[Quantitative lacrimal scintillography in the normal lacrimal drainage system].
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Biomedical subjects
Publications and source records attributed to L Du.
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Previously we reported that ultralow concentrations of dynorphins (10(-16) to 10(-12) M) inhibited lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and proinflammatory cytokines in mouse glia without the participation of kappa-opioid receptors. In the current study using mouse cortical neuron-glia cocultures, we examined the possibility that inhibition of glia inflammatory response by dynorphins might be neuroprotective for neurons. LPS, in a concentration-dependent manner, markedly increased the release of lactate dehydrogenase (LDH), an indicator of cellular injury. Ultralow concentrations (10(-14) to 10(-12) M) of dynorphin (dyn) A-(1-8) significantly prevented the LPS-induced release of LDH, loss of neurons, and changes in cell morphology, in addition to inhibition of LPS-induced nitrite production. Meanwhile, ultralow concentrations (10(-15) to 10(-13) M) of des-[Tyr(1)]-dyn A-(2-17), a nonopioid peptide which does not bind to kappa-opioid receptors, exhibited the same inhibitory effect as dyn A-(1-17). These results suggest that dynorphins at ultralow concentrations are capable of reducing LPS-induced neuronal injury and these neuroprotective effects of dynorphins are not mediated by classical opioid receptors.
In order to investigate the effect of epidural morphine and electroacupuncture (EA) on immune function of postoperative patients, peripheral blood for NK (natural killer) cell activity assay were obtained from patients before and on the 1st, 3rd, 7th day after cholecystectomy. 1 mg morphine injected into epidural space after surgery significantly suppressed NK cell activities via prolonged inhibition and increased the inhibitory intensity of it. EA of "Zusanli (St. 36), Sanyinjiao(Sp. 6), Hegu(L.I.4) and Neiguan(P.6) points enhanced the NK cell activities after epidural injection of morphine. It was further observed that microinjection of 1 microgram/1 microliter naloxone into periaqueductal gray (PAG) partially antagonized the suppression of NK cell activity induced by intrathecal (ith) injection of 40 micrograms/50 microliters morphine, and so does EA of "Zusanli(St. 36)". When EA applied after naloxone microinjected into PAG, the NK cell activity was further augmented as compared to that using EA or PAG microinjection of naloxone alone. The above results suggest epidural morphine combined with EA is a better method to relieve postoperative pain, and opiate receptor in PAG might partially mediate the suppression of NK cell activity induced by intrathecal injection of morphine. Yet, the mechanisms of the attenuation of EA on morphine induced immunosuppression needs further study.
BACKGROUND AND PURPOSE: T2 hyperintensity of the middle cerebellar peduncle (MCP) is described in a number of diseases, including multiple system atrophy (MSA). We hypothesize that mild MCP hyperintensity on fluid-attenuated inversion recovery (FLAIR) imaging can be a normal finding. To our knowledge, a detailed study of the prevalence of this finding in various age groups with the FLAIR sequence has not been described. METHODS: One hundred twenty-two patients underwent an axial FLAIR examination of the brain as part of either a hearing loss or tinnitus work-up (ie, to exclude an acoustic neuroma or a retrocochlear cause). Subjects aged 15-78 years were included to reflect an even spread through the decades and were divided into 6 age groups. A radiologist and an MR imaging fellow graded the examinations subjectively, blinded to age: 0 for normal or 1 for the presence of MCP hyperintensity if the increased signal intensity was greater than that of adjacent pons and cerebellar white matter. Spearman rank correlation test of MCP hyperintensity with age and analysis of variance (ANOVA) were performed. RESULTS: Of 122 patients, we identified 17 with MCP FLAIR hyperintensity. None of these patients had a clinical condition that could cause MCP hyperintensity. MCP hyperintensity did not show a statistically significant correlation with age (r = 0.05, P = .62). Patients were divided into 6 age groups, and ANOVA showed no statistically significant difference in the incidence of MCP hyperintensity between different age groups (P = .95). However, results were highly reproducible with excellent interobserver correlation (r = 0.97, P < .001). CONCLUSIONS: Mild MCP FLAIR hyperintensity can occur normally, and this finding shows no relationship with age.