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Post by itellthefuture777 on Mar 23, 2020 14:32:17 GMT -5
Some information I read online indicated inhaled insulin reduces inflammation of the lung alveolar ..in part... "Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are forms of pulmonary edema that result from robust local and systemic inflammatory states, such as sepsis. The morbidity and mortality associated with ALI and ARDS are significant and the treatment of these conditions presents a formidable challenge. Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. For instance, insulin inhibits NF-kappaB--dependent synthesis of pro-inflammatory factors and attenuates production of ROS. Indeed, intravenous administration of insulin ameliorates pulmonary injury and dysfunction in the LPS model of ALI. Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. We propose that administering inhalable insulin to hyperglycemic ALI/ARDS patients could directly reduce alveolar inflammation while reducing circulating glucose levels"
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Post by itellthefuture777 on Mar 23, 2020 14:35:47 GMT -5
Some information I read online indicated inhaled insulin reduces inflammation of the lung alveolar ..in part... "Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are forms of pulmonary edema that result from robust local and systemic inflammatory states, such as sepsis. The morbidity and mortality associated with ALI and ARDS are significant and the treatment of these conditions presents a formidable challenge. Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. For instance, insulin inhibits NF-kappaB--dependent synthesis of pro-inflammatory factors and attenuates production of ROS. Indeed, intravenous administration of insulin ameliorates pulmonary injury and dysfunction in the LPS model of ALI. Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. We propose that administering inhalable insulin to hyperglycemic ALI/ARDS patients could directly reduce alveolar inflammation while reducing circulating glucose levels" ... This suggested the preferential effects of insulin in reducing the levels of these cytokines and insulin's apparent anti-inflammatory role in counterbalancing the physiologic responses to high glucose [28]. Recently, intravenous insulin treatment showed inhibition on the expression of nuclear factor-kappa B (NF-κB) and TLR4 in a LPS-induced lung injury model [29], but the present results have just confirmed an inference that insulin in an inhaled form capable of reaching the alveoli may exert a local anti-inflammatory effect [30]
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Post by itellthefuture777 on Mar 23, 2020 14:40:02 GMT -5
Some information I read online indicated inhaled insulin reduces inflammation of the lung alveolar ..in part... "Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are forms of pulmonary edema that result from robust local and systemic inflammatory states, such as sepsis. The morbidity and mortality associated with ALI and ARDS are significant and the treatment of these conditions presents a formidable challenge. Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. For instance, insulin inhibits NF-kappaB--dependent synthesis of pro-inflammatory factors and attenuates production of ROS. Indeed, intravenous administration of insulin ameliorates pulmonary injury and dysfunction in the LPS model of ALI. Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. We propose that administering inhalable insulin to hyperglycemic ALI/ARDS patients could directly reduce alveolar inflammation while reducing circulating glucose levels" ... This suggested the preferential effects of insulin in reducing the levels of these cytokines and insulin's apparent anti-inflammatory role in counterbalancing the physiologic responses to high glucose [28]. Recently, intravenous insulin treatment showed inhibition on the expression of nuclear factor-kappa B (NF-κB) and TLR4 in a LPS-induced lung injury model [29], but the present results have just confirmed an inference that insulin in an inhaled form capable of reaching the alveoli may exert a local anti-inflammatory effect [30] youtu.be/okg7uq_HrhQ
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Post by mango on Mar 23, 2020 16:04:02 GMT -5
Some information I read online indicated inhaled insulin reduces inflammation of the lung alveolar ..in part... "Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are forms of pulmonary edema that result from robust local and systemic inflammatory states, such as sepsis. The morbidity and mortality associated with ALI and ARDS are significant and the treatment of these conditions presents a formidable challenge. Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. For instance, insulin inhibits NF-kappaB--dependent synthesis of pro-inflammatory factors and attenuates production of ROS. Indeed, intravenous administration of insulin ameliorates pulmonary injury and dysfunction in the LPS model of ALI. Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. We propose that administering inhalable insulin to hyperglycemic ALI/ARDS patients could directly reduce alveolar inflammation while reducing circulating glucose levels" As sayhey24 has mentioned several times here, many people actually see improvement in lung function following use of Afrezza. Nice finds
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Post by Clement on Mar 23, 2020 16:20:04 GMT -5
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Post by mango on Mar 23, 2020 22:45:54 GMT -5
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Post by peppy on Mar 25, 2020 14:38:33 GMT -5
Some information I read online indicated inhaled insulin reduces inflammation of the lung alveolar ..in part... "Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are forms of pulmonary edema that result from robust local and systemic inflammatory states, such as sepsis. The morbidity and mortality associated with ALI and ARDS are significant and the treatment of these conditions presents a formidable challenge. Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. For instance, insulin inhibits NF-kappaB--dependent synthesis of pro-inflammatory factors and attenuates production of ROS. Indeed, intravenous administration of insulin ameliorates pulmonary injury and dysfunction in the LPS model of ALI. Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. We propose that administering inhalable insulin to hyperglycemic ALI/ARDS patients could directly reduce alveolar inflammation while reducing circulating glucose levels" itellthefuture777mangoAll Do you see/ have you seen any patents for technosphere immunization delivering antibodies?
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Post by mango on Mar 25, 2020 14:55:28 GMT -5
Some information I read online indicated inhaled insulin reduces inflammation of the lung alveolar ..in part... "Acute lung injury (ALI) and the more severe acute respiratory distress syndrome (ARDS) are forms of pulmonary edema that result from robust local and systemic inflammatory states, such as sepsis. The morbidity and mortality associated with ALI and ARDS are significant and the treatment of these conditions presents a formidable challenge. Controlling hyperglycemia with insulin is a core component of patient management in the critically ill. Insulin treatment also exerts beneficial metabolic effects beyond glucose control, as well as non-metabolic effects, in insulin-resistant states. For instance, insulin inhibits NF-kappaB--dependent synthesis of pro-inflammatory factors and attenuates production of ROS. Indeed, intravenous administration of insulin ameliorates pulmonary injury and dysfunction in the LPS model of ALI. Most recently, an inhalable insulin formulation was shown to effectively reduce glucose concentrations with minimal impact on long-term pulmonary function. We propose that administering inhalable insulin to hyperglycemic ALI/ARDS patients could directly reduce alveolar inflammation while reducing circulating glucose levels" itellthefuture777mangoAll Do you see/ have you seen any patents for technosphere immunization delivering antibodies? This one immediately comes to mind patents.google.com/patent/US9410957B2/en
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Post by mango on Mar 25, 2020 14:58:18 GMT -5
Monoclonal antibodies are really cool stuff. This is what I am thinking the ARDS treatment is. They are genetically engineered antibodies that use the innate immune system. Really fascinating to read and learn about.
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Post by mango on Mar 25, 2020 15:11:03 GMT -5
They can be monovalent meaning target one specific epitope on an antigen or bispecific, targeting two different kinds of antigen. Anyways, when the antigen triggers a response, B cells will form clones of cells that will release the same antibodies (immunoglobulins). The antibodies that came from the cloned B cells are the actual monoclonal antibodies. liane did I get that right?
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