Energy metabolism disorders are a critical factor contributing to cognitive dysfunction.Astrocytes,as key suppliers of energy substrates to neurons,help to sustain normal cognitive function via their extensive energy metabolism activities in the brain,coordinated by various energy supply mechanisms.Imbalances in astrocyte-neuron energy metabolism coupling lead to abnormal neuronal activity,thereby driving the pathogenesis and progression of Alzheimer's disease(AD).It is therefore essential to investigate the pathological mechanisms and therapeutic targets associated with AD from the perspective of energy metabolism to support the future development of AD treatments and interventions.Traditional Chinese medicine(TCM),characterized by multi-component and multi-target effects,has shown potential efficacy for regulating cerebral energy metabolism,suggesting that modulating brain energy metabolism may represent a significant pathway by which TCM might ameliorate AD.This review systematically elucidates the mechanistic role of the dysregulation of astrocyte-neuron bioenergetic coupling in the pathogenesis and progression of AD,and critically evaluates recent advancements in therapeutic interventions mediated by TCM.

Energy metabolism disorders are a critical factor contributing to cognitive dysfunction.Astrocytes,as key suppliers of energy substrates to neurons,help to sustain normal cognitive function via their extensive energy metabolism activities in the brain,coordinated by various energy supply mechanisms.Imbalances in astrocyte-neuron energy metabolism coupling lead to abnormal neuronal activity,thereby driving the pathogenesis and progression of Alzheimer's disease(AD).It is therefore essential to investigate the pathological mechanisms and therapeutic targets associated with AD from the perspective of energy metabolism to support the future development of AD treatments and interventions.Traditional Chinese medicine(TCM),characterized by multi-component and multi-target effects,has shown potential efficacy for regulating cerebral energy metabolism,suggesting that modulating brain energy metabolism may represent a significant pathway by which TCM might ameliorate AD.This review systematically elucidates the mechanistic role of the dysregulation of astrocyte-neuron bioenergetic coupling in the pathogenesis and progression of AD,and critically evaluates recent advancements in therapeutic interventions mediated by TCM.

Purpose To investigate the clinicopathological features,diagnosis,differential diagnosis and molecular charac-teristics desmoid fibromatosis the breast(DFB).Methods The clinicopathological data and prognostic information of 26 pa-tients with desmoid fibromatosis of the breast were collected.Their clinical characteristics,histological morphologies,immu-nophenotypes and molecular characteristics were analyzed.Re-sults All the 26 patients were female,with a median age of 34.5 years and an average age of 36.8 years(range from 13 to 69 years).There were 10 cases in left breast,14 cases in right breast and 2 cases in bilateral breast.Isolated and painless breast masses were found in all patients,and 3 cases were ac-companied by nipple depression.Grossly,most of them showed a poorly circumscribed tan-white to gray mass with a trabeculated appearance.Microscopically,all the tumors were composed of mild spindle cells with varying intervals of collagen fiber bun-dles.The boundary between the tumor and the surrounding breast tissue was not clear,and the tumor cells infiltrated adja-cent tissues,such as breast ducts,lobules,adipose tissue,and skeletal muscle.Uniform spindle or oval cells formed in fascicles and interwoven,without atypical or polymorphism;the nuclear chromatin was sparse or vacuolar,with small nucleoli,but mito-ses were rare or absent.Nuclear accumulation of β-catenin was present in 20 of 26 tumors,SMA was variously positive in 20 of 26,desmin was focally positive in 6 of 26;CKpan,CK5/6,p63,CD34,CD10 and S-100 were all negative.The Ki67 index was 5％-10％.The gene mutations of CTNNB1 exon 3 were found in 18 of 26 by Sanger sequencing,including T41A(83.3％),S45P(11.1％)and S45F(5.6％).Two patients also had familial adenomatous polyposis.Local resection was performed in 23 cases,mastectomy was performed in 2 cases,and one case did not require any additional treatment after core needle biopsy.20 cases were followed up for 1-108 months,and no recurrence occurred.Conclusion Desmoid fibromatosis of the breast is rare,and can mimic breast cancer clinically,ra-diologically and histologically.It should be always considered in differential diagnosis for the spindle cell proliferations of the breast.A diagnosis of DFB can be achieved basing on the typi-cal histopathology,immunohistochemistry,history and gene se-quencing.

OBJECTIVE To explore the mechanism of Yishen tongluo formula （YSTLF） in improving abnormal lipid metabolism based on the sterol regulatory element binding proteins （SREBPs） pathway. METHODS Using C57BLKS/J （db/db） mice as model and C57BLKS/J （db/m） mice as normal control， the mechanism of 1， 2.5 and 5 g/kg YSTLF improving abnormal lipid metabolism of db/db mice was investigated by determining the liver coefficient， the contents of serum total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein （LDL） and high-density lipoprotein （HDL）， observing steatosis and lipid accumulation in liver tissue of mice， detecting the protein expressions of SREBP-1 and SREBP-2 as well as mRNA transcription levels of Srebp- 1c， Srebp-2 and their downstream lipid metabolism-related target genes （Fasn， Acc1， Scd5， Fads1， Hmgcr， Dhcr24， Insig-1， Fdps） in liver tissue of mice. Using low-fat cultured human liver cancer cell HepG2 as an in vitro cell model for abnormal lipid metabolism， and 25-HC （SREBPs inhibitor， 10 μmol/L） as the control， the effects of 125， 250 and 500 μg/mL YSTLF on protein expressions of SREBP-1 and SREBP-2 as well as mRNA transcription of SREBP-1c， SREBP-2 and their downstream lipid metabolism-related target genes were investigated to verify the mechanism in vitro. RESULTS 1， 2.5， 5 g/kg YSTLF significantly reduced the levels of TC， TG and LDL， the percentage of lipid droplet-positive region in liver tissue and liver coefficient， significantly down-regulated protein expressions of Pre-SREBP-1， n-SREBP-1， Pre-SREBP-2 and n-SREBP-2， and mRNA transcription of Srebp-1c， Srebp-2 and their downstream target genes in liver tissue， while significantly increased HDL level， with statistical significance （P＜0.05 or P＜0.01）. In the cell experiment in vitro， the expressions of the above-mentioned proteins and genes in the cells treated with YSTLF at 125， 250 and 500 μg/mL for 24 hours were consistent with those in the animal experiment； there was no significant difference in the expressions of the above-mentioned proteins and genes between inhibitor control group and 250， 500 μg/mL YSTLF groups （P＞0.05）. CONCLUSIONS YSTLF can regulate the expression of transcription factor SREBPs， so as to inhibit the high expression of fatty acid and cholesterol synthesis-related genes， promote the degradation of TC and TG， improve the abnormality of lipid metabolism and inhibit lipid accumulation， thus playing the role of lipid-lowering.

Objective To evaluate the association between recurrent miscarriages and insulin resistance.Methods The case-control studies on the association between recurrent spontaneous abortion and insulin resistance from June 1996 to April 2012 were collected from Medline,Elsevier,Chinese Journal Fulltext Database,Chinese Biological Medicine Database,data base of Wanfang,Springer link and EMBASE.RevMan 5.1 software was used for Meta analysis.Results According to the included criteria,7 clinical trials were finally selected.Total 467 cases with recurrent pregnancy loss were enrolled in study group,while 413 women with no history of abnormal pregnancies were enrolled in control group.No significant difference was found in average age and body mass index between the two groups (P ＞ 0.05).Meta analysis results showed that the level of fasting glucose was no statistical difference between study group and control group (WMD =2.27,95％ CI:-1.11 to 5.65,P ＞0.05); fasting insulin level was higher 2.05 mU/L in study group than that of in control group,the difference was statistically significant (WMD =2.05,95％ CI:1.03 to 3.08,P ＜ 0.01).Case number of study group on Homa-insulin resistance ＞ 4.5 was more than that of control group (OR =3.36,95％ CI:1.72 to 6.57,P ＜ 0.01).Case number of study group on glucose/insulin ratio ＜ 4.5 was more than that of the control group,statistical difference was found (OR =3.37,95％ CI:1.90 to 5.99,P ＜ 0.01).Conclusion Insulin resistance is associated with the susceptibility to recurrent miscarriages,and it may contribute to the occurrence of recurrent miscarriages.

Objective To evaluate the contribution of gyrA and parE detection in Ureaplasma genotyping.Methods Sixty Ureaplasma isolates were selected with the Mycoplasma IST kit.The gyrA and parE were amplified by PCR.The DNA was sequenced and compared with the corresponding sequences in GenBank.Results The nucleotide sequence of gyrA had 100% identity in serovar 1,3,6,14 and 100%identity in serovar 2,4,5,7～13,too.But the sequence had 91%identity between the two groups.The nucleotide sequence of parE had 98%～99% identity in serovar 1,3,6,14.And it had 100% identity in erovar 2,5,7,8,11 and 100% identity in serovar4,12,13.But it had only 90% identity between the two groups.Ureaplasma parvum(Up),Ureaplasma urealyticum(Uu)and Up+Uu infection were found 68.3%(41/60),21.7%(13/60)and 10%(6/60) of clinical specimens,respectively.In Up isolates,serovar 3 was 48.8%(20/41).Conclusion Ureaplasma can be divided into two genotypes(Up and Uu)by gyrA analysis.And Up can be divided into four subtypes which correspond to serovar 1,3,6,14,respectively.Serovar 3 is the main isolate in our research.

ObjectiveTo recognize the cranial MRI appearance in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy(CADASIL). MethodsFive patients with CADASIL from two generations in a family underwent routine MRI and MRA examinations.Three patients with CADASIL were confirmed by the Notch3 genetic testing and the vascular pathological Resultsand one was diagnosed on basis of MR and clinical manifestations. The imaging data from 4 patients with CADASIL were analyzed.ResultsFour cases achieved preliminary diagnosis of CADASIL and one was excluded by MRI.In 4 patients with CADASIL,bilateral symmetrical,confluent white matter lesions in the subcortical and Deriventricular regions were seen frequently in the temporal,frontal and parietal lobes,but the occipital lobes were less involved.These lesions appeared as long T1 and long T2 signal.O'Sul]ivan sign was shown in all cases and subcortical lacunar lesions was seen in 2 cases. In the centrum semiovale,well-defined,round or oval cystic infarcts(black holes)were demonstrated in 3 cases and multiple tiny round enlarged perivascular spaces(pepperpot appearance)in all cases.The corpus callosum was involved in all cases,and it was evidently atrophic in 2 cases.The anterior part of internal capsule and external capsule were were present in the basal ganglia and brainstem. Only one case revealed a small infarct in the right cerebellum. Four Datients shared mild or moderate atrophy of brainstem, cerebellum and cerebrum. No marked abnorillalitv of large vessels was seen in all cerebral MRA. ConclusionsThe cranial MRI appearance in CADASIL shows some characteristics.MRI may give some infotznation in the preliminary diagnosis or exclusion of CADASIL.