Distribution of the cytoskeletal protein, Nestin, in acute leukemia.

Nestin is a neuroepithelial stem cell marker that is expressed in some types of tumor cells. Recent reports suggest that Nestin may be closely related to malignant cell proliferation and migration. Acute leukemia (AL) is characterized by a lack of differentiation, which results in uncontrolled proliferation in the bone marrow and accumulation of immature cells. The expression and function of Nestin in AL is unclear. We investigated Nestin immunohistochemical patterns of 87 patients that included 47 cases of acute myeloid leukemia (AML) and 40 cases of acute lymphoblastic leukemia (ALL), and 20 patients in complete remission (CR) from AML or ALL. We also investigated the clinico-pathological features of 87 cases of AL and their CR and overall survival (OS). Nestin was expressed in leukemic blasts and mature granulocytic cells in most cases (39/47) of AML. Conversely, Nestin was expressed in mature granulocytic cells in fewer cases (6/40) of ALL, but not in blasts. Nestin expression appeared in leukemic blasts of AML, but not ALL. Nestin expression in AML blast cells was not associated with CR or OS. We provide evidence that Nestin is expressed in AL and might be a useful immunohistochemical marker for identifying AML and ALL.

The novel peptide apelin lowers blood pressure via a nitric oxide-dependent mechanism.

Apelin is an endogenous ligand of the human orphan receptor APJ. We detected apelin-like immunoreactivity in the adipocytes, gastric mucosa, and Kupffer cells in the liver. We also detected apelin-like immunoreactivity localized within the endothelia of small arteries in various organs. Further, it was found that mean arterial pressure after the administration of apelin-12, apelin-13, and apelin-36 at a dose of 10 nmol/kg in anaesthetized rats was reduced by 26+/-5, 11+/-4, and 5+/-4 mm Hg, respectively. In the presence of a nitric oxide (NO) synthase inhibitor, the effect of apelin-12 on blood pressure was abolished. Furthermore, the administration of apelin-12 (10 nmol/kg) in rats produced a transitory elevation of the plasma nitrite/nitrate concentration from a basal level of 21.4+/-1.6 to 27.0+/-1.5 microM. Thus, apelin may lower blood pressure via a nitric oxide-dependent mechanism.

Apelin peptides block the entry of human immunodeficiency virus (HIV).

The orphan G protein-coupled receptor APJ has been shown to be a coreceptor for human and simian immunodeficiency virus (HIV and SIV) strains. We have determined that some HIV and SIV strains use APJ as a coreceptor to infect the brain-derived NP-2/CD4 cells. Because apelin is an endogenous ligand for the APJ receptor, we examined the inhibitory effects of apelin peptides on HIV infection, and found that the apelin peptides inhibit the entry of some HIV-1 and HIV-2 into the NP-2/CD4 cells expressing APJ. The inhibitory efficiency has been found to be in the order of apelin-36>apelin-17>apelin-13>apelin-12.

Isolation and characterization of a novel endogenous peptide ligand for the human APJ receptor.

In the search for an endogenous ligand of the orphan G protein-coupled receptor APJ, the presence of the ligand in various tissue extracts was examined by measuring the increase in extracellular acidification rate of the cells expressing the APJ receptor as a specific signal induced by the interaction of the receptor and ligand. By monitoring this activity, we isolated an APJ receptor ligand, designated apelin, from bovine stomach extracts. The structures of bovine and human apelin preproproteins were deduced from the sequences of the corresponding cDNAs. The preproproteins consisted of 77 amino acid residues, and the apelin sequence was encoded in the C-terminal regions. Synthetic peptides derived from the C-terminal amino acid sequence of bovine preproapelin were capable of specifically promoting the acidification rate in the cells expressing the APJ receptor in a range from 10(-7) to 10(-10) M, indicating that apelin is an endogenous ligand for the APJ receptor.

[The effect of lesion of nucleus ventromedialis hypothalami on neurogenesis in adult ring doves].

In the present study the effects of lesion hypothalami ventromedialis nucleus (VMN) of ring dove (Streptopelia Risoria) on neurogenesis regarding the lesion-induced change of distribution of proliferating cells in the lateral ventricular zone (LVZ) and new neurons in the non-ventricular zone (VZ) were studied by using [3H] thymidine-autoradiographic and immunohistochemistry methods. The results showed that such lesion not only induced significant increase of neurogenesis in telencephalon (up to 1.62 times of that of the intact doves), but also altered distribution patterns of the newborn neurons. Many of the new neurons confined in neostriatum medialis and pars caudalis of telencephalon, where the rate of neurogenesis in intact dove is very low. Such kinds of neurogenesis in the birds with brain lesions may be region-dependent and somewhat underlie brain repair and alteration of endocrine function after brain injury.

Immunopathologic demonstration of MAC387+ UCHL1+ cells in bullous skin diseases.

Immunopathologic aspects of bullous skin diseases were studied in paraffin sections of thirty-three skin biopsy specimens utilizing monoclonal antibodies directed against histiocytes, helper/inducer T lymphocytes, and Langerhans cells in skin lesions. Laboratory examinations revealed that either more or fewer of the standard number of helper/inducer T lymphocytes (UCHL1+) were observed in the upper dermis in 84.8% of the cases examined, particularly in the various forms of pemphigus; histiocytes (MAC387+) were also found to occur in the upper dermis in 45.5% of the cases and blisters in 27.3% of the cases, particularly in pemphigus erythematosus and dermatitis herpetifomis. In 54.5% of all the cases, both UCHL1+ and MAC387+ cell infiltrates predominated in the upper dermis. These findings suggest that a cell-mediated immune response may also be important in the pathogenesis of bullous skin diseases. It may be possible that antigen from keratinocytes can produce ETAF, and that IL1 activating T lymphocytes and histiocytes also produce IL1 activating T cells, particularly helper/inducer T cells. Such activities would further promote the increase of B cell function and immunoglobulin synthesis.

Significance of pre-S2 protein and its antibody in children with HBV infections.

Pre-S2 protein and its antibody were detected in 130 children with hepatitis B virus (HBV) infection and 30 with T6 hepatitis B (HB) vaccination. The results showed that pre-S2 was positive in most chronic persistent hepatitis (CPH) and chronic active hepatitis(CAH) patients, while anti-pre-S2 was positive in only 8% (2/92 cases) and 11.5% (3/26 cases) respectively. The positive rate of anti-pre-S2 was 78.9% (15/19 cases) in cases at the convalescent stage of acute hepatitis B, 91.7% (55/60 cases) in cases with T6 HB vaccination and 83.3% (25.30 cases) in naturally acquired anti-HBs children, while pre-S2 was not noted. Anti-pre-S2 was negatively related to ALT and positively to anti-HBs (P less than 0.01). The positive relation of pre-S2 to HBsAg was observed. These results suggest that pre-S2 could be a marker for HBV infection, and anti-pre-S2 may indicate a favourable prognosis of HBV infection. There was no correlation between anti-pre-S2 and pathogenic damages induced by HBV.