PubMed Health⌕ Search

Biomedical subjects

Y S Shi

Publications and source records attributed to Y S Shi.

17 recordsLinked to original sources
PubMed2005

Body-centered-cubic Ni and its magnetic properties.

The body-centered-cubic (bcc) phase of Ni, which does not exist in nature, has been achieved as a thin film on GaAs(001) at 170 K via molecular beam epitaxy. The bcc Ni is ferromagnetic with a Curie temperature of 456 K and possesses a magnetic moment of 0.52+/-0.08 micro(B)/atom. The cubic magnetocrystalline anisotropy of bcc Ni is determined to be +4.0x10(5) ergs x cm(-3), as opposed to -5.7x10(4) ergs x cm(-3) for the naturally occurring face-centered-cubic (fcc) Ni. This sharp contrast in the magnetic anisotropy is attributed to the different electronic band structures between bcc Ni and fcc Ni, which are determined using angle-resolved photoemission with synchrotron radiation.

Journal Article↗
PubMed1993

[Hemodilution therapy for cerebral ischemic acidosis].

The four-vessel (bilateral vertebral arteries and carotid arteries) occlusion rabbit models were used as brain ischemia models. At the beginning of reperfusion, blood was withdrawn and replaced with dextran 20 equivalently until various scale hemodilution was achieved and lasted for 30 min. Hematocrits were 31.7 +/- 1.4%, 23.7 +/- 2.8%, 13.7 +/- 2.5% respectively during hemodilution. Before and after reperfusion for 30, 90 and 180 minutes, internal jugular venous blood samples were taken for gas analysis and lactate acid determination. The results showed that pHv of internal jugular vein was improved in limited and medium hemodilution, and lactate acid level was reduced from 160.17 +/- 26.76 mg/dl to 148.83 +/- 18.98 mg/dl in limited hemodilution group, while it was 184.5 +/- 54.21 mg/dl in the controls after reperfusion for 90 minutes. It is suggested that cerebral ischemia acidosis could be improved by hemodilution, in addition to the clearance of lactate acid. However, the shortage of extreme hemodilution, metabolic acidosis, made it limited for clinical practice.

Acidosis↗
PubMed1993

[Observations on serum digoxin-like immunoreactive substances in patients with cor-pulmonale].

The level of endogenous digoxin-like immunoreactive substances (DLIS) was determined with RIA in 27 patients with cor-pulmonale and 10 normal subjects as controls. The results showed that the concentration of serum DLIS was 0.51 +/- 0.18 ng/ml in the controls, 0.82 +/- 0.24 (P < 0.05), 1.45 +/- 0.51 (P < 0.001), and 2.31 +/- 1.22 ng/ml (P < 0.001) in the patients groups with cardiac function grade II (9 cases), III (10 cases) and IV (8 cases) respectively. It has been reported that both endo- and exogenous digoxin-like substances have the same function. Cor-pulmonale patients with heart failure who are treated with digoxin tend to have toxic reactions. We consider the increase in serum endogenous DLIS as the cause. It is suggested that the dosage of digoxin, if it must be used, should be individualized and the serum level monitored if possible, so as to achieve best therapeutic effects with smaller doses.

Adult↗
PubMed1992

Further studies on interactions between periaqueductal gray, nucleus accumbens and habenula in antinociception.

Previous findings from this laboratory with the intracerebral microinjection technique suggested that the periaqueductal gray (PAG), nucleus accumbens, and habenula might constitute a unidirectional loop to play their roles in pain modulation. In the present study we demonstrate that intra-habenular injection of naloxone antagonizes the analgesia elicited by morphine injected into the periaqueductal gray (PAG) and that intra-accumbens injection of naloxone is capable of attenuating the analgesic effects of morphine injected into the habenula. These results indicate that the relationships between these nuclei may be more complex than the putative unidirectional loop.

Analysis of Variance↗
PubMed1992

Naloxone blocks opioid peptide release in N. accumbens and amygdala elicited by morphine injected into periaqueductal gray.

It has been proposed that a serial, unidirectional circuit from the PAG to the N. accumbens and the amygdala are involved in antinociception and that enkephalins (ENK) and beta-endorphin (beta-EP) act as neurotransmitters in this circuitry. In the present study, we measured the release of ENK and beta-EP by simultaneous push-pull perfusion of the N. accumbens and amygdala after microinjection of morphine into the PAG. Morphine administration elicited an increase in immunoreactive ENK and beta-EP in both the N. accumbens and the amygdala, which was antagonized in each nucleus by perfusion with naloxone. These data suggest that the three nuclei were not serially connected and that they may take part in one and the same antinociceptive system with an "all or none" character.

Amygdala↗
PubMed1991

[Cardiovascular reactions mediated by 5-HT1A and 5-HT3 receptors in the spinal cord of conscious rats].

Intrathecal administration (ith) of 5-hydroxytryptamine (5-HT, 1.56, 3.125, 6.25 and 12.5 micrograms/10 microliters) to conscious rats produced a marked dose-dependent hypertensive effect without significant change in heart rate (HR). Ith administration of fluoxetine (10 micrograms/microliters), one of the presynaptic reuptake inhibitors of 5-HT, produced a marked increase in the mean arterial blood pressure (mABP). This effect could be prevented by a pretreatment with cinanserin (25 micrograms ith) as a blocker of 5-HT receptor. It was further observed that ith of 8-OH-DAPT (2.5, 5, 10 micrograms/10 microliters), a 5-HT1A receptor agonist, produced a dose-dependent increase of mABP and lowering of HR. However, ith of 5-HT3 receptor agonist 2-Methylserotonin (25, 50, 100 micrograms/10 microliters), decreased mABP markedly without change in HR. The results indicate that 5-HT in the spinal cord may extra hypertensive effect via 5-HT1A receptor and a hypotensive effect via 5-HT3 receptor. This gives a possible explanation about the conflicting reports concerning the effect of 5-HT in the central nervous system on blood pressure.

Animals↗
PubMed1990

Lumbar intrathecal administration of naloxone antagonizes analgesia produced by electrical stimulation of the hypothalamic arcuate nucleus in pentobarbital-anesthetized rats.

In lightly pentobarbital-anesthetized and acutely-prepared rats, electrical stimulation within the arcuate nucleus of the hypothalamus consistently inhibited the tail-flick responses to noxious heating of the tail. The opioid receptor antagonist, naloxone hydrochloride applied intrathecally at the lumbar level, at dose of 20 micrograms, reversed this inhibition without affecting the baseline pain threshold. The same dose of naloxone, applied to the cervical subarachnoid space, had no effect on the inhibitory modulation by the arcuate nucleus. Naloxone, at doses 2- to 4-fold greater than the intrathecal dose, did not modify the suppression of the tail-flick, when given systemically. With the doses ranging from 5 to 40 micrograms, naloxone showed a dose-dependent blockade of the inhibition produced by stimulation of the arcuate nucleus. These results indicate that an endogenous opioid system is most likely involved in the descending inhibition of spinal nociceptive reflexes, resulting from stimulation of the arcuate nucleus of the hypothalamus.

Analgesia↗
PubMed1986

Studies on the mesolimbic loop of antinociception--II. A serotonin-enkephalin interaction in the nucleus accumbens.

In a previous report we have shown that the antinociceptive effect elicited by microinjection of morphine into the periaqueductal gray is due, at least in part, to the activation of an ascending serotonergic pathway which releases 5-hydroxytryptamine in the nucleus accumbens. We now report that antinociception induced by intra-periaqueductal gray injection of morphine can be attenuated also by the narcotic antagonist naloxone or the enkephalin antibodies administered into the nucleus accumbens, and potentiated by D-phenylalanine, a putative inhibitor of the degradation of enkephalins. Moreover, the antinociceptive effect induced by 5-hydroxytryptamine administered into nucleus accumbens could be blocked by naloxone injected into the same site, whereas the antinociception elicited by intra-accumbens injection of [D-Ala2,D-Leu5]enkephalin was not affected by cinanserin, a 5-hydroxytryptamine blocking agent. It is concluded that morphine administered to the periaqueductal gray is capable of activating an ascending serotonergic pathway to release 5-hydroxytryptamine in the nucleus accumbens, which in turn activates an enkephalinergic mechanism within the same nucleus, resulting in an antinociceptive effect.

Animals↗
PubMedDate not supplied

Intrathecally injected antibody can diffuse into spinal cord.

Antibody microinjection has been widely used to investigate the function of neuropeptides, but the capability of antibody to diffuse in the brain tissue has not been well characterized. The present study was conducted with an immunohistochemical method to determine if the anti-enkephalin serum injected intrathecally could diffuse into the spinal cord. Enkephalin immunoreactivity was observed in laminae I and II in slight amounts after 10 min, in moderate amounts after 30 minutes and very clearly after 60 min of the intrathecal injection of enkephalin antiserum. In addition, marked nonspecific staining was observed in the dorsal part but not in the ventral part of the white matter. These results indicate that antibodies injected intrathecally are capable of diffusing into the spinal cord within a time period of 10-60 min.

Animals↗