Objective To explore the pathological changes of the middle-small arteries and veins of uremic patients in early stage.Methods Forty patients with chronic kidney disease at Ⅴ stage were randomly subjected in our study.Radial artery and cephalic vein about 0.5 to 1 cm in length were obtained by arteriovenous fistula operations.Cephalic veins from 4 trauma patients were taken as control group.Immunohistochemisty with anti-?-SMA(smooth muscle actin-alpha),BMP-2(bone morphology protein-2) and BMP-7(bone morphology protein-7) antibodies,alizarin Bordeaux staining,HE staining and Masson trichrome staining were carried out to investigate calcification and fibrosis.Results Compared with control group,the expressions of ?-SMA and BMP-2 were up-regulated obviously.Masson trichrome staining indicated fibrosis in the vein from uremic patients.Conclusion Fibrosis may be one of the early pathologic changes in the vein from uremic patients,suggesting the venous alterations may be related to cardiovascular disease of uremic patients.

It is a difficult problem of forensic medicine to accurately estimate the post-mortem interval. Entomological approach has been regarded as an effective way to estimate the post-mortem interval. The developmental biology of carrion-breeding flies has an important position at the post-mortem inter-val estimation. Phorid flies are tiny and occur as the main or even the only insect evidence in relatively enclosed environments. This paper reviews the research progress of carrion-breeding phorid flies for esti-mating post-mortem interval in forensic medicine which includes their roles, species identification and age determination of immatures.

Rapid on site evaluation (ROSE) technology of interventional pulmonology includes“cytological ROSE”(C-ROSE) and“microbiological ROSE”(M-ROSE). Recently, this“ROSE”has gradually become one of core technologies in modern interventional pulmonology. In this commentary, perspectives on origin and development, classification and clini-cal value, operational approach, clinical application, and how to carry out effective work related to ROSE were summarized and remarked.

G protein-coupled estrogen receptor(GPER), as a newly discovered estrogen membrane protein-coupled receptor, has attracted much attention in endocrine metabolism research in recent years.Abnormal glucose and lipid metabolism and imbalance of inflammatory response mediated by GPER is one of the pathogenesis mechanisms of various endocrine and metabolic diseases.GPER is expected to become a new drug target for the treatment of coronary atherosclerosis, obesity and diabetes.This article briefly reviews the progress of GPER-mediated estrogen signaling pathway in terms of glucose metabolism, lipid metabolism and inflammation.

Objective To observe the developmental changes of projection and termination of proprioceptive afferent fibers in the mouse spinal cord. Methods Parvalbumin (PV) immunohistochemistry was used to label the proprioceptive afferents. Single and dual immunofluorescence histochemistry were used to examine the growth pattern of proprioceptive afferents and their relationships with motoneurons in the spinal ventral horn (VH). The stained sections were observed under a confocal laserscanning microscope. Results PV-like immunoreactive (LI) proprioceptive fibers first appeared in the dorsal column on embryonic (E) day 14, then entered the gray matter on El5 and reached the intermediate gray matter and VH more obviously on E16. The number and intensity of PV-LI proprioceptive afferent fibers and punctata increased in the VH with age and reached a maximum during earlier postnatal (P) period (P0-P7). After P14, the number and intensity of proprioceptive afferents gradually decreased. The proprioceptive terminals seemed to form close relationship with motoneurons from E17. Conclusion The present study indicates that the somatotopic organization of proprioceptive afferents in the spinal cord is established during the late embryonic and early postnatal stages. These results provide evidence for understanding the development of the reflex movements.

The present study was designed to examine the developmental changes in projection and termination of nociceptive and proprioceptive afferent fibers in the spinal cord by labeling those two fibers with calcitonion gene-related peptide (CGRP) and parvalbumin (PV)separately in mouse embryos and neonatal pups aged embryonic day 15 to posanatal day 3 (E15 -P3). CGRP-like immunoreactive (LI)nociceptive fibers first appeared in the superficial dorsal horn (DH) at E16. The afferent projections extended laterally to the DH and entered into the deep portions of the DH at E17 and E18. After birth, the projection pattern of CGRP-LI fibers remained unchanged but the intensity of afferent terminals increased in the superficial laminae and their branching patterns became more complicated. In addition,CGRP-LI collaterals that projected into the contralateral DH were also examined after E16. Around birth, the contralateral projections were also found originated from the lateral part of the DH. PV-LI proprioceptive afferents were first observed entering the gray matter at E15 and reached the intermediate gray matter (IG) and the ventral horn (VH) more obviously on E16. The number and intensity of PV-LI fibers increased in the the VH with age and reached a maximum during earlier postnatal period ( P0-P3 ). The proprioceptive terminals seemed to form close relationship with motoneurons in the VH from E17. Our results indicate that the somatotopic organization of nociceptive and proprioceptive afferents in the spinal cord both are established during the late embryonic and early postnatal stages. These results help to understand the development of the sensory transmission in more details.

Epidemiologic Studies ; Humans ; Indium ; toxicity ; Occupational Diseases ; epidemiology ; Occupational Exposure ; adverse effects

Dental Implants ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; pharmacology ; Osteogenesis ; Prostheses and Implants ; Simvastatin ; pharmacology ; X-Ray Microtomography

Objective To establish a multi-drug resistant model of temporal lobe epilepsy,and to observe the changes of γ-aminobutyric acid (GABA) receptor expression in the hippocampal tissues so as to explore its effects in pharmacoresistant epileptogenesis.Methods One hundred rats were selected to prepare the amygdaloid kindled model of epilepsy by chronic stimulation of amygaloid basal lateral nucleus.After the kindled model of epilepsy was prepared successfully(n =52),pharmacoresistant epileptic rats were selected according to their response to the phenobabital and phenytoin.The selected pharmacoresistant epileptic rats (n =8)were sacrificed and the hippocampus was removed to determine the GABA receptor expression,and the same number of pharmacosensitive epileptic rats was used as control.Results The pharmacoresistant epileptic rats displayed degenerative and necrotic hippocampal neurons.The arrangement of hippocampal neurons was disordered,and the structural characteristics of the arrangement of the hippocampal neurons disappeared.The gray values of GABAA-positive neurons in the hippocampal tissues (141.15 ± 14.72) increased significantly compared with the pharmacosensitive epileptic rats (92.56 ± 5.17; t =3.380,P =0.006).Western blot method demonstrated that the band of GABAA became narrowed and thin.The relative quantity of GABAA in the hippocampal tissues (0.38 ± 0.08) decreased significantly as compared with the pharmacosensitive epileptic rats (0.88 ± 0.18).A significant difference was observed (t =5.420,P =0.002).Conclusions GABA receptor expression might be decreased in the hippocampal tissues of pharmacoresistant epileptic rats.It might play a certain role in the formation of pharnmacoresistant epilepsy.

BACKGROUND: Adhesion molecules are closely associated with inflammation. Inflammation due to white blood cell (WBC) infiltration and free radical injury following brain ischemia are believed to be important factors contributing to the pathogenesis of multi-infarct dementia.OBJECTIVE: To determine the level of serum adhesion molecules and free radicals in patients with multi-infarct dementia to explore the relationship between their levels and multi-infarct dementia.DESIGN: A case-control trial.SETTING: Department of Neurology, Second Affiliated Hospital of Jilin University.PARTICIPANTS: Totally 82 patients with multi-infarct dementia were hospitalized in the Department of Neurology, Second Affiliated Hospital of Jilin University between January 2000 and December 2004. These patients included 32 cases of mild dementia, 21 of moderate dementia, and 29 of severer dementia. The normal controls were 23 concomitant healthy volunteers who came for routine physical examination.METHODS: Enzyme-linked immunosorbent assay (ELISA) and electron spin resonance were used to determine the level of serum soluble intercellular adhesion molecules (ICAM) and vascular cell adhesion molecules (VCAM), as well as oxygen free radical concentration in the normal controls and patients with multi-infarct dementia, and the association between the severity of the illness and the levels of adhesion molecules and oxygen free radicals was analyzed.MAIN OUTCOME MEASURES: Serum levels of ICAM-1 and VCAM-1 and oxygen free radical concentration in the two groups.RESULTS: Totally 82 patients with multi-infarct dementia and 23 healthy controls were included in this study and all enter the result analysis. In multi-infarct dementia patients, the serum levels of soluble ICAM-1 and VCAM-1 and oxygen free radical concentration [(469.00±76.33), (196.00± 45.91) and (1 103.30±98.96) μg/L, respectively] were significantly higher than those of the control group [(601.00±76.30), (4.018±1.656), and (1.295±0.718) μg/g, respectively, t=5.517-6.754, P ＜ 0.01], and the 3 indices were positively correlated with the severity of dementia (r=0.659 4,r=0.697 2, r=0.649 4, respectively, P ＜ 0.05); serum ICAM-1 and VCAM-1 levels were positively correlated with the concentration of oxygen free radicals (r=0.714 7, r=0.732 4, respectively, P ＜ 0.01).CONCLUSION: Serum ICAM-1, VCAM-1 and oxygen free radicals might be implicated in the pathophysiological development of multi-infarct dementia, and their levels increase in parallel with the severity of dementia.