Lipidomics is an emerging discipline that systematically studies the various types, functions, and metabolic pathways of lipids within living organisms. This field compares changes in diseases or drug impact, identifying biomarkers and molecular mechanisms present in lipid metabolic networks across different physiological or pathological states. Through employing analytical chemistry within the realm of lipidomics, researchers analyze traditional Chinese medicine (TCM). This analysis aids in uncovering potential mechanisms for treating diverse physiopathological conditions, assessing drug efficacy, understanding mechanisms of action and toxicity, and generating innovative ideas for disease prevention and treatment. This manuscript assesses recent literature, summarizing existing lipidomics technologies and their applications in TCM research. It delineates the efficacy, mechanisms, and toxicity research related to lipidomics in Chinese medicine. Additionally, it explores the utilization of lipidomics in quality control research for Chinese medicine, aiming to expand the application of lipidomics within this field. Ultimately, this initiative seeks to foster the integration of traditional medicine theory with modern science and technology, promoting an organic fusion between the two domains.

【Objective】 To clarify the hematological characteristics and current situation of chronic mountain sickness among Tibetan residents in extreme high altitude area (more than 5 000 m above the sea level) of Ali district based on the analysis of physical examination and blood test results. 【Methods】 Totally 250 Tibetan residents were selected by convenient sampling for blood oxygen saturation (SpO2), heart rate, and blood routine examination. Chronic mountain sickness was determined according to the hemoglobin (Hb) level and SpO2. 【Results】 The red blood cell (RBC), Hb and hematocrit (HCT) of the Tibetan residents at 5 200-meter altitude were all higher than the normal physiological reference range of China. Mean red blood cell volume (MCV), mean red blood cell hemoglobin content (MCH), mean red blood cell hemoglobin concentration (MCHC), white blood cell (WBC) and platelet (PLT) were in the upper limit of the reference value. The RBC, Hb, HCT and MCHC of male Tibetan residents were higher than those of females, while PLT was lower than that of females, with significant differences. There were no statistical differences in MCV, MCH or WBC among different genders of Tibetan residents. The SpO2 of the Tibetan residents was about 85% of the normal value, and the males had higher SpO2 than the females in the same age group, and the difference was statistically significant, but the heart rate did not differ significantly. The prevalence rate of chronic mountain sickness in this area was as high as 16.4%, and the prevalence rate of heavy manual workers was significantly higher than that of light manual workers, with significant differences. 【Conclusion】 The high-altitude anoxic environment causes the changes in red blood cells, hemoglobin, and oxygen saturation of local residents, and the prevalence of chronic mountain sickness increases significantly. Labor intensity is one of the risk factors for chronic mountain sickness in high-altitude areas.

Objective To study the effects of NRG2 on cardiac structure and function , we established the cardiac-specific human NRG2 transgenic mice and investigate the effect of NRG2 on cardiac structure and function under pressure overload situation .Methods The transgenic vector was constructed by insertion of the human NRG2 gene under the α-MHC promoter.The transgenic mice were generated by microinjection and were all maintained on a C57BL/6J genetic background .The genotype of transgenic mice was identified by PCR and the expression level of target gene was determined by western blot .Transverse aortic constriction ( TAC) was applied to prepare the pressure overload induced cardiomyopathy mice model .The cardiac structure and function of the transgenic mice were compared and analysized by echocardiographic and pathological observation .Results Transgenic mice with high level of NRG2 in heart tissues were established.The left ventricular wall thickness (LVPWD) was increased, and to 15.6% at 3 months old compared with that of the non transgenic ( NTG) mice.The hypertrophy of left ventricular wall caused by pressure overload was removed due to the expression of NRG2 .Meanwhile, cardiac disarray and fibrosis were increased obviously compared with that of the NTG mice.Conclusion The transgenic expression of NRG2 in heart tissues could shorten the pathological process of hypertrophy, but accelerated the process of heart failure (HF).

Objective To study the effects of transcranial magnetic stimulation (TMS) on learning and memory, and angiogenesis and the dendritic structure of hippocampal CA3 pyramidal neurons after cerebral infarction. Methods Forty-eight male Sprague-Dawley rats were divided into a sham operated group, a model group and a TMS group (n = 16). Rat models of focal cerebral infarction were established with unilateral middle cerebral artery (MCA) suture occlusion in the model and TMS groups. The rats of the TMS group were given 4 weeks of TMS treatment beginning 1 day after the infarction (2 times per day, 30 pulses per time). Their learning and memory abilities were tested with a Y-maze. Angiogenesis and the dendritic structure of their hippocampal CA3 pyramidal neurons were detected after 4 weeks. Results Compared with the model group, learning and memory improved significantly in the TMS group. The average microvessel density of the hippocampus in the TMS group was significantly more than in the model group. The total length of apical dendrites of hippocampal CA3 pyramidal neurons in TMS group was significantly longer than in the model group. Conclusions The improved learning and memory observed following TMS treatment are likely to be related to changes in angiogenesis, the dendritic.structure of the hippocampal CA3 pyramidal neurons, and enhanced synaptic plasticity.

Atherosclerosis is a leading cause of death worldwide, and its mechanisms are still unclear. However, various animal models have significantly advanced our understanding of the mechanisms involved in atherosclerosis and have allowed the evaluation of therapeutic options. The aim of this paper is to review those animal models (i.e., rabbits, mice, rats, guinea pigs, hamsters, avian, carnivores, swine, and, non-human primates) that have been used to study atherosclerosis. Though there is no single perfect animal model that completely replicates the stages of human atherosclerosis, cholesterol feeding and mechanical endothelial injury are two common features shared by most models of atherosclerosis. Further, with the development of genetically modified animals, these models are significantly broadening our understanding of the pathogenesis of atherosclerosis.
Animals ; Atherosclerosis ; epidemiology ; metabolism ; pathology ; Disease Models, Animal ; Humans

In order to investigate the transfer and expression of Snail gene in human bone mesenchymal stem cells (MSCs) and to study effects of Snail gene modification on the CXCR4 expression of human MSCs and their capacity of migration to SDF-1 in vitro, the plasmid PCAGGSneo-Snail-HA or the control vector of PCAGGSneo was transferred into the cells. Fluorescence activated cell sorting analysis, immunofluorescence staining and RT-PCR were used to study the expression of CXCR4 by MSCs. Chemotaxis assays were performed to evaluate the migratory capacity of MSCs-Sna and MSCs-neo to SDF-1 in vitro. For the blocking assay, CXCR4 blocking antibody was added into cell culture. CXCR4 expression was higher in MSCs-Sna than that in MSCs-neo (P < 0.05). Chemotaxis assays showed that SDF-1alpha stimulated migratory activity of MSCs-Sna more than MSCs-neo in vitro (P < 0.05). Moreover, the SDF-1alpha-induced migratory activity of MSCs-Sna was inhibited in a concentration-dependent manner by a CXCR4-blocking antibody. It was concluded that Snail enhanced expression of CXCR4 in MSCs, providing a plausible mechanism for Snail-mediated MSCs transmigration to damaged tissues in vivo where SDF-1 has been shown to be up-regulated as part of injury responses.
Bone Marrow Cells ; cytology ; Cell Movement ; genetics ; Cells, Cultured ; Chemokine CXCL12 ; metabolism ; Humans ; Mesenchymal Stromal Cells ; cytology ; metabolism ; Receptors, CXCR4 ; genetics ; metabolism ; Snail Family Transcription Factors ; Transcription Factors ; genetics ; Transduction, Genetic

The effect of transcranial magnetic stimulation (TMS) on the neurological functional recovery and expression of c-Fos and brain-derived neurotrophic factor (BDNF) of the cerebral cortex in rats with cerebral infarction was investigated. Cerebral infarction models were established by using left middle cerebral artery occlusion (MCAO) and were randomly divided into a model group (n=40) and a TMS group (n=40). TMS treatment (2 times per day, 30 pulses per time) with a frequency of 0.5 Hz and magnetic field intensity of 1.33 Tesla was carried out in TMS group after MCAO. Modified neurological severity score (NSS) were recorded before and 1, 7, 14, 21, and 28 day(s) after MCAO. The expression of c-Fos and BDNF was immunohistochemically detected 1, 7,14, 21, and 28 day(s) after infarction respectively. Our results showed that a significant recovery of NSS (P＜0.05) was found in animals treated by TMS on day 7, 14, 21, and 28 as compared with the animals in the model group. The positive expression of c-Fos and BDNF was detected in the cortex surrounding the infarction areas, while the expression of c-Fos and BDNF increased significantly in TMS treatment group in comparison with those in model group 7, 14, 21, and 28 days (P＜0.05) and 7,14, 21 days (P＜0.01) after infarction, respectively. It is concluded that TMS has therapeutic effect on cerebral infarction and this may have something to do with TMS's ability to promote the expression of c-Fos and BDNF of the cerebral cortex in rats with cerebral infarction.

BACKGROUND: Microglial cells are prominently involved in certain neurologic diseases such as Parkinson disease and Alzeheimer disease. In vitro primary culture is commonly used in studies on the functions of microglia.However, these classical culture methods have some defects including complex procedures and low out-put.OBJECTIVE: To establish a simplified high-output primary culture of microglia.DESIGN: An explorative experiment with microglial cells as the single sample.SETTING: Department of Neurology, Affiliated Union Hospital, Tongji Medical College, Huazhong University of Science and Technology.MATERIALS: The study was finished at the Central Laboratory of Union Hospital from April to October 2004. Microglial cells were obtained from 10 newborn(one day) male Kunming mice that were selected.METHODS: The author' s culture method was based on McCarthy method, we developed a new culture method and made some improvements,including the increased cell density for primary culture and nutritional deprivation. The microlglial cells were isolated with low-concentration trypsin-EDTA(ethylene diamine tetraacetic acid) digestion and immunochemically labeled with MAC-1 antibody, so as to measure the output and purity of microglia.MAIN OUTCOME MEASURES: ① Morphologic features of microglial cells, observed with inverted microscope; ② Purity and activity of microglia cultured with these two methods, were measured immunohistochemically.RESULTS: For microglia cultured with McCarthy method, the culture cycle was 20 days and the output was 2 × l05 cells per flask with a purity of 95% -97%. The new method shortened the culture cycle to 15 days and the output reached 1 × 106 cells per flask with a purity of 96-98%. Cell purity and activity had no significant difference between these two culture methods.CONCLUSION: The new method has a similar purity and activity with classical method; however, it may simplify procedures, shorten cycle, and increase output, and therefore can be a useful method for studies on microglia function and for nerve repair.

BACKGROUND: Studies have shown that mild hypertension and hypothermia both offer cerebral protection against focal cerebral ischemia,and their possible synergistic effect may provide even better neuroprotective effects.OBJECTIVE: To investigate the mechanism of cerebral protection by induced hypertension combined with mild hypothermia against focal cerebral ischemia and reperfusion, through observation of the changes in the infarct volume and blood-brain barrier(BBB) in rats.DESIGN: A randomized controlled experimental study based on experimental animals.SETTING: The departments of neurology of two university hospitals and department of dermatology in a municipal hospital.MATERIALS: The study was carried out in the Laboratory of Department of Neurology, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology and Laboratory of Department of Neurology, People' s Hospital of Wuhan University from March to July 2001. Sixty-four Wistar rats weighing 180 to 230 g were purchased from the Experimental Animal Center of People' s Hospital of Wuhan University.INTERVENTIONS: Sixty-four rats were randomly divided into control group, hypertension group, mild hypothermia group, and combined therapy group, each group consisting of 16 rats. Reperfusion was initiated after a 3-hour focal cerebral ischemia of the 16 rats, and at 2 hour during the ischemia, the rats in the hypertension and mild hypothermia group were treated with hypertension for 3 hours and mild hypothermia, respectively, and those in the combined therapy group received both treatment. The rats in the control group received no treatments for ischemia and reperfusion. Twenty-four hours later, all rats were killed for examination.MAIN OUTCOME MEASURES: The scores of neurological deficits, infarct volume and degree of BBB damage.RESULTS: The scores for neurological deficits, infarct size and volume of Even' s blue staining were 2. 12 ±0. 54, (17.65 ±4.78)%, and(56.63± 10.70) mm3, respectively, in hypertension group, and 2. 14 ±0.69,(16. 21 ± 3.79)%, and(53.52 ± 8.44) mm3 in mild hypothermia group,and 1.78 ±0. 61, (11, 31 ±3.64)%, and 38.45 ±5.25 mm3 in combined therapy group, which were all decreased significantly as compared with the control group[2.70 ±0. 64, (28.34 ±4. 13)%, and(94.87 ± 15.34) mm3].The combined therapy group had the smallest infarct size and volume of Even's blue staining among the three treatment groups( P ＜ 0.05).CONCLUSION: Hypertension and mild hypothermia may reduce the infarct volume and alleviate BBB damage during focal cerebral ischemia and reperfusion in rats, and the effects of combined treatment are more obvious.

Objective To evaluate the effects of TMS on the brain plasticity and functional outcome after cerebral infarction in rats. Methods Twenty-four male Sprague-Dawley rats were divided randomly into a model group and a TMS group. The rat models of focal cerebral infarction were established with unilateral middle cerebral artery (MCA) suture occlusion method. The rats of TMS group were given additional 4 weeks of TMS treatment commenced at!1 day after infarction (2 times per day, 30 pulses per time), while those in the control group were reared in their original living state. Synaptic substructure in the sensori-motor cortex area was assessed morphologically and quantitatively. Results When compared with the model group, the rats in the experimental group had a significant improvement in terms of their neural functions (P