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Biomedical subjects

J Chin

Publications and source records attributed to J Chin.

206 records · Page 12Linked to original sources
PubMedDate not supplied

Can paralytic poliomyelitis be eliminated?

The question of whether paralytic poliomyelitis can be eliminated can be approached either from the theoretic and scientific perspective or from the practical perspective of a program. From the former perspective, the answer is probably yes; from the latter, the answer would be that global eradication of this disease cannot be achieved by the year 2000. The global eradication of smallpox was a remarkable achievement and is held up as an example to show that the deliberate worldwide elimination of a human infectious-disease agent can be scheduled and accomplished. However, there are significant differences in the epidemiology and in the control programs for smallpox and poliomyelitis that make the global eradication of poliomyelitis more difficult. Presently, scarce resources for improving health throughout the world cannot be easily diverted for the specific purpose of eradicating paralytic poliomyelitis. The control of poliomyelitis for the next decade will have to proceed at the same relative pace as other major disease control programs of the World Health Organization, such as the Expanded Programme on Immunization and the International Drinking Water Supply and Sanitation Decade. After 1990, the extent to which these programs have controlled or regionally eliminated paralytic poliomyelitis can be assessed. It may be more appropriate then to ask the question, can paralytic poliomyelitis be eliminated?

Humans↗
PubMedDate not supplied

Diagnostic screening of mitochondrial DNA mutations in Australian adults 1990-2001.

BACKGROUND: Many diverse pathogenic mitochondrial DNA (mtDNA) mutations have been described since 1988. The Melbourne Neuromuscular Research Institute (MNRI) has undertaken diagnostic detection of selected mtDNA mutations since 1990. MtDNA mutations screened have included point mutations associated with Leber's hereditary optic neuropathy (LHON; G3460A, G11778A and T14484C), mitochondrial encephalopathy lactic acidosis and stroke-like episodes (MELAS; A3243G), myoclonus epilepsy and ragged red fibres (MERRF; A8344G) and Leigh's syndrome/neuropathy ataxia retinitis pigmentosa (LS/NARP; T8993C/G). Samples have also been screened for deletions/ rearrangements associated with Kearns-Sayre syndrome (KSS) and chronic progressive external ophthalmoplegia (CPEO). AIMS: To present an audit of the MNRI mtDNA diagnostic service between 1990 and 2001, encompassing 1725 referred patients. METHODS: The detection techniques carried out included polymerase chain reaction amplification of mtDNA combined with restriction fragment length polymorphism analysis for mtDNA point mutation detection, supplemented with selected sequence analysis and Southern blots for the detection of deletions/ rearrangements. Tissues tested included blood, hair and skeletal muscle. RESULTS: Of the 1184 patients screened for MELAS A3243G, 6.17% were positive for the mutation, whereas for MERRF A8344G, 2.21% carried the mutation and for LS/NARP T8993C/G, 0.32% carried the mutation. The outcomes for the LHON mutations were G11778A, 6.60%, T14484C, 5.76% and G3460A, 0.29%. Of the patients referred for KSS and CPEO, 17.72% had deletions/rearrangements. CONCLUSIONS: Overall, the detection rate of mtDNA point mutations was low. The protean clinical features of mitochondrial disorders and the frequency of partial phenotypes lead to requests for tests in many patients with a relatively low likelihood of mtDNA mutations. An improved algorithm could involve mutation screening appropriate to the phenotype using sequencing of selected mtDNA regions in patients with a high likelihood of mtDNA disease. Features increasing the likelihood of mtDNA mutations include the following: (i) a typical phenotype, (ii) a maternal inheritance pattern and (iii) histochemical evidence of mitochondrial abnormality in the muscle biopsy. Efficient laboratory diagnosis of mtDNA disease involves good communication between the physician and laboratory scientists, coupled with screening of the appropriate tissue.

Adult↗
PubMedDate not supplied

TGF-beta1 in Aplysia: role in long-term changes in the excitability of sensory neurons and distribution of TbetaR-II-like immunoreactivity.

Exogenous recombinant human transforming growth factor beta-1 (TGF-beta1) induced long-term facilitation of Aplysia sensory-motor synapses. In addition, 5-HT-induced facilitation was blocked by application of a soluble fragment of the extracellular portion of the TGF-beta1 type II receptor (TbetaR-II), which presumably acted by scavenging an endogenous TGF-beta1-like molecule. Because TbetaR-II is essential for transmembrane signaling by TGF-beta, we sought to determine whether Aplysia tissues contained TbetaR-II and specifically, whether neurons expressed the receptor. Western blot analysis of Aplysia tissue extracts demonstrated the presence of a TbetaR-II-immunoreactive protein in several tissue types. The expression and distribution of TbetaR-II-immunoreactive proteins in the central nervous system was examined by immunohistochemistry to elucidate sites that may be responsive to TGF-beta1 and thus may play a role in synaptic plasticity. Sensory neurons in the ventral-caudal cluster of the pleural ganglion were immunoreactive for TbetaR-II, as well as many neurons in the pedal, abdominal, buccal, and cerebral ganglia. Sensory neurons cultured in isolation and cocultured sensory and motor neurons were also immunoreactive. TGF-beta1 affected the biophysical properties of cultured sensory neurons, inducing an increase of excitability that persisted for at least 48 hr. Furthermore, exposure to TGF-beta1 resulted in a reduction in the firing threshold of sensory neurons. These results provide further support for the hypothesis that TGF-beta1 plays a role in long-term synaptic plasticity in Aplysia.

Animals↗
PubMedDate not supplied

Prevention of bladder tumor formation in mice by a novel bone marrow-derived factor, reptimed.

BACKGROUND: Reptimed is a novel, species-conserved, bone marrow-derived molecule which possesses anti-neoplastic activity. Previously, we established an orthotopic murine bladder tumor (MBT-2) model and reported accurate documentation of the presence and the extent of intravesical involvement of bladder tumor implants using magnetic resonance imaging (MRI) (1). Herein, we investigated the activity of exogenously administered Reptimed in the MBT-2 model. MATERIALS AND METHODS: Intravesicular and intraperitoneal administration of Reptimed concurrently with and following transurethral tumor cell implantation was performed and MBT-2 tumor response was assessed at several time points post tumor implant. RESULTS: Serial MRI scans of Reptimed-treated mice at days 14 to 33 post tumor transplant revealed significant inhibition of bladder tumor growth with no significant tumor growth observed by MRI on day 33 post-implant. The corresponding histological examination of the whole mount bladder sections revealed similar inhibitory effects of Reptimed with respect to the topography and depth of intravesical tumor involvement. In contrast, control, untreated bladders revealed extensive exophytic tumors with deeply invasive transitional cell carcinoma. CONCLUSIONS: These studies demonstrate the anti-tumor effect of Reptimed and highlight its importance as a potential therapy for cancer.

Administration, Intravesical↗
PubMedDate not supplied

Secretion of a soluble T cell promoting factor by the human prostate adenocarcinoma cell line DU-145.

INTRODUCTION: A variety of cancers suppress host immune defenses by secretion of soluble factors. Conditioned media (CM) from numerous cancer cell lines possess the ability to suppress proliferation of activated T cells. The effects of CM from the prostate cancer cell line DU-145 on T cell activation was investigated. MATERIALS AND METHODS: Human PBMC, purified T cells and Jurkat T cells were treated with DU-145 CM. Proliferation, cell cycle, apoptosis, Fas expression/and cytokine secretion were assessed by thymidine incorporation, flow cytometry and ELISA. RESULTS: DU-145 CM increased proliferation of concanavalin-A (ConA) activated peripheral blood mononuclear cells (PBMC) increasing the percentage of cells in the S/G2 phase of cell cycle. Treatment of the Jurkat T cell line with DU-145 CM induced a potent proliferative response. ConA-induced proliferation of purified T cells from human PBMC and murine splenocytes was augmented in a dose-dependent manner by addition of DU- 145 CM. DU- 145 CM treatment of ConA-activated T cells induced an increase in interleukin-2 (IL-2) production. The soluble factor(s) responsible for promoting T cell proliferation was dependent on protein synthesis by the DU- 145 cells and possessed a molecular weight greater than 10 kDa. CONCLUSION: DU- 145 cells secrete a soluble factor(s) > 10 kDa, whose production is dependent on protein synthesis and which acts as a promoter of T cell activation.

Adenocarcinoma↗
PubMedDate not supplied

Transjugular intrahepatic portosystemic stent-shunt.

The transjugular intrahepatic portosystemic stent-shunt is a non-surgical method for creating a portosystemic shunt. Early reports suggest that it is effective for treating portal hypertension and variceal bleeding. This review describes the technique and discusses the indications and complications.

Angioplasty, Balloon↗