动物的的变态

变态是动物学中一个较重要的专用名词,有关内容在中学课本也多处涉及到。现择要介绍一点动物变态的知识,供动物学教学参考。何谓动物的变态动物由于外在和内在的原因,个体形态发生变化,这叫变态。但动物学所讲的变态,是狭义地从发生学角度理解,即胚胎不直接转变为成体,而是在后期发育过程中,先形成形态、生理、生态方面特殊的幼体,行独立生活和生长,以后在某阶段发生急剧变化,转变为成体。青     

活的不可培养的细菌的研究进展

活的不可培养微生物(VBNC)即一些微生物明显地丧失了可培养的特性,但是保留了自身原有的代谢活力,并且在一定条件下,又可以回复到可培养的状态。从VBNC细菌的诱导条件、生物学特性和检测方法3个方面对VBNC细菌研究进展做一综述。     

真核细胞的基因的组织

一、真核细胞基因的基本结构 1.转录单位: 从已知的数十种基因的顺序,可得出一个具有功能的基因的共同规律,在基因5’端-25至-75区,有CCAAT和TATAAA区(后者又称ATA box或Hogness box),相当于促进子区(Promotor),为体外转录所必需。     

高频率的波动对于种子的萌发和植物的发育的影响

本文主要是以理论和试验来说明音波对植物的生长发育和种子萌发所起的影响。在农业实践上音波所起的作用,据现在所知:有缩短植物成熟期,加速萌芽和增强植物的生长发育等。这一些非但具有理论和实践上的意义,同时在今後把物理科学应用到农业科学中开辟了极广阔的前程。     

由吸附的缩氨酸诱导的细胞膜的形变

研究了由一系列相互平行的吸附在细胞膜上的缩氨酸引起的膜的弹性形变,以及膜对缩氨酸的包裹行为,得到膜的平衡方程,用它可以来处理大尺度的形变,弯曲能量、吸附能量和弹性形变的相互竞争导致膜对缩氨酸发生从不吸附到部分吸附乃至完全包裹的结构转变．在膜的形变很小的时候,可以得到系统能量的解析解。     

远古的人们是怎样认识自己的起源的

人是从那里来的? 回答这个问题,你也许会说这有什么困难——人是从古猿变来的;甚至你还会进一步说,在这个从猿到人的转变过程中,劳动起着决定性的作用。然而这个现在看来比较明了的道理,恰是经历了多么漫长的认识过程才达到的呵!现在让我们首先来谈谈,远古的人们是怎样认识自己的起源的。最初的原始人可能还想不到自己的起源在人类诞生的最早时期,“最初的、从动物界分离出来的人,在一切本质方面是和动物本身一样不自由的”(恩格斯:《反杜林论》),这些最初的原始人为艰苦     

敲除pckA基因的结核杆菌引起的免疫反应的研究

研究结核杆菌pckA基因编码的磷酸烯醇型丙酮酸羧激酶(PEPCK)诱导机体产生的保护性免疫反应。用敲除pckA基因的牛结核杆菌BCG和野生型BCG分别感染小鼠,取肝、肺、脾进行病理分析,并进行脾细胞培养,检测CD4 、CD4 /CD8 、细胞因子IFNI-γI、L-12和TNF等。用敲除pckA基因的BCG感染的小鼠比野生型BCG感染的小鼠体内产生的结核结节少且不典型,炎性程度低。野生型BCG感染的小鼠脾脏内的CD4 T细胞和CD4 /CD8 、细胞因子IFN-γ、IL-12、TNF均明显高于敲除pckA基因BCG感染的小鼠。pckA基因为结核杆菌生长所必需,其编码产物PEPCK能够刺激机体产生免疫反应,是一种很好的疫苗候选分子。     

分离的蚕豆细胞核的RNA聚合酶活力的研究

利用Triton X-100对叶绿体膜的作用,可快速地从蚕豆幼叶制备较纯净的细胞核,它具有较高的RNA聚合酶活力。比较了两种分离核的方法,证明利用匀浆法制备的核具有较高的活力。核活力与发育时期有关系,茎端和第1对幼叶的核活力显著高于第2和第3对叶片的核活力。此外,核活力明显地受反应液内锰离子的抑制。     

霸王的原生质体培养的研究

目的：为利用原生质体融合技术转移霸王抗旱基因。方法：采用酶解法分离霸王原生质体,比较了霸王子叶和愈伤组织游离原生质体的产量和活力,不同渗透压和起始密度对原生质体分裂频率的影响。结果：愈伤组织游离的原生质体产量和活力均高于子叶,原生质体产率可达2.4×106个/g.FW,活力达89%。采用液体浅层培养,在附加2,4-D（2mg/L）、6-BA（1.0mg/L）、2%蔗糖和甘露醇（0.4mol/L）的DPD培养基中,原生质体分裂频率最高,达68.6%。转移到附加2-iP（3mg/L）、KT（1.0mg/L）、6-BA（1.0mg/L）的分化培养基上,获得2个再生苗。结论：采用酶解法游离霸王愈伤组织,可获得高活力和高分裂频率的霸王原生质体。     

Characterization of monoclonal antibodies raised against the latent nuclear antigen of human herpesvirus 8

Human herpesvirus 8 (HHV-8; also designated Kaposi's sarcoma-associated herpesvirus) is the likely etiological agent of Kaposi's sarcoma (KS). HHV-8 encodes a latent nuclear antigen (LNA) which is the product of the viral gene orf 73. LNA is recognized by most infected patient sera and is the basis of current immunofluorescence assays used in epidemiological studies of HHV-8 infection. Here we describe the characterization of four monoclonal antibodies raised to the C-terminal third of LNA-glutathione S-transferase fusion proteins. These monoclonal antibodies recognized discrete linear epitopes within the C terminus and repetitive region of LNA, detected antigen in primary effusion lymphoma (PEL) cells, and precipitated a 220- to 230-kDa protein doublet corresponding to LNA from HHV-8-infected PEL cell lines. In situ immunocytochemistry of KS lesions with these antibodies show that LNA is extensively expressed in KS spindle cells.     

Monocytes in Kaposi's sarcoma lesions are productively infected by human herpesvirus 8.

PCR analysis and serological studies demonstrated a close association between Kaposi's sarcoma (KS)-associated herpesvirus, or human herpesvirus 8 (HHV-8), and the development of Kaposi's sarcoma (KS). The majority of the KS cells were shown to be latently infected by the virus. In this study we investigated which type of cell is productively infected in KS lesions. In situ hybridization was performed with strand-specific RNA probes complementary to the sequences coding for the minor capsid protein (VP23) of HHV-8. The VP23 gene is specifically expressed during the lytic or replicative period of the virus life cycle, and therefore it is a useful marker to detect productively infected cells. By in situ hybridization of KS lesions, a strong hybridization signal was detected only in a small subset of the KS cells of the lesions. Simultaneous application of immunohistochemical staining and in situ hybridization identified the virus-replicating cells to be of monocytic origin. Productively infected monocytes may be an important reservoir for transmission of the virus and for the increase and maintenance of the high load of HHV-8 generally observed in nodular KS lesions during late stages of infection.     

Viruses, cancer and AIDS

Patients with AIDS are at risk of lymphoma and Kaposi's sarcoma. These tumours are associated with the gamma herpesviruses, Epstein-Barr virus (EBV) and human herpesvirus 8 (HHV-8), although a proportion of AIDS lymphomas lacks both viruses. EBV and HHV-8 are latent in the tumour cells, with genes that play a direct role in driving cell proliferation. Human immunodeficiency virus, in contrast, while being the greatest risk factor for lymphoma and Kaposi's sarcoma, acts indirectly, mainly by causing immune suppression, as immunosuppressed transplant patients are at risk for the same types of tumour.     

Genotypic analysis on the ORF-K1 gene of human herpesvirus 8 from patients with Kaposi's sarcoma in Xinjiang, China

Human herpesvirus 8 (HH'V-8) is thought to be essential for the development of all forms of Kaposi's sarcoma (KS). HHV-8 DNA is present virtually in all KS tumor biopsy samples. Genes at both ends of the HHV-8 genome have been shown to vary considerably. Seve nmajor molecular subtypes of HHV-8 were defined based on the amino acid sequence of the open reading frame K1 (ORF-Kl), generally known as A, B, C, D, E, E and Z. Most strains collected worldwide were clustered into two subtypes (A and C). Here, the Kl/VRl region of HHV-8 was amplified by nested PCR in 22 (81.48%) of 27 cases from Xinjiang Uygur Autonomous Region, a province in northwest-ern China. Phylogenetic analysis on the basis of the KI/VRI amino acid sequence indicated that the majority of these KS patients were infected by subtype C HHV-8 (n = 18, including 15 belonging to the C2 group), and several by subtype A (n = 4, including 3 being the Al group). This is the fast report of subtype A HHV-g in China. Furthermore, the correlations between different forms and lesions of KS and different subtypes of HHV-8 were analyzed. The findings showed that subtype A HHV-8 resulted in significantly more frequent mucosal KS lesions than subtype C. However, there was no obvious correlation between different forms of KS and different subtypes of HHV-8.     

Human herpesvirus 8 (HHV-8/KSHV) and hematologic malignancies

Human herpesvirus 8 (HHV-8), also defined Kaposi's sarcoma (KS)-associated herpesvirus, was identified by Chang and colleagues in 1994 using purely molecular techniques, before any serological evidence or virus isolation in cell culture could be achieved. HHV-8 is unique among herpesviruses because its prevalence in the general population is low and because it possesses the richest weaponry of viral oncogenes and tumor-promoting factors ever described. Eleven HHV-8-specific genes are homologs of cellular genes, which were hijacked from the host during a long parallel evolution, and at least five of such genes show both in vitro and in vivo transforming ability. HHV-8 is the causative agent of KS, but it has also been associated with different hematologic malignancies, including primary effusion lymphoma (PEL), multicentric Castelman's disease (MCD), MCD-related immunoblastic/plasmablastic lymphoma and various atypical lymphoproliferative disorders. Although low-level silent infection was detected in bone marrow stromal cells from patients with multiple myeloma, a role of HHV-8 in this disease is unlikely. As seen with KS, the incidence of HHV-8-associated lymphoproliferative disorders is increased in the setting of human immunodeficiency virus infection.     

Alpha interferon inhibits human herpesvirus 8 (HHV-8) reactivation in primary effusion lymphoma cells and reduces HHV-8 load in cultured peripheral blood mononuclear cells

Infection by human herpesvirus 8 (HHV-8) is associated with the development of Kaposi's sarcoma (KS). Since regression of KS can be achieved by treatment of the patients with alpha interferon (IFN-alpha), we analyzed the effects of IFN-alpha or anti-IFN-alpha antibodies (Ab) on HHV-8 latently infected primary effusion lymphoma-derived cell lines (BCBL-1 and BC-1) and on peripheral blood mononuclear cells (PBMC) from patients with all forms of KS and from at-risk subjects. IFN-alpha inhibited in a dose-dependent manner the amplification of HHV-8 DNA in BCBL-1 cells induced to lytic infection with tetradecanoyl phorbol acetate (TPA). This effect was associated with the inhibition of the expression of HHV-8 nut-1 and kaposin genes that are induced early and several hours, respectively, after TPA treatment. In addition, IFN-alpha inhibited virus production and/or release from BCBL-1 cells. Inhibition of nut-1 and kaposin genes by IFN-alpha was also observed in BC-1 cells induced with n-butyrate. Conversely, the addition of anti-IFN-alpha Ab to TPA-induced BCBL-1 cells resulted in a larger number of mature enveloped particles and in a more extensive cytopathic effect due to the neutralization of the endogenous IFN produced by these cells. IFN was also produced by cultured PBMC from HHV-8-infected individuals, and this was associated with a loss of viral DNA during culture. However, the addition of anti-IFN-alpha Ab or anti-type I IFN receptor Ab promoted the maintenance of HHV-8 DNA in these cells that was associated with the detection of the latency-associated kaposin RNA. Finally, the addition of IFN-alpha reduced the HHV-8 load in PBMC. Thus, IFN-alpha appears to have inhibitory effects on HHV-8 persistent infection of PBMC. These results suggest that, in addition to inhibiting the expression of angiogenic factors that are key to KS development, IFN-alpha may induce KS regression by reducing the HHV-8 load and/or inhibiting virus reactivation.     

Distribution of 'promoter' sandflies associated with incidence of classic Kaposi's sarcoma

The patchy geographical distributions of classic Kaposi's sarcoma (KS) and human herpesvirus type 8 (HHV-8), better known as Kaposi's sarcoma-associated herpesvirus (KSHV) remain unexplained. It has been proposed that certain species of bloodsucking insects ('promoter arthropods') promote the reactivation of HHV-8/KSHV and facilitate both HHV-8/KSHV transmission and KS development. This hypothesis was tested by sampling the presence and density of human-biting Diptera with CDC light traps in two areas of Sardinia with contrasting incidence rates of classic KS. In total, 11 030 specimens (99.9% sandflies and 0.1% mosquitoes) belonging to 10 species were collected from 40 rural sites. Five of these species are considered to be possible promoter arthropods because of the irritation their bites cause: Phlebotomus perniciosus Newstead; Phlebotomus perfiliewi Parrot (Diptera: Psychodidae); Aedes berlandi Seguy; Culiseta annulata (Schrank) and Culex theileri Theobald (Diptera: Culicidae). Five species are probable 'non-promoters' because their bites are not particularly irritating: Culiseta longiareolata (Macquart); Culex pipiens s.l .; Anopheles algeriensis Theobald; Anopheles maculipennis s.l. , and Anopheles plumbeus Stephens. A significant correlation was found between the geographical distribution of promoter arthropods and incidence rates of KS (Spearman's r = 0.59 ,P < 0.01). Promoter arthropods were more likely to be caught in areas with cutaneous leishmaniasis and a past high prevalence of malaria, and in areas of limestone, acid volcanic soil and cereal cultivation. The study supports the association between promoter arthropods and classic KS, which may explain the geographic variability of KS and HHV-8/KSHV, and highlights the links with a number of variables previously associated with the incidence of KS.     

Kaposi's sarcoma and human chorionic gonadotropin: mechanisms,moieties and mysteries

Kaposi's Sarcoma (KS) is a highly angiogenic neoplasm associated with infection by the human gamma-herpesvirus, HHV-8 or Kaposi's sarcoma herpes virus (KSHV). When in 1872 the Hungarian scientist Moritz Kaposi described the sarcoma, which was later named after him, he was dealing with a rare dermatologic disease. Today, KS is a more common pathology due to its high incidence in AIDS, in immuno-suppressed transplantation patients and, in its endemic form, in Africa. The introduction of highly active antiretroviral therapy (HAART) has led to a drastic reduction of KS incidence in HIV-infected patients, but in some cases KS resists the treatment. KS is more common in men than in women. The observation of spontaneous remissions during pregnancy stimulated investigations into the potential anti-KS activity of the pregnancy hormone human chorionic gonadotropin (hCG). The variable effect in clinical trials using urinary preparations of the hormone (u-hCG) has led to the hypothesis that contaminating moieties present in these preparations may account for the anti-KS effect observed in vitro. While the discrepancy between laboratory tests and clinical trials remains a mystery, little is known about potential anti-KS mechanisms of the hormone itself and/or other active moieties present in u-hCG.     

Genotypic analysis on the ORF-K1 gene of human herpesvirus 8 from patients with Kaposi's sarcoma in Xinjiang,China

Human herpesvirus 8(HHV-8) is thought to be essential for the development of all forms of Kaposi's sarcoma(KS).HHV-8 DNA is present virtually in all KS tumor biopsy samples.Genes at both ends of the HHV-8 genome have been shown to vary considerably.Seven major molecular subtypes of HHV-8 were defined based on the amino acid sequence of the open reading frame K1(ORF-K1),generally known as A,B,C,D,E,F,and Z.Most strains collected worldwide were clustered into two subtypes(A and C).Here,the K1/VR1 region of HH...     

The Biology of Kaposi＇s Sarcoma-Associated Herpesvirus and the Infection of Human Immunodeficiency Virus

Kaposi sarcoma-associated herpesvirus (KSHV),also known as human herpesvirus 8 (HHV-8),is discovered in 1994 from Kaposi's sarcoma (KS) lesion of an acquired immunodeficiency syndrome (AIDS)patient.In addition to its association with KS,KSHV has also been implicated as the causative agent of two other AIDS-associated malignancies:primary effusion lymphoma (PEL) and multicentric Castleman's disease (MCD).KSHV is a complex DNA virus that not only has the ability to promote cellular growth and survival for tumor development,but also can provoke deregulated angiogenesis,inflammation,and modulate the patient's immune system in favor of tumor growth.As KSHV is a necessary but not sufficient etiological factor for KS,human immunodeficiency virus (HIV) is a very important cofactor.Here we review the basic information about the biology of KSHV,development of pathogenesis and interaction between KSHV and HIV.