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Biomedical subjects

Yan Wen

Publications and source records attributed to Yan Wen.

At least 19 recordsLinked to original sources

Adolescent depression as a systemic multimorbidity catalyst: integrated genetic and metabolic pathway analysis.

BACKGROUND: Although adolescent depression has been linked to individual chronic conditions, its broader role in shaping multimorbidity risk remains understudied. METHODS: A total of 87,562 UK Biobank participants were included, of whom 18,851 had documented adolescent depression. Cox proportional hazards models were applied to evaluate associations between adolescent depression and 24 chronic diseases, followed by stratified analyses by sex and age. Two-sample Mendelian randomization (MR) was then conducted to infer causality for diseases showing significant associations. Genomic colocalization analyses were performed using relevant GWAS data to identify shared causal variants. Mediation analyses were performed to detect possible mediating factors, including the frailty index, KDM biological age acceleration, allostatic load and 30 circulating biomarkers. RESULTS: Adolescent depression was associated with elevated risk for 12 chronic diseases, with strongest associations for hypothyroidism (HR = 1.29 [1.18-1.42]), diabetes (HR = 1.25 [1.13-1.38]) and chronic obstructive pulmonary disease (COPD) (HR = 1.74 [1.50-2.01]). Risks were notably higher among females and younger adults. MR confirmed likely causal relationships for hypothyroidism (OR = 1.45 [1.03-2.05]), diabetes (OR = 1.01 [1.01-1.02]) and COPD (OR = 1.04 [1.02-1.06]). Genomic colocalization revealed a shared genetic signal at the CDSN/PSORS1C1 locus between adolescent depression and hypothyroidism. Mediation analyses revealed disease-specific pathways: creatinine for hypothyroidism, testosterone for diabetes, KDM biological ageing for COPD and frailty index across all three conditions. CONCLUSIONS: Adolescent depression confers systemic vulnerability through genetic and metabolic mechanisms, with amplified risks in females and individuals aged ≤55 years. These findings support early, integrated interventions to mitigate long-term multimorbidity.

Humans↗

Genetic heterogeneity affects the risk of incident depression, comorbidity, and response to environment: A prospective trajectory study.

BACKGROUND: Depression exhibits significant heterogeneity in its genetic underpinnings. The role of genetic components in the development of depression and its comorbidities remains insufficiently explored. METHODS: First, depression risk loci from a large-scale genome-wide meta-analysis were annotated to Gene Ontology (GO) terms by functional enrichment. GO-based polygenic risk scores (GO-PRS) were then calculated for individuals in the UK Biobank. Principal component analysis (PCA) was applied for dimensionality reduction, followed by cluster analysis to identify genetic subtypes of depression. Multistate models were applied to assess the impact of genetic patterns on the trajectory from healthy status to incident depression, and depression to 26 subsequent diseases, as well as the associations between environmental factors and disease trajectories across genetic subtypes. RESULTS: Participants were categorized into three genetic subtypes: immune-dominant, neuro-dominant, and comprehensive-risk. Significant differences in risk of depression and subsequent diseases, and susceptibility to environmental factors were observed across subtypes. Comprehensive-risk subtype showed higher risks of depression compared to immune-dominant (HR: 1.10, 95% CI: 1.05-1.15) and neuro-dominant subtype (HR: 1.12, 95% CI: 1.08-1.16). Comprehensive-risk subtype exhibited higher risks of transition from depression to subsequent diseases, such as anemia compared to immune-dominant subtype, and diseases of the digestive system compared to neuro-dominant subtype. Environmental factors were more strongly associated with the transition from depression to subsequent diseases in immune-dominant and comprehensive-risk subtypes, including cardiovascular, respiratory, and metabolic diseases. CONCLUSIONS: Our findings highlight the genetic heterogeneity of depression and comorbidities, and shed light on how genetic components modulate responses to environmental factors.

Humans↗

Polygenic enrichment analysis in multi-omics levels identifies cell/tissue specific associations with schizophrenia based on single-cell RNA sequencing data.

OBJECTIVE: Understanding the specific cellular origin and tissue heterogeneity in schizophrenia is critically important for exploring the disease etiology. This study aims to investigate these aspects by performing multiple analyses based on omics data. METHOD: We performed single-cell disease relevance score (scDRS) algorithm to link brain single-cell RNA sequencing (scRNA-seq) with schizophrenia risk across multi-omics scales at single-cell resolution. This approach identified cell types with overexpression of schizophrenia-related genes implicated by multi-omics panels (ATAC-seq, RNA-seq, TWAS, and GWAS). Schizophrenia-related genes from these multi-omics panels were extracted and combined with scRNA-seq data to calculate scDRS. Subsequently, the cell-type vs. disease association and tissue heterogeneity were assessed using scDRS for each omics panel. RESULTS: We identified two novel cell subpopulations in the brain that differentially express SCUBE3 (59 cells, 7.0 %) and FN1 (21 cells, 2.5 %). At the individual cell level, schizophrenia-associated cell subpopulations included microglial cell associated with ATAC-seq panel (Passociation = 0.002, Pheterogeneity = 0.009) and deep layer neuron suggestively associated with GWAS panel (Passociation = 0.033, Pheterogeneity = 0.017). At the brain tissue level, microglial cell was significantly associated with cortical plate in ATAC-seq panel (Passociation = 0.002, Pheterogeneity = 0.011). Gene level analysis identified several genes associated with schizophrenia across multi-omics panels. CONCLUSIONS: Our study outlines the signature of cell subpopulations, brain regions, and disease risk genes in schizophrenia at single-cell resolution across multi-omics scales. These findings provide a reference for future precision medicine approaches targeting specific cell types and brain regions in schizophrenia.

Schizophrenia↗

Do extracellular matrix protein expressions change with cyclic reproductive hormones in pelvic connective tissue from women with stress urinary incontinence?

BACKGROUND: To evaluate differential expression of transforming growth factor (TGF-beta1), latent transforming factor-binding proteins (LTBP-1, LTBP-2) and elastin microfibril components (fibrillin-1 and fibrillin-2) in vaginal tissue from women with stress urinary incontinence (SUI). METHODS: In this case-control study, vaginal tissue from women in both phases of the menstrual cycle was obtained. Messenger RNA (mRNA) expressions of LTBP-1, LTBP-2, fibrillin-1, fibrillin-2 and TGF-beta1 were determined by relative real-time quantification PCR. Tissue localization was analysed by immunohistochemistry, and semiquantitative protein expression was evaluated by Western blot analysis. RESULTS: Vaginal wall fibroblasts synthesized all proteins tested. LTBP-1, LTBP-2 and TGF-beta1 co-localized with elastin microfibrils, fibrillin-1 and fibrillin-2 in the extracellular matrix. LTBP-1 mRNA and protein expressions were higher in control versus women affected with SUI in the proliferative phase (P = 0.04), while in the secretory phase, mRNA expression in cases was higher (P = 0.04). Fibrillin-1 mRNA was higher in women affected by SUI versus controls in both phases, but no statistical differences in fibrillin-1 protein expression were observed between the two groups in either phase. LTBP-2 and TGF-beta1 mRNA expressions showed the same trends as LTBP-1. CONCLUSION: LTBP-1, LTBP-2, TGF-beta1, fibrillin-1, and fibrillin-2 expressions are hormonally regulated in vaginal wall fibroblasts and differ in women affected by SUI when compared to controls. These data suggest a mechanism to regulate TGF-beta1 activity in pelvic connective tissue.

Case-Control Studies↗

Regulation of cyclooxygenase activity in cultured endometrial stromal cells by granulocyte-macrophage colony-stimulating factor.

OBJECTIVE: To assess the ability of granulocyte-macrophage colony-stimulating factor (GM-CSF) to regulate cyclooxygenase (COX) enzyme activity and prostaglandins (PGs) synthesis, specifically PGE2 production in stromal cells, neither of which have been addressed in the literature. DESIGN: Prospective study. SETTING: Department of obstetrics and gynecology at a university hospital. PATIENT(S): Human luteal phase endometrium was obtained from surgical specimens (n = 6) for clinical indications. INTERVENTION(S): Confluent stromal cells were stimulated with GM-CSF. MAIN OUTCOME MEASURE(S): Expression of COX mRNA, COX enzyme activity, and PGE2 level in cultured stromal cells. RESULT(S): Confluent stromal cell cultures treated with P and E2 for 9 days were stimulated with GM-CSF. After treatment of 12 hours, low-dose GM-CSF (0.001-0.1 ng/mL) increased COX-2 mRNA levels in stromal cell, whereas high dose GM-CSF (1-100 ng/mL) decreased COX-1 and COX-2 mRNA levels. After treatment of 48 hours, low concentrations of GM-CSF (0.001-0.1 ng/mL) increased total COX and COX-2 enzyme activity, whereas high concentrations of GM-CSF (1-100 ng/mL) inhibited COX and COX-2 activity; The PGE2 levels decreased by 31% to 393.3 pg/mL (P < .05) with concentrations of GM-CSF increasing from 1 ng/mL to 100 ng/mL. CONCLUSION(S): There appeared to be a biphasic pattern of COX-2 enzyme response to GM-CSF with low concentrations increasing activity and high concentrations inhibiting activity. It is possible that GM-CSF may provide critical regulation of PG production in the preimplantation period.

Cells, Cultured↗

[Study on changes in circulatory renin-angiotensin system in rats with endotoxemia].

OBJECTIVE: To investigate the changes in circulatory renin-angiotensin system (RAS) in rats with endotoxemia and explore its mechanism. METHODS: Ninety Wistar rats were randomly divided into normal control group (n=10) and endotoxemia groups (n=80). The endotoxemia group was further divided into subgroups of 2, 4, 8, 12, 24, 48, 72 hours and 7 days after injection of lipopolysaccharide (LPS) into the abdominal cavity (each n=10). The rats were sacrificed at different time points after LPS (10 mg/kg) challenge. Contents of plasma LPS, plasma renin activity (PRA), plasma angiotensin II (A II), angiotensin-converting enzyme (ACE), tumor necrosis factor-alpha (TNF-alpha), and interleukin-10 (IL-10) were determined. RESULTS: (1) Plasma LPS, TNF-alpha and IL-10 reached highest levels 2 hours after LPS injection, and they returned to normal levels 7 days, 8 hours and 8 hours after LPS challenge respectively. (2) The levels of plasma PRA, A II and ACE reached highest levels 2, 8 and 8 hours after LPS challenge respectively, and they returned to normal levels 12, 24 and 72 hours after LPS injection, respectively. CONCLUSION: During endotoxemia, there is a series of inflammatory reactions and anti-inflammatory reactions, and a large number of cytokines and inflammatory mediators are released. At the same time, the circulating RAS is activated, which causes constriction of blood vessel and dysfunction of the microcirculation aggravating hypoxia of cells. The study of the changes in RAS is significant to interpreting the pathogenetic mechanism of endotoxemia in rats.

Angiotensins↗

[A testing method of assessing the protein-removing effect of the contact lenses' protein -removing care solution].

OBJECTIVE: Testing the protein-removing effect of the protein-removing care solution on the protein precipitation of the soft contact lenses. METHOD: Soak the lenses into the artificial-tears to simulate the protein absorption, test the absorbency of cleaned protein at the wavelength of 280 nm by UV spectrophotometer, and compute the percentage of protein. RESULT: Testing results of the percentage of the cleaned protein are repeatable. CONCLUSION: This experimental method can be used to evaluate the cleaning effect of the protein- removing care solution, but still needs much improvements.

Contact Lens Solutions↗

[Preliminary study on the genotyping of Mycobacterium leprae on 50 isolates from China].

OBJECTIVE: To understand the genotypic mapping of Mycobacterium leprae identified in China and to compare with those from other countries to select suitable alleles for epidemiological investigation in the transmission chain of leprosy. METHODS: Various number of tandem repeat(VNTR) in genomic DNA of Mycobacterium leprae was used in the present genotyping study. 33 skin biopsies from Wenshan prefecture,Yunnan province and 17 from other parts of China were studied. DNA extracted from skin biopsies of leprosy patients was subjected to PCR followed by agarose gel analysis and DNA sequencing to determine the number of repeats. RESULTS: Loci GGT-5,12-5,21-3 and 23-3 were as highly homogenous as 100%; The homogeneity of loci AC-8, 18-8, 27-5 and rpoT were 97%, 94%, 97% and 85% respectively. Loci GTA-9, AC-9 and 6-7 showed significant allelic diversity in isolates and the diversity of GTA-9 in Mycobacterium leprae isolated from China was also different from those identified other countries. We had subjected loci GTA-9 and the ten loci to phylogenetic tree analysis respectively. CONCLUSION: The present study revealed that the genotype of Mycobacterium leprae identified from China was close to the strains from the Philippines and India although a few loci were somehow differentiate. Locus 12-5 manifested as only 3 copies in China whereas 4-5 copies predominating in other countries. 12-5 locus might serve as a useful marker to diffrentiate Chinese strains from those in other countries. However, further study on the diversity of GTA-9 was needed in China. The molecular typing of Mycobacterium leprae from different geographic areas might be useful in studying the transmission of leprosy.

Alleles↗

Microarray analysis of differentially expressed genes in vaginal tissues from women with stress urinary incontinence compared with asymptomatic women.

BACKGROUND: The pathophysiology of pelvic floor dysfunction resulting in stress urinary incontinence (SUI) in women is complex. Evidence suggests that there is also a genetic predisposition towards SUI. We sought to identify differentially expressed genes involved in extracellular matrix (ECM) metabolism in vaginal tissues from women with SUI in the secretory phase of menses compared with asymptomatic women. METHODS: Tissue samples were taken from the periurethral vaginal wall of five pairs of premenopausal, age-matched SUI and continent women and subjected to microarray analysis using the GeneChip Human Genome U133 oligonucleotide chip set. RESULTS: Extensive statistical analyses generated a list of 79 differentially expressed genes. Elafin, keratin 16, collagen type XVII and plakophilin 1 were consistently identified as up-regulated ECM genes. Elafin, a serine protease inhibitor involved in the elastin degradation pathway and wound healing, was expressed in pelvic fibroblasts and confirmed by Western blot, quantitative competitive PCR and immunofluorescence cell staining. CONCLUSIONS: Genes involved in elastin metabolism were differentially expressed in vaginal tissue from women with SUI, suggesting that elastin remodelling may be important in the molecular aetiology of SUI.

Adult↗

Exogenous granulocyte-macrophage colony-stimulating factor promotes follicular development in the newborn rat in vivo.

BACKGROUND: Expression and selective cellular localization of granulocyte-macrophage colony-stimulating factor (GM-CSF) and its receptor in ovarian tissue imply an autocrine/paracrine role in ovarian function. Evidence indicating a functional role for GM-CSF in ovarian follicular cell function has been provided by studies with GM-CSF knockout (GM-/-) mice, which suggest that GM-CSF influences events associated with murine follicular maturation. METHODS: Immature female rats were treated with GM-CSF, FSH or saline for 5 or 10 days. Ovaries were collected for histologic examination and immunostaining determination of CYP17, a theca cell marker. In addition, ovarian section slides were evaluated by immunofluorescence for CD45, an ovarian leukocyte marker. To investigate the possible mechanism of GM-CSF action on follicular development, theca-interstitial cells (T-I) were separated and cultured. Cells were treated with increasing concentrations of GM-CSF, then evaluated for CYP17 mRNA and protein expression assays. RESULTS: After 10 days of treatment with GM-CSF, the number of small preantral and large preantral follicles was significantly increased compared with the control group (P < 0.05). Similarly, treatment with FSH increased the number of small preantral and large preantral follicles (P < 0.05). CD45 expression measured by immunofluorescence was not different in the three groups, indicating that the distribution of leukocytes was unchanged. In addition, CYP17 was increased in the T-I cells both in vivo and in vitro after GM-CSF treatment. CONCLUSION: The present results suggest that GM-CSF may play a significant role in follicular development.

Animals↗

Preliminary experience with low concentration of granulocyte-macrophage colony-stimulating factor: a potential regulator in preimplantation mouse embryo development and apoptosis.

PURPOSE: To investigate the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the development of preimplantation mouse embryos. METHODS: Mouse 2-cell embryos were collected and cultured in P-1 medium supplemented with GM-CSF at different concentrations. Using reverse transcription-polymerase chain reaction, expression Bcl-2 and Bax mRNA in blastocyst were evaluated in the GM-CSF group and control group. Apoptosis detection was performed using the in situ apoptosis detection kit in mouse blastocysts. The statistical significance of the data was analyzed using t-test and chi-square test. RESULTS: The development of blastocyst increased to 89% in the addition of GM-CSF (0.125 ng/mL), compared to controlled group (80%). The number of cells staining for apoptosis was lower in GM-CSF group than that in the control group. Bcl-2 expression was found to be upregulated in blastocysts in the GM-CSF supplemented group compared to the control group. CONCLUSION: These results suggest that GM-CSF might be an important regulator in embryo development.

Animals↗

Elastin metabolism in pelvic tissues: is it modulated by reproductive hormones?

OBJECTIVE: The purpose of this study was to investigate the effect of relaxin on extracellular matrix protein expression in pelvic fibroblasts that were cultured from women with stress urinary incontinence compared with asymptomatic control subjects. STUDY DESIGN: Periurethral vaginal wall fibroblasts from premenopausal women with stress urinary incontinence and continent women (in both the proliferative and secretory phase of the menstrual cycle) were stimulated with increasing concentrations of relaxin (0-500 ng/mL). The supernatant was sampled for matrix metalloproteinase-2 and -9 by zymography. Tissue inhibitors of metalloproteinase-1 and -2 and alpha-1 antitrypsin were evaluated with Western blot. Total elastase activity was measured by generation of free amino groups from succinylated elastin. Increasing concentrations of alpha-1 antitrypsin were added to cell lysate to evaluate total elastase activity inhibition. RESULTS: Proliferative-phase stress urinary incontinence fibroblasts demonstrated an increase in matrix metalloproteinase-2 and no change in matrix metalloproteinase-9 and tissue inhibitors of metalloproteinase-1 and -2 expressions with increasing relaxin concentrations. Cells from control subjects showed increased expression of matrix metalloproteinase-2 and -9, but no change in tissue inhibitors of metalloproteinases. Secretory-phase stress urinary incontinence fibroblasts showed no response in matrix metalloproteinase or tissue inhibitors of metalloproteinase expressions with relaxin stimulation. Secretory-phase control fibroblasts reacted by increasing matrix metalloproteinase-2 and -9 and tissue inhibitors of metalloproteinase-2. With respect to total elastase activity and alpha-1 antitrypsin expression, increasing doses of relaxin appear to increase elastolytic activity in stress urinary incontinence cells by decreasing the expression of alpha-1 antitrypsin in proliferative phase cells or increasing the total elastase activity in secretory phase cells. Fibroblast total elastase activity was inhibited by increasing concentrations of alpha-1 antitrypsin. CONCLUSION: Elastase activity appears to be increased in relaxin-stimulated stress urinary incontinence fibroblasts by either decreased inhibitor (alpha-1 antitrypsin) production or increased elastase activity.

Adult↗

The structure-anticoagulant activity relationships of sulfated lacquer polysaccharide: effect of carboxyl group and position of sulfation.

Regiospecific oxidation of the primary hydroxyl groups in lacquer polysaccharide (LPL, Mw 6.85 x 10(4)) and its NaIO4 oxidation derivatives (LPLde) to C-6 carboxy groups was achieved with NaOCl in the presence of Tempo and NaBr. Sulfate groups were incorporated into the oxidated polysaccharides using Py.SO3 complex as a reagent. Reactivity of polysaccharide hydroxyl group was C-6 > C-2 > C-4. Sulfate groups were mainly linked to the second hydroxy at C-2 in the products. The results of APTT assay showed after incorporation of carboxyl groups into lacquer polysaccharides, the intrinsic coagulation pathway was promoted, and all sulfated polysaccharides had very weak anticoagulant activity within the scope of studied DS (0.39-1.11). These indicated that carboxyl groups and sulfate groups had the synergistic action. At the same time, the anticoagulant activity increased very slowly with the DS in the second hydroxy. This indicated that 6-O-SO3- in the side chains took an important role in the anticoagulant activity.

Anticoagulants↗

[The effects of bilirubin concentration on laminin and epidermal growth factor expression in lung tissue and type II pneumocytes in smoking rats model].

OBJECTIVE: To explore the effects of bilirubin on expression of laminin (Ln) and epidermal growth factor (EGF) in lung tissue and in type II pneumocytes (ATII) in smoking rats. METHODS: 36 healthy Wistar rats were randomly divided into three groups: a normal group, a smoking-induced emphysema model group (model group), and a bilirubin group (n = 12, for each group). According to XU San-lin method, rats both in the model group and the bilirubin group were exposed to smoke for a total of 6 months. Rats in the bilirubin group were pretreated with indirect bilirubin (20 mg.kg(-1).d(-1)) before exposed to smoke once a day. All animals were sacrificed six months later. ATIIwere isolated, purified and cultured. Ln in ATII culture medium was determined by radioimmunoassay (RIA). We detected Ln in lung tissue with indirect immunofluorescence technique and EGF with immunochemistry. RESULTS: In the model group, Ln content in ATII culture medium and in lung tissue [(5.0 +/- 0.3) mg/ml, 5.67 +/- 0.26] increased significantly compared with those in the normal group [(3.2 +/- 0.5) mg/ml, 2.01 +/- 0.74; P < 0.05, respectively]. In the bilirubin group, the two indexes [(3.9 +/- 0.7) mg/ml, 4.18 +/- 0.63] decreased significantly compared with those in the model group (P < 0.05, respectively), which was higher than the normal group (P < 0.05). Expression of EGF in lung tissue of the model group (0.43 +/- 0.09) increased significantly compared with that of the normal group (0.14 +/- 0.02; P < 0.05). The expression of EGF in the bilirubin group (0.34 +/- 0.03) decreased significantly compared with the model group (P < 0.05), which was higher than that of the normal group. CONCLUSIONS: Bilirubin was shown to be able to promote the reconstruction of extracellular matrix by decreasing the expression of Ln and EGF in lung tissue and in ATII in the development of emphysema.

Animals↗

[Prospective clinical study on serum immunity in IgG-antibodies positive patients convalescent from severe acute respiratory syndrome].

OBJECTIVE: To investigate the serum immunological characteristics in patients convalescent from severe acute respiratory syndrome (SARS). METHODS: In the 1 st, 3 rd, 6 th month after their discharge, eg. SARS-IgG, T cell subsets, blood routine, and the blood biochemistry were systemically determined in SARS convalescent patients. RESULTS: The SARS-antibodies could be used as the diagnostic evidence. During the 6 months after discharge, the titers of SARS-antibodies were high, but they lowered along with passage of time. At the first recheck, the CD4(+) lymphocyte count was lower than normal level in 55.9% of patients, the CD3(+) lymphocyte count was lower than normal level in 31.2% of patients, and the CD8(+) lymphocyte count was lower than normal level in 14.0% of patients. At the second recheck, the levels of T cell subsets recovered to normal level in the most patients. CONCLUSION: T cell subsets, and the number of leukocyte are abnormal in some patients convalescent from SARS. All the indexes examined recover to normal levels half year after discharge. Therefore, it is necessary to follow up the changes in the levels of SARS-antibodies.

Adolescent↗

[Clinical study of relationship between serum procalcitonin and severity of multiple organ dysfunction syndrome].

OBJECTIVE: To study the correlation between serum procalcitonin (PCT) level and severity of multiple organ dysfunction syndrome (MODS). METHODS: Sixty-one patients with MODS were enrolled in this study. They were divided into infection group and non-infection group. Serum PCT were measured using an immunoluminometric assay. Acute physiology and chronic health evaluation II (APACHE II) scores and Marshall scores of the two groups were recorded and the relationship between PCT levels and APACHE II scores as well as Marshall scores was analysed. RESULTS: Serum PCT levels in patients with MODS were higher. Serum PCT [13.01(2.73, 64.79) microg/L], APACHE II [(17.50+/-5.35) scores] and Marshall score [(6.38+/-2.46) scores] of infection group were significantly higher than non-infection group [1.50 (0, 2.98) microg/L, (14.67+/-3.01) scores, and (4.62+/-2.01) scores, respectively, P<0.05 or P<0.001]. Serum PCT of infection group and non-infection group did not show correlation with APACHE II (r=0.175, P=0.281; r=0.071, P=0.759). Serum PCT of all patients with MODS showed positive correlation with Marshall score (r=0.514, P<0.001), and correlation index of infection group was higher (r=0.535, P<0.001). Serum PCT of non-infection group did not show correlation with Marshall score (r=0.003, P=0.991). CONCLUSION: Serum PCT has clinical values in judgment of the severity of infected patients complicated by MODS.

APACHE↗

[Prospective 2-year clinical study of patients with positive IgG-antibodies after recovering from severe acute respiratory syndrome].

OBJECTIVE: To investigate the clinical characteristics of patients recovering from severe acute respiratory syndrome (SARS) during 2 years after the infection. METHODS: The antibody of SARS-IgG, T cell subsets, chest CT, and the pulmonary function were observed in patients 1 month, 3 months, 6 months, and 2 years after convalescence from SARS. RESULTS: In the 20 SARS cases, the level of antibodies was found to descend gradually and slowly during 2 years after convalescence. In the majority of patients T cell subsets recovered completely to normal range at the second examination. At the first re-examination, the rate of abnormal chest CT was 65%, and the main abnormal images included ground glass opacities, thickening of inter-lobular and intra-lobular septa, distorted lobular structure, thickened bronchovascular bundles, thickened pleura, arc shadow under the pleura, bronchiolar dilation, and honey comb like shadows. The rate of abnormal chest CT was 30% at the 4 fourth examination. At the first re-examination, the abnormal rate of KCO was highest, accompanied by abnormalities of forced expiratory volume in 1 second (FEV1) and the diffusing capacity of the lung for carbon monoxide (DLCO), and it began to recover since the third examination. CONCLUSION: The level of SARS-IgG descends slowly, and it may last for a long time. The recovery of chest CT to normal may take a long time. The abnormality in pulmonary functions manifests mainly as impairment of diffusion function. Further research on SARS is necessary.

Adolescent↗