PubMed Health⌕ Search

Biomedical subjects

Min Qiao

Publications and source records attributed to Min Qiao.

13 recordsLinked to original sources

Blood-oxygen-level-dependent magnetic resonance signal and cerebral oxygenation responses to brain activation are enhanced by concurrent transient hypertension in rats.

Neuronal activation results in increases in blood-oxygen-level-dependent (BOLD) signal increases in magnetic resonance images, increases in cerebral blood flow (CBF), and changes in tissue oxygenation. We hypothesized that transient hypertension concurrent with neuronal activation would interfere with the normal physiological responses to neuronal activation potentially leading to additive responses. Anesthetized rats were prepared for functional magnetic resonance imaging studies in which increases in BOLD signal were measured in response to: (1) electrical forepaw stimulation, (2) different graded levels of transient hypertension produced with norepinephrine, and both 1 and 2. In other experiments with a similar protocol, changes in CBF and cortical oxyhemoglobin (oxyHb) and deoxyhemoglobin (deoxyHb) were measured using Laser Doppler Flowmetry and near-infrared (IR) spectroscopy. BOLD signal within the sensory-motor cortex increased during forepaw stimulation. These matched increases in CBF and oxyHb and decreases in deoxyHb. During moderate or severe transient hypertension, there was a blood pressure-dependent increase in BOLD signal, CBF, and oxyHb; and a decrease in deoxyHb. When transient hypertension and forepaw stimulation were combined, the responses of oxyHb, deoxyHb, or BOLD signal were generally a summation of each response. In contrast, the CBF response to forepaw stimulation was relatively unaffected by transient hypertension. We conclude that during stimulation with concurrent hypertension, the normal changes in tissue oxygenation that accompany neuronal activation are enhanced by the increases produced by hypertension despite an excellent autoregulation of CBF. The latter could reflect highly transient decreases in oxygen consumption or likely a redistribution of flow through more nonexchange vessels.

Animals↗

DNA damage and repair process in earthworm after in-vivo and in vitro exposure to soils irrigated by wastewaters.

In this study, DNA damage to earthworms (Eisenia fetida) after in vivo exposure to contaminated soils was measured by detecting DNA strand breakages (DSBs) and causality was analyzed through fractionation based bioassays. A non-linear dose-response relationship existed between DNA damage and total soil PAHs levels. DNA damage, measured with the comet assay, and its repair process, were observed. To identify the chemical causality, an in vitro comet assay using coelomocytes was subsequently performed on the fractionated organic extracts from soils. The results showed that the PAHs in the soils were responsible for the exerting genotoxic effects on earthworms. When normalized to benzo(a)pyrene toxic equivalent (TEQ(BaP)), the saturation dose in the dose-response curve was about 10ng TEQ(BaP) g(-1) soil (dw).

Animals↗

Identification of Ah receptor agonists in sediment of Meiliang Bay, Taihu Lake, China.

Deterioration of ecosystem and water quality in Taihu Lake, the third largest freshwater lake in China, is of great concern in China. However, most evaluations on water and sediment were carried out by chemical analysis, which could hardly gain information on the risk stressors affecting the system. Sediment samples from Meiliang Bay, Taihu Lake were assayed for AhR-mediated EROD induction using a rat hepatoma cell line (H4IIE). The known AhR agonists including PCDD/Fs, PCBs, and PAHs were analyzed by instruments. The cause-effect relationship between the observed EROD activity and chemical concentrations of AhR agonists and their dose-effect relationship were examined. Our results showed that sediment extracts could induce significant AhR effects, and the chemical-derived TCDD equivalents (TEQ(cal)) were significantly correlated to bioassay-derived TCDD equivalents (TEQ(bio)) (R = 0.85, p < 0.01). Among different contributors, PAHs could account for 70-93% and PCDD/Fs could contribute less than 30% of TEQ(cal). PCBs exhibited almost no contribution. Therefore, integration of EROD bioassay and chemical analysis provided an effective way for identifying the potential risk stressors. Underthis circumstance, a quantitative dose--effect relationship between TEQ(PAH) and EROD activity could be established, suggesting that the observed AhR effect was mostly derived from PAHs. The implication is that the EROD assay and the identified risk stressors (PAHs) may be used in lieu of detailed environmental analysis to follow the progression of a remediation strategy.

Animals↗

Transient blood pressure changes affect the functional magnetic resonance imaging detection of cerebral activation.

Functional magnetic resonance imaging (fMRI) provides an indirect measure of cerebral activation that could be altered by factors directly affecting cerebral blood flow independent of changes in neuronal activation. Presently, we investigate how changes in blood pressure (BP) affect the activation detected with fMRI. fMRI scans were acquired in 33 rats under control conditions and following transient BP increases (norepinephrine, IV) or decreases (arfonad, IV) with and without electrical stimulation of the forepaw. Voxels correlating to either the stimulation or the change in BP time courses were identified. During transient hypertension, irrespective of forepaw stimulation, BP increases (i.e., >10 mm Hg) produced a transient increase in the blood oxygen level-dependent (BOLD) intensity resulting in a significant numbers of voxels correlating to the BP time courses (P < 0.05), and the number of these voxels increased as BP increased, becoming substantial at BP > 30 mm Hg. The activation patterns with BP increases and stimulation overlapped spatially resulting in an enhanced cerebral activation to simultaneous forepaw stimulation (P < 0.05). BP decreases (>10 mm Hg) produced corresponding decreases in BOLD intensity, causing significant numbers of voxels correlating to the BP decreases (P < 0.005), and these numbers increased as BP decreased (P < 0.001). The BP decreases and stimulation time courses and responses were distinct, and hypotension did not affect the detection of the activation response to forepaw stimulation. The results indicate that substantial hypertension accompanying a stimulation paradigm produces a BOLD response that enhances the cerebral activation detected, whereas hypotension does not affect the detection of neuronal activation but does produce responses that could be interpreted as a 'deactivation'.

Adrenergic alpha-Agonists↗

Organchlorinated pesticides in surface sediments of Meiliang Bay in Taihu Lake, China.

The concentration level of organochlorine pesticides (OCPs) in sediments from Taihu Lake, China was investigated to evaluate the potential ecological risk. A total of 48 surface sediment samples were collected in Taihu Lake. Meiliang Bay in Taihu Lake was selected due to its importance as a drinking water source for nearby cities. Results show that the concentrations of various pesticides in sediments were in the range of 0.1-107.3 ng/g for HCH, 3.5-50.5 ng/g for endosulfan sulfate, 2.7-23.0 ng/g for endosulfan II and 0.3-59.3 ng/g for DDT. Among the OCPs, HCHs and DDTs were the most dominant contamnants in the sediments. Cyclodiene compounds were also the main pesticides in Taihu lake besides HCH and DDT. Among the cyclodiene compounds, heptachlor and endosulfan sulfate prevailed in most of the sediments. Moreover, the frequencies of detection for the metabolites of PAHs were higher than those of parent compounds, depicting that the sediments have been contaminated historically. The results obtained in this study shown that there still exist a variety of OCPs residues in Taihu Lake and Meiliang Bay.

China↗

Evolution of magnetic resonance imaging changes associated with cerebral hypoxia-ischemia and a relatively selective white matter injury in neonatal rats.

We hypothesized that a combination of quantitative magnetic resonance imaging (MRI) sequences would detect a differential evolution of hypoxic-ischemic changes in white matter compared with gray matter in a recently developed model of unilateral mild cerebral hypoxia-ischemia in the 7-d-old rat. Using this model, which involved unilateral carotid artery occlusion and exposure to hypoxia for 45-50 min, maps of apparent diffusion coefficients of water (ADC), T1, T2, and cerebral blood flow (CBF) were acquired either before hypoxia-ischemia or at 1, 24, or 48 h and at 7 d post-hypoxia-ischemia followed by brain processing for histology. At 1 h post-hypoxia-ischemia, MRI changes in white matter ipsilateral to the hypoxia-ischemia were not as pronounced as those in gray matter. However, increases in T1, T2 and ADC and decreases in CBF within white matter enhanced over time, with changes being maximal at 48 h post-hypoxia-ischemia, whereas changes in the cortical gray matter normalized over this time. By 7 d post-hypoxia-ischemia, there were no differences in ADC, T1, T2, or CBF between hemispheres despite there being histologic changes in white matter within the hypoxic-ischemic hemisphere including increased glial proliferation and reactivity, reduced myelin basic protein, and increased cell death. The results demonstrate that increases in ADC and T2 observed subacutely in the days following hypoxia-ischemia are associated with rather selective white matter damage and suggest that diffuse white matter hyperintensities and increased ADC reported in infants are transient MRI changes post- hypoxia-ischemia.

Animals↗

[Comparison between biomimetic sampling technique using semipermeable membrane device and bioconcentration in caged fish for polycyclic aromatic hydrocarbons].

Semipermeable membrane device (SPMD) was recently accepted to estimate the time-integrated concentrations of bioavailable hydrophobic organic compounds (HOCs) in a similar manner as lipophilic bioconcentration. However few field researches were carried out to verify the similarities of SPMD and fish in concentrating HOCs from water. In present work, SPMD and caged crucian carps (Carassius auratus) were deployed side-by-side at five sites in Meiliang Bay, Taihu Lake for 32 days and concentrations of polycyclic aromatic hydrocarbons (PAHs) in SPMD and fish were analyzed. The results showed that the composition of PAHs and relative concentration of individual PAH in SPMD and fish were quite similar. There was significant correlation between bioconcentration factors (lg BCF) and device concentration factors (lg DCF) for concentrations of PAHs (p < 0.0001). However in a quantitative analysis, lipid-normalized concentrations of PAHs in SPMD and fish were similar, and the ratios of the concentrations of PAHs in fish and SPMD were ranged from 0.47 to 4.12. In summary, SPMD could be the surrogate to estimate PAHs levels in fish in fresh water lake.

Animals↗

Composition, sources, and potential toxicological significance of PAHs in the surface sediments of the Meiliang Bay, Taihu Lake, China.

Twenty-five surface sediment samples were collected from Meiliang Bay, Taihu Lake, China, in 2003. The concentrations of 16 polycyclic aromatic hydrocarbons (PAHs), identified as priority pollutants by the USEPA, were determined by gas chromatography equipped with a mass spectrometry detector (GC-MS). Total concentrations of the PAHs ranged from 1207 to 4754 ng/g dry weight. Sediment samples with the highest PAH concentrations were from the northern site of the bay, which is in proximity to the incoming PAH source; the PAH levels in the southern part were relatively low. The observed PAH levels were higher than those in river sediments in China but were lower than those found in sediments of urban areas and harbors. According to the observed molecular indices, PAHs originated largely from the high-temperature pyrolytic process, whereas the petrogenic process was more commonly responsible for PAH contamination in harbors. A good correlation existed between the benzo[a]pyrene level and the total PAH concentration (r=0.97), making benzo[a]pyrene a potential molecular marker for PAH pollution. According to the numerical effect-based sediment quality guideline (SQGs) of the United States, the levels of PAHs at most studied sites in Meiliang Bay, except some sites in the northern part of the bay, should not exert adverse biological effects. In the northern part of the bay, the PAH levels at sites 21 and 22 exceed the effects range low (ERL) and could thus cause acute biological impairments, in comparison with the sediment quality guidelines. The total PAH levels were expressed as the B[a]P toxicity equivalents (TEQs(carc)) and compared to the contaminated sediments from Guba Pechenga, Barents Sea, Russia.

China↗

White matter damage precedes that in gray matter despite similar magnetic resonance imaging changes following cerebral hypoxia-ischemia in neonatal rats.

We hypothesized that the cerebral injury produced by hypoxia-ischemia (HI) in neonatal rats would differ in white compared with gray matter as detected histologically or with magnetic resonance (MR) imaging methods. Maps of T2 and the apparent diffusion coefficient (ADC) of water were acquired in 1-week-old rats at times prior to cerebral HI (right carotid artery occlusion plus 1.5 h of hypoxia), within the last 5-10 min of HI, and 1 h or 24 h after HI. Near the end of HI, ADC decreased and T2 increased in both cortical gray and subcortical white matter within the cingulum of the HI hemisphere. One hour after HI, ADC partially recovered, but T2 remained increased and then increased further by 24 h post-HI. In contrast to the similar MR responses in white and gray matter, histological evidence for irreversible cell damage occurred in white matter earlier than in gray matter within the HI hemisphere. At 1 h post-HI, rarefied or disrupted nerve fibers and an increase in TUNEL-positive cells were observed within white matter in the cingulum, whereas neurons within the cortical gray matter appeared normal. By 24 h post-HI, damage was apparent in both white and gray matter. Thus, MR imaging detected acute tissue edema following cerebral HI in both gray and white matter but did not distinguish between the early irreversible tissue injury detected histologically in white but not gray matter in this rather severe model of neonatal encephalopathy.

Age Factors↗

Magnetic resonance imaging of differential gray versus white matter injury following a mild or moderate hypoxic-ischemic insult in neonatal rats.

Selective white matter injury in the pre-mature infants suggests it has a greater susceptibility to hypoxia-ischemia. To investigate whether white matter injury would predominate following a mild hypoxic-ischemic insult, 7-day-old rats underwent either mild or moderate hypoxia-ischemia and magnetic resonance imaging 24 h later. Mild and moderate hypoxia-ischemia were produced by unilateral carotid artery occlusion plus exposure to hypoxia for either 45-50 or 90 min at ambient temperatures of 34.5 or 35.5 degrees C, respectively. Following mild hypoxia-ischemia, there was a significant increase in T(1) and T(2) within periventricular white matter (e.g. corpus callosum) in the hemisphere ipsilateral to the occlusion compared to that contralaterally and less of an increase within gray matter (e.g. cortex and striatum). This corresponded to relatively selective white matter injury detected histologically. Following a moderate hypoxia-ischemia, both gray and white matter was severely injured with marked increases in T(1) and T(2) occurring in both white and gray matter regions ipsilateral to the hypoxia-ischemia. We conclude that a mild insult, consisting of a short duration of hypoxia-ischemia at a slightly lower body temperature than a moderate hypoxic-ischemic insult, produces enhanced injury in white matter and a relative sparing of gray matter.

Animals↗

Correspondence of AQP4 expression and hypoxic-ischaemic brain oedema monitored by magnetic resonance imaging in the immature and juvenile rat.

Whether the water channel protein AQP4 is involved in the very early cell swelling and brain oedema observed with cerebral hypoxia-ischaemia (HI) and whether this response depends on the maturity of brain were investigated by comparing regional changes in AQP4 protein expression and signal intensity on magnetic resonance (MR) images in immature and juvenile brains. Maps of T2 and the apparent diffusion coefficient (ADC) of water were acquired in 1- and 4-week-old rats at times prior to HI, within the last 5 min of HI and 1 h or 24 h afterwards. AQP4 expression assessed with Western blotting was not significantly reduced until 24 h post-HI irrespective of age. However, AQP4 immunostaining was decreased at the end of HI and at 1 h or 24 h after HI in the hemisphere ipsilateral to the occlusion with changes being similar in both age groups and coinciding well with regional reductions in ADC. IgG immunostaining to assess blood-brain barrier integrity and T2 were unchanged at early time points in 4-week old rats despite decreases in AQP4 immunostaining. Thus, at early time points there were decreases in AQP4 detected with immunostaining but not Western blotting methods. However, the good correlation between alterations in ADC and AQP4 immunostaining suggests that changes in the AQP4 are involved in some of the early changes in brain water distribution observed in hypoxia-ischemia, and supports the speculation that AQP4 is involved in the transport of water across the perivascular membranes into the vascular lumen.

Aging↗

Development of acute edema following cerebral hypoxia-ischemia in neonatal compared with juvenile rats using magnetic resonance imaging.

We hypothesized that the evolution of cerebral edema accompanying cerebral hypoxia-ischemia is dependent on age and that such differences would be detectable using magnetic resonance imaging methods. Thus we examined in immature and juvenile rats the relationship between hypoxic-ischemic changes in T1 and T2 and the alterations in brain water content, as assessed by differences in tissue wet-dry weights. One- and 4-wk-old rats were anesthetized and subjected to unilateral carotid artery occlusion and subsequent exposure to hypoxia (8% oxygen). T1 and T2 maps were acquired at 9.4 T, and then brain water content was measured in sham controls or in hypoxic-ischemic animals before, during, and 1 or 24 h after hypoxia-ischemia. In sham controls, T1, T2, and proton density decreased with increasing age, corresponding to an ontogenic decrease in water content. In 1-wk-old rats, increases in T1 and T2 were observed during and at 1 and 24 h after hypoxia-ischemia, corresponding to elevations in water content. In 4-wk-old rats, T1 and water content increased during and at 1 and 24 h after hypoxia-ischemia whereas T2 was not increased until 24 h after hypoxia-ischemia. Regression analysis showed that T1 correlated better with total water content than T2. In both immature and older brain, an increase in total brain water develops acutely and persists after an episode of cerebral hypoxia-ischemia, and T1 imaging detects this change better than T2. Hypoxic-ischemic changes in T2 are age dependent, reflecting other physicochemical changes of water in the tissue than water content alone.

Acute Disease↗

Transient hypoxia-ischemia in rats: changes in diffusion-sensitive MR imaging findings, extracellular space, and Na+-K+ -adenosine triphosphatase and cytochrome oxidase activity.

PURPOSE: To investigate the correlation between diffusion-weighted (DW) magnetic resonance (MR) image changes with alterations in extracellular volume and changes in cytochrome oxidase and Na(+)-K(+)-adenosine triphosphatase (ATPase) activity at various times during and after cerebral hypoxia-ischemia in neonatal and juvenile rats. MATERIALS AND METHODS: One- and 4-week-old rats were randomly assigned to control or transient cerebral hypoxia-ischemia (ie, right carotid artery occlusion plus exposure to 8% oxygen) groups. Hypoxic-ischemic changes compared with normal ipsilateral brain tissue on DW images and the apparent diffusion coefficient of water were measured during and at 1 and 24 hours after hypoxia-ischemia ended. Hypoxic-ischemic changes in extracellular space and ipsilateral versus contralateral differences in Na(+)-K(+)-ATPase and cytochrome oxidase activity were measured. RESULTS: Hyperintensities on DW images obtained during hypoxia-ischemia correlated well (P <.05) with extracellular space reductions, which occurred 15 minutes earlier in the brains of 4-week-old rats than in the brains of 1-week-old rats. Similarly, within 1 hour after hypoxia-ischemia ended, DW image and extracellular space changes normalized. In contrast, Na(+)-K(+)-ATPase and cytochrome oxidase activity decreased in some regions during hypoxia-ischemia and remained reduced 1 hour after the end of hypoxia-ischemia. Twenty-four hours after signal intensity normalization, hyperintense areas reappeared on DW images, and Na(+)-K(+)-ATPase and cytochrome oxidase activity remained decreased. CONCLUSION: Signal intensity alterations with diffusion-sensitive MR imaging during and after transient hypoxia-ischemia are closely associated with a corresponding shrinkage and reexpansion of the extracellular space, irrespective of age. Mechanisms other than Na(+)-K(+)-ATPase changes may induce the early cell volume changes detected with diffusion-sensitive MR imaging.

Animals↗