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Objective:To investigate the nutritional risk and the incidence of malnutrition in children with recurrent abdominal Henoch Schonlein purpura(HSP), and observe the changes in the incidence of malnutrition after nutritional intervention.Methods:We retrospectively analyzed 90 children diagnosed with recurrent HSP in our hospital from 2017 to 2019.The cases were divided into two groups according to whether nutritional intervention was performed.The cases from January 2017 to May 2018 were chosen as the control group( n=42), and the cases from June 2018 to December 2019 were chosen as the experimental group( n=48). Based on the treatment of the primary disease, the high nutritional risk cases in experimental group were treated with extensively hydrolysed infant formula for nutritional intervention.The children were evaluated for nutritional risk with the STRONGkids nutrition tool.According to the score results, they were divided into high nutritional risk group and medium nutritional risk group.The Z score was used to evaluate malnutrition, and the degree of malnutrition was compared at admission and discharge. Results:Eighty-one children (90.0%) with recurrent abdominal allergic purpura had a high nutritional risk, 9 cases (10.0%)had a medium nutritional risk.There was no significant difference in the incidence of moderate and severe malnutrition between experimental group and control group at admission[39.6% (19/48) vs.40.5% (17/42), P>0.05]. The incidence of moderate and severe malnutrition in control group was higher than that in experimental group at discharge[66.7% (28/42) vs.22.9% (11/48), P<0.05]. Conclusion:In children with recurrent abdominal HSP, due to severe gastrointestinal symptoms and a high incidence of high nutritional risk, nutritional intervention with extensively hydrolysed infant formula can avoid the occurrence or aggravation of iatrogenic malnutrition during hospitalization.
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Objective To investigate the clinical and pathological characteristics of Henoch-Sch?nlein purpura nephritis with diffuse capillary endothelial cell proliferation as pathological manifestation. Methods The clinical manifestations and pathology of capillary endothelial proliferative purpura nephritis (DEP-HSPN) diagnosed by renal biopsy were retrospectively analyzed in 50 children in recent 5 years. Results The pathological lesions in 50 cases included simple DEP-HSPN in 11 cases (7 males and 4 females) and capillary endothelial cell proliferation combined with crescents formation (non-simple DEP-HSPN) in 39 cases (27 males and 12 females). There was no significant difference in the course of disease and age between the two groups (P>0.05). The clinical type of 11 cases of simple DEP-HSPN was type Ⅲ. In 39 cases of non-simple DEP-HSPN, 16 cases were type Ⅲ and 23 cases were type Ⅴ. All of the children had hematuria and proteinuria. The incidence of gross hematuria, urine red blood cell count, 24 h urine protein, and serum creatinine levels in children with non-simple DEP-HSPN were significantly higher than those in simple DEP-HSPN group, but the plasma albumin level was significantly lower than that in simple DEP-HSPN group. It was easy to have crescent formation in DEP-HSPN, and the rate of crescent formation was 11.1％ (5.0％-27.6％). The incidence of segmental lesions and renal tubular interstitial damage was low. All children had non simple IgA deposits in the mesangial area. In the 50 children treated for 1 year, 22 had complete remission, 28 had asymptomatic hematuria, and none had active nephropathy and renal insufficiency. In 32 cases of non-simple DEP-HSPN, the 24 h urinary protein, plasma albumin level, and the incidences of gross hematuria and microscopic hematuria were statistically different before treatment and 1, 3, 6, 12 months after treatment (P<0.01). The 24 h urine protein and gross hematuria gradually decreased with the prolongation of treatment, while the level of plasma albumin was gradually increased. Conclusions DEP-HSPN is characterized by gross hematuria and proteinuria. The onset is acute and it is easy to have crescent formation. When combined with crescent formation, the clinical symptoms are more severe. The combination of strong immunosuppressive agents and long-term sequential follow-up treatment is effective in acute stage. The prognosis is good.
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BACKGROUND:Human umbilical cord mesenchymal stem cel s belong to a special class of stem cel s with a limited number, which are difficult to isolate and purify. Importantly, there is a lack of clinical understanding of biological characteristics of human umbilical cord mesenchymal stem cel s. OBJECTIVE:To study the bioactive properties and cardiomyocyte-like differentiation of human umbilical cord mesenchymal stem cel s. METHODS:Under a sterile col ection, umbilical cord blood of newborn from cesarean section was col ected to isolate human mesenchymal stem cel s by digestion using col agenase II. Immunohistochemical staining was used to detect cel surface markers and observe morphological characteristics, and MTT assay used to detect cel proliferation and draw cel growth curve. Cel s grown to 70%-80%confluence were treated with 10μmol/L 5-azacytidine for 24 hours. RESULTS AND CONCLUSION:One week after adherent tissue culture, human umbilical cord mesenchymal stem cel s were seen, and then the cel s cultured in culture medium showed colony growth. Within 24 hours of cel seeding, cel s at passages 3 and 10 were at latency period and then grew logarithmical y with a doubling time of 30 hours. Immunocytochemical staining showed that passage 3 cel s at over 90%confluence expressed CD44 and CD29, rather than CD28 and CD31.Three weeks after induced culture, the cel s with the absence of processes grew irregularly;after 4 weeks, the cel s were round in shape and expressed cardiac-specific immune markers. Taken together, isolated human umbilical cord mesenchymal stem cel s with strong proliferative ability have the basic biological characteristics of mesenchymal stem cel s, which are capable of differentiating into cardiomyocyte-like cel s induced by 5-azacytidine.
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Objective:To construct the mammalian CO-expression plasmid pBudCE4.1-LMP-1-LMP-3,and to detect the expression of the plasmid in vitro.Methods:Fragments of LMP-1 gene and Fragments of LMP-3 gene were gained from the Company,and were constructed respectively into the plasmid vector Puc57,The inserted target genes in plasmid were verified by nucleotide sequencing and enzymes.fragments of LMP-1 gene were constructed firstly into the plasmid vector pBudCE4.1,fragments of LMP-3 gene were constructed into the plasmid vector pBudCE4.1-LMP-1 after iden tification with nucleotide sequencing and enzymes.MSCs cell line was transfected with this Co-expression plasmid using lipofectin reagent.according to the transfect situation,the MSCs were divided into 5 groups,the non-transfected group(Group A),the group transfected by empty vector(Group B),the group transfected by LMP-1(Group C),the group transfected by LMP-3(Group D)and the group transfected both LMP-1 and LMP-3(Group E).the expression of LMP-1 and LMP-3 were detected by RT-PCR and Western blot technique.Results:The plasmids Puc57-LMP-1、Puc57-LMP-3 and pBudCE4.1-LMP-1-LMP-3 were obtained successfully and verified by nucleotide sequencing and enzymes.After transfection with this mammalian Co-expression plasmid,the LMP-1 and LMP-3 molecules were expressed in MSCs cells.The results of RT-PCR and Western Blot were measured with the grey value.To the expression of mRNA and protein of LMP-1,the diferences between groups A、B and groups C、D、E were significant(P0.05);To the expression of mRNA and protein of LMP-3,the diferences between groups A、B and groups C、D、E were significant(P0.05).Conclusion:the constructed mammalian Co-expression plasmid pBudCE4.1-LMP-1-LMP-3 can express LMP-1 and LMP-3 molecules in vitro at the same time.