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Objective:To investigate the relationship between inherited dysplasminogenemia and cerebral infarction (CI) by phenotype and gene mutation analysis of 2 inherited dysplasminogenemia pedigrees.Methods:Retrospective analysis was carried out on clinical data of 2 patients diagnosed with CI who were treated in the Department of Neurology, the First Affiliated Hospital of Wenzhou Medical University in January and March 2021, and peripheral venous blood samples were collected from proband 1 and his family members (8 subjects, 4 generations in total) and proband 2 and her family members (5 subjects of 3 generations in total), and their plasminogen (PLG) activity (PLG:A), protein C activity, protein S activity, antithrombin activity and the content of PLG antigen (PLG: Ag), fibrinogen, D-dimer and fibrinogen degradation products were measured for definite diagnosis. All 19 exons,5′ and 3′ untranslated regions of PLG were amplified with polymerase chain reaction, and the amplification products were analyzed by direct DNA sequencing. The results were compared with human PLG reference sequences published in the National Center for Biotechnology Information database using Chromas software to find the mutation sites, and confirmed by reverse sequencing.Results:Both of the 2 patients with confirmed CI had a young onset, and PLG: A was reduced to 21% in the proband 1 and to about 50% in 4 family members; PLG: A was reduced to about 50% in the proband 2 and 2 family members; PLG:Ag and the above tests were essentially normal in both probands and family members. Gene analysis showed that the proband 1 had the homozygous mutation of c.1858G>A in exon 15, the 4 family members of the proband 1, proband 2 and her 2 family members had the heterozygous mutation of c.1858G>A in exon 15, which resulted in a mutation of alanine at position 620 in PLG to threonine (p.Ala620Thr).Conclusions:The decrease of PLG:A was caused by the p.Ala620Thr missense mutation of PLG gene. Proband having CI may be related to the inhibition of fibrinolytic function in the organism due to the p.Ala620Thr missense mutation.
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Objective To observe the changes of tear film stability,goblet cell and mucin 5AC expression in conjunctivochalasis patients,and explore the mechanism of conjunctivochalasis.Methods Conjunctivochalasis patients (30 cases) and single age-related cataract patients (15 cases) were collected as conjunctivochalasis group and normal control group.Eye symptom assessment (OSDI score),tear break-up time (BUT),Schirmer Ⅰ test,tear fern crystallization tests were performed for all the selected persons.Conjunctival rescent-shaped resections were made for all the conjunctivochalasis patients.Conjunctival tissue samples were stained by HE staining,AB staining,mucin 5AC immunohistochemical staining from the conjunctivochalasis group and norral control group respectively,and then statistical analysis was made.Results The OSDI score in the conjunctivochalasis group (37.80 ± 8.94) was significantly higher than that in the normal control group (11.40 ±4.08) (P ＜0.01).BUT in the conjunctivochalasis group (6.70 ± 2.76) s was significantly lower than that in the normal control group (13.67 ± 3.48) s (P ＜ 0.01).Schirmer Ⅰ test in the conjunctivochalasis group (6.23 ± 3.13) mum was significantly lower than the normal control group (13.40 ± 3.74)mm (P ＜ 0.01).Tear ferbing crystallization of the conjunctivochalasis group was decreased significantly compared with the normal control group (x2 =14.309,P =0.003).Light microscopic showed that conjunctival thickness was thinned,collagen fibers were less,elastic fiber was reduced,the lamina propria and interstitial were congestion and edema,the number of goblet cells was significantly reduced,and the positive staining of mucin 5AC staining was significantly lower in the conjunctivochalasis group than in normal control group (x2 =9.499,P =0.023).Conclusion For patients with conjunctivochalasis,the tear film function is affected,goblet cells are decreased,tear fern crystallization is decreased,mucin 5AC content is decreased,which finally leads the excessive conjunctival relaxation and abnormal ocular surface and tear.
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BACKGROUND:Abnormal immunological function is possibly observed after cardiac valve replacement. However, effect of continuous venovenous hemofiltration on immunological function after cardiac valve replacement is rarely reported. OBJECTIVE:To observe the effect of continuous venovenous hemofiltration on the cellular immune function in patients with multiple organ dysfunction syndrome after cardiac valve replacement. METHODS:Thirty-one patients with multiple organ dysfunction syndrome after cardiac valve replacement in Xijing Hospital, the Fourth Military Medical University of Chinese PLA, from August 2008 to July 2009, were included in this study. They were treated with continuous venovenous hemofiltration using AV600 hemofilter and were divided into two groups:survival group (17 survivors) and death group (14 deaths). In addition, 16 healthy blood donors served as the control group. RESULTS AND CONCLUSION:The duration of acute renal failure before continuous venovenous hemofiltration of survival group was significantly lower than that of death group (P<0.05). Before continuous venovenous hemofiltration, the CD4+/CD8+ratio and Th1/Th2 ratio of survival group and death group were lower than that of control group (P<0.05), and lymphocyte apoptosis rate and Fas/FasL antigen expression were higher than that of control group (P<0.05). This evidence suggested the presence of immunosuppression state and Th1/Th2 disbalance. During continuous venovenous hemofiltration, the CD4+/CD8+ratio and Th1/Th2 ratio of survival group were gradual y increased (P<0.05), while lymphocyte apoptosis rate and Fas/FasL antigen expression were gradual y decreased (P<0.05) at 24 hours. The above changes were observed in both survival group and death group, but emerged latter in death group. Continuous venovenous hemofiltration can improve cellular immune function, maintain the balance of T lymphocyte subsets and Th1/Th2, down-regulate Fas/FasL expression on the surface of lymphocyte membrane, and decrease lymphocyte apoptosis rate in patients with multiple organ dysfunction syndrome after cardiac valve replacement. Early continuous venovenous hemofiltration can improve patients’ prognosis.
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Objective To evaluate the clinical effects of intra-lamellar orbicularis dissecting micro-traumatic double eyelid surgery for the treatment of adolescent upper eyelid trichiasis. Methods Three cutaneous micro-incisions following intra- and sub-lamellar orbicularis dissections were performed and the deep orbieularis and suborbicularis fat pad between the intended eyelid crease and 1 mm above the eyelid margin were resected. The subcutaneous orbicularis was fixed to the exposed levator aponeurosis at the medial, center and lateral regions. For the quantitative analysis, the entire eyelid margins' eyelashes were equally divided into three sections and the eyelashes lift-up angle (LA), the body curl-up angle (BC) and the end curl-up angle (EC) were compared before and after surgery in each section, respectively. Results One hundred and fourteen eyes of 57 cases were followed up during 24-30 months. Compared to the LA before surgery and 2 years after surgery, it was changed from (26.37±9.67)° to (55.42± 10.03)° in section Ⅰ , and from (22.03±11.64)° to (50.03±10.02)° in section Ⅱ , and from (25.31±8.01)° to (64.05±8.33)° in section Ⅲ. There were no significant changes of BC and EC during following-up. Con-clusions For the adolescent upper eyelid trichiasis, the intra-lamellar orbicularis dissecting micro-trau-matic double eyelid surgery could acquire satisfactory aesthetic appearance and stable eyelashes'position at the same time.
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BACKGROUND:Comeal graft endothelial cell density may decline spontaneously at a super-physiological speed after penetrating keratoplasty (PKP),even if no corneal rejection happens,and this is chronic corneal allograff dysfunction (CCAD).OBJECTIVE:To investigate the effects of topical corticosteroid treatment on chronic corneal allograft dysfunction after PKP.DESIGN,TIME AND SETTING:A controlled clinical analysis was performed at the Department of Ophthalmology,Tongji Hospital,Tongji University from May 2004 to May 2009.PARTICIPANTS:A total of 54 patients (eyes) who underwent PKP were included in this study.METHODS:Tobramycin-dexamethasone eyedrops was applied 6 times per day as an initial dosage and tapered during 4 months.Thereafter,drug withdrawal group and long term group were randomly divided.Treatments were ceased in the drug withdrawal group but were continued in the long-term group with a dosage of twice per day till 12 months after surgery.MAIN OUTCOME MEASURES:Corneal graft endothelial cell density was followed up.The mean follow up pedod was 3.12±0.28years.RESULTS:The corneal graft endothelial cell density of drug withdrawal and long term groups was dramatically declined within 36 months after PKP.At every time point,the endothelial cell density was significantly decreased compared to the last follow up (all P＜0.01 ).The endothelial cell density was decreased from (2 428±2.11) cells/mm~2 and (2 791±2.29) cells/mm~2 to (1 424±124) cells/mm~2 and (1 614±114) cells/mm~2 in the drug withdrawal and long-term groups,respectively.There was significant difference in endothelial cell density between the two groups no matter prior to surgery or at each time points after surgery,but the declination trends of two groups were basically the same,indicating that graft loss of endothelial cell density was not impacted by topical corticosteroid treatment after PKP (P＞0.05).CONCLUSION:Chronic corneal allograft dysfunction after PKP is independent of topical corticosteroid treatment.
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Objective To estimate the relationships between lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and cerebral feeding artery athemsclemsis.Methods The blood samples were obtained from 148 atheroselerosis patients (atheroselerosis group) and 40 normal controls (control group).Activity of plasma Lp-PLA2 and traditional factors were determined.Logistic and regression model was adopted to analyze the roles of Lp-PLA2 and generally inflammatory risk factors in athemselemsis.Results Lp-PLA2 activity was significantly higher in atheroselerosis group than that in control group [(29.84±3.50)lesion number showed positive correlation with Lp-PLA2 (r=0.491,P＜0.01 and r=0.249,P=0.026).Adjusted other risk factors,Lp-PLA2 was an independent risk factor in cerebral feeding artery atherosclerosis.Conclusion Lp-PLA2,a novel inflammatory marker,is an independent risk factor of cerebral feeding artery atherosclerosis.
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Objective To investigate the effects of total anthraquinone in rheum on aquaporin 2 and aquaporin 4 expression in rat kidney and explore its diuresis mechanism.Methods Thirty-two SD rats were randomly divided into control group,low dose group,medium dose group and high dose group.Total anthraquinone in rheum was administered to rats at different doses.Urinary volume of 24 h,Na+ concentration and osmolality were detected.Rats were sacrificed 5 days later.Blood samples were taken from the abdominal aorta to detect blood biochemical indicators. Kidneys of rats were removed to detect AQP2, AQP4 expression through immunohistochemistry,Western blot,and RT-PCR. Results Compared with control group,there were significantly increased 24 h urine output of rats in medium and high dose group[(16.21±1.96),(18.16±1.8) ml vs(13.85±1.25)ml,P＜0.05].24 h urine output in low-dose group did not change significantly.AQP2 protein and mRNA expression were significantly decreased in rats'kidneys of medium and high dose group (P＜0.01),The AQP4 protein and mRNA expression was significantly down-regulated in high dose group (P＜0.01).In medium does group,the AQP4 protein expression was down-regulated (P＜0.01),without significant decrease in the mRNA expression.Protein and mRNA expression of AQP2 and AQP4 did not significantly change in low dose group.Conclusion Total anthraquinone in rheum can reduce the expression level of AQP2 and AQP4 in rat kidney,which is probably one mechanism of diuresis caused by rheum.