66 research outputs found
Low temperature fluid blender
Blender supplies hydrogen at temperatures from 289 deg K to 367 deg K. Hydrogen temperature is controlled by using blender to combine flow from liquid hydrogen tank /276 deg K/ and gaseous hydrogen cylinder /550 deg K/. Blenders are applicable where flow of controlled low-temperature fluid is desired
Hydrogen-air ignition torch
The design and operation of a hydrogen-air ignition torch presently being used to burn off excess hydrogen that accumulates in the scrubber exhaust ducts of two rocket engine test facilities at the NASA Lewis Research Center in Cleveland, Ohio, is described
Low-cost high-temperature brazing material
Commercially available nickel-copper wire containing 6 and 12 percent nickel is used in high temperature furnace brazing of rocket engine parts. Brazed joints have properties comparable to or better than those brazed with more expensive materials, and cost savings are substantial
Hydrogen-oxygen Torch Ignitor
The hydrogen-oxygen torch igniter described herein has been successfully used for many years at various NASA Lewis Research Center rocket test facilities to provide ignition for rocket engine research hardware. This igniter is inexpensive, simple to operate, and has demonstrated very good reliability. It has been used as an ignition source for rocket engines that utilized a variety of propellant combinations; some of these engines developed up to 40,000 lb of thrust
ΠΠΎΠ½ΠΊΡΡΠ΅Π½ΡΠΎΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΡ ΠΏΡΠΎΠ΄ΡΠΊΡΠΈΠΈ Β«Π¨Π°Π½Ρ Π°ΠΉ Π’ΠΎΠ±Π°ΠΊΠΊΠΎ Π³ΡΡΠΏΠΏΒ» Π½Π° ΡΡΠ½ΠΊΠ΅ ΡΠ°Π±Π°ΡΠ½ΡΡ ΠΈΠ·Π΄Π΅Π»ΠΈΠΉ
ΠΠΊΡΡΠ°Π»ΡΠ½ΠΎΡΡΡ ΡΠ°Π±ΠΎΡΡ Π·Π°ΠΊΠ»ΡΡΠ°Π΅ΡΡΡ Π² ΡΠΎΠΌ, ΡΡΠΎ Π² ΡΡΠ»ΠΎΠ²ΠΈΡΡ
ΡΠΆΠ΅ΡΡΠΎΡΠ΅Π½ΠΈΡ ΠΊΠΎΠ½ΠΊΡΡΠ΅Π½ΡΠ½ΡΠΉ Π±ΠΎΡΡΠ±Ρ Π»ΡΠ±Π°Ρ ΠΊΠΎΠΌΠΏΠ°Π½ΠΈΡ Π²ΡΠ½ΡΠΆΠ΄Π΅Π½Π° ΡΠΏΡΠ°Π²Π»ΡΡΡ ΡΠ²ΠΎΠ΅ΠΉ ΠΊΠΎΠ½ΠΊΡΡΠ΅Π½ΡΠΎΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΡΡ Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠ°Π½Π½ΠΎΠΉ ΠΊΠΎΠ½ΠΊΡΡΠ΅Π½ΡΠ½ΠΎΠΉ ΡΡΡΠ°ΡΠ΅Π³ΠΈΠΈ.
Π ΠΏΡΠΎΡΠ΅ΡΡΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈΡΡ ΠΈΠ·ΡΡΠ΅Π½ΠΈΠ΅ ΠΈ ΡΠΈΡΡΠ΅ΠΌΠ°ΡΠΈΠ·Π°ΡΠΈΡ ΠΈΠ½ΡΠΎΡΠΌΠ°ΡΠΈΠΈ ΠΏΠΎ ΠΏΡΠ΅Π΄ΠΌΠ΅ΡΡ ΠΈ ΠΎΠ±ΡΠ΅ΠΊΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ. ΠΡΡΠΎΡΠ½ΠΈΠΊΠΈ ΠΈΠ½ΡΠΎΡΠΌΠ°ΡΠΈΠΈ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»Π΅Π½Ρ Π² ΡΠΏΠΈΡΠΊΠ΅ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Π½ΡΡ
ΠΈΡΡΠΎΡΠ½ΠΈΠΊΠΎΠ².
ΠΠ°ΡΡΠ½Π°Ρ Π½ΠΎΠ²ΠΈΠ·Π½Π° ΡΠ°Π±ΠΎΡΡ Π·Π°ΠΊΠ»ΡΡΠ°Π΅ΡΡΡ Π² ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠ΅ ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄Π°ΡΠΈΠΉ ΠΏΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΡ ΠΊΠΎΠ½ΠΊΡΡΠ΅Π½ΡΠΎΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΠΈ ΡΠ°Π±Π°ΡΠ½ΠΎΠΉ ΠΊΠΎΠΌΠΏΠ°Π½ΠΈΠΈ.
ΠΡΠΎΠ³ΠΎΠΌ ΡΠ°Π±ΠΎΡΡ ΡΡΠ°Π»ΠΈ ΡΠ΅ΠΊΠΎΠΌΠ΅Π½Π΄Π°ΡΠΈΠΈ ΠΏΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΡ ΡΡΠΎΠ²Π½Ρ ΠΊΠΎΠ½ΠΊΡΡΠ΅Π½ΡΠΎΡΠΏΠΎΡΠΎΠ±Π½ΠΎΡΡΠΈ ΠΊΠΎΠΌΠΏΠ°Π½ΠΈΠΈ "Π¨Π°Π½Ρ
Π°ΠΉ Π’ΠΎΠ±Π°ΠΊΠΊΠΎ Π³ΡΡΠΏΠΏ".
Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ Π±ΡΠ΄ΡΡ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½Ρ Π² Π΄Π΅ΡΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ ΠΊΠΎΠΌΠΏΠ°Π½ΠΈΠΈ "Π¨Π°Π½Ρ
Π°ΠΉ Π’ΠΎΠ±Π°ΠΊΠΊΠΎ Π³ΡΡΠΏΠΏ".The urgency of the work lies in the fact that in the context of toughening of competitive struggle, any company is forced to manage its competitiveness on the basis of the developed competitive strategy.
During the research, the study and systematization of information on the subject and object of the study was conducted. Sources of information are listed in the list of sources used.
The scientific novelty of the work is to develop recommendations for increasing the competitiveness of the tobacco company.
The work resulted in recommendations for increasing the level of competitiveness of the Shanghai Tobacco Group.
The results of the research will be applied to the activities of the Shanghai Tobacco Group
Neurovascular dysfunction in vascular dementia, Alzheimerβs and atherosclerosis
Efficient blood supply to the brain is of paramount importance to its normal functioning and improper blood flow can result in potentially devastating neurological consequences. Cerebral blood flow in response to neural activity is intrinsically regulated by a complex interplay between various cell types within the brain in a relationship termed neurovascular coupling. The breakdown of neurovascular coupling is evident across a wide variety of both neurological and psychiatric disorders including Alzheimerβs disease. Atherosclerosis is a chronic syndrome affecting the integrity and function of major blood vessels including those that supply the brain, and it is therefore hypothesised that atherosclerosis impairs cerebral blood flow and neurovascular coupling leading to cerebrovascular dysfunction. This review will discuss the mechanisms of neurovascular coupling in health and disease and how atherosclerosis can potentially cause cerebrovascular dysfunction that may lead to cognitive decline as well as stroke. Understanding the mechanisms of neurovascular coupling in health and disease may enable us to develop potential therapies to prevent the breakdown of neurovascular coupling in the treatment of vascular brain diseases including vascular dementia, Alzheimerβs disease and stroke
Data from: Ξ²-adrenergic receptor-dependent alterations in murine cardiac transcript expression are differentially regulated by gefitinib in vivo
Ξ²-adrenergic receptor (Ξ²AR)-mediated transactivation of epidermal growth factor receptor (EGFR) has been shown to promote cardioprotection in a mouse model of heart failure and we recently showed that this mechanism leads to enhanced cell survival in part via regulation of apoptotic transcript expression in isolated primary rat neonatal cardiomyocytes. Thus, we hypothesized that this process could regulate cardiac transcript expression in vivo. To comprehensively assess cardiac transcript alterations in response to acute Ξ²AR-dependent EGFR transactivation, we performed whole transcriptome analysis of hearts from C57BL/6 mice given i.p. injections of the Ξ²AR agonist isoproterenol in the presence or absence of the EGFR antagonist gefitinib for 1 hour. Total cardiac RNA from each treatment group underwent transcriptome analysis, revealing a substantial number of transcripts regulated by each treatment. Gefitinib alone significantly altered the expression of 405 transcripts, while isoproterenol either alone or in conjunction with gefitinib significantly altered 493 and 698 distinct transcripts, respectively. Further statistical analysis was performed, confirming 473 transcripts whose regulation by isoproterenol were significantly altered by gefitinib (isoproterenol-induced up/downregulation antagonized/promoted by gefinitib), including several known to be involved in the regulation of numerous processes including cell death and survival. Thus, Ξ²AR-dependent regulation of cardiac transcript expression in vivo can be modulated by the EGFR antagonist gefitinib
Data from: Ξ²-adrenergic receptor-dependent alterations in murine cardiac transcript expression are differentially regulated by gefitinib in vivo
Ξ²-adrenergic receptor (Ξ²AR)-mediated transactivation of epidermal growth factor receptor (EGFR) has been shown to promote cardioprotection in a mouse model of heart failure and we recently showed that this mechanism leads to enhanced cell survival in part via regulation of apoptotic transcript expression in isolated primary rat neonatal cardiomyocytes. Thus, we hypothesized that this process could regulate cardiac transcript expression in vivo. To comprehensively assess cardiac transcript alterations in response to acute Ξ²AR-dependent EGFR transactivation, we performed whole transcriptome analysis of hearts from C57BL/6 mice given i.p. injections of the Ξ²AR agonist isoproterenol in the presence or absence of the EGFR antagonist gefitinib for 1 hour. Total cardiac RNA from each treatment group underwent transcriptome analysis, revealing a substantial number of transcripts regulated by each treatment. Gefitinib alone significantly altered the expression of 405 transcripts, while isoproterenol either alone or in conjunction with gefitinib significantly altered 493 and 698 distinct transcripts, respectively. Further statistical analysis was performed, confirming 473 transcripts whose regulation by isoproterenol were significantly altered by gefitinib (isoproterenol-induced up/downregulation antagonized/promoted by gefinitib), including several known to be involved in the regulation of numerous processes including cell death and survival. Thus, Ξ²AR-dependent regulation of cardiac transcript expression in vivo can be modulated by the EGFR antagonist gefitinib
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