Regulating the gene: From genetic consumption to regulatory trust

In this article, we examine the changing terms on which genetics-based technologies in two areas agriculture (Genetically Modified Organism, GMOs) and health (genetic diagnostics) have been regulated. These are used to illustrate and examine the proposition that shifts in the politics of governance and regulation (associated in part with the advent of the negotiation state) have meant that the responsibility for the social management of new technology is increasingly shared between the state and the consumer. However, this redistribution of the social management of risk, we argue, fails to establish a sufficient basis for a legitimate regulatory trust. We suggest that trust will depend on embedding broad social values and a self-critical agenda within the regulatory regime itself.     

Regulatory volume response of erythrocytes exposed to a gradual and slow decrease in medium osmolality

 A sudden decrease in external medium osmolality (90 mosmol/kg) causes an immediate swelling of trout erythrocytes, followed by a regulatory volume decrease (RVD) due to activation of both a KCl cotransporter and a taurine transport pathway. Here, we determined how trout red cells respond when they are exposed to a gradual and slow decrease in medium osmolality (80 mosmol/kg at a rate of 0.7 mosmol/kg per min). Erythrocytes were unable to regulate their volume efficiently when swollen gradually and it increased continuously throughout the experimental period (120 min). As long as volume was increased slowly by 15–25%, regulatory pathways remained essentially inactivated, erythrocytes losing no significant amount of intracellular osmotically active solutes. Above this swelling threshold, a response was triggered but the quantity of solutes lost via the regulatory pathways was still not sufficient to counterbalance the continuous entry of water due to the slow and gradual decrease in medium tonicity. Received: 18 January 1999 / Received after revision: 10 February 1999 / Accepted: 11 February 1999     

Short-term and long-term results after early treatment with the castillo morales stimulating plate

The present study is divided into 2 parts: The first explains the concept of stimulating plate therapy at the Muenster Clinic and the second presents a longitudinal study of mouth and tongue posture in trisomy 21 children treated with this concept.47 children underwent a pre-treatment examination (Rec1), and 38 attended a first follow-up examination (Rec2) after an average of 4 months of stimulating plate treatment. The second follow-up examination (Rec3) was on average 53 months after the end of treatment and covered 18 patients. Data acquisition was based on standardized parent questionnaires and standardized clinical examination records. Rec2 showed in part a highly significant improvement in orofacial appearance. These results were confirmed by the parent interview, according to which the mouth and tongue posture improved in 76.3% of the children during the time they were wearing the plate. Even when the plate was not in place, the result remained stable in 65.8% of the patients. Up to Rec3, further improvement was recorded in some results. The symptoms: mouth mostly wide open and tongue mostly protruding way over lips were reduced. The number of children whose tongue was mostly in the oral cavity increased correspondingly.At Rec3, the parents also rated the mouth posture in 88.9% and the tongue posture in 77.7% of the children as stable or further improved.It can be concluded from the results of this study that stimulating plate treatment in combination with physiotherapy provides a long-term improvement in the mouth and tongue posture of children with Down's syndrome.     

恒力法测量制动对兔髌韧带截面面积的影响

目的：介绍一种测量软组织截面面积的装置和方法。方法：用测微仪对膝关节制动前后兔髌韧带截面面积进行反复测量。结果：测微仪的变异系数在０．９％以下,制动６周后髌韧带的截面面积明显增大。结论：兔髌韧带截面面积的这种变化与组织的胶原代谢水平相关     

进行期银屑病患者活性氧代谢变化探讨

目的：探讨进行期银屑病患者活性氧代谢变化。方法：采用细胞化学发光分析技术测定患者及健康对照组外周血淋巴细胞化学发光强度（ Ｌｙｃｌ）及多形核白细胞化学发光强度（ Ｐ Ｍ Ｎｃｌ）,同时测定血浆超氧化物歧化酶（ Ｓ Ｏ Ｄ）、全血谷胱甘肽过氧化物酶（ Ｇ Ｓ Ｈ Ｐｘ）以及血浆丙二醛（ Ｍ Ｄ Ａ）含量。结果：银屑病患者 Ｌｙｃｌ及 Ｐ Ｍ Ｎｃｌ较对照组显著增强（ Ｐ＜ ０．０５）,血浆 Ｓ Ｏ Ｄ活力明显增强（ Ｐ＜ ０．０５）, Ｍ Ｄ Ａ 浓度较对照组明显增高（ Ｐ＜ ００５）。全血 Ｇ Ｓ Ｈ Ｐｘ 活力较对照组显著下降（ Ｐ＜ ０．０５）。结论：进行期银屑病患者细胞功能改变,机体活性氧代谢增强,抗氧化功能下降,组织细胞损伤加快。活性氧损伤可能是该病患者皮损炎症的重要原因。     

Reactive oxygen species in NMDA receptor-mediated glutamate neurotoxicity

In search of endogenous protective substances that inhibit neurotoxic action of glutamate and nitric oxide (NO), we found that brain-derived neurotrophic factor (BDNF), acting on TrkB receptor tyrosine kinase, inhibited neurotoxicity induced by glutamate and NO donors in cultured cortical neurons. In co-cultures of the mesencephalon and striatum, projection of mesencephalic dopamine neurons to the striatum attenuated N-methyl-d-aspartate (NMDA)-induced cytotoxicity in dopamine neurons themselves. Growth factors such as neurotrophins, which the target cells in the striatum would synthesize and secrete, may offer the protection of dopamine neurons against glutamate neurotoxicity.     

Studies on LH modulated 8kDa peptide involved regulation of testosterone production in rat Leydig cells

Aim: To demonstrate the role of the 8 kDa peptide in regulation of testosterone production by mt Leydig cells. Meth-ods: A peptide similar to 8 kDa peptide purified from immature rat Leydig cells was isolated and purified from rat lungcytosol. Immunological and structural similarity between the peptides purified from lung and Leydig cells was estab-lished by Western blot and tryptic map comparison respectively. Results: Addition of the 8 kDa peptide 10, 50, 100;and 150 ug decreased the production of testosterone in Leydig cells dose-dependently. But the addition of the peptide150 ug along with hCG had no effect on hCG-stimulated increase in testosterone production. Conclusion: In vitro ad-dition of the peptide purified from lung cytosol to adult rat Leydig cells resulted in a concentration-dependent decrease inbasal testosterone production although it had no effect on hCG-stimulated testosterone production. (Asian J Androl1999 Dec; 1: 191-194)     

Dexamethasone effects on cerebral protein synthesis prior to and following hypoxia-ischemia in immature rat

We hypothesized that the neuroprotection against cerebral hypoxic-ischemic damage observed with dexamethasone treatment in immature rats is related to a change in cerebral protein synthesis. Six-day-old Wistar rats were injected with either vehicle (10 ml/kg) or dexamethasone (0.1 mg/kg) 24 h prior to cerebral hypoxia-ischemia. Local cerebral protein synthesis (incorporation of 14C-leucine into proteins) was measured in 7-day-old rats during normoxia, during hypoxia-ischemia, and after hypoxia-ischemia which was produced with right carotid artery ligation and 2-h exposure to 8% O2. In normoxic controls, cerebral protein synthesis was similar in dexamethasone and vehicle-treated animals. During hypoxia-ischemia, local cerebral protein synthesis decreased markedly (p < 0.0001) in ischemic regions ipsilateral to the occlusion, irrespective of treatment. After hypoxia-ischemia, protein synthesis declined even further in vehicle-treated animals. Reductions in protein synthesis were substantially more severe in vehicle- than dexamethasone-treated animals, particularly after hypoxia-ischemia (p < 0.0001). Thus, neuroprotection with dexamethasone is not related to a reduction in basal levels of cerebral protein synthesis, but is associated with an improved protein synthesis during and following hypoxia-ischemia.     

Ischemic "cross" tolerance in hypoxic ischemia of immature rat brain

The phenomenon of ischemic tolerance has been closely associated with the expression of heat shock proteins but recently, stress tolerance not related to hsp72 has been reported. In the present study, we focused on ischemic tolerance induced by hypoxia and hyperthermia in neonatal rat brain and analyzed the expression of hsp72. In a neonatal rat model of hypoxic ischemia (H-I), preconditioning by whole-body hyperthermia or hypoxia was induced 24 h prior to the ischemia. Brain damage was histologically evaluated and the expressions of hsp72 were analyzed. Hyperthermic preconditioning at 41 degrees C for 15 min, as well as hypoxic preconditioning with 8% hypoxia for 3 h, had almost complete neuroprotective effects. However, we failed to detect the expression of hsp72 in any of preconditioning. Only the H-I insult itself induced hsp72 in the dorsal striatum and slightly in the thalamus and the hippocampus. Hyperthermic preconditioning has neuroprotective effects which are comparable to hypoxic preconditioning in immature brain. The expression of hsp72 is not likely necessary for the ischemic tolerance in immature brain.     

Reactive oxidant species in piriform cortex extracellular fluid during seizures induced by systemic kainic acid in rats

Kainic acid (KA) administered systemically to rats produces seizures and brain damage. We measured an increase in reactive oxidant species (ROS) during KA-induced seizures in the extracellular fluid (ECF) of the piriform cortex, a brain region known to be subsequently damaged. Intracerebral microdialysis samples were collected and assayed for isoluminol-dependent chemiluminescence before and after injection of KA (16 mg/kg, ip). Hydrogen peroxide (H₂O₂) concentrations were calculated from catalase-sensitive chemiluminescence, the difference between total and catalase-resistant chemiluminescence. During generalized tonic-clonic seizures, both total and catalase-resistant chemiluminescence increased significantly in samples from brain ECF. Catalase-resistant chemiluminescence, most likely produced by ascorbic acid, increased for a full hour during sustained seizure activity. H₂O₂ concentrations showed a trend towards elevation during seizures. Increased ROS suggest that oxidative stress occurs in brain ECF during sustained seizure activity.