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Biomedical subjects

G Su

Publications and source records attributed to G Su.

47 records · Page 3Linked to original sources

[A preliminary report on changes in micro-circulation of conjunctiva in patients with high altitude pulmonary edema].

Micro-circulation of conjunctiva was investigated in 36 patients with high altitude pulmonary edema (HAPE) and 21 healthy subjects who arrived recently in high land and were the controls, and plasma angiotensin II (AT II) and aldosterone (ALD) were determined in 16 patients with HAPE and in the control group. The results show that the concentrations of plasma AT II, ALD in patients with HAPE are obviously higher than those of the healthy individuals (P < 0.001), the degree of changes in micro-circulation of conjunctiva in patients with HAPE is directly proportional to the degree of severity of HAPE, and the higher the concentrations of plasma AT II and ALD, the severer the degree of changes in micro-circulation.

Adolescent↗

High level expression of Shiga toxin B subunit of Shigella dysenteriae serotype 1 in Escherichia coli.

In this study the gene encoding the Shiga toxin (Stx) was cloned from the chromosomal DNA of Shigella dysenteriae serotype 1 (W30864). The Stx gene was located in a 4.5kb EcoRI fragment. The biological assay revealed that the hybrid plasmid pMGC001 containing the Stx gene could produce Shiga toxin. The amount of Stx was 16 times more than that produced by its parent. The cloned strain showed cytotoxic, entorotoxic and neurotoxic activities. The gene for Stx-B subunit was subcloned into a plasmid vector pJLA503 from the plasmid pMGC001. The B subunit could be expressed at high level in E. coli and has been purified in large quantities. The polyclonal and monoclonal antibodies against B subunit were raised. Western blot showed that they could react specifically to the B subunit.

Bacterial Toxins↗

[Secretive export of StxB/HlyA (CT) fusion protein and B subunit specific antibody responses in mice].

In this study, the Shiga toxin B subunit has been fused to haemolysin A C-terminus. The fusion protein StxB/HlyA(CT) can be exported to the external medium not only from E. coli K-12 but also from S. typhimurium aroA strain SL3261. When the plasmid pUC18 was used as vector, StxB/HlyA(CT) was toxic to hosts. But the fusion protein was stable and safe to hosts when the pUC18 was replaced with pBR322. The fusion protein can be expressed and exported to the external medium under either the aerobactin promoter or beta-lactomase promoter. Oral and i.p. immunization of mice with StxB/HlyA(CT) carrying S. typhimurium aroA strain SL3261 resulted in significant B subunit specific mucosal and serum antibody responses. This the first report demonstrating that foreign polypeptides fused to the 23kD C-terminus of E. coli haemolysin A can be exported from attenuated Salmonella Vaccine strains and that such exported polypeptides can result in antigen specific immune responses.

Animals↗

[Oligonucleotide directed in vitro mutagenesis].

In this study, a method for oligonucleotide directed in vitro mutagenesis was described. It includes the following steps: clone of the gene to be mutated into the phagemid pGCI; preparation of single strand template; design and synthesis of mutated oligonucleotides; synthesis of double strand DNA. Using this method, a new BamHI site was originated at the N terminal of Stx-B and BglII site at the C terminal of Stx-B. It is ready to fuse the Stx-B gene to LamB. This method is a very useful tool for genetic engineering.

Base Sequence↗

Relation between plasma atrial natriuretic peptide (ANP) and glomerular ANP receptors in 5/6 nephrectomized rats.

Chronic renal failure (CRF) was induced in male wistar rats (Group I) by 5/6 nephrectomy and the sham-operated ones served as control (Group II). The results showed that in Group I, plasma atrial natriuretic peptide (ANP) levels increased progressively as the Scr was elevated. Plasma R-A rose simultaneously compared to the normal (P less than 0.001). At the 20th week after operation, urine volume and Na decreased significantly (P less than 0.05). The number of glomerular receptors decreased markedly at the 12th week (P less than 0.05) and 20th week (P less than 0.01). Our data suggest that in 5/6 nephrectomized rats, the elevation of plasma ANP level might be partly caused by the damage of glomerular ANP receptors, and the elevated plasma ANP could not play its role in diuresis, natriuresis, blood pressure depression and R-A inhibition as a result of the damage of kidney ANP receptors.

Animals↗