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Objective:To comprehensively evaluate the correlation between migraine and the risk of hemorrhagic stroke using Meta-analysis.Methods:The published observational studies on migraine and the risk of hemorrhagic stroke in PubMed, EMbase, Cochrane library, Chinese Biomedical Database, China Journal Full-text Database, Wanfang Database and VIP Database were retrieved by computers. The retrieval time limit was from the establishment of the databases to December 31, 2019. Two reviewers independently conducted the literature screening and data extraction, and evaluated the quality according to Newcastle Ottawa scale. Stata SE 12.1 software was used for Meta-analysis.Results:Six case-control studies and 7 cohort studies met the inclusion criteria, all of which were in English. The results of Meta-analysis showed that exposure to migraine increased the risk of hemorrhagic stroke (odds ratio [ OR] 1.47, 95% confidence interval [ CI] 1.23-1.76; P<0.001). Sensitivity analysis showed that the results were robust. Subgroup analysis showed that migraine with aura ( OR 1.38, 95% CI 1.05-1.81; P=0.019), migraine without aura ( OR 1.46, 95% CI 1.19-1.80; P<0.001), male ( OR 2.10, 95% CI 1.72-2.56; P<0.001) and female ( OR 1.53, 95% CI 1.22-1.92; P<0.001) migraine could increase the risk of hemorrhagic stroke. Conclusion:Regardless of the gender of patients and presence or absence of migraine aura, migraine can significantly increase the risk of hemorrhagic stroke.
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Clonal hematopoiesis is a common aging_associated biological state. The incidence of malignant neoplasms for the patients with clonal hematopoiesis of indeterminate potential (CHIP) is 0.5%-1% every year. Potential factors of clonal progression in hematopoietic cells have been summarized, including disordered endogenous immunity caused by the augmentation of proliferative pressure, chromosomal instability caused by telomeres short; the amplification of clonal stem cells, acquisition of new mutations, and aging_associated changes in hematopoietic stem cells, including altered DNA damage response, an altered transcriptional program and epigenetic alterations while failing to support healthy hematopoiesis. CHIP is a vascular risk factor driven by interactions between clonal monocytes_macrophages and the endothelium, as well as a neoplastic progression risk factor driven by the acquisition of additional somatic mutations in the context of many other influences on hematopoiesis and clonal balance. Strategies to reduce the clonal burden associated with CHIP and to inhibit the key inflammatory pathways leading to atherosclerosis could improve the prognosis of the patients.
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Myelodysplastic syndromes (MDS) are clonal disorders characterized by the accumulation of complex genomic abnormalities that defined disease phenotype,prognosis,and the risk of transformation to acute myeloid leukemia.The clinical manifestations and prognosis of patients with different phenotypes arevary different,and the overall survival varies from several months to several years.Prognostic scoring systems are important staging tools that aided physicians in their treatment recommendations and decision-making and could help patients understand their disease trajectory and expectations.These models and others use mainly clinical variables that are obtained from bone marrow biopsy and peripheral blood measurements.Adding gene mutation data into current models might improve the total predictive power.The search for an optimal way to merge the clinical and genomic data in a sophisticated and highly accurate model remains a work in progress.A comprehensive geno-clinical model that could translate the use of genomic data into clinical practice would finally be established.This paper mainly introduces the progress of the gene mutations and prognosis models of MDS in the 60th American Society of Hematology (ASH) Annual Meetings were reviewed.
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The myelodysplastic syndromes (MDS) are collectively the most common myeloid neoplasms,and the clonal hematopoiesis presented in MDS results in bone marrow failure.An understanding of the MDS gene mutation profile can help to understand the biological significance of MDS and can be used for early diagnosis of disease,precise risk stratification,interpretation of pathogenesis,and improvement of treatment options.As the pathological features of MDS are gradually elucidated,individualized and effective treatment options are improved,and the targeted drug therapy may improve the prognosis of MDS patients.This article introduces the progress of MDS gene mutations and targeted therapy in the 60th American Society of Hematology (ASH) Annual Meeting.
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The support treatment of low-risk myelodysplastic syndromes (MDS) patients whose revised international prognostic score system (IPSS-R) is defined as 3.5 points remains the main treatment. The erythropoiesis stimulating agent (ESA) is the best choice for patients with del (5q) MDS as long as the endogenous erythropoietin (EPO) level is less than 500 U/L (preferably<200 U/L). The application of EPO for patients with treatment failure or relapsed after transfusion, chooses are immunosuppressant, transforming growth factor beta inhibitors and lenalidomide. Del (5q) syndrome could benefit from lenalidomide, and some patients after discontinuation of treatment still have been stable in peripheral blood. Thrombocytopenia caused serious hemorrhage rarely; thrombopoietin receptor analogs could reduce bleeding and improve the platelet count. These drugs can be used in patients with bone marrow blast counts of < 0.05. If treatment failed or advanced to high-risk MDS or transformed to acute myeloid leukemia, allogeneic hematopoietic stem cell transplantation might be required. Combined with reports in the 59th American Society of Hematology (ASH) Annual Meeting, this article describes the treatment strategies for low-risk MDS.
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Myelodysplastic syndromes (MDS) is a clinical heterogeneous disease characterized by impaired hematopoietic function and morphologic abnormalities of the bone marrow. Genomic studies show that MDS is usually driven by a series of multistep somatic cell genetic processes that affect the core genome. By definition, reproducible MDS drives mutations leading to cloning advantage. In addition, exposure factors, such as cytotoxic chemotherapy or genetic propensity of the reproductive system, could affect the pathogenesis and clinical outcomes of the disease. Combined with the reports in the 59th American Society of Hematology (ASH) Annual Meeting, the article introduces the genetic characteristics of MDS, in order to improve the diagnosis of MDS and the understanding of the pathogenesis of treatment-related MDS as well as the genetic tendency of MDS in the reproductive system.
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The treatment of patients with myelodysplastic syndromes (MDS) has included primarily supportive care (blood transfusions, colony stimulating agents, iron chelation, etc.) and new drugs, including 5-azacytidine, deoxyazacytidine, and lenalidomide. For those who are no longer benefiting from these agents, there is nearly nothing to do with effective therapies. When those drugs are ineffective, what the doctors could do is optimizing the delivery of hypomethylating agents (HMT) by dosing appropriately, sequencing appropriately, and using thoughtful combinations; as well as improving drug formulations (oral formulations and/or novel formulations) and working toward better selection of patients for best upfront mutation-directed therapy. Hopefully, the drug targeting and patient selection for optimal HMT treatment of MDS will be improved. Furthermore, ongoing research is focused on identifying unique agents to rescue MDS patients who have progressed despite HMT. Agents such as rigosertib are now focused on its application in specific MDS populations who might most likely benefit from this therapeutic approach [primary refractory and high-risk international prognostic scoring system (IPSS) patients]. Doctors eagerly await results of single-agent programmed death 1 (PD-1) and its inhibitors, or combination with HMT to the upfront and relapsed MDS setting. For the minority of patients who have specific targetable mutations, the selective agents (IDH1/2) are highly promising. Bone marrow transplantation remains the only offer for cure, but is depressingly unrealistic given the majority of the elderly and frail patients at the time of MDS progression.
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The treatment of patients with myelodysplastic syndromes (MDS) has included primarily supportive care (blood transfusions, colony stimulating agents, iron chelation, etc.) and new drugs, including 5-azacytidine, deoxyazacytidine, and lenalidomide. For those who are no longer benefiting from these agents, there is nearly nothing to do with effective therapies. When those drugs are ineffective, what the doctors could do is optimizing the delivery of hypomethylating agents (HMT) by dosing appropriately, sequencing appropriately, and using thoughtful combinations; as well as improving drug formulations (oral formulations and/or novel formulations) and working toward better selection of patients for best upfront mutation-directed therapy. Hopefully, the drug targeting and patient selection for optimal HMT treatment of MDS will be improved. Furthermore, ongoing research is focused on identifying unique agents to rescue MDS patients who have progressed despite HMT. Agents such as rigosertib are now focused on its application in specific MDS populations who might most likely benefit from this therapeutic approach [primary refractory and high-risk international prognostic scoring system (IPSS) patients]. Doctors eagerly await results of single-agent programmed death 1 (PD-1) and its inhibitors, or combination with HMT to the upfront and relapsed MDS setting. For the minority of patients who have specific targetable mutations, the selective agents (IDH1/2) are highly promising. Bone marrow transplantation remains the only offer for cure, but is depressingly unrealistic given the majority of the elderly and frail patients at the time of MDS progression.
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This paper reports a case of Ancylostoma duodenale parasitized in the hepatic flexure of colon and the case was misdiagnosed at the beginning. The causes of misdiagnosis are analyzed and the laboratory examination methods of hookworm are summarized.
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New progress of treatment of low-risk myelodysplastic syndromes (MDS) reported in the 58th American Socienty of Hematology (ASH) Annual Meetings was reviewed. Anemia is a single common symptom of low-risk MDS, and erythropoietic-stimulating agents (ESA) may be effective. The dose and duration of erythropoietic-stimulating agents (ESA) are critical to determine efficacy. If the treatment of ESA failed, the available options may include lenalidomide (approved for del5q positive cases), hypomethylating agents and a rather large number of experimental agents. The choice for the second-line treatment must consider the biologic, cytogenetic and molecular-identified characteristics of individual patient, as well as frailty and comorbidities. Other cytopenias rarely appear alone. Thrombomimetic agents for thrombocytopenia has been proposed in clinical trials, but there were some safety issues. Although neutropenia is targeted symptomatically with growth factor supportive care, the immunosuppressive therapy is indicated mainly for pancytopenic and hypoplastic low-risk MDS. Finally, hematopoietic stem cell transplantion is the curative option also for low-risk MDS, but it should be carefully evaluated to balancing toxicity and the possibility of survival advantage.
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Progress of World Health Organization (WHO) reclassification of myelodysplastic syndromes (MDS) in the 57th American Society of Hematology annual meetings were reviewed. A revision to the 4th edition of the WHO classification of MDS will be enacted in mid-2016. Based on recommendations of the Clinical Advisory Committee, proposals for change included abandoning the routine names of 'refractory anemia/cytopenia', expressing the prognostic significance of gene mutations in MDS, revising the diagnostic criteria for MDS entities with ring sideroblasts based on the detection of SF3B1 mutations, modifying the cytogenetic criteria for MDS with isolated del (5q), reclassifying the erythroid/myeloid type of acute erythroleukemia, and recognizing the familial link in some cases of MDS.
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Research progress of somatic mutations and the response to the treatment of de novo myelodysplastic syndromes (MDS) patients in the 57th American Society of Hematology (ASH) annual meetings was reviewed. The optimal methods and therapy time for patients with high-risk de novo MDS remained an area of ongoing investigation. The clinical prognostic scoring system does not include the molecular genetic abnormalities and DNA metlylation of histone/nuclear chromatin modifications, which may predict the effect of hypomethylation (HMA). Treatment of HMA may change the expression of genes related with prognosis, and the response rate to the HMA treatment was significantly increased for TET2-mutated patients with high-variant allele frequencies. The overall grade of recommendation for choosing HMA therapy over induction chemotherapy in high-risk MDS based on molecular genetic mutations was 2C, according to less-associated toxicity and increased responses primarily in TET2-mutated disease. Further prospective studies are needed to evaluate the long-term effects of HMA therapy, particularly in TET2-mutated patients.
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Objective To compare the differences of platelet(PLT) count between the optical method (PLT‐O) and electrical impedance method (PLT‐I) ,using microscopic method (PLT‐M) as a standard method ,and to analyze the alarm information of in‐strument .Methods Both of PLT‐O and PLT‐M of 468 cases of patient specimens were detected by Sysmex XE‐2100 automatic hematocyte analyzer ,and which were compared with PLT‐M .The counts and morphology of red blood cells and platelets were de‐tected by microscopic method .The alarm information of red blood cells and platelets were recorded .Results In non‐hematopathy group ,there was no significant difference among PLT‐M ,PLT‐I and PLT‐O (P=0 .071) .In hematopathy group ,PLT‐I was signifi‐cantly different from both PLT‐M and PLT‐O (P0 .05) .There were 149 cases occurring platelets alarm and 127 cases occurring red blood cells alarm in hematopathy group , which was consistent with the results of microscopic method .Conclusion When the value of PLT is below the normal reference range ,counting error of PLT‐I is large and the value of PLT should be rechecked or corrected using PLT‐M and PLT‐O .Re‐exam‐ination should be performed when alarm information is displayed .
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Objective:To explore the relationship between sleep structure changes and state or trait anxiety in patients with insomnia.Methods:Investigations were conducted with the State-trait Anxiety Inventory (STAI) and whole-night ploysomnography (PSG) recorded in 31 patients with insomnia and 20 normal controls.Repeated examinations were conducted in return visits 3～4 months after discharge.Results:Compared to control group,the patients with insomnia had decreased sleep time[(333.71±84.33) min vs.(403.65±19.29) min] and sleep efficiency[(70.41±17.35) % vs.(83.45±4.42) %],and increased sleep latency[(39.48±24.24) min vs.(19.65±8.57) min],REM sleep latency[(106.60±42.89) min vs.(86.80±12.25) min],proportion of S_1 sleep time[(25.36±14.22) % vs.(8.86±1.77) %]and awakening times[(4.45±2.51)vs.(1.75±1.07)].The proportions of S_(3+4) time[(7.38±9.70) % vs.(13.78±4.24) %] and REM sleep time reduced[(14.54±5.61) % vs.(19.18±2.14)%] (Ps<0.05).According to the STAI,scores of both state anxiety[(47.94±8.96) vs.(39.15±4.51)] and trait anxiety[(49.94±8.90) vs.(42.05±7.13)] were significantly higher in insomnia group than in control group (Ps<0.05).State anxiety was positively correlated with sleep latency (r=0.42),REM sleep latency (r=0.25),awakening times (r=0.44) and proportion of S_1 sleep time (r=0.34) (Ps<0.05),and negatively correlated with proportion of REM sleep time (r=-0.41,P<0.01).Trait anxiety was positively correlated with sleep latency (r=0.37,P<0.01) and wakefulness frequency (r=0.29,P<0.05).In return visits,the sleep structure improved,state anxiety score reduced,and trait anxiety had no significant changes.Conclusion:Patients with insomnia have significant sleep structural changes and higher state and trait anxiety.Their sleep structural changes are possilly related to state and trait anxiety.
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Objective To investigate the composite of chitosan(CS) and polyvinyl alcohol (PVA) as scaffold carrier for rabbit chondrocytes nurture and growth.Methods The third passage of chondrocytes were seeded in CS/PVA gel scaffold and 24,48 and 72 h after which cytoactive and toxicity were determined by MTT respectively.After one,two and three weeks,the growing status and morphology of chondrocytes in CS/PVA gel were observed with scaning electron microscope (SEM) and laser confocal scanning fluorescence microscope (LCSM).Results The third passage of chondrocytes in CS/PVA gel scaffold remained high proliferation ability.MTT measuring cell activity and virulence,the result showed that the number of cells obviously increased with the time,with statistical significance of difference between each groups (P＜0.05),without side effect to cells by the material.Observation of scaning electron microscope and confocal laser scanning fluorescence microscope showed that chondrocytes grew well with the scaffold of CS/PVA gel.Conclusion CS/PVA mixed gel material can be used as scaffold for rabbit chondrocytes growing for repairing cartilages defect in tissue engineering.