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1.
Zool Res ; 44(3): 451-466, 2023 May 18.
Article En | MEDLINE | ID: mdl-36994536

Chronic liver injury leads to progressive liver fibrosis and ultimately cirrhosis, a major cause of morbidity and mortality worldwide. However, there are currently no effective anti-fibrotic therapies available, especially for late-stage patients, which is partly attributed to the major knowledge gap regarding liver cell heterogeneity and cell-specific responses in different fibrosis stages. To reveal the multicellular networks regulating mammalian liver fibrosis from mild to severe phenotypes, we generated a single-nucleus transcriptomic atlas encompassing 49 919 nuclei corresponding to all main liver cell types at different stages of murine carbon tetrachloride (CCl 4)-induced progressive liver fibrosis. Integrative analysis distinguished the sequential responses to injury of hepatocytes, hepatic stellate cells and endothelial cells. Moreover, we reconstructed cell-cell interactions and gene regulatory networks implicated in these processes. These integrative analyses uncovered previously overlooked aspects of hepatocyte proliferation exhaustion and disrupted pericentral metabolic functions, dysfunction for clearance by apoptosis of activated hepatic stellate cells, accumulation of pro-fibrotic signals, and the switch from an anti-angiogenic to a pro-angiogenic program during CCl 4-induced progressive liver fibrosis. Our dataset thus constitutes a useful resource for understanding the molecular basis of progressive liver fibrosis using a relevant animal model.


Endothelial Cells , Liver Cirrhosis , Mice , Animals , Endothelial Cells/metabolism , Liver Cirrhosis/chemically induced , Liver Cirrhosis/genetics , Liver Cirrhosis/metabolism , Liver Cirrhosis/veterinary , Carbon Tetrachloride/toxicity , Cell Communication , Mammals
2.
World J Gastroenterol ; 18(33): 4627-8, 2012 Sep 07.
Article En | MEDLINE | ID: mdl-22969239

Gastrointestinal complications caused by herpes zoster are extremely rare. Here, we described a case of abdominal distention caused by herpes zoster. The patient was a 59-year-old female who suffered from unexplained paroxysmal and a burning pain on the right part of her waist and abdomen, accompanied by abdominal distention. Intestinal pseudo-obstruction was diagnosed by abdominal radiography. Distention of the right abdominal wall was still apparent after one month. In this report, we found that recovery from abdominal distention caused by herpes zoster is difficult and may require surgical intervention.


Abdomen/pathology , Herpes Zoster/complications , Intestinal Pseudo-Obstruction/diagnostic imaging , Intestinal Pseudo-Obstruction/etiology , Aza Compounds/therapeutic use , Fasting , Female , Fluid Therapy , Fluoroquinolones , Humans , Intestinal Pseudo-Obstruction/therapy , Middle Aged , Moxifloxacin , Quinolines/therapeutic use , Radiography, Abdominal , Treatment Outcome , Vitamin B 12/analogs & derivatives , Vitamin B 12/therapeutic use
3.
Opt Express ; 17(26): 23530-5, 2009 Dec 21.
Article En | MEDLINE | ID: mdl-20052060

A packaging scheme utilizing omni-directional reflective (ODR) optical coating is described to enhance the light extraction of near UV excited, phosphor-converted LEDs. A simple 1D model was developed to analyze the spectra of the extracted light measured with an integration-sphere as a function of phosphor layer concentration and thickness. Quantitative determination of the absorption coefficients at the pump and fluorescent light wavelength along with the conversion coefficient of phosphors were obtained. The reflection of the ODR film and the back reflector are also characterized. These parameters are then used for efficiency optimization of the present packaging scheme. A maximum enhancement of 40% can be expected with the materials and the configuration used in the present work.


Lenses , Lighting/instrumentation , Semiconductors , Computer-Aided Design , Equipment Design , Equipment Failure Analysis , Light , Scattering, Radiation
4.
Zhonghua Yi Xue Za Zhi ; 86(37): 2639-42, 2006 Oct 10.
Article Zh | MEDLINE | ID: mdl-17198592

OBJECTIVE: To evaluate the effects of transcranial magnetic stimulation (TMS) on the brain plasticity and its role in functional outcome in cerebral infarction. METHODS: Twenty male SD rats underwent suture of the unilateral middle cerebral artery (MCA) so as to establish focal cerebral infarction models and then were randomly divided into 2 equal groups: model group, to be reared in the original living state, and TMS group, given in addition TMS treatment 1 day after infarction 2 times per day and 30 pulses per time for 4 weeks. Twenty-eight days after the rats were killed. Four rats from each group underwent microscopy of the brain to measure the dendritic structure of the pyramidal cells quantitatively. Other 4 rats from each group underwent electron microscopy of the brain to measure the parameters of synaptic interface in the sensorimotor cortex. Neural function scoring was conducted 24 hours after the establishment of model and before being killed. RESULTS: There was no significant difference in the neural function 24 h after the establishment of models, however, 28 days after the score of neural function of the TMA group was 0.58 +/- 0.49, significantly lower than that of the model group (0.92 +/- 0.28, P < 0.05). The total dendritic length, number of dendritic branching points, and dendritic density in layer V pyramidal cells within the undamaged motor cortex of the TMS group were 898 microm +/- 127 microm, 6.6 +/- 1.5, and 0.75/microm +/- 0.19/microm, all significantly higher than those of the model group (788 microm +/- 112 microm, 5.8 +/- 1.5, and 0.60/microm +/- 0.16/microm, P < 0.05 or < 0.01). Electron microscopy showed that the synaptic curvatures and post-synaptic density of the TMS group were 1.06 +/- 0.08 and 64 +/- 13 respectively, both significantly higher than those of the model group (1.02 +/- 0.06 and 54 +/- 12 nm respectively, P < 0.05 and P < 0.01), and the synapse cleft width of the TMS group was 19.5 +/- 2.1, significantly narrower than that of the model group (23.3 +/- 2.3, P < 0.01). CONCLUSION: TMS promotes the improvement of neural functions of the rats with cerebral ischemia by the potential mechanism that TMS strengthen the compensatory roles of the synaptic interface and dendritic structure in the undamaged sensorimotor cortex area and increase synaptic plasticity.


Cerebral Infarction/physiopathology , Dendrites/ultrastructure , Synapses/ultrastructure , Transcranial Magnetic Stimulation , Animals , Cerebral Infarction/pathology , Cerebral Infarction/therapy , Disease Models, Animal , Male , Microscopy, Electron, Transmission , Pyramidal Cells/diagnostic imaging , Rats , Rats, Sprague-Dawley , Ultrasonography
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