Objective To get more diagnostic informa ti on from the acute cerebral infarct, We used1HMRS and TCD to investigate the r elationship between the metabolites in the infarct, the infarct volume, blood f low velocity and blood flow to the infarct, and the clinical neurologic deficit. MethodsFifteen patients with acute cerebral infarct underwent1HMRS and TCD examinations. Clinical neurologic deficit score was c ollected from every patient record at the time of the1HMRS and TCD study. Inf arct volume (V/ml) was determined with machine software automatically. A PRESS a cquisition was used for1HMRS. The peak areas of N,Lac,Cr,Cho in the lesi on region were compared with those in the contralateral side. TCD was performed for measuring Vs, Vm of encephalic blood vessels on both sides, and the responsi ble cerebral blood flow was estimated by Vs. ResultsT here were significant decrease of N,Cr,Vm and ECBF in the lesion region when c ompared with the contralateral side( P

Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg(-1)·mL(-1)) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression.

Objective To evaluate the clinical efficacy and safety of different full spectrum light times in treating patients with Alzheimer's disease (AD).Methods A total of 127 AD patients with sleep disorder were randomly divided into a blank group (n=34),a 30 min group (n=31),a 60 min group (n=33) and a 120 min group (n=29).After one month treatment by 10 000 lux full spectrum fluorescent light,the improvements of sleep quality,excessive daytime sleepiness,cognitive ability,mental state,dementia degree were graded by Pittsburgh sleep quality index (PQSI),Epworth sleepiness scale (ESS),Neuropsychiatric inventory (NPI),mini-mental state examination (MMSE),global deterioration scale (GDS).The scores were compared among the groups before the treatment and after the treatment respectively.Results (1) Compared with before treatment,the scores of PQSI,ESS,NPI of the 30 min group,60min group and 120min group were statistically significant (in 30 min group 14.4 ±5.2vs 11.7±4.9,14.4±4.1 vs 11.8±3.7,14.2±1.3 vs 10.9±1.7,t=2.071,2.609,8.446.P=0.043,0.011,0.000; in 60 min group13.4±4.0 vs 8.1±3.7,14.5±3.0 vs 9.4±2.0,13.7±5.8 vs 8.7±4.3,t=5.650,8.209,3.902,all P＜0.01 ;in 120 min group 14.0±3.2 vs 7.0±2.3,14.7-±2.3 vs 7.0± 1.9,14.9±3.6 vs 8.1±3.7,t=9.474,13.926,7.062,all P＜0.01),but the scores of MMSE,GDS were not statistical significances(all P＞0.05).(2)Compared with the blank group,the scores of PQSI,ESS,NPI of 30 min group,60 min group and 120 min group were statistically significant (30 min group t=1.936,4.524,2.482,P=0.031,0.000,0.016.60 min group t=5.945,5.153,7.319,all P=0.000.120 min group t=7.896,6.767,10.776,all P=0.000), but the scores of MMSE,GDS were not statistical significances(all P＞0.05).(3)Compared with the 30 min group,the scores of PQSI,ESS,NPI of 60 min group and 120 min group were statistically significances (60 min group t =3.288,2.694,3.354,P=0.002,0.009,0.001.120 min group t=4.615,3.930,6.303,all P =0.000),the scores of MMSE,GDS were not statistical significances (all P＞0.05).Compared with the 60 min group,the scores of ESS of 120 min group was statistically significant(t=4.854,P=0.000),but the scores of PQSI,NPI,MMSE,GDS were not statistical significances (all P ＞ 0.05).Conclusion It is demonstrated good curative effects that light therapy treat patients on AD patients in the matter of sleep quality,excessive daytime sleepiness,mental state,but have not apparent effect for their cognitive ability and dementia degree.And the effect of light therapy with 60 or 120 minutes is better than that of 30 minute,illumination time of 120 minutes is superior to that of 60 minutes in improving excessive daytime sleepiness.Light therapy has no obvious impacts in the cognitive ability and the degree of dementia in the patients with AD and has not appear obvious adverse reaction in the process of treatment.

Objective To evaluate the capability of Turbo inversion recovery magnitude (TIRM) magnetic resonance neurography (MRN) in the diagnosie of sacral plexus injury by comparing MRN findings with surgical results.Methods Ten patients with sacral plexus injury confirmed surgically underwent conventional T1WI,T2WI,TIRM and coronal TIRM MRN before operations from June,2011 to December,2012.The MRI data and surgical data were analyzed retrospectively to observe nerve injury.Results The coronal TIRM MRN images displayed 93 trunks of sacral plexus,of which 37 were confirmed injury by operation.The MRI findings were as follows:6 trunks involved continuous nerves,but with thickening and blurred margin,as well as abnormal high signal intensity;22 trunks were continuous,but with distortion,stiffness and adhesion accompanied by heterogeneous signal intensity and structural disorder;3 trunks showed complete loss of continuity,absence of normal signal,accompanied by retraction;and 3 trunks involved formation of traumatic neurofibroma.The coincidence of injured nerve trunks diagnosed by MRN with surgical findings amounts to 81.08％ (30/37).Conclusion MR with coronal TIRM imaging is effective in the diagnosis and depiction of sacral plexus injury,therefore it can be used as conventional sequence in sacral plexus examination to detect sacral plexus avulsion.

BACKGROUND:hIL-24, a tumor suppressor gene, can stimulate immune responses, inhibit the growth of tumor cel s, and the formation of tumor vessels, and induce cel apoptosis. OBJECTIVE:To explore the effects of hIL-24 gene on the proliferation and apoptosis of fibroblasts in the keloid and the underlying mechanisms. METHODS:Al the keloid specimens col ected from 13 patients were used for fibroblast culture and indentification. Fibroblast of the keloid was transfected with or without hlL-24 lentivirus. Subsequently, mRNA expressions of transforming growth factor-β, Smad3, proliferating cel nuclear antigen, matrix metal oproteinase-2,-9, and metal opeptidase inhibitor 1 were determined. RESULTS AND CONCLUSION:Immunofluorescent staining and flow cytometry showed that vimentin antibody was expressed positively in cytoplasma of fibroblast cultures, and the purity was more than 97.8%. Western blot assay showed that hIL-24 expression was significantly increased in the transfected fibroblasts. Quantitative PCR showed that the overexpression rate of hIL-24 in fibroblasts was 81.7%and mRNA expressions of transforming growth factor-β, Smad3, proliferating cel nuclear antigen, matrix metal oproteinase-2, and-9 were significantly decreased, while metal opeptidase inhibitor 1 mRNA expression was significantly increased in hIL-24 transfection group compared with control group (P<0.05). These findings suggest that hIL-24 gene inhibits the expressions of proliferating cel nuclear antigen, matrix metal oproteinase-2, and-9 in fibroblasts, and the underlying mechanism may involves TGF-β/Smad3 pathway.

Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg(-1)·mL(-1)) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression.
Animals ; Brain Ischemia ; metabolism ; Disease Models, Animal ; Granulocyte Colony-Stimulating Factor ; metabolism ; Hyperlipidemias ; metabolism ; Male ; Neuroprotective Agents ; metabolism ; Rats ; Rats, Sprague-Dawley

Objective: : EID3 (EP300-interacting inhibitor of differentiation) was identified as a novel member of EID family and plays a pivotal role in colorectal cancer development. However, its role in glioma remained elusive. In current study, we identified EID3 as a novel oncogenic molecule in human glioma and is critical for glioma cell survival, proliferation and invasion. Methods: : A total of five patients with glioma were recruited in present study and fresh glioma samples were removed from patients. Four weeks old male non-obese diabetic severe combined immune deficiency (NOD/SCID) mice were used as transplant recipient models. The subcutaneous tumor size was calculated and recorded every week with vernier caliper. EID3 and AMP-activated protein kinase α1 (AMPKα1) expression levels were confirmed by real-time polymerase chain reaction and Western blot assays. Colony formation assays were performed to evaluate cell proliferation. Methyl thiazolyl tetrazolium (MTT) assays were performed for cell viability assessment. Trypan blue staining approach was applied for cell death assessment. Cell Apoptosis DNA ELISA Detection Kit was used for apoptosis assessment. Results: : EID3 was preferentially expressed in glioma tissues/cells, while undetectable in astrocytes, neuronal cells, or normal brain tissues. EID3 knocking down significantly hindered glioma cell proliferation and invasion, as well as induced reduction of cell viability, apoptosis and cell death. EID3 knocking down also greatly inhibited tumor growth in SCID mice. Knocking down of AMPKα1 could effectively rescue glioma cells from apoptosis and cell death caused by EID3 absence, indicating that AMPKα1 acted as a key downstream regulator of EID3 and mediated suppression effects caused by EID3 knocking down inhibition. These findings were confirmed in glioma cells generated patient-derived xenograft models. AMPKα1 protein levels were affected by MG132 treatment in glioma, which suggested EID3 might down regulate AMPKα1 through protein degradation. Conclusion : Collectively, our study demonstrated that EID3 promoted glioma cell proliferation and survival by inhibiting AMPKα1 expression. Targeting EID3 might represent a promising strategy for treating glioma.

Objective To investigate the expression change and their clinical role of triggering receptor expressed on myeloid cells-1 (TREM-1) in patients with severe thoracic trauma.Methods A prospective cohort study was conducted to analyze the clinical data of 52 patients with severe thoracic trauma (trauma group) hospitalized from October 2016 to May 2017.The peripheral anticoagulant blood samples were collected at days 1,3,5,7 and 14 after trauma.Meanwhile,10 healthy volunteers were enrolled in control group and their blood samples were collected once.According to injury severity score (ISS),the patients were divided into ISS low-score group (＜ 20 points,n =15) and high-score group (≥20 points,n =37).The patients were assigned to traumatic non-sepsis group (n =34) and traumatic sepsis group (n =18) by the latest definition and standard of sepsis 3.0 issued by the Society of Critical Care Medicine (SCCM)/European Society of Intensive Care Medicine (ESICM).The expressions of TREM-1 on neutrophils and monocytes were measured by flow cytometry.Pairwise comparisons were done between trauma group and healthy volunteers,ISS low-score group and ISS high-score group,and traumatic sepsis group and non-sepsis group,respectively.The accuracy of traumatic sepsis prediagnosis by TREM-1 was evaluated by the area under receiver operating characteristic curve (AUC).Results Trauma group had 41 males and 11 females,with age of (45.9 ± 12.4) years,Abbreviated Injury Scale (AIS) of (3.5 ± 0.6) points and Injury Severity Score (ISS) of (23.6 ± 8.5) points.Control group had eight males and two females,with the age of(29.1 ± 2.8) years.Compared to control group,trauma group had slightly lower TREM-1 expressions in neutrophils and significantly higher expressions in monocytes at days 1 to 14 (all P ＜ 0.01).ISS high-score group had slightly lower TREM-1 expressions in neutrophils than ISS low-score group at days 1 to 7,with significant difference at day 1 (P ＜ 0.05).ISS high-score group had slightly higher TREM-1 expressions in monocytes than ISS lowscore group at days 1 to 14,with significant difference at day 14 (P ＜ 0.05).Compared to traumatic non-sepsis group,traumatic sepsis group had significantly lower TREM-1 expressions in neutrophils at days 1 to 14 (all P ＜ 0.05).Traumatic sepsis group had slightly lower expressions in monocytes than traumatic non-sepsis group at days 1 to 7,with significant difference at day 3 (P ＜ 0.05).AUC and 95％ CI evaluating the role of neutrophils TREM-1 in traumatic sepsis prediagnosis were 0.852 (0.738,0.966) at day 1,0.835 (0.721,0.948) at day 3,0.797 (0.654,0.939) at day 5,0.756 (0.599,0.914) at day 7,and 0.707 (0.525,0.888) at day 14,respectively.Conclusions After severe thoracic trauma,the expressions of TREM-1 are decreased in neutrophils but increased in monocytes.TREM-1 might be used to assess the injury severity and has certain value in prediagnosis for traumatic sepsis.

Objective: To investigate the therapeutic effect of free superficial circumflex iliac artery perforator (SCIP)flap for reconstruction of soft tissue defects secondary to resection of retromolar and lateral buccal squamous cell carcinoma. Methods: From January 2014 to January 2017, eight patients with retromolar and lateral buccal squamous cell carcinoma received radical resection and reconstructed with SCIP flap immediately. CTA and color Doppler sonography were routinely performed before the surgery. According to the size of the defect in the recipient area, the flap vascularized by the perforator vessel was carefully prepared and transferred to the buccal-pharynx-palate composite defect. The recipient area and donor area were sutured tightly after arteriovenous anastomosis under microscope. The survival and functional recovery of the flap were observed after operation. Results: The flap sizes ranged from 5 cm× 6 cm to 7 cm×9 cm.The mean diameter of the superficial circumflex iliac arteries was 0.65 mm. And the mean diameter of the veins was 1.2 mm. The mean arterial pedicle length was 7.0 cm, and the venous pedicle length was 8.0 cm. Eight flaps were all survived. The shape of the buccal-parapharyngeal-palate was good and the mouth opening was normal after operation. Conclusions Superficial circumflex iliac artery perforator flap was a good choice for repairing the defect of parapharyngeal squamous cell carcinoma in the posterior molar region.

The clinical application of doxorubicin (DOX) in cancer chemotherapy is limited by its life-threatening cardiotoxic effects. Chrysophanol (CHR), an anthraquinone compound isolated from the rhizome of L., is considered to play a broad role in a variety of biological processes. However, the effects of CHR׳s cardioprotection in DOX-induced cardiomyopathy is poorly understood. In this study, we found that the cardiac apoptosis, mitochondrial injury and cellular PARylation levels were significantly increased in H9C2 cells treated by Dox, while these effects were suppressed by CHR. Similar results were observed when PARP1 activity was suppressed by its inhibitors 3-aminobenzamide (3AB) and ABT888. Ectopic expression of PARP1 effectively blocked this CHR׳s cardioprotection against DOX-induced cardiomyocyte injury in H9C2 cells. Furthermore, pre-administration with both CHR and 3AB relieved DOX-induced cardiac apoptosis, mitochondrial impairment and heart dysfunction in Sprague-Dawley rat model. These results revealed that CHR protects against DOX-induced cardiotoxicity by suppressing cellular PARylation and provided critical evidence that PARylation may be a novel target for DOX-induced cardiomyopathy.