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Biomedical subjects

H Lai

Publications and source records attributed to H Lai.

At least 73 records · Page 4Linked to original sources

Intraseptal microinjection of beta-funaltrexamine blocked a microwave-induced decrease of hippocampal cholinergic activity in the rat.

Acute (45 min) exposure to pulsed (2 microseconds pulse width, 500 pulses per second) 2450-MHz microwaves at a power density of 1 mW/cm2 (whole body specific absorption rate 0.6 W/kg) microwaves caused a decrease in cholinergic activity in the hippocampus of the rat as measured by the sodium-dependent high-affinity choline uptake. Microinjection of beta-funaltrexamine (1 microgram) into the septum before microwave exposure blocked this effect. These data indicate that mu-opioid receptors in the septum mediate a microwave-induced decrease in cholinergic activity in the hippocampus and support our hypothesis that microwaves at a whole body SAR of 0.6 W/kg can activate endogenous opioids in the brain.

Animals↗

Single- and double-strand DNA breaks in rat brain cells after acute exposure to radiofrequency electromagnetic radiation.

We investigated the effects of acute (2-h) exposure to pulsed (2-micros pulse width, 500 pulses s(-1)) and continuous wave 2450-MHz radiofrequency electromagnetic radiation on DNA strand breaks in brain cells of rat. The spatial averaged power density of the radiation was 2mW/cm2, which produced a whole-body average-specific absorption rate of 1.2W/kg. Single- and double-strand DNA breaks in individual brain cells were measured at 4h post-exposure using a microgel electrophoresis assay. An increase in both types of DNA strand breaks was observed after exposure to either the pulsed or continuous-wave radiation, No significant difference was observed between the effects of the two forms of radiation. We speculate that these effects could result from a direct effect of radiofrequency electromagnetic energy on DNA molecules and/or impairment of DNA-damage repair mechanisms in brain cells. Our data further support the results of earlier in vitro and in vivo studies showing effects of radiofrequency electromagnetic radiation on DNA.

Animals↗

Mortality in prostate cancer.

PURPOSE: We evaluated in patients with prostate cancer whether treatment is associated with in decreased mortality and whether the association of treatment with mortality varies with calendar time. MATERIALS AND METHODS: Using the 146,979 prostate cancer patients from the 1973 to 1990 public use tape of the Surveillance, Epidemiology and End Results program, we performed survival analysis and multivariate proportional hazards modeling to estimate the relative risk of disease specific and overall mortality. RESULTS: In men with prostate cancer, advanced age, black race, high tumor stage and not having treatment were independently associated with disease specific and overall mortality. The relative risk of mortality in treated patients decreased significantly from 1973 to 1990. CONCLUSIONS: The fact that advanced age and black race are associated with disease specific mortality (even when treatment and stage are controlled) is a new observation, which suggests that tumor biology and/or response to treatment is worse in elderly and black men. Overall, the data are consistent with the hypothesis that treatment of prostate cancer is associated with lower disease specific and overall mortality rates. The decreases in relative mortality in treated patients from 1973 to 1990 indirectly support the theory that changes in patterns of care from 1973 to 1990 had a beneficial effect on mortality. This observation implies that future studies should account for calendar time when interpreting outcomes data.

Aged↗

Marriage and mortality in prostate cancer.

PURPOSE: We evaluated the association of marital status and survival in patients with prostate cancer. MATERIALS AND METHODS: Using the 146,979 prostate cancer patients of the 1973 to 1990 public use tape of the Surveillance, Epidemiology and End Results program we performed survival analysis and multivariate proportional hazards modeling to estimate the relative risk of mortality. RESULTS: Married patients had significantly longer median survival than those who were divorced, single, separated or widowed. In models that controlled for age, stage, race and treatment, married patients had a significantly lower risk of mortality than those who were divorced, single, separated or widowed. CONCLUSIONS: Several hypothetical models can explain the association of marital status and mortality in men with prostate cancer. The most attractive model relies on the putative salutary effects of being married on social support and/or mood. A social support and depressed mood model of mortality raises the possibility that in prostate cancer quality of life determines quantity of life. Understanding the relationships among marital status, social support, mood and mortality could open the way to rational strategies for postponing death in men with prostate cancer.

Aged↗

[Applied anatomical study of the lingual nerve].

The lingual nerve and its adjacent structures were observed and measured on 32 adult cadavours. Its length was 69.7 mm and it was divided, bounded by the internal pterygoid muscle, into three segments and the length and diameter of them were respectively measured. According to its relationship with the lingual nerve, the submandibular ganglion can be classified into fusion type (being 46.9%) and free type (being 53.1%), and its superoinferior and transeversal diameters were separately measured to be 2.7 and 2.9 mm. The lingual nerve and its lingual branches were closely related to submandibular duct and there were two intersects. The relation and clinical significance of the third segment of lingual nerve and its neighbor structures were studied.

Adult↗

Oral administration of dihydroartemisinin and ferrous sulfate retarded implanted fibrosarcoma growth in the rat.

In the presence of iron, dihydroartemisinin forms free radicals and causes cell death. Since most cancer cells have high rates of iron intake, dihydroartemisinin would have selective cytotoxic effect on cancer cells. The present experiment was designed to study the effect of dihydroartemisinin and ferrous sulfate on the growth of implanted fibrosarcoma in the rat. We found that the growth rate of the tumor was significantly retarded by daily oral administration of ferrous sulfate followed by dihydroartemisinin. No significant tumor growth retardation effect was observed in rats treated with either dihydroartemisinin or ferrous sulfate alone. The drug treatment did not significantly affect body weight compared with untreated tumor-implanted animals and no apparent toxic effect was observed after drug treatment. An artemisinin analog-ferrous salt combination may provide a novel approach for cancer therapy.

Administration, Oral↗

Selective cancer cell cytotoxicity from exposure to dihydroartemisinin and holotransferrin.

Rapid cell death, as evidenced by a decrease in cell counts, was observed when molt-4-lymphoblastoid cells, a human leukemia cell line, were exposed to holotransferrin (12 microM) and dihydroartemisinin (1-200 microM). Incubation with either compound alone was significantly less effective. Significantly less cell death was observed when normal human lymphocytes were exposed to a combination of these 2 drugs. Probit analysis of dose-response functions shows that the drug combination is approximately 100 times more effective on molt-4 cells than lymphocytes (LD50s for molt-4 and lymphocytes were 2.59 microM and 230 microM, respectively). This drug combination may provide a novel approach for cancer treatment.

Artemisinins↗

Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells.

Levels of DNA single-strand break were assayed in brain cells from rats acutely exposed to low-intensity 2450 MHz microwaves using an alkaline microgel electrophoresis method. Immediately after 2 h of exposure to pulsed (2 microseconds width, 500 pulses/s) microwaves, no significant effect was observed, whereas a dose rate-dependent [0.6 and 1.2 W/kg whole body specific absorption rate (SAR)] increase in DNA single-strand breaks was found in brain cells of rats at 4 h postexposure. Furthermore, in rats exposed for 2 h to continuous-wave 2450 MHz microwaves (SAR 1.2 W/kg), increases in brain cell DNA single-strand breaks were observed immediately as well as at 4 h postexposure.

Analysis of Variance↗

Ethanol-induced single-strand DNA breaks in rat brain cells.

Male Sprague-Dawley rats were intubated with 4 g/kg body weight of ethanol (in a 20%, v/v, water solution). Brain cells were analyzed for single-strand DNA breaks at various post-ethanol administration time points using an alkaline microgel electrophoresis assay. Results showed a significant increase in single-strand DNA breaks in brain cells that peaked at approx. 4 h and returned to control level within 6 h after ethanol administration.

Administration, Oral↗

Effects of ECS on DNA single-strand breaks in rat brain cells.

We conducted a series of experiments to evaluate possible molecular mechanisms by which electroconvulsive therapy, a commonly used treatment for depression, may exert its adverse effects such as amnesia. We assessed the effects of repeated electroconvulsive shocks (ECS) alone and in combination with low-level radiograph irradiation on DNA single-strand breaks in cells in the rat brain, using a sensitive alkaline microgel electrophoresis assay method. Our results show that ECS, when administered alone, had no significant effects on DNA single-strand breaks in cells in either the hippocampus or the rest of the brain. However, repeated ECS when combined with a low-level radiograph irradiation produced a small but significant increase in DNA single-strand breaks in rat brain cells.

Animals↗

Demyelination and ethnicity: experience at the University of British Columbia Multiple Sclerosis Clinic with special reference to HTLV-I-associated myelopathy in British Columbian natives.

Since its creation in 1980, the Multiple Sclerosis Clinic at the University of British Columbia has actively followed over 2,500 patients from the Canadian province of British Columbia (BC) who have clinically definite multiple sclerosis (MS). These patients include 2,496 European Caucasians from a BC population of 3,858,505 (prevalence 64.7/100,000) in contrast with 92 patients of other ethnic origin (prevalence 14.6/100,000). Prevalence was higher in South Asians (15.7 from a population of 114,355) than in East Asians (6.25 from 287,845). Among individuals with native ancestry, MS was not rare when there was also European ancestry (46 cases from a population of 94,615), but MS was not encountered in pure-blooded natives (0 cases from 74,420 individuals). In contrast, among 5 patients with HTLV-I-associated myelopathy (HAM), 4 (from a population of 74,420) were of single native ancestry and only 1 (from a population of 94,615) was of multiple ancestry, including native ancestry. HAM was not found among Caucasians. This preliminary account clearly establishes that HAM is linked to native ancestry and that MS is linked to Caucasian ancestry.

British Columbia↗

Microwave irradiation affects radial-arm maze performance in the rat.

After 45 min of exposure to pulsed 2450 MHz microwaves (2 microseconds pulses, 500 pps, 1 mW/cm2, average whole body SAR 0.6 W/kg), rats showed retarded learning while performing in the radial-arm maze to obtain food rewards, indicating a deficit in spatial "working memory" function. This behavioral deficit was reversed by pretreatment before exposure with the cholinergic agonist physostigmine or the opiate antagonist naltrexone, whereas pretreatment with the peripheral opiate antagonist naloxone methiodide showed no reversal of effect. These data indicate that both cholinergic and endogenous opioid neurotransmitter systems in the brain are involved in the microwave-induced spatial memory deficit.

Analysis of Variance↗

NS-3, a TRH analog, reverses repeated ECS-induced deficits in water maze performance in the rat.

Rats given five consecutive daily electroconvulsive shock (ECS) treatments and trained to run in the Morris water maze, starting three days posttreatment, showed deficits in learning and memory functions. Treatment before each training session with the thyrotropin-releasing hormone (TRH) analog NS-3 [(CG-3703), (3R),(6R)-6-methyl-5-oxo-3-thiomorphorinyl-l-histidyl-l-prolinamid e tetrahydrate] reversed these behavioral deficits. The possible use of TRH and its analogs as therapeutic treatment for the cognitive dysfunctions resulting from electroconvulsive shock treatment for depression and the possible involvement of central cholinergic systems in the cognitive dysfunctions are discussed.

Animals↗

Effects of a 60 Hz magnetic field on central cholinergic systems of the rat.

We studied the effects of an acute (45 min) exposure to a 60 Hz magnetic field on sodium-dependent, high-affinity choline uptake in the brain of the rat. Decreases in uptake were observed in the frontal cortex and hippocampus after the animals were exposed to a magnetic field at flux densities > or = 0.75 mT. These effects of the magnetic field were blocked by pretreating the animals with the narcotic antagonist naltrexone, but not by the peripheral opioid antagonist, naloxone methiodide. These data indicate that the magnetic-field-induced decreases in high-affinity choline uptake in the rat brain were mediated by endogenous opioids in the central nervous systems.

Animals↗

ECT and TRH: cholinergic involvement in a cognitive deficit state.

In this paper we describe the findings from two preliminary experiments, a human and an animal study, investigating whether thyrotropin-releasing hormone (TRH) can mitigate electroconvulsive therapy (ECT)-induced cognitive deficits. Our results suggest further explorations of TRH and its analogs as possible therapeutic agents for these deficits. We speculate that the major cause of the ECT-induced cognitive deficits is a decrease in cholinergic transmission in the central nervous system. Treatments such as TRH, which enhance cholinergic activity, can reverse the cognitive deficits.

Adult↗

Single vs. repeated microwave exposure: effects on benzodiazepine receptors in the brain of the rat.

We studied the effects of single (45 min) and repeated (ten daily 45-min sessions) microwave exposures (2450-MHz, 1 mW/cm2, average whole-body SAR of 0.6 W/kg, pulsed at 500 pps with pulse width of 2 microseconds) on the concentration and affinity of benzodiazepine receptors in the cerebral cortex, hippocampus, and cerebellum of the rat. We used a receptor-binding assay with 3H-flunitrazepam as ligand. Immediately after a single exposure, an increase in the concentration of receptor was observed in the cerebral cortex, but no significant effect was observed in the hippocampus or cerebellum. No significant change in binding affinity of the receptors was observed in any of the brain-regions studied. In rats subjected to repeated exposures, no significant change in receptor concentration was found in the cerebral cortex immediately after the last exposure, which may indicate an adaptation to repeated exposures. Our data also show that handling and exposure procedures in our experiments did not significantly affect benzodiazepine receptors in the brain. Because benzodiazepine receptors in the brain are responsive to anxiety and stress, our data support the hypothesis that low-intensity microwave irradiation can be a source of stress.

Animals↗