环境内分泌干扰物与多囊卵巢综合征关系的研究进展

环境内分泌干扰物（EED）广泛存在于日常生活中，是一类可以干扰激素行为的外源性化学物。EED可以结合人体内不同的受体，通过多种机制增强或抑制体内正常的内分泌功能，从而引发多种疾病。多囊卵巢综合征（PCOS）病因复杂，已有研究结果表明PCOS的发生与环境因素有关。相关流行病学和基础实验研究表明，EED参与PCOS的发生、发展，但具体作用机制仍需进一步研究。现就EED与PCOS的关系及可能的相关作用机制进行阐述，总结EED与PCOS的关系,为干预PCOS患者的生活方式并阻断疾病发生提供新的线索。     

The Protective Effects of Up-Regulating Prostacyclin Biosynthesis on Neuron Survival in Hippocampus

Cellular arachidonic acid (AA), an unsaturated fatty acid found ubiquitously in plasma membranes, is metabolized to different prostanoids, such as prostacyclin (PGI₂) and prostaglandin E₂ (PGE₂), by the three-step reactions coupling the upstream cyclooxygenase (COX) isoforms (COX-1 and COX-2) with the corresponding individual downstream synthases. While the vascular actions of these prostanoids are well-characterized, their specific roles in the hippocampus, a major brain area for memory, are poorly understood. The major obstacle for its understanding in the brain was to mimic the biosynthesis of each prostanoid. To solve the problem, we utilized Single-Chain Hybrid Enzyme Complexes (SCHECs), which could successfully control cellular AA metabolites to the desired PGI₂ or PGE₂. Our in vitro studies suggested that neurons with higher PGI₂ content and lower PGE₂ content exhibited survival protection and resistance to Amyloid-β-induced neurotoxicity. Further extending to an in vivo model, the hybrid of PGI₂-producing transgenic mice and Alzheimer’s disease (AD) mice showed restored long-term memory. These findings suggested that the vascular prostanoids, PGI₂ and PGE₂, exerted significant regulatory influences on neuronal protection (by PGI₂), or damage (by PGE₂) in the hippocampus, and raised a concern that the wide uses of aspirin in cardiovascular diseases may exert negative impacts on neurodegenerative protection.

Our study intended to understand the crosstalk of prostanoids in the hippocampus, a major brain area impacted in AD, by using hybrid enzymes to redirect the synthesis of prostanoids to PGE₂ and PGI₂, respectively. Our data indicated that during inflammation, the vascular mediators, PGI₂ and PGE₂, exerted significant regulatory influences on neuronal protection (by PGI₂), or damage (by PGE₂) in the hippocampus. These findings also raised a concern that the widely uses of non-steroidal anti-inflammatory drugs in cardiovascular diseases may exert negative impacts on neurodegenerative protection.

     

Prevention and treatment of pressure ulcers/injuries: The protocol for the second update of the international Clinical Practice Guideline 2019

Aim

The European Pressure Ulcer Advisory Panel, the Pan Pacific Pressure Injury Alliance, and the National Pressure Ulcer Advisory Panel are updating the ‘Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline’ (CPG) in 2019. The aim of this contribution is to summarize and to discuss the guideline development protocol for the 2019 update.

Use of monoclonal antibodies as sensitive and specific probes for biologically active human gamma-interferon.

Mouse monoclonal antibodies B1 and B3 are specific for natural and Escherichia coli-derived recombinant human gamma-interferon (IFN-gamma). The two antibodies recognize different epitopes of the IFN-gamma molecule and do not compete with each other's binding. We have used these two antibodies to construct a solid-phase, sandwich immunoradiometric assay for human IFN-gamma. Purified antibody B1 was coated on polystyrene beads (0.64 cm in diameter) and used as the solid-phase immunoadsorbent and antibody B3 was labeled with 125I and used as tracer. This assay can be completed in about 4 hr and is capable of detecting IFN-gamma levels in human serum or tissue culture fluids as low as 0.1 NIH reference unit/ml. Recombinant human IFN-gamma derived from E. coli was detectable at a concentration of 0.02 ng/ml. The assay appears to be specific for the biologically active forms of IFN-gamma, since after exposure to pH 2, 37 degrees C, or 56 degrees C, biological activity and reactivity in the immunoradiometric assay decreased in parallel. The immunoradiometric assay can be employed for the analysis of the structural characteristics of the human IFN-gamma molecule.     

A nested case-control study on treatment-related risk factors for early relapse of tuberculosis

This nested case-control study aimed at evaluating treatment-related risk factors of relapse of tuberculosis under a service program of directly observed treatment. Out of 12,183 patients with pulmonary tuberculosis who completed treatment within 1 year, 113 relapsed within 30 months after commencement of therapy. The overall 30-month relapse rate was 0.9% (95% confidence interval [CI] 0.8-1.1%). On matching 113 cases with 226 control subjects in a conditional logistic model, thrice-weekly treatment increased the risk of relapse in comparison with daily treatment (odds ratio 3.92, 95% CI 1.78-8.63), whereas prolonging both intensive phase and overall treatment by 50% or more protected against relapse (odds ratio 0.24, 95% CI 0.08-0.70). When pretreatment culture was positive and cavitation was absent, the 30-month relapse rate for standard thrice-weekly regimen was 1.1% (95% CI 0.6-2.0%). The corresponding rates in the presence of cavitation were 7.8% (95% CI 4.0-14.6%) for standard thrice-weekly regimen; 3.3% (95% CI 1.9-5.5%) for standard daily regimen; 0.5% (95% CI 0.1-2.6%) for extended thrice-weekly regimen; and 0.4% (95% CI 0.1-0.9%) for extended daily regimen. Further studies are required to reduce the risk of relapse under program settings.     

Effectiveness of anemia and chronic kidney disease as predictors for presence and severity of coronary artery disease in patients undergoing stress myocardial perfusion study

Chronic kidney disease (CKD) and anemia portend a higher risk of cardiac events and mortality. We sought to ascertain whether coronary artery disease (CAD) by myocardial perfusion single-photon emission computed tomography is more common in patients with CKD (glomerular filtration rate < or =60 ml/min/1.73 kg/m(2)) and/or anemia (hemoglobin level < or =13 g/L) and the impact of different degrees of CKD. One thousand five hundred eighty patients (mean age 65 +/- 10 years) underwent gated myocardial perfusion single-photon emission computed tomography and clinical evaluation. Patients were divided into 4 groups (group 1, no anemia/no CKD, n = 800; group 2, anemia/no CKD, n = 195; group 3, CKD/no anemia, n = 332; group 4, anemia/CKD, n = 253). Multivariate logistic regression analysis was undertaken to examine the association of these diagnoses with abnormal myocardial perfusion single-photon emission computed tomogram. Compared with patients with neither diagnosis, an abnormal scan was more common in those with anemia or CKD. Patients with anemia and CKD exhibited more severe CAD (mean summed stress score 6.8 vs 4.7, p <0.01). Established high-risk findings were more prevalent in patients with anemia and/or CKD, including a summed stress score > or =8, transient ischemic dilation, or a left ventricular ejection fraction < or =40% (group 1 28%, group 2 38%, group 3 38%, group 4 48%, all p values <0.01). Patients with moderate CKD demonstrated an increased risk of an abnormal scan (odds ratio 2.66, p <0.0001). After adjustment in multivariate analysis, anemia and CKD each remained predictors for an abnormal scan. The association was stronger in those with the 2 conditions (odds ratio for high-risk scan 1.89, p = 0.0002). In conclusion, in patients with suspected CAD, anemia and CKD are predictors of myocardial perfusion single-photon emission computed tomographic markers for worsened outcomes. The relation was independent of other risk factors, supporting the inclusion of anemia and CKD in global risk assessment for patients with suspected CAD.     

Intracranial hemorrhage after carotid angioplasty: a pooled analysis.

PURPOSE: To use a pooled analysis of the literature to find the incidence of and characteristics common to intracranial hemorrhage (ICH) associated with carotid artery stenting (CAS). METHODS: A search of the English-language literature (1996-2005) was performed in PubMed to find cases of CAS-associated ICH. Information was derived from the identified case studies in 5 categories and 19 aspects: (1) incidence of CAS-associated ICH; (2) demographic data (sex, age, symptom presentation, and presence of preexisting hypertension); (3) imaging data (side of lesion, degree of maximal stenosis, lesion location, status of the contralateral carotid artery, collateral circulation, and preprocedural imaging features); 4) procedure-related characteristics (antithrombotic medication, use of cerebral protection devices, residual stenosis, symptoms, interval from the procedure to ICH, type of ICH, and blood pressure changes); and (5) clinical outcome. RESULTS: Fifty-four cases of CAS-associated ICH were reviewed: 51 cases from 36 published articles and our own 3 cases. The incidence of CAS-associated ICH was 0.63% (95% CI 0.38% to 0.97%) in studies consisting of >100 cases, which was significantly lower (p<0.0001) than that of case series consisting of <100 cases (2.69%, 95% CI 1.75% to 3.94%). Distinctive features included symptomatic lesions, severe stenosis (> or =90%), maximal stenosis in the internal carotid artery (ICA) distal to the bifurcation, and preexisting cerebral infarction. CONCLUSION: The incidence of CAS-associated ICH was significantly lower in series consisting of >100 cases. More caution should be directed toward patients with symptomatic lesions, severe stenosis, maximal ICA stenosis distal to the carotid bifurcation, and preexisting cerebral infarction.     

Encephalopathy and acute axonal sensorimotor polyneuropathy following acute pancreatitis: a case report and review of the literature

A case of a 22-year-old woman with rare neurologic complications including encephalopathy and acute axonal sensorimotor polyneuropathy in the course of acute pancreatitis is reported. The encephalopathy emerged 3 weeks after the onset of the illness with complete remission being noted 1 week later. The polyneuropathy presented as quadriplegia and respiratory failure that required intubation and partially remitted gradually. There was no pancreatic lesion, no major pancreatic surgery, no sepsis, and no multiple organ failure, all of which had been proposed as the predisposing factors. Severe inflammatory response syndrome (SIRS) that developed during the clinical course of this patient might have induced these neurologic complications.