Objective To explore the characteristics and significance of functional connectivity (FC) of affective network (AN) in patients with postpartum depression (PPD) under resting state. Methods A total of 23 patients with PPD (PPD group) and 28 healthy postpartum women (control group) were examined using resting-state fMRI. As two critical nodes of AN, amygdala (AMYG) and subgenual anterior cingulate cortex (sgACC) were selected as the regions of interest (ROI) to analyze the differences of functional connectivity strength (FCS) of two regions from other brain regions between two groups, followed by Pearson correlation analysis on the abnormal FCS and the Edinburgh postnatal depression scale (EPDS) score in PPD group. Results Compared to the control group, the patients in PPD group showed the extensively reduced FCS (P<0.05, Alphasim correction) between AMYG and frontal cortex, temporal cortex, hippocampus, cerebellum and orbitofrontal cortex, while there were enhanced FCS (P<0.05, Alphasim correction) between sgACC and parietal cortex, occipital cortex, thalamus, superior temporal gyrus and cingulate cortex. Moreover, in PPD group, the reduced FCS between left AMYG and left medial orbitofrontal cortex was negatively correlated with EPDS scores (r=-0.62, P=0.02). Conclusion Patients with PPD have dysfunctional connectivity of AN in multiple brain regions. The weaker FCS between left amygdala and left medial orbitofrontal cortex is, the more severe depression. The dysfunctional connectivity of AN may provide an effective mechanism-based biomarker underlying PPD.

BACKGROUND:Ola rats is a kind of rats with genovariation, who displays Wallerian degeneration after peripheral neuroaxonal damage that is slower than that normal 6J rats, thereby additional damage factor may help fully understand the property of Ola rats.OBJECTIVE: To observe the effect of acrylamide on the degeneration and regeneration of sciatic nerve medullated fibers following crush injury of C57BL/Ola (Ola) rat and C57BL/6J (6J) rat.DESIGN: Randomized controlled experiment.SETTING: Department of Neurology,Second People's hospital of Shenzhen; Department of Neurology of First hospital of Jilin University MATERIALS: This experiment was carried out in the neurological department in the University of Occupational and Environmental, Japan from January to June 1996. Twelve adult Ola rats and 6J rats were adopted and evenly randomly divided into experimental group and comparison group.METHODS: Rats were subjected to general anaesthesia, and then the proximal section of sciatic nerve was exposed and frustrated with hemostatic forceps for 10 s before suture. Rats in the experimental group were given intraperitoneal injection of acrylamide in a total dosage of 350 mg, which replaced by the same volume of physiological saline in comparison group.At 14 days after sciatic nerve torsion injury, all rats were anaesthetized again and the distal section of sciatic nerve was obtained and cut into slices, meanwhile the cross sectional area, the density and size frequency distribution of medullated fibers, as well as the number of medullated fibers in each nerve were determined.MAIN OUTCOME MEASURES: The density and size frequency distribution of sciatic nerve medullated fibers, as well as the number, the maximum diameter and the mean diameter of medullated fibers in two group of 0la rats and 6J rats.RESULTS: Totally 12 Ola rats and 6J rats entered the result analysis.① No Ola rat displayed Wallerian degeneration; But medullated fiber degeneration and following neonatal small diameter medullated fibers could be observed in 6J rats. ②In the experimental group, the total density of sciatic nerve medullated fibers in 6J rats was lower than that of Ola rat (P ＜ 0.05) ;with the total number of medullated fibers in 6J rats also less than that of Ola rat (P ＜ 0.01 ), which predominated by obviously reduced big diameter fibers (P ＜ 0.01); The mean diameter of medullated fiber in 6J rats was also obviously smaller than that of 0la rat (P ＜ 0.01 ).CONCLUSION: The Wallerian degeneration is extremely slow in Ola rat after torsion injury, which cannot be affected by acrylamide; while acrylamide has obvious inhibition on the axonal neogenesis in 6J rat after torsion injury.

BACKGROUND: Vascular endothelial growth factor (VEGF) can accelerate neovascularization and, as a multifunctional cytokine, performs critical functions via its receptors in angiogenesis.OBJECTIVE: To investigate the expression of VEGF and its receptor FLT-1 and FLK-1 mRNA during the early stage of acute focal cerebral brain ischemia, and examine the relationship between the timing and location of their expressions.DESIGN: Randomized controlled study.SETTING: Department of Neurology of the First Hospital Affiliated to Jilin University and Teaching and Research Section of Pathology, Bethune Medical College of Jilin University.MATERIALS: This study was carried out between June 2001 and April 2002. Totally 130 adult SD rats were selected, with male and female in half, and randomly divided into normal control group (n=10), sham operation group (n=10), and cerebral ischemia group (n=110). The rats in cerebral ischemia group were further divided equally into 11 subgroups and examined at 0, 1, 2, 3, 6, 24, 48 hours and 1, 2, 3, 4 weeks after cerebral ischemia model establishment, respectively.METHODS: Permanent middle cerebral artery occlusion (MCAO) model was established in rats in cerebral ischemia group by ligation of the left common carotid artery, while the rats in the sham operation group received no artery ligation but with identical other treatments. The rats in the control group did not have any treatment. Reverse transcriptional (RT) PCR was used to detect the expression of VEGF and its receptor mRNA at different time points after ischemic model establishment, and neovascularization in the rats'brain was observed.MAIN OUTCOME MEASURES: ① Expression of VEGF and its receptor mRNA and ② neovascularization in the brain tissue at different time points of cerebral ischemia.RESULTS: Data of the 130 mice were statistically analyzed without losses.At 3, 6, 24, and 48 hours of ischemia, the number of cells positive for VEGF expression was 31.13±2.21, 43.11±2.43, 85.41±2.75 and 98.66±1.76 in each vision filed in the surrounding ischemic region, greater than the numbers in the central ischemic region at the corresponding time points (13.32±1.31, 19.40±3.22, 47.63±2.45, 57.32±3.35 in each vision field, respectively, P ＜ 0.05). VEGF mRNA expression gradually decreased since 48 hours after model establishment till recovering the control level by 2weeks. The expression of VEGF receptor FLT-1 mRNA, determined by the number of positive cells in each vision field at 3, 6, 24, and 48 hour after the ischemia in each vision field for FLK-1 mRNA at these time points in the peripheral ischemic regions, higher than those in the central ischemic regions (P ＜ 0.05), which recovered the control level 3 weeks after the ischemia (P ＜ 0.05). At 48 hours and 1 week after the ischemia, the number of microvessels in each vision field was 47.2±2.11 and 199.2±3.45 in the peripheral ischemic region, significantly higher than the number in the central ischemic region (29.4±2.37 and 76.6±4.62, P ＜ 0.05).CONCLUSION: VEGF and its receptors FLT-1 and FLK-1 mRNA are expressed in the neurons, glial cells and endothelial cells during the early stage of acute focal cerebral ischemia, and the expressions are significantly enhanced in response to ischemia, exhibiting temporal and spatial expression patterns.

OBJECTIVETo investigate the etiology, pathology, and mechanism of pathogenesis of Moyamoya disease.

METHODSA total of 15 human autopsies were analyzed. In addition, in order to create an animal model of the disease, 21 Japanese rabbits were divided randomly into two groups and subjected to injections of horse serum either intravenously or locally in the area of the sympathetic ganglia. Pathological and immunohistochemical characteristics were observed.

RESULTSThe pathological features of the autopsies and the animal models both involved intima hyperplasia and stenosis or even occlusion of the lumen in the terminal ends of the internal carotid artery and the anterior and middle cerebral arteries. Disconnections or even breakages of the inner layer of the lumen were also observed, without an obvious inflammatory response. Hyperplasic smooth muscle cells of the medial membrane had extended inward through broken portions of the internal elastic lamina, with intima cell hyperplasia resulting in lumen stenosis. The hyperplastic vascular walls were positive for IgG and IgM.

CONCLUSIONSThe etiology of Moyamoya disease may involve allergic angiitis. A possible mechanism is that proximal portions of the circle of Willis first develop chronic stenosis or occlusion, leading to compensatory small vessel proliferation, which perforates into the cerebral parenchyma.

Adolescent ; Adult ; Animals ; Carotid Artery, Internal ; pathology ; Child ; Humans ; Hyperplasia ; Male ; Middle Aged ; Middle Cerebral Artery ; pathology ; Moyamoya Disease ; etiology ; pathology ; Rabbits ; Tunica Intima ; pathology

OBJECTIVETo explore the changes of brain energy metabolism following acrylamide (ACR) poisoning.

METHODSCreatie kinase (CK), adenosine triphosphate (ATP), adenosine diphosphate(ADP), adenosine 5'-monophosphate(AMP) and glucose contents in brain were observed in O1a mice and 6J mice following ACR intoxication by enzyme analytical method.

RESULTSATP, CK and glucose levels decreased transiently in O1a mice, while ATP level in 6J mice was significantly decreased (1.76 mumol/g, P < 0.01), as compared to the control (2.53 mumol/g) but ADP and AMP were increased, glucose was decreased. The activity of CK in poisoned group (1.13 mumol/g, P < 0.01) was lower than that of control (3.16 mumol/g and lasted for 5 weeks).

CONCLUSIONThe influence of ACR on O1a mice was slight and reversible but on 6J mice was severe and lasting. There was severe damage to the potential energy supply compensation, which might be the biochemical basis of neuron damage induced by acrylamide.

Acrylamide ; poisoning ; Adenosine Triphosphate ; analysis ; Animals ; Brain ; drug effects ; metabolism ; Creatine Kinase ; analysis ; Energy Metabolism ; drug effects ; Glucose ; analysis ; Mice

Objective To investigate the relationship between axon degeneration of Goll’s column system and Amyloid ? protein (A?) deposit sludge. Methods A? protein deposition in area of axon degeneration of Goll’s columns was measured by using immunohistochemical method.Results There was found strong positive round like A? deposit in the area of axon degeneration of Goll’s column system of GAD mouse. Spheroid appeared in the area of medullar nucleus of the Goll's column system at an age of 4 weeks. However the A? was negative and 9 weeks later, it became positive in partial spheroid and formed a strong round like material and became more and more standing up with age increase. The material mentioned above appeared consistently progressive in degeneration of axon in sequence.Conclusion It was suggested that the deposition of A? should be the result secondary to degeneration of nervous axon and be closely correlated with axon degeneration.

Objective　To observe the differential pathological changes in Purkinje cells of the cerebellum in Ola mice and 6J mice after acrylamide intoxication. Methods　Purkinje cells were studied by light microscope and electron microscope. Results　Under light microscope,Purkinje cells in 6J mice were densely stained and irregular in cell shape.Under electron microscope,parts of the plasma membrane projection containing some smooth tubular endoplasmic reticula were found occasionally,and the membrane became split and thickened.These abnormal changes were not found in Ola mice. Conclusion　Acrylamide intoxication may induce pathological changes in Purkinje cells of 6J mice which may be the pathological basis of ataxia.

Objective　To observe the differential pathological changes in Purkinje cells of the cerebellum in Ola mice and 6J mice after acrylamide intoxication. Methods　Purkinje cells were studied by light microscope and electron microscope. Results　Under light microscope,Purkinje cells in 6J mice were densely stained and irregular in cell shape.Under electron microscope,parts of the plasma membrane projection containing some smooth tubular endoplasmic reticula were found occasionally,and the membrane became split and thickened.These abnormal changes were not found in Ola mice. Conclusion　Acrylamide intoxication may induce pathological changes in Purkinje cells of 6J mice which may be the pathological basis of ataxia.

Objective :To observate the axon changes in pathology of Ola mice,compared with those of 6Jmice. Methods:The peroneal nerve and sural nerve were studied by light-microscope and electronmi-croscope. Results :In light-microscope,the total transverse fascicular area was significantly large ;density ofmyelinated fibers was significantly less;the maximal diameter of myelinated fibers was significantly less;minimal diameter of myelinated fibers had no changens in 6J mice. The Ola mice were nomal. In electronmi-croscope observation, the neurofilament was accumulated within axons. Conclusion: In Ola mice treatedwith ACR,the like-Wallerian degeneration wes delayed. However,in 6J mice the neurofilament and mito-chondria accumulation was found within axons.

Objective To invectigate the etiology and pathogenesis of intracranial aneurysm. Methods Four experimental animal models of intracranial aneurysm were established with normal horse serum injected into veins or the neck regions, or into both common carotid arteries which were narrowed, by using silk ligature or noradrenalin injection into the neck regions. Results Ten intracranial aneurysms were found in the experimental animal model.Conclusion The immunological response,arteryischemia and continuous vasospasm may be considered the direct pathogenic factors of the intracranial aneurysm.