Macrophages have plastic and diverse phenotypes and functions, and they play different roles in host defense, tissue homeostasis and repair, development, and various pathologic processes. Although the classically activated macrophage (M1) and alternatively activated macrophage (M2) phenotypes are widely accepted, most macrophages under physiologic and pathologic conditions are polarized to a continuum of states between the M1 and M2 extreme phenotype poles. In recent years, research on the regulatory mechanisms of M1 and M2 macrophages has made great progress, preliminarily elucidating the role of cellular metabolic reprogramming in macrophage polarization and the role of glycolytic enzymes in controlling inflammatory macrophages. The knowledge lays the foundation for elucidating the mechanisms in the regulation of macrophage functional phenotypes. Tumor-associated macrophages play important roles in the development of tumors. The macrophages in the microenvironment of hematologic malignancies have unique features, and a deep study on them will provide new thoughts and clues for clinical diagnosis and therapeutics.

The tumors originate from transformation cells caused by gene mutations. These cells are frequently kept at dormant state or detected and cleared by the immune surveillance. The research data show that the hallmarks of tumors and aging share many similarities, which is the biological basis for tumors as aging-related diseases. With the increase of tumor initiation cells and the decline of immune function in the elderly, the morbidity and mortality of tumors steadily increase. The core mechanisms are inflammaging and immunosenescence in the elderly. This article reviews recent advances in the field of tumorigenesis, inflammaging and immunosenescence, which elucidates the hypothesis and possible mechanism that tumors are aging-related diseases.

B-cell lymphomas are a group of highly heterogeneous malignancies. The phenotypes of different subtypes depend on the differentiation stage and genetic changes of B-cell, which reflects in the immunophenotype, karyotype and tumor microenvironment changes, especially the differences in the cellular composition of microenvironment. This article reviews the characteristics of B-cell lymphoma cells and the cellular composition of microenvironment, discusses the role of tumor microenvironment cells in the occurrence and development of B-cell lymphoma, which provides new ideas for clinical diagnosis and treatment.

Human herpes virus (HHV) spreads widely in a latent-infected way. HHV is divided into 3 kinds and 8 types. Herpes simplex caused by HHV-1 and HHV-2, varicella-zoster caused by HHV-3 and Epstein-Barr virus (EBV) known as HHV-4 and recognized firstly as human tumor virus, are well known in the field of virology. With the application of hematopoietic stem cell transplantation , cytomegalovirus (HHV-5) and HHV-6 have gained an increasing attention. The biological characteristic of HHV is latent infection in a long time and HHV can be reactivated in some immunocompromised individuals. Clarification of latent infection mechanism will help provide targets for therapy and lay a foundation for clinical treatment. This paper summarizes the clinical significance of HHV infection. Taking the mechanism of EBV latent infection as an example, the pathway and significance as well as strategy of co-evolution of organism and virus will be discussed in order to provide clues for prevention and therapy.

Half a century ago,it was confirmed that leukemia could be induced by retroviruses in some animals.There are numerous en-dogenous retroviruses in the human genome.However,retrovirus-related human adult T-cell leukemia is only endemic in some local areas. Recently,an extensive study on apolipoprotein B mRNA editing enzyme catalytic polypeptide 3(APOBEC3)family members has revealed the resistance mechanism in human to retrovirus-induced leukemia.The Epstein-Barr virus is widely spread in the human population and exists as a latent infection in the human body for a long time.It is closely associated with the occurrence and development of some lymphomas and solid tumors,indicating its tumorigenicity.The relationship between other viral infections and leukemia/lymphoma remains unclear. The interaction may be mediated by complex,multistep,and indirect networks,which need to be further illuminated.

Human herpesvirus 6 (HHV-6) is recognized as a ubiquitous dsDNA virus in human with widespread cell tropism in vivo, which could induce lifelong latent infection and be reactivated in some immunocompromised individuals leading to serious diseases. With the increasing application of hematopoietic stem cell transplantation (HSCT), it is obvious that HHV-6 reactivation has a close relationship with several complications including encephalitis after transplantation. On the other hand, among about 1 % infected people, HHV-6 and subtelomeric region of cell chromosomes in the state of endogenous persistent infection play a part in activated virus infection. As the detection methods make a great progress in HHV-6 detection, clinical data reveals the relationship between HHV-6 reactivation and lots of chronic diseases, especially lymphoma, leukemia as well as some chronic hematopoietic and immunological diseases.

Allee effect is a phenomenon in ecology characterized by a correlation between population size or density and the mean individual fitness of population or species.It is consistent with density dependent phenomenon in biomedical field.Recently,Allee effect has been studied by theoretical biologist in detail for oncology biological research.Leukemia cells,which reside in organic microenvironment,show an obvious Allee effect.The authors compared Allee effect with density dependent growth of leukemia cells based on their work experience and literature data.No principle distinction was found between these two terms.In this paper,Allee effect in leukemia cell culture and leukemia,especially in minimal residual disease,will be discussed in the view of ecology.The association between Allee effect and leukemogenesis and relapse dynamics will also be explored in the future research.

Dormant follicular lymphoma, prostate carcinoma and breast carcinoma are frequently detected by autopsy of non-tumor patients. Dormancy of malignant cells in hematopoietic malignancies is associated with genesis, development and treatment of these diseases. Dormancy is the universally applied strategy by living organism during survival competition. As the in vivo neoplasm, tumor cells keep this property. Recently, much attention has been paid to the mechanisms of tumor dormancy. These studies not only have theoretical significance, provide new ways for the prevention and treatment of tumors, but also help the understanding of over-diagnosis, over-treatment and provide clues for precise medicine. This paper reviewed cellular mechanism of tumor cell dormancy,immunological and vascular regulation of dormant tumors. The clinical significance,application of these mechanisms and direction of further study, which will provide new clues for the treatment of hematopoietic malignancies, were also discussed.

Objective To evaluate the correlation between serum uric acid with cognitive disorder after acute cere?bral infarction by prospective study. Methods Four hundred consecutively enrolled patients of acute cerebral infarction were divided into no cognitive impairment group and cognitive impairment group according to the assess of Montreal Cog?nitive Assessment (MoCA). Univariate analysises were conducted in the potential risk factors of cognitive impairment in?cluding age, sex, smoking, alcohol, hypertension, diabetes, dyslipidemia, level of education, infarction in key parts, atrial fibrillation, serum uric acid, blood homocysteine between two groups. The statistically significant indicators in univariate analysises were used as independent variables and the scores of MoCA were used as the dependent variable to conduct multiple linear regression analysis. The assessment on the risk of cognitive impairment after cerebral infarction were con?ducted according to serum uric acid, sex, age and TOAST classification further. Results Serum uric acid was indepen?dent risk factors of cognitive disorder after acute cerebral infarction. The risk of cognitive disorder after acute cerebral in?farction was significantly increased in patients with high level of serum uric acid than with normal level and the relative risk was 1.35,95%CI(1.098,1.660). Especially for the young, male or patients with cerebral infarction in classification of small artery occlusion, the risk increased further, and the relative risk was 1.513, 95%CI(1.092, 2.096)1.412, 95%CI (1.125, 1.771)and 1.464, 95%CI(1.128, 1.900)respectively. Conclusion Exaltation of Serum uric acid was indepen?dent risk factor of cognitive disorder after acute cerebral infarction. The risk of cognitive disorder after acute cerebral in?farction was significantly increased in patients with high level of serum uric acid than with normal level, and especially for the young, male and patients with cerebral infarction in classification of small artery occlusion, the risk increased fur?ther.

Cancer stem cells (CSCs) are units in cancer evolution.The elucidation the origin of CSCs has great significance on prevention and treatment of cancers.This paper discusses possible origins,genetic pathways and mechanisms of CSC on the basis of the literature and authors' research.Normal stem cells could be malignantly transformed to CSC through long term accumulation of gene mutations.Induction to pluripotent stem cells by reprogramming is a possible pathway for somatic cells to become CSCs.Dedifferentiation of cancer cells to CSCs is another pathway.Epithelial-mesenchymal transition (EMT),which is an important mechanism for cellular plasticity,plays important roles in cancer metastasis and stemness of cancer cells.Cell-fusion inducing EMT could be a mechanism for the genesis of CSCs.Infection of some virus is also related to the genesis of CSCs.The complexity of cancer biology was also discussed.