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The critical speed for bending-torsional flutter can be increased by decreasing the unbalance of the airfoil [i], i .e. , by moving the center of mass of each spanwise element closer to the stiffness axis. This can be achieved by adding balance masses ahead of the stiffness axis or even by adding a single concentrated mass at a certain section of the airfoil. The size and situation of the mass have a definite influence on the magnitude of the critical flutter speed. In the usual design calculation for bending-torsional flutter of an airfoil by the Bubnov-Galerkin method [I], an equivalent two-degree-of-freedom system is introduced. The va r i ab l e s in this s y s t e m a r e two "gene r a l i z e d " coord ina tes c o r r e s p o n d i n g to two p r e s c r i b e d modes : bending and to r s ion of the a i r fo i l . The p a r a m e t e r s of the "equiva len t" s y s t e m a r e the values of the fol lowing quant i t ies : the mass of the a i r fo i l , its m o ment of ine r t i a , its bending and to r s iona l s t i f fness , and the s ta t ic m o m e n t d e s c r i b i n g the ine r t i a l coupl ing between bending and to r s ion . Acco rd ing to the Bubnov-Ga le rk in method, the ef fec t of the balance m a s s on the c r i t i c a l f lu t t e r speed is as fol lows. The ins ta l la t ion of a ba lance m a s s changes the p a r a m e t e r s of the "equ iva len t " t w o d e g r e e o f f r e e d o m sys t em, i nc r ea s ing the e f fec t ive m a s s and momen t of iner t ia and d e c r e a s i n g the ef fec t ive coef f ic ien t of i n e r t ia coupling between the " g e n e r a l i z e d " bending and t o r s ional coord ina te s . The d e c r e a s e in coupling leads to a d e c r e a s e in the amount of e n e r g y f r o m the a i r flow, and hence the c r i t i c a l f lu t t e r speed is d e c r e a s e d . A method of de t e rmin ing the c r i t i c a l f lu t t e r speed of an a i r fo i l based on the d i r e c t solut ion of the equations for bend ingto r s iona l v ib ra t ions by means of an analog compute r was d e s c r i b e d in [2]. This method makes no assumpt ions about the types of v ibra t ion . The a c c u r a c y of the solut ion depends only on the extent to which the equat ions d e s c r i b e an actual wing, the a c c u r a c y in spec i fy ing the p a r a m e t e r s and ae rodynamic f o r c e s , and the machine e r r o r s . This method is used below to det e r m i n e the c r i t i c a l f lu t t e r speed, toge the r with the f requency and type of the f lu t t e r modes of an a i r fo i l with ba lance m a s s . The r e s u l t s obtained a r e c o m p a r e d with the c o r r e s p o n d i n g r e s u l t s given by the BubnovGalerk in method. It is shown that for the given example (also c o n s i d e r e d in [2]) of a un i fo rm a i r fo i l t h e r e a r e d i s c r e p a n c i e s be tween the two methods , at l e a s t for ce r t a in b a l a n c e r p a r a m e t e r s . 1. The equat ions for the bend ing to r s iona l v i b r a tion of a long un i fo rm a i r fo i l a r e [1]

In acute and chronic experiments staged on cats and rabbits a study was made of the role played by various portions of the brain in the reaction of respiration to aminazine. In administration of this preparation in a dose of 2–3 mg/kg to cats and in a dose of 8–10 mg/kg to rabbits no significant shifts occurred in the frequency and nature of respiratory movements. The use of hypnotics, acting as a depressive agent on the brain cortex, did not change the reaction of respiration to aminazine. In decerabrated anaimals, aminazine injection led to marked respiratory disturbances. Such animals often perish, the cause of death being repsiratory arrest. Evidently, weakly pronounced respiratory reactions following aminazine administration in intact animals were the result of considerable compensatory capacities of the higher portions of the brain in respiratory regulation.

Cardiovascular and respiratory disturbances occuring in chlorpromazine administration are more pronounced in decerebrated animals than in the intact ones. Antagonistic relationships of chlorpromazine and adrenaline (according to the indices of arterial pressure and respiration) developed in decerebrated animals without significant differences from the animals with an intact central nervous system.