The Kobe journal of the medical sciences 

About: The Kobe journal of the medical sciences is an academic journal published by Kobe University. The journal publishes majorly in the area(s): Cancer & SMA*. It has an ISSN identifier of 0023-2513. Over the lifetime, 905 publications have been published receiving 8125 citations. The journal is also known as: Hyogo Journal of Medical Sciences.

Leptin stimulates rat aortic smooth muscle cell proliferation and migration

Abstract: Leptin, a peptide secreted from adipose tissue, plays an important role in the regulation of food intake and energy expenditure. In obese patients, plasma leptin levels are elevated and obesity is one of the major risk factors for cardiovascular diseases. Therefore, in this study, we investigated the effect of leptin on vascular smooth muscle cell (VSMC) functions. Cultured rat aortic VSMC expressed 130-kDa short form of leptin receptor. Leptin stimulated both proliferation and migration of VSMC. Leptin stimulated phosphorylation and activation of mitogen-activated protein (MAP) kinases, and also increased phosphatidylinositol (PI) 3-kinase activity. Further, two distinct PI 3-kinase inhibitors, wortmannin and LY294002 inhibited the migratory effect of leptin. These results demonstrate that leptin is a proliferative and migratory factor for VSMC, implying that leptin may play a role in the formation and development of vascular lesions.

Osteoblast differentiation and bone formation gene expression in strontium-inducing bone marrow mesenchymal stem cell.

Abstract: Osteoblastic differentiation from human mesenchymal stem cell (hMSCs) is an important step of bone formation. We studied the in vitro induction of hMSCs by using strontium ranelate, a natural trace amount in water, food and human skeleton. The mRNA synthesis of various osteoblast specific genes was assessed by means of reverse transcription polymerase chain reaction (RT-PCR). In the hMSCs culture, strontium ranelate could enhance the induction of hMSCs to differentiate into osteoblasts. Cbfa1 gene was earlier expressed on day 4 of cell culture (the control group, on day 14) and osteonectin on day 11 (control, on day 21). The early Cbfa1 expression indicates that strontium could enhance osteoblastic differentiation. The detection of osteonectin using strontium induction indicates the role of strontium in enhancing bone remodeling, bone structure stabilization of hydroxyapatite molecule and collagen fibril organization. The cultured hMSCs in the presence of strontium expressed genes of bone extracellular matrix: collagen type I, bone sialoprotein and osteocalcin on the same days as control (same medium with no strontium). Concentration of strontium ranelate has been recommended to be optimized in between 0.2107 - 21.07 μg/ml whereas the high concentration up to 210.7 μg/ml have delayed effect on osteoblastic differentiation with delayed expression on Cbfa1 and osteonectin, and inhibitory effect on bone sialoprotein expression. In addition, strontium could help cell expansion by maintaining cell proliferation rate of hMSCs and osteoblast lineage. We recommend that the strontium is an important factor for inducing mesenchymal stem cells to differentiate into osteoblasts with further enhancement on bone formation. This model might provide a useful cell source for tissue engineering and bone repair.

The role of human papilloma virus in the molecular biology of cervical carcinogenesis.

Abstract: Research exploring the E6-p53 and E7-pRb model has resulted in the identity of the viral gene's actions on numerous cellular proteins and processes normally involved in cell growth and proliferation. Specially, several findings have established the various ways by which the HPV-infected cell may escape controls governing cell growth and proliferation, including the fidelity of the host cell's genome and apoptosis. A large body of knowledge already generated in this area supports the view that high-risk HPV types have the ability to transform cells into a malignant phenotype. Such ability, however, is not sufficient to actually and inevitably produce cervical carcinoma, as indicated by the frequent spontaneous clearance of HPV infection and the long delay between the onset of persistent infection and emergence of the malignancy. Delay in the participation of cofactors has been suggested as explanation in this regard. However, it remains unclear how and when cofactors or factors that are innate in the HPV-infected cells launch the host cells into an irreversible progression to carcinoma.