De Jane Marcet ao visconde de Vilarinho de São Romão: conversas sobre química no século XIX / From Jane Marcet to the Viscount of Vilarinho de São Romão: conversations about chemistry in the nineteenth century

Resumo O livro de Jane Marcet Conversations on chemistry foi adaptado e publicado em português, em 1834, por António Teixeira Girão, por meio da tradução da adaptação de Anselme Payen, publicada em 1825. Nessa versão, Girão introduz grande número de notas e novo capítulo. Este artigo analisa o conteúdo científico e as circunstâncias da publicação da obra de Girão, no contexto das diversas formas em que Conversations foi adaptado em diferentes datas e países. Para isso, foi realizada uma compilação das edições acessíveis em bibliotecas públicas de todo o mundo. Na análise, são também abordadas problemáticas da autoria, tradução e adaptação, assim como questões de gênero, envolvidas na edição científica no século XIX.

Abstract Jane Marcet's Conversations on chemistry was adapted and published in Portuguese by António Teixeira Girão in 1834, based on a translation of Anselme Payen's adaptation, released in 1825. Girão added many notes and a new chapter to his version. The article analyzes the scientific content and circumstances surrounding publication of Girão's book within the context of the diverse approaches used in adapting Conversations at different moments in time and in different countries. The analysis draws from our compilation of editions accessible online at public libraries around the world. It also explores issues related to authorship, translation, adaptation, and gender in scientific publishing in the nineteenth century.

Expression of cell cycle inhibitors in canine prostate with proliferative inflammatory atrophy and carcinoma / Expressão de inibidores do ciclo celular na próstata canina com atrofia inflamatória proliferativa e carcinoma

Gene expression of CDKN1A, CDKN1B, and TP53, and immunostaining of p21, p27 and p53 were evaluated to verify the role of these cell cycle inhibitors in canine prostates with proliferative inflammatory atrophy-PIA and prostatic carcinoma-PC. Seventy samples, 15 normal, 30PIA and 25PC. Regarding number of p27 and p53 labeled cells, difference between normal and PIA and PC was observed, as well as between PIA and PC for p53. Immunostaining intensities of p21, p27 and p53 were different when comparing normal tissues to PIA and PC. Sixteen cDNA of canine prostatic FFPE tissue were subjected to RT-PCR and RT-qPCR, four normal, three PIA, and nine PC. CDKN1A mRNA was detected in four PC by RT-PCR, and it was overexpressed when compared to normal by RT-qPCR, in one PIA and six PC. CDKN1B mRNA was detected in three PC by RT-PCR and it was overexpressed in three PC and decreased in one PC. TP53 mRNA was overexpressed in one PIA and three PC. In conclusion, when overexpressed in canine prostate with premalignant and malignant, p21 and p27 play a role controlling cell proliferation, working as a protective factor in the evolution of PIA to PC, and in the PC development, even in the presence of altered p53.(AU)

A expressão gênica de CDKN1A, CDKN1B e TP53, assim como imunomarcação de p21, p27 e p53 foram realizadas a fim de verificar o papel desses inibidores do ciclo celular na próstata canina com atrofia inflamatória proliferativa (PIA) e carcinoma prostático (PC). Foram obtidas70 amostras de próstata canina, sendo 15 de tecido normal, 30 de PIA e 25 de PC. Quanto ao número de células imunomarcadas foi observada diferença entre amostras normais, com PIA e PC para p27 e p53, assim como entre PIA e PC para p53. Para a intensidade de imunomarcação houve diferença entre os tecidos normais e com PIA e PC para p21, p27 e p53. Foram obtidas dezesseis amostras de cDNA a partir de amostras de próstatas caninas embebidas em parafina para a realização da RT-PCR e RT-qPCR, sendo quatro normais, três com PIA, e nove com o PC. O gene CDKN1A foi detectado em quatro das amostras com PC por RT-PCR, e pela RT-qPCR este estava superexpresso em uma PIA e em seis PC quando da comparação com o tecido prostático normal. O CDKN1B foi detectado em três PC por RT-PCR e pela RT-qPCR estava superexpresso em três PC e reduzido em um PC. O TP53 foi detectado em todas as próstatas caninas com PIA e PC por RT-PCR, sendo também superexpresso em uma glândula com PIA e em três com PC. Concluiu-se que p21 e p27 quando superexpressas na próstata canina com lesões pré-malignas (PIA) e malignas (PC) desempenham ação no controle da proliferação celular, possivelmente atuando como fator de proteção na evolução da PIA para PC, e no desenvolvimento do PC, mesmo na presença de p53 alterada. Assim, o próximo passo é avaliar essas proteínas do ciclo celular em casos de PC canino com metástase.(AU)

Expression of EGF receptors in canine prostate with proliferative inflammatory atrophy and carcinoma / Expressão de receptores EGF na próstata canina com atrofia inflamatória proliferativa e carcinoma

ABSTRACT: Gene expression of ErbB1 and ErbB2, and immunostaining of EGFR (Her1) and Her2 (c-erbB-2) were evaluated in this study to ascertain whether these receptors are involved in the evolution of canine premalignant and malignant prostatic lesions, as proliferative inflammatory atrophy (PIA) and prostatic carcinoma (PC). With regards to the intensity of EGFR immunostaining, there was no difference between normal prostatic tissue and tissues with PIA or PC. In relation to Her2 immunostaining, there were differences between normal prostatic tissue and those with PIA and PC, as also differences between prostates with PIA and PC. There was no correlation between EGFR and Her2 immunostaining. ErbB1 gene product was detected in two normal tissue samples, in one with PIA, and in all samples with PC. ErbB2 mRNA was recorded in two canine samples with PIA, in all with PC, but was not detected in normal prostatic tissue. It was concluded that EGFR and Her2 play roles in canine PIA and PC, suggesting that those receptors may be involved in canine prostatic carcinogenesis.

RESUMO: A expressão gênica de ErbB1 e ErbB2 e a imunomarcação de EGFR (Her1) e Her2 (c-erbB-2) foram avaliadas para verificar o envolvimento desses receptores em lesões pré-malignas e malignas da próstata canina, como a atrofia proliferativa inflamatória (PIA) e o carcinoma prostático (PC). Em relação à intensidade de imunomarcação para EGFR, não houve diferença entre o tecido prostático normal e com PIA e PC. Em relação a Her2, observou-se diferença de imunomarcação entre o tecido prostático normal e aqueles com PIA e PC e entre os com PIA e PC. Não houve correlação entre EGFR e Her2. O gene ErbB1 foi detectado em duas amostras normais, uma de PIA e em todas as amostras de PC. O gene ErbB2 foi detectado em duas amostras de PIA e em todas as amostras de PC, não sendo detectado no tecido prostático normal. Conclui-se que EGFR e Her2 atuam nas lesões de PIA e PC, sugerindo o envolvimento destes na carcinogênese da próstata canina.

Plano Individual de Atendimento (PIA) na perspectiva dos técnicos da semiliberdade / The Individual Plan of Care (IPC) from the point of view of technicians who deal with semi-liberty

Este artigo apresenta uma leitura do trabalho das equipes técnicas com o Plano Individual de Atendimento (PIA). Contextualiza o PIA no cenário das medidas socioeducativas, que teve início como projeto de vida e se formalizou enquanto dispositivo previsto na Lei n. 12.594/2012. Discute-se a importância do instrumento, bem como os impasses do seu uso a partir da concepção das equipes das Casas de semiliberdade, considerando as especificidades presentes no cumprimento desta determinação judicial. Por fim, expõem-se reflexões sobre o trabalho com o PIA, propondo recursos para garantir, além da formalização, a individualização da medida do adolescente.

This article is an analysis of the work accomplished by the technical teams working with the Plano Individual de Atendimento (PIA) - Individual Plan of Care (IPC). It contextualizes IPC in the scenario of Social and Educational Procedures. IPC started as a life project, and it was formalized as a provision in Law 12.594/2012. The importance of the instrument is discussed, as well as the impasses to its use from the conceptions of the teams working at Casas de semiliberdade (Semi-liberty Houses). The specificities to abide by that judicial determination are considered. Finally, there are some thoughts about the work with IPC, and resources are proposed in order to ensure not only the formalization, but also the individualization of the teenager procedure.

Caracterização histomorfológica da atrofia inflamatória proliferativa na próstata canina / Histomorphological characterization of proliferative inflammatory atrophy in canine prostate

A atrofia inflamatória proliferativa (PIA) é uma lesão prostática pré-maligna de grande ocorrência na próstata humana e, mais recentemente, também observada em cães. Esta pesquisa teve por objetivo verificar os aspectos histomorfológicos da PIA na próstata canina. Foram utilizadas 43 próstatas de cães adultos, de várias raças e portes, e com histórico ou não de doença prostática. Os focos de PIA apresentaram epitélio displásico, formado por ácinos atróficos e com mais de uma camada de células de morfologia atípica, especialmente anisocitose, anisocariose, citoplasma reduzido, núcleo volumoso e com nucléolo evidente. As alterações epiteliais eram sempre acompanhadas de infiltrado inflamatório intersticial periacinar predominantemente linfocitário. Foi observado um índice de 65 por cento de PIA. Destes, 39 por cento corresponderam à PIA com infiltrado inflamatório discreto, 42 por cento à PIA com infiltrado moderado e 19 por cento à PIA com infiltrado acentuado. Dessa forma, foi possível caracterizar a PIA prostática canina e constatar alta ocorrência dessa alteração nos cães examinados. Considera-se de grande importância a caracterização histomorfológica da PIA em cães, já que essa lesão vem sendo estudada na próstata humana quanto ao potencial pré-maligno. Ressalta-se ainda a possibilidade de utilização da próstata do cão como modelo experimental da PIA humana, considerando a semelhança dessa afecção prostática em ambas as espécies.

Proliferative inflammatory atrophy (PIA) is a premalignant prostatic change with high occurrence in human prostate and it has been recently observed in dogs. This research aimed to verify the morphologic aspects of the PIA in canine prostate. It was studied 43 glands of adult dogs of several breeds and sizes and with or without a history of prostatic disease. PIA focus was characterized by dysplastic epithelium, atrophic acini formed by several layers of cells with variable degrees of anisocytosis, anisokaryosis, reduced amount of cytoplasm and nuclei with prominent nucleoli. The epithelial changes were always accompanied by periacinar interstitial infiltrate composed of mononuclear cells, especially lymphocytes. The histomorphological evaluation showed occurrence of 65 percent of PIA. Out of these, 39 percent were PIA with discrete inflammatory infiltration, 42 percent PIA with moderate infiltrate and 19 percent PIA with marked infiltration. Thus, it was possible to characterize the PIA in the canine prostate which had high occurrence. The histomorphological characterization of canine PIA is considered of great importance because the premalignant characteristic of it have been studied in human prostate. The canine prostate can be used as an experimental model of human PIA, because the lesion is similar in both species.

Activation of adenosine A_1 receptor inhibits glucose-induced cardiomyocyte hypertrophy / 中国药理学通报

Aim To demonstrate the effects and mechanism of adenosine A1 receptor agonist R(-)-N6-(2-phenylisopropyl) adenosine(R-PIA) on high glucose(HG)-induced myocardial hypertrophy by in vitro cultured myocardial cells from neonatal rats.Methods The protein content was assayed by the method of Lowry. The expression of p-ERK1/2 and ERK1/2 was determined by Western blot.The [Ca~(2+)]I transient changes of cell loaded Fura-2/AM were measured by Till image system.Results 1 μmol·L~(-1) R-PIA and U0126 inhibited similarly HG-induced increase of the protein content and [Ca~(2+)]I transient along with the relative expression of p-ERK1/2.These responses were completely abolished by adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine(CPDPX).Conclusion Adenosine A1 receptor stimulation significantly inhibits HG-induced myocardial hypertrophy by mediating ERK1/2 pathway and Ca~(2+).

The Effects of Intrathecal Adenosine A1 Receptor Agonists (R-PIA) on the Morphine Tolerance in a Rat Model of Postoperative Pain / 대한마취과학회지

BACKGROUND: Analgesic tolerance to opioids has been described in both experimental and clinical conditions, which may limit their clinical utility. This study investigated the effects of intrathecal adenosine A1 receptor agonist (R-PIA) on spinal morphine tolerance. METHODS: SD rats were given intrathecal injections of saline 10microliter, R-PIA 10microgram, morphine 10microgram, or R-PIA plus morphine combinations for 7 days (R-PIA given for days 1-7; days 1-3; or days 5-7). Antiallodynic testing using von Frey filaments was carried out before and 30 minutes after the drug injection. On day 8, an antiallodynic dose-response curve was constructed and the 50% effective dose (ED(50)) for morphine (given alone) was calculated for each study group. RESULTS: The coinjection group of R-PIA with morphine blocked the development of tolerance, as shown by the preservation of morphine antiallodynia over 7 days the concomitant decrease in the ED(50) values on day 8, compared with the morphine-alone group. Although additive analgesia over days 1-7 cannot be ruled out, the reductions of the ED(50) in the R-PIA and morphine combination group suggest some suppression of tolerance. CONCLUSIONS: These results suggest that intrathecal R-PIA prevents the development of spinal opioid tolerance. Future studies will be needed to examine the respective roles of supraspinal and peripheral sites of R-PIA and morphine interaction, and to investigate the mechanisms underlying the action of R-PIA on opioid tolerance.

Effects and Mechanism of Adenosine A_1 Receptor Agonist on Isoproterenol Induced Hypertrophy in Cultured Neonatal Rats Myocardial Cells / 中华高血压杂志

Objective To demonstrate the inhibitory effect of adenosine A_1 receptor agonist R(-)-N6-(2-phe- nylisopropyl) adenosine (R-HA) and cross-talk between adenosine A_1 receptor and CaMKII on Isoproterenol (Iso)- induced hypertrophy in cultured myocardial cells in neonatal rats.Methods The protein synthesis was determined by incorporation of [~3H]-leucine into myocyte protein.The expression of CaMK Ⅱ ? B was determined by Western- blot.The [Ca~(2+)]i transient was measured in myocytes loaded with fura-2 by the spectrofluorometric method. Results R-PIA (1?mol/L) inhibited Iso(10 ?mol/L)-induced increase of [~3 H-]-leucine incorporation [(R-PIA: 974.8?58.6) vs (Iso:1220.8?240.5) count per min per well,P

The Effect of ATP-sensitive Potassium Channel on R-PIA Induced Mechanical Antiallodynia in a Peripheral Neuropathic Rat / 대한통증학회지

BACKGROUND: Nerve ligation injury may produce mechanical allodynia, but this can be reversed after an intrathecal administration of adenosine analogues. In many animal and human studies, ATP-sensitive potassium channel blockers have been known to reverse the antinociceptive effect of various drugs. This study was performed to evaluate the mechanical antiallodynic effects of spinal R-PIA (Adenosine A1 receptor agonist) and the reversal of these effects due to pretreatment with glibenclamide (ATP-sensitive potassium channel blocker). Thus, the relationship between the antiallodynic effects of R-PIA and ATP-sensitive potassium channel were investigated in a neuropathic model. METHODS: Male Sprague Dawley rats were prepared by tightly ligating the left lumbar 5th and 6th spinal nerves and implantation of a chronic lumbar intrathecal catheter for drug administration. The mechanical allodynia was measured by applying von Frey filaments ipsilateral to the lesioned hind paw. And the thresholds for paw withdrawal assessed. In study 1, either R-PIA (0.5, 1 and 2microgram) or saline were administered intrathecally for the examination of the antiallodynic effect of R-PIA. In study 2, glibenclamide (2, 5, 10 and 20 nM) was administered intrathecally 5 min prior to an R-PIA injection for investigation of the reversal of the antiallodynic effects of R-PIA. RESULTS: The antiallodynic effect of R-PIA was produced in a dose dependent manner. In study 1, the paw withdrawal threshold was significantly increased with 2microgram R-PIA (P < 0.05). In study 2, the paw withdrawal threshold with 2microgram R-PIA was significantly decreased almost dose dependently by intrathecal pretreatment of 5, 10 and 20 nM glibenclamide (P < 0.05). CONCLUSIONS: These results demonstrated that an intrathecal injection of ATP-sensitive potassium channel blockers prior to an intrathecal injection of adenosine A1 receptors agonist had an antagonistic effect on R-PIA induced antiallodynia. The results suggest that the mechanism of mechanical antiallodynia, as induced by an intrathecal injection of R-PIA, may involve the ATP-sensitive potassium channel at both the spinal and supraspinal level in a rat nerve ligation injury model.

The Mechanical Antiallodynic Effect of intrathecal Morphine and R-Phenylisopropyl-Adenosine in Rats with Spinal Nerve Ligation / 대한마취과학회지

BACKGORUND: A nerve ligation injury may produce a pain syndrome including mechanical allodynia. Usually the antiallodynic effect of morphine is diminished in a neuropathic rat model. However, in a previous study, spinal morphine was found to have an antiallodynic effect in a neuropathic rat model. Therefore, the present study was performed to observe the mechanical antiallodynic effects of spinal morphine and R-PiA, and to investigate the relationship between the two. METHODS: Male SD rats were prepared by tightly ligating the left L5 and L6 spinal nerve and by implanting a lumbar intrathecal catheter. in study 1, each of the 5 groups (morphine at 3 or 10mug, adenosine A1 receptor agonist (R-PiA) at 3 or 10mug, or saline) were administered intrathecally to examine changes in the mechanical allodynia threshold. in study 2, selective adenosine A1 receptor antagonist (DPCPX 10mug) was administered to investigate the reversal of the mechanical antiallodynic effect in the 4 treated groups. in study 3, we observed the pretreatment effect of DPCPX 10mug. The mechanical allodynic thresholds for left hindpaw withdrawal to von Frey hairs were assessed and converted to %MPE. RESULTS: in study 1, the mechanical allodynic threshold was significantly increased in a similar pattern by intrathecal morphine (3, 10mug) and R-PiA (3, 10mug) (P<0.05). in study 2, the allodynic threshold of morphine was insignificantly decreased by intrathecal DPCPX pretreatment. The mechanical allodynic threshold of R-PiA 3mug was decreased by intrathecal DPCPX (P<0.05). in study 3, the antiallodynic effect of morphine was not influenced by DPCPX pretreatment. CONCLUSiONS: intrathecal morphine and R-PiA produced the antiallodynic effect. The antiallodynic effect of morphine was slightly decreased by DPCPX 10mug. Therefore, it was suggested that the antiallodynic effect of morphine might be, at least in part, mediated by adenosine in a rat model of spinal nerve ligation.

The Interaction of Morphine and Adenosine Receptor Agonists on Antiallodynia in Rats with a Nerve Ligation Injury / 대한마취과학회지

BACKGROUND: A Nerve ligation injury may produce a pain syndrome that includes tactile allodynia. Reversal effects on tactile allodynia have been demonstrated after an intrathecal administration of adenosine analogues or morphine. Adenosine receptor agonists have been known to have antinociceptive and antiallodynic effects in many animal and human studies. We examined the drug interactions between morphine and adenosine agonists in a rat model of a nerve ligation injury. METHODS: Male Sprague Dawley rats were prepared with a tight ligation of the left lumbar 5 th and 6 th spinal nerves and chronic lumbar intrathecal catheter implantation for drug administration. We measured the tactile allodynia by applying von Frey filaments ipsilateral to the lesioned hindpaw. Thresholds for paw withdrawal were assessed. Morphine (1 - 30ng), adenosine (1 - 30ng) and R-PIA (0.1 - 10ng) were administered to obtain the dose-response curves and the 50% effective dose (ED50). Fractions of ED50 values were administered to establish the ED50 of drug combinations. Drug interactions were evaluated by the fractional and isobolographic analyses. Allodynic thresholds for left lesioned hindpaw withdrawal to the von Frey hairs test were assessed and converted to % maximal possible effect (%MPE). RESULTS: The antiallodynic effect of morphine, adenosine, and R-PIA were produced in a dose dependent manner. The antiallodynic effects of combinations showed a similar pattern. Isobolographic analysis revealed a synergistic interaction for the morphine-R-PIA combination but not for the morphine-adenosine combination. However, fractional analysis produced a synergistic result for two combination groups. CONCLUSIONS: The results demonstrated that intrathecal co-administration of adenosine A1 receptors agonist and morphine showed the synergistic effect on nerve ligation injury induced allodynia.

Sequence analysis and prokaryotic expression system construction of PIA genes isolated from Neisseria gonorrhoeae / 中国病理生理杂志

AIM: To analyze the nucleotide and putative amino acid sequences of PIA genes isolated from N. gonorrhoeae and to construct the prokaryotic expression system of PIA gene.METHODS: The entire PIA genes from 9 strains of N. gonorrhoeae were amplified by using high fidelity PCR. The target amplification fragments were sequenced after T-A cloning. Homology comparison of the nucleotide and putative amino acid sequences of PIA genes from the isolates with the reported sequences in GenBank was then performed. A prokaryotic expression system of PIA gene was constructed. Different dosages of IPTG were applied to induce the expression of the target recombinant protein (rPIA) and 10% SDS-PAGE plus Bio-Rad Agarose Image Analysor was used to determine the expression level of rPIA. rPIA was extracted using Ni-NTA affinity chromatography and the purified effect was detected by SDS-PAGE.RESULTS: In comparison with the reported PIA gene sequences (GenBank No: L19962), the homologies of nucleotide and putative amino acid sequences of PIA genes from the isolates were 99.6%-100% and 99.1%-100%, respectively, which indicated that all the isolates were belonging to serovars IA6. Output of rPIA was as high as 50.1% of the total bacterial proteins. The purified rPIA only showed a single target protein fragment in gel.CONCLUSION: Serovar IA6 is dominant in the local N. gonorrhoeae isolates and sequences of the encoding gene are relatively conserved. The constructed prokaryotic expression system is able to express rPIA with high efficiency, which may lay a foundation for further development of serological detection kit and vaccine of N. gonorrhoeae.

The therapeutic effect of frequency spectrum equipment of the rat epilepsy model and the influence on the pia microcirculatory blood flow volume / 中国康复理论与实践

@#The epilepsy symptom and the pia microcirculatory blood flow volume (PMBFV) were investigated in epilepsy rat model induced by strychnine and the changes after treatment by using faradized frequency spectrum therapeutic equipment were observed. The epilepsy symptom was improved and the PMBFV increased after treatment. The convulsion seizure time was delayed, the seizure frequency and convulsion time were reduced, and the epilepsy even was not appeared in some cases. Results suggested that this improvement might be related to the change of PMBFV.

Emergency Coronary Artery Bypass Grafting for Acute Coronary Syndrome / 日本心臓血管外科学会雑誌

Emergency coronary artery bypass grafting (CABG) for the treatment of acute coronary syndrome is still associated with increased operative risk and postoperative morbidity. Thirty-five patients underwent CABG for the treatment of medically refractory unstable angina (UAP), 42 patients for acute myocardial infarction (AMI) and 7 patients for post-infarction angina (PIA). The UAP patients received 2.8 distal anastomoses on average. Five patients (14%) died postoperatively, 3 of them due to perioperative myocardial infarction (PMI). In the AMI patient group, 29 patients were in shock and 3 patients were in cardiac pulmonary arrest (CPA) preoperatively. They received an average of 2.8 distal anastomoses. Fourteen patients (33%) died postoperatively. Ten of them died of postoperative myocardial failure. The operative mortality was extremely high in the shock state patient group (41%) and CPA state patients group (100%). Poor operative results were anticipated in those patients whose infarct-related artery was not recanalized preoperatively. All patients survived the CABG in the PIA group. It was concluded that reduction in mortality in the group of patients undergoing emergency CABG required highly refined myocardial preservation techniques to prevent PMI and to limit intraoperative myocardial damage, as well as powerful mechanical assist systems to provide support in cases of the postoperative myocardial failure.

Analysis of Unsuccessfully Operated Patients in Microvascular Decompression for Hemifacial Spasm

Seventy six patients with hemifacial spasm(HFS) were operated with microvascular decompression(MVD) at Soonchunhyang University Hospital from January, 1987 to June, 1994. We report an analysis of 30 patients who were not relieved from or had a recurrence of their symptoms immediately after MVD. 1) 14 patients(46.7%) showed delayed remission. Among them, 8 patients improved within 3 months and 1, after 6 months. 5 patients reoperated, at which time incomplete decompression of small vessels were identified in 4 patients. The vessels were then completely decompressed at the facial nerve root exit zone(FNREZ) and the surrounding pia-arachoid membrane were incised. 2) 12 patients(40%) showed partial remission. Among them, 9 patients did not show complete remission after the operation and continued to show only partial remission during the follow-up periods. 3 patients showed the same severity of HFS after the operation but 2 patients improved spontaneously at first and then at 3 months postoperatively. 3) 4 patients(13.3%) showed recurrence. The symptoms of one patient right 1 month after the operation, and 3 patients at 3 months. These findings suggest that the ideal time to evaluate the surgical outcome of MVD for HFS is 3 months or later after the operation, and that the procedure of opening up the piaarachnoid menbrane at FNREZ may be effective for a complete remission.

Ischemic postconditioning ameliorates pia mater microcirculation in rats subjected to cerebral ischemia reperfusion / 中国病理生理杂志

AIM:To investigate the ameliorative effect of ischemic postconditioning (I-postC) on pia mater microcirculation in rats subjected to cerebral ischemia reperfusion (I/R) and its mechanisms. METHODS:Thirty-two male Wistar rats were randomly divided into sham,I/R,I-postC,and ischemic preconditioning (IPC) groups. The global cerebral I/R injury was induced by shunting carotid artery in rats. Pia mater microcirculation and cerebral microcirculatory perfusion were measured after reperfusion. The content of soluble intercellular adhesion molecule-1 (sICAM-1) in plasma was detected using enzyme linked-immunosorbent assay (ELISA). Myeloperoxidase (MPO),malondialdehyde (MDA),and superoxide dismutase (SOD) in cerebral tissue were detected. The expressions of vascular endothelial cell cadherin (VE-cadherin) and NF-?B p65 in cerebral tissue were assayed by Western blotting. RESULTS:(1) The disturbance of the blood flow in microvessel induced by I/R was improved significantly by I-postC. In addition,I-postC alleviated significantly the decrease in diameters of microvesseles,cerebral microcirculatory perfusion and cerebral VE-cadherin content induced by I/R (P

AN EXPERIMENT ON THE INTERRELATIONSHIP BETWEEN THE BULBAR CONJUNCTIVAL MICROCIRCULATION DISTUBANCE AND PSAl MICROCIRCULATION DISTURBANCE / 第二军医大学学报

The animal model of the bulbar conjunctival and pral microcirculation disturbance induced by high molecular weight dextran in rabbit were reported In this experiment.The interre'ationship between the bulbar conjunctival microcired ation disturbance and the pial miciocirculation disturbance, has been observed. We found that the occurrence of the buibar conjunctival microcirculation was earlier than the pial microcirculation. The degrees of abnormal bulbar conjunctival micro-circulation were more prominent. than that of the pial one, however, the degrees of erythrocyte aggregation in the bulbar conjunctiva Was similar to that of the cerebral microcirculation. The experiment showed the bulbar conjunctival microciculation disturbance, to some degree may reflect the degree of the cerebral microcirulation disturbance in living animals.