Dynamical Models of Extreme Rolling of Vessels in Head Waves

Rolling of a ship is a swinging motion around its length axis. In particular vessels transporting containers may show large amplitude roll when sailing in seas with large head waves. The dynamics of the ship is such that rolling interacts with heave being the motion of the mass point of the ship in vertical direction. Due to the shape of the hull of the vessel its heave is influenced considerably by the phase of the wave as it passes the ship. The interaction of heave and roll can be modeled by a mass-spring-pendulum system. The effect of waves is then included in the system by a periodic forcing term. In first instance the damping of the spring can be taken infinitely large making the system a pendulum with an in vertical direction periodically moving suspension. For a small angular deflection the roll motion is then described by the Mathieu equation containing a periodic forcing. If the period of the solution of the equation without forcing is about twice the period of the forcing then the oscillation gets unstable and the amplitude starts to grow. After describing this model we turn to situation that the ship is not anymore statically fixed at the fluctuating water level. It may move up and down showing a motion modeled by a damped spring. One step further we also allow for pitch, a swinging motion around a horizontal axis perpendicular to the ship. It is recommended to investigate the way waves may directly drive this mode and to determine the amount of energy that flows along this path towards the roll mode. Since at sea waves are a superposition of waves with different wavelengths, we also pay attention to the properties of such a type of forcing containing stochastic elements. It is recommended that as a measure for the occurrence of large deflections of the roll angle one should take the expected time for which a given large deflection may occur instead of the mean amplitude of the deflection

FINE STRUCTURE PECULIARITIES OF MEDULLARY EPITHELIAL CELLS AND THEIR RELATION TO THYMUS LYMPHOPOIESIS

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SOME ULTRASTRUCTURAL PECULIARITIES OF THE NUCLEI OF THYMUS EPITHELIAL CELLS

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FINE STRUCTURE OF THE THYMUS EPITHELIAL CELLS OF A MOUSE IN THE PERINATAL PERIOD

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VIRUS LIKE PARTICLES IN THYMUS EPITHELIAL CELLS OF CONVENTIONAL MICE

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COMPARATIVE STUDY OF THE VACUOLE APPARATUS IN EPITHELIAL CELLS OF A MOUSE THYMUS GLAND

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ULTRASTRUCTURAL CHARACTERISTICS CF THYMOCYTE MICROENVIRONMENT

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Short-interval amygdala kindling in neonatal rats.

The kindling paradigm provides a powerful tool for studying the generation, propagation and generalization of seizures. Such reproducible quantitative paradigms are a prerequisite for the experimental study of epilepsy in the developing brain. Kindling has been extensively utilized as a model of limbic seizures in the adult rat; amygdala short-interval kindling has been studied in > or = 15-day-old rats. We applied the short-interval kindling method, i.e., stimulation at every 15 min, to 7-12-day-old rats. Stage-5 behavioral seizures were achieved even in 7-day-old rats; however, the progression of behavioral kindling differed somewhat from that of older rats. Correlation of electrographic discharges and behavioral phenomena was inversely related to age. Reliable progressive amygdala discharges were difficult to assess in most < or = 10-day-old rats. Spontaneous seizures occurred relatively frequently in younger age groups. The amygdala short-interval kindling paradigm is reproducibly and reliably applicable to rats during the 2nd postnatal week. The presence of progressive focal to bilateral-generalized seizures suggests a significant functional maturity of the amygdala-limbic circuitry at this age

Inhibition of pituitary-adrenal secretion by a corticotropin releasing hormone antagonist in humans.

Corticotropin releasing hormone (CRH) is the primary modulator of ACTH release from the pituitary, and a neuromodulator in limbic and autonomic brain regions. Dysfunction of CRH-mediated neurotransmission is emerging as a critical mechanism in several disorders. Therefore, modulation of CRH availability at receptor sites is a potentially powerful therapeutic tool. Inhibitory analogues of CRH have been tested in rodents and primates, but their safety and hormonal effects in humans are unknown. We administered a CRH-antagonist, alpha-helical-CRH-(9-41) to six individuals. Each received two intravenous infusions: 50 micrograms kg-1 on day 1, and 100 micrograms kg-1 on the following morning. These doses block both endocrine and central effects of CRH in experimental animals. ACTH, cortisol, electrolytes, glucose and autonomic parameters were monitored in comparison with control values. Infusion of CRH antagonist did not alter heart rate, blood pressure, temperature or plasma electrolytes and glucose. Pre-infusion plasma ACTH levels averaged 26.8 +/- 6.7 pg ml-1 on day 1, and 29.0 +/- 5.8 pg ml-1 on day 2. Post-infusion values were 11.8 +/- 2 and 11.5 +/- 2.4 pg ml-1, significantly lower than pre-infusion levels. Plasma cortisol levels, which averaged 21.4 +/- 4 micrograms dl-1 on the first morning and 22.9 +/- 4.2 on the second, also decreased significantly after CRH antagonist infusions (to 14.0 +/- 2.9 micrograms dl-1 on day 1, and 13.9 +/- 3.0 micrograms dl-1 on day 2). Hormonal changes were transient, and circadian rhythm was not affected. Though not measured formally, euphoria, anxiety or somnolence were not observed. In conclusion, CRH antagonist administration to adults reduces hormonal secretion by pituitary corticotrophs, with resulting decrease in plasma ACTH and cortisol

Ontogenic study of lithium-pilocarpine-induced status epilepticus in rats.

Lithium is known to potentiate the ability of pilocarpine to induce status epilepticus in rats. The goal of this study was to determine whether lithium could potentiate pilocarpine-induced seizures in developing animals. Behavioral, electroencephalographic (EEG), and histopathological changes induced by systemic administration of lithium (3 meq/kg) followed 20 h later by pilocarpine (3, 10, 30, 60 mg/kg) were studied in 3-30-day-old rats. Lithium followed by pilocarpine (30 and 60 mg/kg) induced hyperactivity, tremor, loss of postural control and scratching but no electrographic seizures in 3-8-day-old rats. In the 7-10-day-old animals pretreatment with lithium and pilocarpine 60 mg/kg induced status epilepticus with sustained myoclonus and continuous bilateral synchronous spike and sharp wave, but doses of pilocarpine lower than 60 mg/kg had no effect. The susceptibility to lithium-pilocarpine-induced status epilepticus increased markedly during the third postnatal week of life. During this time period, rats treated with lithium (3 meq/kg) plus pilocarpine 10 mg/kg exhibited behavioral and EEG manifestations of status epilepticus. The same combination of lithium and pilocarpine failed to induce status epilepticus either before or after the third week of life. Histopathological analysis of the brains of the animals used in these studies failed to demonstrate the widespread damage reported in adult rats that have undergone lithium-pilocarpine-induced status epilepticus