Trade-offs between acquired and innate immune defenses in humans

Immune defenses provide resistance against infectious disease that is critical to survival. But immune defenses are costly, and limited resources allocated to immunity are not available for other physiological or developmental processes. We propose a framework for explaining variation in patterns of investment in two important subsystems of anti-pathogen defense: innate (non-specific) and acquired (specific) immunity. The developmental costs of acquired immunity are high, but the costs of maintenance and activation are relatively low. Innate immunity imposes lower upfront developmental costs, but higher operating costs. Innate defenses are mobilized quickly and are effective against novel pathogens. Acquired responses are less effective against novel exposures, but more effective against secondary exposures due to immunological memory. Based on their distinct profiles of costs and effectiveness, we propose that the balance of investment in innate versus acquired immunity is variable, and that this balance is optimized in response to local ecological conditions early in development. Nutritional abundance, high pathogen exposure and low signals of extrinsic mortality risk during sensitive periods of immune development should all favor relatively higher levels of investment in acquired immunity. Undernutrition, low pathogen exposure, and high mortality risk should favor innate immune defenses. The hypothesis provides a framework for organizing prior empirical research on the impact of developmental environments on innate and acquired immunity, and suggests promising directions for future research in human ecological immunology.     

Participation of angiotensin II in learning and memory. III. Interactions of angiotensin II with GABAergic drugs

The experiments were carried out on male albino rats trained and tested for retention (24 hr later) in a shuttle-box. Angiotensin II (AT II) 0.10 micrograms intracerebroventricularly (i.c.v.), gamma-aminobutyric acid (GABA) 100 micrograms i.c.v., bicuculline 0.5 and 1.0 mg/kg intraperitoneally (i.p.), and picrotoxin 0.5 and 1.0 mg/kg i.p. administered independently or in combinations immediately after training. AT II was found to improve retention. GABA also facilitated retention. Combination of AT II + GABA potentiated the memory-improving effect of AT II. Bicuculline and picrotoxin at a dose of 0.5 mg/kg did not affect retention, while at a dose of 1.0 mg/kg they improved it. Combinations of AT II + bicuculline (0.5 mg/kg) and AT II + picrotoxin (0.5 mg/kg) abolished the retention-improving effect of AT II. Bicuculline (0.5 mg/kg) or picrotoxin (0.5 mg/kg) abolished the retention-facilitating effect of the combination of AT II + GABA as well as the potentiating action of GABA on the memory effect of AT II. These results suggest the participation of GABAergic transmission in the CNS in the mechanisms of the long-term memory-improving effect of AT II.     

麦冬类中药组织切片计算机三维重建图鉴

利用计算机技术实现麦冬类中药组织连续切片三维重建与动态显示,为计算机辅助生药学鉴定和教学提供了新的三维图像技术和研究资料。     

Gastro-oesophageal reflux disease: Medical or surgical treatment? Report of an interactive workshop

Gastroesophageal reflux disease (GERD) is the most common disease of the upper gastrointestinal tract. With the introduction of proton pump inhibitors medical treatment of GERD has been significantly improved. However, the development of laparoscopic antireflux surgery resulted in an increasing interest of surgeons in this disease. An interactive meeting was organized in order to develop an agreement between gastoenterologists and surgeons regarding therapeutic decisions and this is the main topic of this paper.     

Mechanisms of tizanidine action on spasticity

This investigation estimated the mechanisms of tizanidine action on spasticity using a battery of neurophysiological methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with tizanidine-mean daily dose 15.8 ± 5.6 mg for a mean of 23.3 ± 4.8 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of neurophysiological methods was used to analyze different mechanisms of spasticity: for alpha motoneuron excitability – the F wave parameters; for presynaptic inhibition – the ratio of H reflex amplitudes before and after vibration of the achilles tendon (Hvibr/Hmax); for common interneuron activity – the flexor reflex parameters. Our results revealed that tizanidine reduces spastically increased muscle tone, but has no influence on muscle force, tendon reflexes, Babinski sign and ankle clonus. Tizanidine is supposed to act by increasing the presynaptic inhibition and decreasing of alpha motoneuron excitability. When spasticity has decreased presynaptic inhibition and increased motoneuron excitability, it is better to treat with tizanidine.     

Electrophoresis of NADH-dependent oxidoreductase (diaphorase) in boar spermatozoa: Elektrophorese der NADH-abhängigen Oxydoreduktase (Diaphorase) in Eberspermatozoen

Two forms of NADH-dependent oxidoreductase (diaphorase [EC.1.6.99.-]) are established in boar spermatozoa. The first form is typical for soluble proteins with a varying electrophoretic profile, while the other form for sedimental proteins with a specific, slowly-moving fraction, which is not common for the soluble form. The two enzyme forms have a close isoelectric point (pI5.5-6.0) and they can not be inhibited by dicumarol 10(-5) mol l-1 and FAD 10(-4) mol l-1. The molecular mass of the soluble form of the enzyme is 28, 37, 46 and 67 kD, while of the sedimental form it is 220, 250 and 260 kD, respectively.     

Studies on antifungal agents. In vitro activity of novel cis-5-alkoxy (or acyloxy)alkyl-3-phenyl-3-(1H-imidazol-1-ylmethyl)-2-methylisoxazolidine derivatives

The synthesis and in vitro antifungal activity of a novel series of cis-5-alkoxy(or acyloxy)alkyl-3-phenyl-3-(1H-imidazol-1-ylmethyl)- 2-methylisoxazolidine derivatives (6a-n) are described. The 5-[(4-chlorobenzyloxy)methyl] analogue 6h and the two 5-acyloxymethyl derivatives 6k,l demonstrated the best overall potency. Against Candida stellatoidea, the minimum inhibitory concentrations (MIC's) for 6h,k,l ranged between 0.7 and 2.0 micrograms/ml. The corresponding value for the standard drug ketoconazole was 7-20 micrograms/ml.