Biomedical subjects

H Qui

Publications and source records attributed to H Qui.

6 recordsLinked to original sources

PubMed2000

Pharmacological vitrectomy.

Pharmacological vitrectomy refers to the use of enzymes in an effort to liquefy vitreous and to weaken the adhesion of vitreous cortex to the internal limiting membrane during or before performing vitreous surgery. It is well known that the vitreoretinal interface plays important roles in developing many blinding diseases. To make the vitreous surgery easier for better outcome or to avoid vitrectomy, plasmin, dispase, and chondroinase have been used to promote the disinsersion of vitreous cortex to the internal limiting membrane, a basement membrane of Muller cells. On the other hand, hyaluronidase has been used clinically to facilitate the clearance of vitreous hemorrhage liquefying vitreous body and developing posterior vitreous detachment. This article reviews enzymes as an intraoperative adjunctive agent in vitrectomy.

Collagenases↗

PubMed1996

[A synthetical mouth study of 105 Uygur people above 100 years of age].

Oral examination was performed in 105 Uygur people aged 100 to 135 years. Among them there were 77 males and 28 females. Results were as follows: the teeth loss rate was 100.0%, edentulous rate 54.3%, dental caries 70.5%, periodontal disease 52.4%, normal labial-buccal mucosa 65.7%, fissured tongue 74.3%, no smoking 86.7%, no drinking 94.3%, and all of them had neither history of dental extration nor restoration. This study may provide data for investigating secret of human longevity.

Aged↗

PubMed1995

Azido-iodo-phenyl-analogs of 2',5'-dideoxy-adenosine as photoaffinity ligands for adenylyl cyclase.

Azidoiodophenyl-analogs of 2',5'-dideoxyadenosine were synthesized and tested as potential 'P'-site selective affinity probes for adenylyl cyclases. The 3'-substituted analogs included: 1: 3'-[(4-nitrophenyl)-acetyl]-2',5'-dideoxy-adenosine 2: 3'-[(4-nitrophenyl)-butyryl]-2',5'-dideoxyadenosine 3: 3'-[(4-azido-3-iodophenyl)-acetyl]-2',5'-dideoxyadenosine and 4: 3'-[(4-azido-3-iodophenyl)-butyryl]-2',5'-dideoxyadenosine. The azidoiodo-phenyl-analogs inactivated adenylyl cyclase irreversibly and in a light-dependent manner. This was observed with detergent-dispersed enzyme from rat brain, purified native enzyme from bovine brain, and recombinant Type I bovine adenylyl cyclase expressed in membranes from fall army worm ovarian (Sf9) cells. Inactivation of the recombinant enzyme was inversely dependent on ATP concentration and was not completely prevented by 2',5'-dideoxyadenosine. Inhibition kinetics with the recombinant enzyme in the absence of light suggested two sites of inhibition, whereas with the native Type I enzyme inhibition kinetics exhibited a straightforward noncompetitive mechanism. Occupation of either or both sites by ligand protected the enzyme against denaturation by UV-irradiation per se. The data are consistent with inactivation of the recombinant enzyme occurring both through the 'P'-site and the catalytic active site, but suggest that this is a characteristic of the recombinant enzyme and is not dependent on the probes per se. The data suggest the potential for independent interactions of such ligands with different sites on a given enzyme and also with other enzymes containing adenosine or adenine nucleotide binding domains.

Adenosine Triphosphate↗

PubMed1992

[Effect of electrical stimulation of the area postrema on plasma renin activity and renal sympathetic nerve activity in rabbits].

68 urethan-anesthetized rabbits were prepared for registration of changes of respiration, arterial blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) due to stimulation of area postrema (AP) by rectangular pulse trains each lasting for 4 s for every 30 s. During 40 min of such a stimulation paradigm the venous blood samples were collected for radioimmunoassay of plasma renin activity (PRA) (both pre- and post-stimulation), RSNA registered and processed by a computer. Animals were divided into three groups: (1) with AP stimulation only (n = 47); (2) AP stimulation after bilateral renal denervation (n = 13); (3) AP stimulation after propranolol injection (n = 8). In Group I, a 91% increase in PRA, an augmentation of RSNA, a rise of BP and a decrease of HR were observed, while respiration did not show obvious change. In Group II, hemodynamic and RSNA response was similar to that in Group I, but PRA was not changed significantly. In Group III, the effects on BP, HR, respiration and RSNA showed no remarkable changes compared with Group I, but significant inhibition of the response of PRA [from 0.65 +/- 0.07 ng/(ml.h-1) to 0.72 +/- 0.10 ng/(ml.h-1), P > 0.05] was observed. The results mentioned above suggested that electrical stimulation of AP may induce an increase in renin release and renal sympathetic nerve activity and hemodynamic changes in rabbits.

Animals↗

PubMedDate not supplied

Spinal cord neural anatomy in rats examined by in vivo magnetic resonance microscopy.

BACKGROUND AND OBJECTIVES: Magnetic resonance microscopy (MRM) is a technique that is worthwhile for anesthesiologists because it allows spinal cord and plexus anatomy to be visualized three dimensionally and followed over time in the same animal. For example, the long-term effect of indwelling intrathecal or plexus catheters can be studied in situ, and convective and diffusive forces within intrathecal, epidural, or nerve sheath spaces can be investigated. Further, diffusion-weighted MRM, which measures an "apparent diffusion coefficient" (ADC), can be used to track the presence of ischemia, hypoperfusion, or cytotoxic edema. This study investigates problems associated with the use of in vivo MRM for spinal cord and peripheral nerve studies in the rat. METHODS: Twenty-one anesthetized female Fisher CDF rats were used. Group 1 (n=7) was used for anatomic three-dimensional studies. Groups 2 (n=4), 3 (n=4), and 4 (n=6) were used for measurements of the ADC. Group 2 served as controls, group 3 received lumbar intrathecal catheters, and group 4 received cervical intrathecal catheters. RESULTS: Cervical spine, lumbar spine, and spinal nerves and ganglia were accurately visualized with MRM. As a rule, spinal cord gray and white matter were better demonstrated using diffusion-weighted proton stains. By contrast, T2-weighted proton staining superiorly demonstrated structures surrounding the spinal cord. In groups 3 and 4, indwelling intrathecal catheters did not affect the spinal cord ADC, indicating normal blood flow and no cytotoxic edema. Contrast studies revealed nonhomogeneous distribution of contrast predominately in the lateral and ventral intrathecal space. CONCLUSION: Three-dimensional diffusion-weighted MRM displays cervical and lumbar spine anatomy accurately in vivo. Apparent diffusion coefficients measurements are feasible in rat cervical spinal cord with intrathecal catheters. Spinal cord ADCs are unaffected by intrathecal catheters, indicating normal spinal cord perfusion.

Animals↗

PubMedDate not supplied

In vivo diffusion-weighted magnetic resonance microscopy of rat spinal cord: effect of ischemia and intrathecal hyperbaric 5% lidocaine.

BACKGROUND AND OBJECTIVES: Pathophysiologic mechanisms underlying persistent neurologic deficits after continuous spinal anesthesia using hyperbaric 5% lidocaine are still not well understood. It has been suggested that high-dose intrathecal lidocaine induces irreversible conduction block and even ischemia in white matter tracts by breakdown of the blood-nerve barrier. In this study, we use diffusion-weighted magnetic resonance microscopy to characterize the effect of intrathecal hyperbaric 5% lidocaine in rat spinal cord. The parameter measured with DWM, is an "apparent diffusion coefficient," (ADC), which can be used to exclude the presence of ischemia. METHODS: Female Fischer CDF rats were used. Group 1 (n = 5) was exposed to ischemia, group 2 (n = 7) was exposed to intrathecal 5% hyperbaric lidocaine, and group 3 (n = 5) was exposed to intrathecal 7.5% glucose. Diffusion-weighted MR images in group 1 were acquired before and after ischemia induced by cardiac arrest and in groups 2 and 3 rats prior to and during perfusion of the spinal catheter with either 5% hyperbaric lidocaine or 7.5% glucose. RESULTS: Ischemia decreased the ADC by 40% in gray matter and by 30% in white matter of spinal cord. Continuous intrathecal anesthesia with hyperbaric 5% lidocaine did not affect the spinal cord ADC. Further, 7.5% intrathecal glucose had no effect on ADCs in gray or white matter of spinal cord. CONCLUSIONS: Ischemia reduced the ADC in both spinal cord white and gray matter. Hyperbaric 5% lidocaine did not affect the spinal cord ADC during the first 1.5 hours. We suggest that 5% hyperbaric lidocaine does not induce irreversible neurologic deficits by causing spinal cord ischemia.

Anesthetics, Local↗