Results The frequencies of rs4244285 GG (45.83% vs. 63.64%,Χ 2=4.766,P=0.029) and rs4244285 A allele (34.03% vs. 22.73%,Χ 2=4.695,P=0.030) were significantly higher in stroke group than in control group. There were no significant differences in the distribution of the alleles of rs4986893 or the rs4244285 GA and AA between these two groups (all P>0.05). After the conventional cerebrovascular risk factors including gender,age,body mass index,smoking,and total cholesterol were adjusted,Logistic regression analysis showed that rs4244285 A allele significantly increased the stroke risk [the additive model AA vs. GG:OR=2.564,95%CI=1.181-5.566,P=0.017;the dominant model AA/AG vs. GG:OR=2.763,95%CI=1.343-5.685,P=0.006].Conclusion CYP2C19 genetic polymorphism may be associated with the increased risk of cerebral infarction in the elderly,although future well-designed studies with larger sample sizes are warranted.

[Role of biological protective dressing in microskin grafting in rabbit].

OBJECTIVE: To study the effect of biological protective dressing made from porcine peritoneum in covering wounds with microskin grafts. METHODS: Twenty New Zealand rabbits were divided into ten couples according to the random number table. Rabbits in each couple underwent surgery at the same time. A piece of full-thickness skin of 5 cm in diameter was removed symmetrically from the left and right sides of the back of each rabbit, thus forming two wounds with full-thickness skin defect. One fifth of one piece of skin of one rabbit was cut into tiny pieces of 0.2-0.5 mm in size (microskin). Then the microskin pieces were spread on the two wounds of the donor rabbit with the microskin/wound area ratio 1:10. The two wounds of each rabbit covered with microskin were divided into two groups according to the random number table. One wound was covered with biological protective dressing prepared with porcine peritoneum as experiment group, and the other was covered with the rest allograft in full size obtained from the other rabbit of each couple as control group. The general condition of wound was observed at post operation week (POW) 1-4. Wound healing rate was calculated at POW 3 and 4. Wound healing time was recorded. Specimens were harvested from wounds for histological observation at POW 1-4. Data were processed with paired t test. RESULTS: (1) At POW 1, the biological protective dressings were found to attach firmly to the wounds in experiment group without obvious inflammatory response; the allografts survived well on the wounds in control group. At POW 2, the coverings attached well to the wounds of both groups, but became drier and darker as compared with those at POW 1. At POW 3, some wounds of the two groups healed when the coverings desiccated and separated. At POW 4, all the wounds of both groups healed without obvious difference in appearance. (2) The wound healing rates of the experiment and control groups were respectively (92.8 ± 6.2)% and (91.3 ± 7.3)% (t = 0.54, P > 0.05) at POW 3 and (98.1 ± 2.3)% and (97.0 ± 4.6)% (t = 0.38, P > 0.05) at POW 4. (3) The wound healing time was (25.0 ± 3.9) d in experiment group and (24.8 ± 2.3) d in control group. The difference between them was not statistically significant (t = 0.82, P > 0.05). (4) Histological observation showed that wounds of the two groups were all infiltrated by inflammatory cells, and new blood vessels were observed at POW 1 and 2. The survived microskin proliferated under the coverings. At POW 3 and 4, the coverings on the wounds of two groups were gradually degenerated and became necrotic and separated from the wound beds, while the wounds underneath were re-epithelialized. CONCLUSIONS: The effect of biological protective dressing in covering wounds grafted with microskin is as good as that of the allograft, as they both help the auto-microskin proliferate and repair the wound. It could be considered to be new biological material for clinical application.