Objective To assess the relationship between single nucleotide polymorphisms of FcεRIαgene and atopic dermatitis. Methods Genomic DNA samples were extracted from peripheral blood of 97 patients with atopic dermatitis and 283 normal human controls. The polymorphism at the distal promoter region of FcεRIα gene was determined by PCR-ligase detection reaction assay followed by gene sequencing. Results A G/T polymorphism was observed at position rs61828219 in the promoter region of FcεRIα gene, while all the tested individuals were homozygous for T/T at position rs12135235 and A/A at position rs36233780 in the promoter region of FcεRIα gene. The mutation frequency at position rs61828219 was 1.04% and 2.17% in patients with AD and normal human controls, respectively (both P ＞ 0.05). Conclusions In the Chinese Han population, there is a G/T polymorphism at position rs61828219 in FcεRIα gene promoter region, which is unlikely related to the development of AD; however, no polymorphism is detected at position rs12135235 or rs36233780.

Objective To investigate the clinical characteristics,surgical treatment and outcome for patients with duodenal stromal tumor.Methods Data of 40 patients with stromal tumor of duodenum were reviewed retrospectively.Results All patients received resection including local resection in 14 cases,segmental resection of the duodenum in 17 cases,and pancreaticoduodenectomy in 9 cases.38 cases were followed-up,and two were lost.The median follow-up was 59 months (range 3-240 mos).The 1,3,and 5-year overall survival rates were 92％,76％ and 68％,respectively.No recurrence was found in very-low-risk tumor (n =1) and low-risk turmors (n =4).The 1,3,and 5-year overall survival rates for intermediate-risk tumors were 95％,80％ and 70％,respectively;and those were 69 ％,31％,and 0 for high-risk tumors,respectively.14 of 33 cases (42％) suffered from recurrence after radical resection for intermediate or high-risk tumors.33 postoperative cases received treatment with Imatinib (Glivec) for more than one year,and one case developed recurrence at 2.5 years after operation.4 patients with synchronous liver metastasis received palliative resection and Imatinib,and two survived more than 1 year.Conclusion Surgery is the first choice for duodenal stromal tumor,and Imatinib should be administered for high-risk disease after surgery.

Objective:To establish the fingerprint analysis method for the root of Rosa laevigata Michx from different regions by UPLC. Methods:The column was ACQUITY UPLC? Phenyl(2.1 mm × 100 mm,1.7 μm). The mobile phase consisted of methanol-water with gradient elution. The flow rate was 0. 2 ml·min-1 , the detection wavelength was 210 nm, the column temperature was 30℃, and the injection volume was 3 μl. Results:The fingerprint consisted of 15 common peaks. The range of similarity for twelve bat-ches of the root of R. laevigata Michx was 0. 489-0. 942. And the reference fingerprint of the root of R. laevigata Michx was estab-lished by UPLC. Conclusion:The fingerprint method is simple and reproducible, which can provide basis for the quality control and the medicinal resources exploration.

Objective:To investigate the clinical efficacy of redo rectal resection and coloanal anastomosis.Methods:The retrospective and descriptive study was conducted. The clinicopatholo-gical data of 49 patients who underwent redo rectal resection and coloanal anastomosis for the treatment of local recurrence of tumors and failure of colorectal or coloanal anastomosis after rectal resection in the Sixth Affiliated Hospital of Sun Yat-sen University from November 2012 to December 2021 were collected. There were 32 males and 17 females, aged 57(range,31-87)years. Redo rectal resection and coloanal anastomosis was performed according to the patient′s situations. Observa-tion indicators: (1) surgical situations; (2) postoperative situations; (3) follow-up. Measurement data with normal distribution were represented as Mean± SD, and measurement data with skewed distri-bution were represented as M( Q1, Q3) or M(range). Count data were described as absolute numbers or percentages. Results:(1) Surgical situations. All 49 patients underwent redo rectal resection and coloanal anastomosis successfully, with the interval between the initial surgery and the reopera-tion as 14.2(7.1,24.3)months. The operation time and volume of intraoperative bold loss of 49 patients in the redo rectal resection and coloanal anastomosis was 313(251,398)minutes and 125(50,400)mL, respectively. Of the 49 patients, there were 38 cases receiving laparoscopic surgery including 12 cases with transanoscopic laparoscopic assisted surgery, 11 cases receiving open surgery including 2 cases as conversion to open surgery, there were 20 cases undergoing Bacon surgery, 14 cases undergoing Dixon surgery, 12 cases undergoing Parks surgery, 2 cases undergoing intersphincter resection and 1 case undergoing Kraske surgery, there were 20 cases undergoing rectum dragging out excision and secondary colonic anastomosis, 13 cases undergoing dragging out excision single anastomosis, 12 cases undergoing rectum dragging out excision double anastomosis, 4 cases undergoing first-stage manual anastomosis, there were 21 cases with enterostomy before surgery, 16 cases with prophylactic enterostomy after surgery, 12 cases without prophylactic enterostomy after surgery. The duration of postoperative hospital stay of 49 patients was (14±7)days. (2) Postoperative situations. Fifteen of 49 patients underwent postoperative complications, including 8 cases with grade Ⅱ Clevien-Dindo complications and 7 cases with ≥grade Ⅲ Clevien-Dindo complications. None of 49 patient underwent postoperative transferring to intensive care unit and no patient died during hospitalization. Results of postoperative histopathological examination in 23 patients with tumor local recurrence showed negative incision margin of the surgical specimen. (3) Follow-up. All 49 patients underwent post-operative follow-up of 90 days. There were 42 cases undergoing redo rectal resection and coloanal anastomosis successfully and 7 cases failed. Of the 37 patients with enterostomy, 20 cases failed in closing fistula, and 17 cases succeed. There were 46 patients receiving follow-up with the median time as 16.1(7.5,34.6)months. The questionnaire response rate for low anterior resection syndrome (LARS) score was 48.3%(14/29). Of the patients who underwent redo coloanal anastomosis and closure of stoma successfully, there were 9 cases with mild-to-moderate LARS.Conclusion:Redo rectal resection and coloanal anastomosis is safe and feasible for patients undergoing local recurr-ence of tumors and failure of colorectal or coloanal anastomosis after rectal resection, which can successfully restore intestinal continuity in patients and avoid permanent enterostomy.

Fractures are frequently occurring diseases that endanger human health. Crucial to fracture healing is cartilage formation, which provides a bone-regeneration environment. Cartilage consists of both chondrocytes and extracellular matrix (ECM). The ECM of cartilage includes collagens and various types of proteoglycans (PGs), which play important roles in maintaining primary stability in fracture healing. The PG form of dentin matrix protein 1 (DMP1-PG) is involved in maintaining the health of articular cartilage and bone. Our previous data have shown that DMP1-PG is richly expressed in the cartilaginous calluses of fracture sites. However, the possible significant role of DMP1-PG in chondrogenesis and fracture healing is unknown. To further detect the potential role of DMP1-PG in fracture repair, we established a mouse fracture model by using a glycosylation site mutant DMP1 mouse (S89G-DMP1 mouse). Upon inspection, fewer cartilaginous calluses and down-regulated expression levels of chondrogenesis genes were observed in the fracture sites of S89G-DMP1 mice. Given the deficiency of DMP1-PG, the impaired IL-6/JAK/STAT signaling pathway was observed to affect the chondrogenesis of fracture healing. Overall, these results suggest that DMP1-PG is an indispensable proteoglycan in chondrogenesis during fracture healing.

The blood-brain barrier (BBB) is a tight boundary formed between endothelial cells and astrocytes, which separates and protects brain from most pathogens as well as neural toxins in circulation. However, detailed molecular players involved in formation of BBB are not completely known. Dentin matrix protein 1 (DMP1)-proteoglycan (PG), which is known to be involved in mineralization of bones and dentin, is also expressed in soft tissues including brain with unknown functions. In the present study, we reported that DMP1-PG was expressed in brain astrocytes and enriched in BBB units. The only glycosylation site of DMP1 is serine89 (S89) in the N-terminal domain of the protein in mouse. Mutant mice with DMP1 point mutations changing S89 to glycine (S89G), which completely eradicated glycosylation of the protein, demonstrated severe BBB disruption. Another breed of DMP1 mutant mice, which lacked the C-terminal domain of DMP1, manifested normal BBB function. The polarity of S89G-DMP1 astrocytes was disrupted and cell-cell adhesion was loosened. Through a battery of analyses, we found that DMP1 glycosylation was critically required for astrocyte maturation both in vitro and in vivo. S89G-DMP1 mutant astrocytes failed to express aquaporin 4 and had reduced laminin and ZO1 expression, which resulted in disruption of BBB. Interestingly, overexpression of wild-type DMP1-PG in mouse brain driven by the nestin promoter elevated laminin and ZO1 expression beyond wild type levels and could effectively resisted intravenous mannitol-induced BBB reversible opening. Taken together, our study not only revealed a novel element, i.e., DMP1-PG, that regulated BBB formation, but also assigned a new function to DMP1-PG.
Animals ; Astrocytes ; cytology ; metabolism ; Blood-Brain Barrier ; cytology ; metabolism ; Cells, Cultured ; Extracellular Matrix Proteins ; genetics ; metabolism ; Female ; Glycosylation ; Male ; Mice ; Proteoglycans ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

In the original publication, the label of Fig. 2C should be read as "GFAP/lectin/DAPI" not "DMP1/GFAP/lectin/DAPI".