OBJECTIVETo investigate the relationship between codon 54 gene polymorphism of the host defense molecule, mannose-binding protein (MBP), and the patterns of glomerular immune deposition in IgA nephropathy (IgAN).

METHODSIgAN patients with different patterns of glomerular immune deposition were selected and divided into two groups. Group A consisted of 77 patients with glomerular IgA and C3 deposits, and Group AGM consisted of 70 patients with glomerular IgA, IgG, IgM, C3 and Clq deposits. Clinical features and laboratory relevant data of all patients were collected. One-hundred and forty healthy adults were recruited as normal controls. The MBP gene codon 54 GGC/GAC polymorphism was investigated by using polymerase chain reaction and restriction fragment length polymorphism.

RESULTSThe genotype frequency of GGC/GAC heterozygotes was significantly higher in Group AGM as compared with that of Group A (41.4% vs 19.5%, P < 0.01) or normal subjects (41.4% vs. 26.4%, P < 0.05), while no difference was found in the distribution of MBP genotypes between Group A and normal subjects. GAC allele frequency was also higher in Group AGM than that in Group A (0.24 vs. 0.14, P < 0.05) or normal subjects (0.24 vs. 0.15, P < 0.05). The variant allele (GAC) was markedly associated with Group AGM (OR = 1.95, 95% CI: 1.06 - 3.58). In both Group A and Group AGM, more patients carrying the variant allele had episodes of upper respiratory or gastrointestinal infections prior to the onset of IgAN than those with wild homozygotes (GGC/GGC).

CONCLUSIONSGenetic variation of the host defense molecule, MBP, may be involved in the formation of the diverse patterns of glomerular immune deposition in IgAN. The variant allele of the MBP gene may partially account for abundant immune deposits in some IgAN patients.

Adult ; Alleles ; Carrier Proteins ; genetics ; Collectins ; DNA ; genetics ; Female ; Gene Frequency ; Genetic Variation ; Genotype ; Glomerulonephritis, IGA ; genetics ; immunology ; Humans ; Kidney Glomerulus ; immunology ; pathology ; Male ; Polymorphism, Restriction Fragment Length

OBJECTIVETo explore the relationship of plasminogen activator inhibitor-1 (PAI-1) gene -675 4G/5G and beta fibrinogen gene -455 G/A variations to glomerular microthrombosis(T) in lupus nephritis(LN).

METHODSOne hundred and one patients with biopsy proven LN were divided into two groups according to the presence or absence of glomerular microthrombus, i.e. group LN+T(n=46) and group LN-T(n=55). The genotypes of PAI-1 gene and beta fibrinogen gene were profiled by polymerase chain reaction-sequence length polymorphism (PCR-SLP) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) respectively. Clinical baseline data at the time of renal biopsy were collected. Normal controls consisted of 128 unrelated healthy adults. The etiologic fractions (EF) were calculated for estimating the contribution of risk genotypes of the two candidate genes to an increase in susceptibility to glomerular microthrombosis in LN patients.

RESULTSBoth the 4G/4G genotype and the 4G allele of PAI-1 gene occurred more frequently in group LN+T (47.83% and 0.685) than in group LN-T (23.64% and 0.507)(P<0.05) and normal controls (28.13% and 0.570) (P<0.05). The PAI-1 4G/4G genotype was significantly associated with microthrombosis (OR=2.96, 95%CI:1.26-6.92). Besides, the prevalence of the genotypes carrying the A allele of beta fibrinogen gene, i.e. G/A and A/A, as well as the prevalence of the A allele per se, was increased in group LN+T (47.83% and 0.261) versus group LN-T (27.27% and 0.145)(P<0.05). LN patients carrying the A allele had a high risk of glomerular thrombosis(OR=2.44, 95%CI:0.98-5.59). In addition, the presence of the PAI-1 4G/4G genotype together with the A allele of the beta fibrinogen gene was found to be a greater risk factor (OR=4.5, 95%CI: 1.34-15.12) for glomerular thrombosis in LN than the 4G/4G genotype or the A allele alone. The pooled EF (45.98%) for the risk genotypes of both PAI-1 gene and beta fibrinogen gene was also higher than that for the risk genotypes of either gene (31.67% and 28.23%).

CONCLUSIONThe above findings indicated that genetic variations in PAI-1 and beta fibrinogen loci might represent risk factors for glomerular microthrombosis in LN. They may have synergetic impact and present gene dosage effect on the susceptibility to this pathological subphenotype.

Adolescent ; Adult ; Alleles ; Capillaries ; pathology ; Confidence Intervals ; Female ; Fibrinogen ; genetics ; Gene Dosage ; Humans ; Kidney Glomerulus ; pathology ; Lupus Nephritis ; complications ; genetics ; Male ; Middle Aged ; Odds Ratio ; Plasminogen Activator Inhibitor 1 ; genetics ; Polymorphism, Genetic ; Thrombosis ; complications ; genetics

Objective: We used polysomnography (PSG) monitoring and neuropsychological scales to explore the characteristics of coronavirus disease-2019 (COVID-19) patients diagnosed with post-traumatic stress disorder (PTSD) in Wuhan, two years after the onset of the COVID-19 pandemic. Methods: A total of 42 patients in the Sleep Medicine Center were diagnosed with insomnia between December 2021 and May 2022; they were divided into the PTSD group (patients with PTSD diagnosed with insomnia after COVID-19 infection) and the non-PTSD group (patients with insomnia without PTSD). A healthy control group was simultaneously included. Results: The PTSD group was more significant than the non-PTSD group in partial manifestations of sleep disorders, neuropsychological clinical symptoms, and partial PSG data. Patients with different COVID-19 subtypes showed significant differences in the course of disease, sleep disorders, neuropsychological clinical symptoms, relevant scale scores, and PSG data analysis. Conclusion The emotional anxiety and depression of COVID-19 patients diagnosed with PTSD two years after the COVID-19 pandemic in Wuhan are more significant, and will not be self-alleviated with the passage of time. It is necessary to continue to pay attention to the PTSD symptoms and sleep psychology of COVID-19 infected patients, and take appropriate measures. Patients with severe and critical COVID-19 have more severe sleep and mental disorders, and there is a significant correlation between the duration of the disease and the severity of mental and mental disorders and sleep disorders after recovery.

This article aimed to summarise the clinical experience of Professor XIONG Jibai in treating henoch-schonlein purpura （HSP） from the perspective of "simultaneous treatment of wind and blood". HSP was devided into acute phase and transitional phase in clinic. It was considered that the wind pathogen exists throughout the disease course， and the treatment is guided by the "four methods of treating blood" in TANG Rongchuan's Treatise on Blood Syndromes - Blood Vomiting （《血证论·吐血》）， which are stanching bleeding， expelling stasis， tranquilising blood， and tonifying blood. In the acute phase， wind-heat damaging collateral symdrome and blood-heat frenetic flow syndrome are common， which could be treated by the method of cooling blood to dispel wind， and eliminating stasis to stop bleeding， with self-prescribed modified Ziping Xiaofeng Powder （紫萍消风散）； in the transitional phase， syndrome of effulgent fire due to yin deficiency and syndrome of qi deficiency failing to control are common， which could be treated by the method of tranquilising blood and tonifying deficiency， with modified Zhibai Dihuang Decoction （知柏地黄汤） and Guipi Decoction （归脾汤）. At the same time， it is believed that wind-related medicinal has the function of eliminating stasis， stanching bleeding， and cooling blood， and the wind-related medicinal should be used throughout the treatment.