Objectives:Analyze the clinical characteristics of patients with primary antiphospholipid syndrome (PAPS) progressing to systemic lupus erythematosus (SLE).Explore the risk factors for the progression from PAPS to SLE.Methods:The clinical data of 262 patients with PAPS enrolled in Peking Union Medical College Hospital from February 2005 to September 2021 were evaluated. Assessments included demographic data, clinical manifestations, laboratory tests (serum levels of complement, anti-nuclear antibodies, anti-double-stranded DNA antibodies), treatment, and outcomes. Kaplan-Meier analysis was used to calculate the prevalence of SLE in patients with PAPS. Univariate Cox regression analysis was employed to identify the risk factors for PAPS progressing to SLE.Results:Among 262 patients with PAPS, 249 had PAPS (PAPS group) and 13 progressed to SLE (5.0%) (PAPS-SLE group). Univariate Cox regression analysis indicated that cardiac valve disease ( HR=6.360), positive anti-double-stranded DNA antibodies ( HR=7.203), low level of complement C3 ( HR=25.715), and low level of complement C4 ( HR=10.466) were risk factors for the progression of PAPS to SLE, whereas arterial thrombotic events ( HR=0.109) were protective factors ( P<0.05 for all). Kaplan-Meier analysis showed that the prevalence of SLE in patients suffering from PAPS with a disease course>10 years was 9%-15%. Hydroxychloroquine treatment had no effect on the occurrence of SLE in patients with PAPS ( HR=0.753, 95% CI 0.231-2.450, P=0.638). Patients with≥2 risk factors had a significantly higher prevalence of SLE compared with those with no or one risk factor (13-year cumulative prevalence of SLE 48.7% vs. 0 vs. 6.2%, P<0.001 for both). Conclusions:PAPS may progress to SLE in some patients. Early onset, cardiac-valve disease, positive anti-dsDNA antibody, and low levels of complement are risk factors for the progression of PAPS to SLE (especially in patients with≥2 risk factors). Whether application of hydroxychloroquine can delay this transition has yet to be demonstrated.

OBJECTIVE To provide ideas and reference for the treatment and pharmaceutical care of infective endocarditis （IE） caused by Micrococcus luteus complicated with severe pneumonia. METHODS The clinical pharmacist participated in the treatment of a patient with IE caused by M. luteus complicated with severe pneumonia； all anti-infective treatment plans were agreed upon after the doctor invited the clinical pharmacist for consultation. After the implementation of the plan， the clinical pharmacist conducted pharmaceutical care of effectiveness and safety for the plan， including adopting suitable drug， adjusting the dose of vancomycin by using parameters such as steady-state valley concentration and creatinine clearance rate， monitoring renal function and adverse drug reactions. RESULTS IE caused by M. luteus was cured after surgery and full treatment with anti-bacterial drugs， the severe pneumonia was improved， and the decline of renal function caused by drugs and the primary disease were recovered； clinical pharmacists had ensured the effect of anti-infection treatment by assisting in the formulation of treatment plans and the implementation of pharmaceutical care， avoiding further renal damage and solving the problem of cefoperazone sulbactam- related drug fever. CONCLUSIONS IE caused by M. luteus is relatively serious， and the treatment drug can be vancomycin and rifampicin. During the treatment， it is necessary to monitor the renal function， and adjust the dose of vancomycin or change other drugs； anti-infection pharmaceutical care provided by clinical pharmacists can guarantee the effectiveness and safety of anti- infection plan， and avoid the occurrence of severe adverse drug reactions.

Objective:To improve the understanding of the relationship between antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE).Methods:The clinical characteristics and process of diagnosis and treatment of a case was reported and analyzed. This patient was initially diagnosed as antiphospholipid syndrome and later developed new skin lesion and positive anti-dsDNA antibody, which made the diagnosis of systemic lupus erythematosus.Results:A 15-year-old girl suffered acute pulmonary embolism, lower extremity deep vein thrombosis, and high titer of anti-phospholipid antibody, but negative for other autoantibodies. So primary antiphospholipid syndrome was diagnosed. Symptoms were improved after thrombolysis and anticoa-gulation treatment. During the follow-up period, the patient developed malar erythema, lymphocytopenia, proteinuria, positive ANA, anti-dsDNA antibody, and reduced complement level. So she was diagnosed with systemic lupus erythematosus. After glucocorticoid pulse therapy and immunosuppressants treatment, the symptoms were relieved and lupus disease activity was decreased.Conclusion:A few primary APS patients can progress into SLE. Patients with risk factors such as a younger age of onset, positive ANA and positive Coomb's test results should be closely followed up.

OBJECTIVE： To study the relationships of polymorphism of MTRR gene rs1801394 locus and SLCO1B1 gene rs11045879 locus with drug concentration of methotrexate （MTX） and high-dose MTX （HD-MTX）-induced ADR in acute lymphoblastic leukemia （ALL） children. METHODS： From Oct. 2015 to Sept. 2018， 70 ALL hospitalized children of Han nationality in Sichuan area who received HD-MTX treatment and were in consolidation chemotherapy were selected retrospectively from Sichuan People’s Hospital. The blood concentration of MTX at 48 and 72 hours after administration was measured by EMIT. The genetic typing of MTRR gene rs1801394 locus and SLCO1B1 gene rs11045879 locus were detected with real-time PCR. The relationships of the polymorphism of MTRR gene and SLCO1B1 gene with MTX blood concentration [dose-corrected concentration （c48 h/D，48 h）， the proportion of children with different concentration of MTX （≤0.1， ＞0.1 μmol/L）] and ADR （such as myelosuppression， liver function damage， gastrointestinal response， mucosal damage， rash， etc.） were analyzed. Binary Logistic regression analysis for the correlation of ADR with different influencing factors （gene polymor- phism， blood concentration of MTX， immunophenotyping， body mass index， etc.） was carried out by Wald method. RESULTS： Totally 31， 32， 7 children with MTRR gene AA， AG and GG genotype， while 23， 37， 10 children with SLCO1B1 gene TT， TC and CC genotype were detected. The distribution of each genotype in 70 children conformed to Hardy-Weinberg equilibrium （P＞0.05）. There was no significant difference in c48 h/D（48 h） of children and the proportion of children with different concentration of MTX （72 h） among difterent genotypes of MTRR and SLCO1B1 gene （P＞0.05）. There was statistical significance in the incidence of liver function injury in children with different genotypes of MTRR gene （P＜0.05）， and the AA genotype was significantly higher than the AG+GG genotype （P＜0.05）. There was no correlation of MTRR gene polymorphism with the incidence of other ADR， neither SLCO1B1 gene polymorphism with the incidence of ADR （P＞0.05）. The results of Binary Logistic regression analysis showed that liver function damage in ALL children was related to the gene polymorphism of MTRR； gastrointestinal reaction was related to whether the plasma concentration was more than 0.1 μmol/L at 72 h； mucosal damage was related to the immune type and BMI of children； the occurrence of skin allergy was correlated with body weight of children（P＜0.05）. CONCLUSIONS： Gene polymorphism of MTRR rs1801394 locus may associated with the occurrence of HD-HTX-induced liver function injury in ALL children， but its polymorphism and gene polymorphism of SLCO1B1 rs11045879 locus are not related to MTX blood concentration in ALL children.

Objective: To investigate the role of granulocyte-colony stimulating factor (G-CSF) on the regulation of inflammatory cytokines in neonatal hypoxic-ischemic brain damage(HIBD) rat model, and to explore the possible mechanism involved in G-CSF neuroprotective effect via the mammalian target of Rapamycin/p70 ribosomal S6 protein kinase (mTOR/p70S6K) signaling pathway. Methods: A group of postnatal day 7 (P7) Sprague-Dawley rat pups (90 cases) were randomly divided into sham-operated group, hypoxia-ischemia(HI) group, G-CSF group, Rapamycin (RAP) group and control group, and the improved Rice method was used to establish a neonatal rat model of HIBD.One hour before HI induction, Rapamycin was administered intraperitoneally with a dose of 250 μg/kg, and the control group was given equal volume of ethanol injected intraperitoneally.One hour after HI, a dose of 50 μg/kg of G-CSF was injected intraperitoneally into the G-CSF group, Rapamycin group and control group.The same volume of normal saline was injected intraperitoneally into HI group and sham-operated group.Forty-eight hours after HI, Western blot was used to detect the protein levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-10, and the mTOR/p70S6K signaling pathway in brain tissue.Neuron injury of the hippocampal CA1 region and the cortex was assessed by Nissl staining, and infarct volume detected by 2, 3, 5-triphenyltetrazolium chloride staining. Results: The G-CSF group and control group were associated with significantly reduced infarction volume compared to the HI group [(12.87±1.54)%, (11.90±1.31)% vs.(24.21±3.28)%], and the differences were statistically significant(P<0.05). There was an increased positive neuron cell number in the ipsilateral hemispheres of the hippocampal CA1 region in the G-CSF group and the control group [(61.00±4.90) cell/field and (61.67±6.40) cell/field] and cortex [(92.67±6.68) cell/field and (90.17±4.45) cell/field] compared with those in HI group [(42.62±4.46) cell/field and (70.83±6.97) cell/field], and the differences were all statistically significant (all P<0.05). The expression levels of TNF-α and IL-1β were significantly decreased in the G-CSF group and the control group, compared with those in HI group(TNF-α: 0.67±0.07, 0.55±0.05 vs.0.86±0.05; IL-1β: 0.65±0.06, 0.52±0.10 vs.0.86±0.06), and the differences were all statistically significant (all P<0.05). There was increased expression levels of IL-10, p-mTOR/mTOR and p-p70S6K/p70S6K in the G-CSF group and the control group, compared with those in HI group (IL-10: 0.68±0.04, 0.62±0.05 vs.0.34±0.02; p-mTOR/mTOR: 0.53±0.02, 0.51±0.01 vs.0.26±0.01; p-p70S6K/p70S6K: 0.89±0.03, 0.90±0.03 vs.0.55±0.02), and the differences were all statistically significant(all P<0.05). There was an increased infarct volume in Rapamycin group [(25.70±1.50)%], compared with the G-CSF group and the control group, and there were decreased number of positive neuron cell count in the hippocampal CA1 region [(40.67±3.50) cell/field] and cortex [(68.33±8.17) cell/field], increased expression levels of TNF-α and IL-1β (0.97±0.06 and 0.98±0.10, respectively), decreased expression levels of IL-10, p-mTOR/mTOR and p-p70S6K/p70S6K (0.21±0.02, 0.30±0.01 and 0.55±0.01, respectively) in the Rapamycin group, and the differences were all statistically significant (all P<0.05). Conclusions G-CSF may inhibit inflammatory responses after HIBD by up-regulating the mTOR/p70S6K signaling pathway in neonatal HI encephalopathy.

Objective To investigate the effects of granulocyte-colony stimulating factor (G-CSF) on neuronal apoptosis after hypoxia-ischemia brain damage (HIBD) and the possible role of the mTOR/p70S6K signaling pathway in neonatal rats.Methods Ninety seven-day-old Sprague-Dawley rats were assigned into 5 equal groups (n=18):sham group,HIBD group,G-CSF group,rapamycin group and ethanol group by random number table method.Pups were subjected to unilateral carotid artery ligation followed by 2hrs hypoxia or sham surgery.HIBD animals received normal saline,G-CSF (50 μg/kg),G-CSF combined with rapamycin (250 μg/kg) or ethanol (vehicle for rapamycin).Pups were euthanized 48hrs post-HIBD to quantify the percentage of brain infraction area.The pathomorphologic changes in the hippocampal CA 1 area and cortex were observed by Nissl staining.Neuronal cell death was determined using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL).mTOR,activated mTOR (p-mTOR),p70S6K,activated p70S6K (p-p70S6K),Cleaved Caspase-3 (CC3),Bax,and Bcl-2 were quantified using Western blot analysis.Results G-CSF treatment resulted in significantly reduced percentage of brain infraction area (P＜0.05) and neuronal apoptosis in the hippocampal CA1 area and cortex (P＜0.05) after HIBD in neonatal rats.However,rapamycin administration reversed the neuroprotective effect of G-CSF.G-CSF administration ameliorated the pathomorphologic damage in the ipsilateral hemisphere.Compared with the HIBD group,the Nissl stained neurons significantly increased in the G-CSF group (P＜0.05).Furthermore,G-CSF increased the expression ofp-mTOR,p-p70S6K and Bcl-2 but decreased the expression levels of CC3 and Bax in the ipsilateral hemisphere,which were all significantly reversed by rapamycin (P＜0.05).Conclusion G-CSF may attenuate caspase activation and reduce neuronal apoptosis by up-regulating the activity of mTOR/p70S6K signaling pathway after experimental HIBD in rat pups.

OBJECTIVE: To comprehensively evaluate the interventional effect on unexpected injury among children and adolescents in China, and to provide scientific basis for the injury control strategy.
 METHODS: Meta analysis was utilized to analyze the selected literatures. After heterogeneity test of the data, a relevant model was chosen to estimate the combined effect values relative risk (RR) and the corresponding 95% confidence interval (95% CI). Subgroup analysis were performed based on the intervention measures, objects and places. Sensitivity and publication bias were analyzed.
 RESULTS: A total of 18 papers were included in the Meta analysis with a sample size of 32 599. The combined RR value was 0.54 (95% CI 0.44 to 0.68). Subgroup analysis showed that the RR value of health education and comprehensive intervention were 0.59 and 0.50, respectively, with no significant difference between them (P>0.05). The RR values of the interventions in school alone, in school and community or in community alone were 0.51, 0.78 or 0.63. The RR values on children alone, children and parents or parents alone were 0.53, 0.65 or 0.35. The differences were significant when the interventions were performed among different places or objects (P<0.05). Sensitivity analysis revealed that meta-analysis results were relatively stable.
 CONCLUSION The targeted interventions were significant in the prevention of unexpected injuries among children and adolescents. It is worth further promoting and spreading.
Adolescent ; Child ; China ; Humans ; Schools ; Wounds and Injuries ; epidemiology ; prevention & control

Objective To understand health literacy levels in elderly people aged 60 years and above in Hunan, and explore factors related to health literacy.Methods Hunan residents aged 60 years and above were randomly recruited by the multistage stratified cluster sampling method.A total of 611 elderly people from 13 counties of Hunan were included in the study, which was conducted through questionnaires.Results The median health literacy score for elderly people aged 60 years and above was 51.00 (4-90), and it was lower than that for people under 60 years old, which was 56.00.Single factor analysis found that education level, occupation, number of family members, and household income each had an influence on health literacy scores (H=59.526, 20.609, 17.214, and 50.749, respectively;P=0.000, 0.002, 0.001 and 0.000, respectively).The number of people with basic health literacy accounted for 10.6％ (65/611) of the total.Multiple logistic regression analysis found that chronic disease was a factor affecting basic health literacy.Compared with elderly people without chronic diseases, a higher percentage of people with basic health literacy was among elderly people with chronic diseases (OR =1.870, 95％ CI: 1.037-3.373).Conclusions The health literacy level is lower in elderly people aged 60 years and above than those under 60 years old in Hunan.Only 10.6％ (65/611) of them show basic health literacy.Education level, occupation, number of family members, and household income are the factors related to health literacy.Health education about healthy lifestyle and behavior as well as chronic disease prevention and control should be increased in order to improve the health literacy level in elderly people.

Objective To explore the effect of docosahexaenoic acid (DHA) on long-term learning and memory disorders and potential mechanism in rats after hypoxic ischemic brain damage. Methods Sixty neonatal 7-day-old SD rats were ramdonly divided into three groups: group S (sham operation+vehicle treatment), group C (hypoxic-ischemic brain damage [HIBD]+vehicle treatment) and group D (HIBD+DHA treatment). After left common carotid artery was isolated and ligated for 2.5 h, rats of group C and group D were put into a condition which oxygen concentration was about 8%for 2 h;rats in the group S were only isolated the left carotid artery, without ligation or hypoxia treatment;rats in the group D were intraperitoneally injected DHA of 15 mg/kg after modeling, and rats in the group S and group C were intraperitoneally injected equivalent volume of vehcle, once a day for 10 consecutive days. The pathomorphology changes of the hypocampal CA1 area, and marginal division of striatum were observed by Nissl staining 48 h after modling; the apoptosis cells were measured by TUNEL;immunohistochemical method was used to detect the expressions of Bax and Caspase-3 positive cells in the two brain areas. Morris water maza test was used to evaluate the long-term lerning and momory functions of 2-month-old rats, and the expressions of N-methyl-D-aspartate receptor 1 (NMDAR1) positive cells were detected by immunohistochemical method. Results The pathomorphology damage was significantly improved, the expressions of Bax and Caspase-3 positive cells and the neuron apoptosis in hypocampal CA1 areas and marginal division of striatum in group D were all signficantly decreased as compared with those in the group C (P<0.05). Rats in group D had significantly decreased escape latency as compared with those in group C in Morris water maze test (P<0.05), and the expression of NMDAR1 positive cells in the two brain areas of group D was significantly increased as compared with that in the group C (P<0.05). Conclusion DHA has the ameliorative effect on long-term learning and memory disorders after hypoxic ischemic brain damage in rats, which may be associated with inhibitory action of cell apoptosis at early phase and up-regulation of expression of NMDA1 at the late phase.

Purpose To improve the understanding of features and diagnostic value of PET/CT imaging in primary tracheal cancer as it is a rare disease.Materials and Methods The18F-FDG PET/CT image data of 11 patients with primary tracheal cancer confirmed pathologically were retrospectively analyzed. The contrast-enhanced CT scan was performed in 9 patients. The PET/CT and contrast-enhanced CT imaging data were analyzed.Results Out of the 11 cases, 5 were adenoid cystic carcinoma, 4 were squamous cell carcinoma and 2 were adenocarcinoma. Endotracheal round or elongated uptake lesions were found in PET imaging. The maximum standardized uptake value of adenoid cystic carcinoma, squamous cell carcinoma and adenocarcinoma were 4.5±1.2, 8.1±1.7 and 4.5±2.4, respectively. The accuracy of diagnosis of PET/CT was 100%(11/11). Soft tissue density nodule or mass in trachea was found in CT scan. The accuracy of CT diagnosis was 81.8% (9/11). Among the 9 patients who underwent enhanced CT scan, 3 had significantly enhanced lesions and 6 had moderate enhanced ones. Mediastinal lymph node metastasis was found in 1 patient. There was no distant metastasis in all the 11 patients.Conclusion Primary tracheal cancer has features of PET/CT imaging such as soft tissue nodules or mass in tracheal lumen or on its walls accompanied by FDG increase. The utilization of metabolic and anatomic imaging of PET/CT has great significance in clinical diagnosis and therapy of primary tracheal cancer.