Biomedical subjects

Weiwei Hu

Publications and source records attributed to Weiwei Hu.

7 recordsLinked to original sources

PubMed2006

Neuroprotective effect of carnosine on necrotic cell death in PC12 cells.

The nervous tissue of many vertebrates, including humans, can synthesize beta-alanyl-L-histidine (carnosine). The biological functions of carnosine are still open to question, although several theories supported by strong experimental data have been proposed. The objective of this study was to examine the effects of carnosine on neurotoxicity in differentiated rat pheochromocytoma (PC12) cells. Neurotoxicity was induced by N-methyl-D-aspartate (NMDA), which caused time- and concentration-dependent cell death as measured by MTT and LDH assays. Pretreatment with carnosine significantly prevented the neurotoxicity in a concentration-dependent manner. The protective effect of carnosine was antagonized by the H1 receptor antagonist pyrilamine, but not by the H2 receptor antagonist cimetidine. In addition, alpha-fluoromethylhistidine, a histidine decarboxylase inhibitor, slightly reversed the protective action of carnosine. These results indicate that carnosine can effectively protect against NMDA-induced necrosis in PC12 cells, and its protection may in part be due to the activation of the postsynaptic histamine H1 receptor. The study suggests that carnosine may be an endogenous protective factor and calls for its further study as a new anti-excitotoxic agent.

Animals↗

PubMed2006

Histamine protects against NMDA-induced necrosis in cultured cortical neurons through H receptor/cyclic AMP/protein kinase A and H receptor/GABA release pathways.

Using histamine and the H3 receptor antagonist thioperamide, the roles of histamine receptors in NMDA-induced necrosis were investigated in rat cultured cortical neurons. Within 3 h of intense NMDA insult, most neurons died by necrosis. Histamine reversed the neurotoxicity in a concentration-dependent manner and showed peak protection at a concentration of 10(-7) m. This protection was antagonized by the H2 receptor antagonists cimetidine and zolantidine but not by the H1 receptor antagonists pyrilamine and diphenhydramine. In addition, the selective H2 receptor agonist amthamine mimicked the protection by histamine. This action was prevented by cimetidine but not by pyrilamine. 8-Bromo-cAMP also mimicked the effect of histamine. In contrast, both the adenylyl cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-purine-6-amine and the cAMP-dependent protein kinase inhibitor N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinolinesulfonamide reversed the protection by histamine. Thioperamide also attenuated NMDA-induced excitotoxicity, which was reversed by the H3 receptor agonist (R)-alpha-methylhistamine but not by pyrilamine and cimetidine. In addition, the protection by thioperamide was inhibited by the GABA(A) receptor antagonists picrotoxin and bicuculline. Further study demonstrated that the protection by thioperamide was due to increased GABA release in NMDA-stimulated samples. These results indicate that not only the H2 receptor/cAMP/cAMP-dependent protein kinase pathway but also the H3 receptor/GABA release pathway can attenuate NMDA-induced neurotoxicity.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2005

Optical phased-array beam steering controlled by wavelength.

A scheme for optical phased-array beam steering controlled by wavelength is proposed. In this scheme, the optical scanning device consists of arrayed optical waveguides with specific length differences, by which the desired phase slope that results in optical beam steering is formed at the ends of the waveguides and can be changed by varying the optical wavelength. By introducing the concept of irregularly spaced arrays, sidelobes can be dramatically suppressed regardless of large center-to-center interelement spacing. The absolute phase difference between adjacent elements plays a vital role in optical beam steering, and the relation between the nonuniform length difference and the corresponding center-to-center spacing among elements is found.

Journal Article↗

PubMed2005

Effect of oxygen-glucose deprivation on degranulation and histamine release of mast cells.

The purpose of this study was to investigate the effect of oxygen-glucose deprivation (OGD) on degranulation and histamine release of mast cells. Cultured mast cells were exposed to OGD for 1, 2, 4, 8, or 16 h. At 2 h of OGD exposure, the degranulation percentage of mast cells had increased and subsequently showed a progressive further increase, associated with a similar change in lactate dehydrogenase release. Histamine release increased significantly from 1 h of OGD exposure. These results indicate that OGD induces mast cells to degranulate, possibly via a cytotoxic response. This in vitro ischemic model of mast cells might clarify their roles in the pathological processes induced by cerebral ischemia.

Animals↗

PubMed2005

Is decompressive craniectomy for malignant middle cerebral artery territory infarction of any benefit for elderly patients?

BACKGROUND: Malignant middle cerebral artery (MCA) infarction is characterized by mortality rate of up to 80%. The aim of this study was to determine the value of decompressive craniectomy in patients who present with malignant MCA territory infarction and to compare functional outcome in elderly patients with younger patients. METHODS: Patients with malignant MCA territory infarction treated in our hospital between January 1997 and March 2003 were included in this retrospective analysis. The National Institutes of Health Stroke Scale (NIHSS) assessed neurologic status at admission, operation, and at 1 week after surgery. All patients were followed up for assessment of functional outcome by the Barthel Index (BI) and the modified Rankin Scale (RS) at 3 to 9 months after infarction. RESULTS: Twenty-five patients underwent decompressive craniectomy. The mortality was 7.7% in younger patients (ages <60 years) compared with 33.3% in elderly patients (ages >/=60 years) (P > .05). All patients had significant decrease of NIHSS after surgery (P < .001). At follow-up, younger patients who received surgery had significantly better outcome with mean BI of 75.42 and Rankin score of 3.00; however, none of the elderly survivors had a BI score above 60 or a Rankin score below 4. CONCLUSION: Decompressive craniectomy in younger patients with malignant MCA territory infarction improves both survival rates and functional outcomes. Although survival rates were improved after surgery in elderly patients, functional outcome and level of independence were poor.

Age Factors↗

PubMed2004

Pharmacological effects of carcinine on histaminergic neurons in the brain.

1 Carcinine (beta-alanyl histamine) is an imidazole dipeptide. The present study was designed to characterize the pharmacological effects of carcinine on histaminergic activity in the brain and on certain neurobehavior. 2 Carcinine was highly selective for the histamine H3 receptor over H1 or H2 receptor (Ki (microM)=0.2939+/-0.2188 vs 3621.2+/-583.9 or 365.3+/-232.8 microM, respectively). 3 Carcinine at a dose of 20 mg kg(-1) slightly increased histidine decarboxylase (HDC) activity in the cortex (from 0.186+/-0.069 to 0.227+/-0.009 pmol mg protein(-1) min(-1)). In addition, carcinine (10, 20, and 50 mg kg(-1)) significantly decreased histamine levels in mice brain. 4 Like thioperamide, a histamine H3 receptor antagonist, carcinine (20, 50 microM) significantly increased 5-HT release from mice cortex slices, but had no apparent effect on dopamine release. 5 Carcinine (20 mg kg(-1)) significantly inhibited pentylenetetrazole-induced kindling. This inhibition was completely reversed by (R)-alpha-methylhistamine, a representative H3 receptor agonist, and alpha-fluromethylhistidine, a selective HDC inhibitor. 6 Carcinine (20 mg kg(-1)) ameliorated the learning deficit induced by scopolamine. This amelioration was reversed by (R)-alpha-methylhistamine as evaluated by the passive avoidance test in mice. 7 Like thioperamide, carcinine dose-dependently increased mice locomotor activity in the open-field test. 8 The results of this study provide first and direct evidence that carcinine, as a novel histamine H3 receptor antagonist, plays an important role in histaminergic neurons activation and might be useful in the treatment of certain diseases, such as epilepsy, and locomotor or cognitive deficit.

Animals↗

PubMed2004

Effect of cerebral ischemia on brain mast cells in rats.

The purpose of this study was to investigate the effect of transient cerebral ischemia on brain mast cells in rats. The mast cells decreased significantly at 1 h, 2 h, 4 h and 7 days after ischemia. At 1 day following ischemia, the increase of the number of mast cells in the middle aspect of the thalamus (bregma -2.80 to -3.16 mm) was twice as that of other regions in the thalamus. In addition, histamine contents increased significantly in the thalamus and striatum after ischemia. These results indicate that brain mast cells participate in the pathological process after ischemia.

Animals↗