Osteoporosis, as a progressive metabolic bone disease, can lead to fractures in patients, especially elderly patients, and seriously affect the quality of life of patients and even threaten the lives of patients. Existing drug treatment can reduce the risk of fracture in patients, reduce bone loss, but can not rebuild the microstructure of damaged bone. Therefore, despite the use of existing therapeutic drugs, many patients still suffer from fractures or the risk of fractures is still high. There is an urgent need for new osteoporosis therapies that can improve bone structure, with the goal of further reducing fracture risk. In addition, recombinant teriparatide [rh PTH(1-34)], a parathyroid hormone (PTH) drug that has recently been approved for clinical use in China, can not only increase the formation of new bone, but also repair the microstructure of bone and improve the cortical bone. Geometry reduces the incidence of vertebral fractures and also reduces the incidence of non-vertebral fractures.
Mechanism of action PTH is secreted by the parathyroid gland and is an important regulator of blood calcium concentration. Decreased blood calcium concentration can stimulate the synthesis and secretion of PTH. PTH has three effects: increased bone calcium release; reduced calcium removal from the kidney; stimulation of 1,25(OH)2D3 (increases calcium absorption).
Although a major role of PTH is to stimulate bone resorption by osteoclasts, studies have provided compelling evidence that osteogenic cells of the osteoblast line are a major target of PTH.
The intermittent use of PTH increases the number of osteoblasts and increases bone formation. Experiments have shown that the increase in the number of mature rat osteoblasts stimulates periosteal cells that do not have bone turnover activity, allowing them to function like osteoblasts.
According to research reports, daily injection of PTH to mice can prolong the lifespan of mature osteoblasts. Its action pathway is to prevent apoptosis, increase the number of osteoblasts, accelerate bone formation and increase bone mass.
The effect of PTH on bone depends on the way the systemic medication is used. The daily administration of PTH once stimulated the formation of new bone on the trabecular and cortical bone surfaces by preferentially stimulating the activity of osteoblasts rather than the activity of osteoclasts. This effect of PTH can rapidly increase bone mass and increase bone turnover index. By increasing the formation of new bone, PTH can improve the bone's microstructure, increase bone mass, and increase bone strength, thereby reducing the risk of fractures. Although many factors are involved in the process of bone formation, the selective down-regulation of osteoclast differentiation factor (RANKL) and the stimulation of osteoblasts secreting osteoprotegerin (OPG) seem to play a key role. On the contrary, endogenous PTH is persistently excessive, such as severe hyperparathyroidism, which is harmful to the bone because the stimulation of bone resorption is greater than the stimulation of bone formation.
Clinical studies Teriparatide 20 μg was treated in a study involving 1326 patients who had similar baseline factors and 25-hydroxyvitamin D values ​​associated with new vertebral fractures compared with placebo. The relative risk of ≥ 1 new vertebral fracture in the group and the 40 μg treatment group was reduced by 65% ​​and 69%, respectively.
In another fracture prevention trial involving 1637 postmenopausal women (1326 patients had an appraisal baseline X-ray and X-rays reviewed, 55 of them had at least one new moderate or severe vertebrae Fractures. Baseline factors associated with new vertebral fractures and blood 25-hydroxyvitamin D values ​​were similar.) Compared to the placebo group, there was at least 1 new occurrence of teriparatide in the 20 μg and 40 μg treatment groups. The relative risk of moderate or severe vertebral fractures was reduced by 90% and 78%, respectively; the relative risk of ≥ 2 new non-vertebral fragility fractures was reduced by 53% and 54%, respectively.
In the fracture prevention trial, the overall difference in adverse events between treatment groups was not statistically significant (P = 0.098). Compared with the placebo group, the total incidence of adverse events during the treatment period was significantly lower in the teriparatide 20 μg/d treatment group (P=0.047).
There was no statistically significant difference in the incidence of dizziness in each treatment group. Dizziness was the most commonly reported adverse neurological event. Dizziness was reported in 33 patients (6.1%) in the placebo group, 50 (9.2%) in the 20 μg group, and 44 (8.0%) in the 40 μg group (P=0.144). .
The incidence of nausea and headache in the 20 μg group was similar to that in the placebo group, with 3% of patients reporting leg cramps. The 40 μg group reported significantly more nausea and headache than the placebo group (P<0.001). The incidence of leg paralysis in the 40 μg group was similar to that in the placebo group.
126 patients (7.7%) withdrew due to adverse events: 32 patients (5.9%/544 patients) in the placebo group, 30 patients (6.5%/541 patients) with teriparatide 20 μg, and 40 μg of teriparatide There were 59 cases (10.7%/552 cases) in the group.
Studies and discussions of preclinical studies have shown that as a synthetic drug, intermittent use of PTH may stimulate the reconstruction of osteoblasts and bone. Clinical trials have demonstrated that intermittent use of PTH can rapidly and dramatically increase bone mineral density (BMD) and prevent new fractures.
PTH is effective for both men and women and is effective for both primary osteoporosis and glucocorticoid-induced osteoporosis.
In summary, PTH can improve the microstructure of cortical bone and trabecular bone, thereby improving the biomechanical properties of bone and reducing the risk of new fractures.
Related Links Treatment and prevention of osteoporosis drugs are divided into two major categories based on their mechanism of action: one is bone resorption inhibitors, and the other is drugs that stimulate bone formation. Drugs that inhibit bone resorption include: estrogens and estrogens + progestogens, selective estrogen receptor modulators (eg, raloxifene, Evita), calcitonin, and bisphosphonates (alendronate phosphate, and risperidone Salts, zoledronic acid, etc.); drugs that stimulate bone formation include fluoride (which can significantly increase bone density, but at the same time increase bone density, its brittleness also increases significantly, resulting in a decrease in bone strength, which is not currently used), Parathyroid hormone. Others include drugs that have a combination of action mechanisms: active vitamins and lanthanum levulinate. At the same time, calcium and vitamin D are recommended for all women at risk of osteoporosis.
Mechanism of action PTH is secreted by the parathyroid gland and is an important regulator of blood calcium concentration. Decreased blood calcium concentration can stimulate the synthesis and secretion of PTH. PTH has three effects: increased bone calcium release; reduced calcium removal from the kidney; stimulation of 1,25(OH)2D3 (increases calcium absorption).
Although a major role of PTH is to stimulate bone resorption by osteoclasts, studies have provided compelling evidence that osteogenic cells of the osteoblast line are a major target of PTH.
The intermittent use of PTH increases the number of osteoblasts and increases bone formation. Experiments have shown that the increase in the number of mature rat osteoblasts stimulates periosteal cells that do not have bone turnover activity, allowing them to function like osteoblasts.
According to research reports, daily injection of PTH to mice can prolong the lifespan of mature osteoblasts. Its action pathway is to prevent apoptosis, increase the number of osteoblasts, accelerate bone formation and increase bone mass.
The effect of PTH on bone depends on the way the systemic medication is used. The daily administration of PTH once stimulated the formation of new bone on the trabecular and cortical bone surfaces by preferentially stimulating the activity of osteoblasts rather than the activity of osteoclasts. This effect of PTH can rapidly increase bone mass and increase bone turnover index. By increasing the formation of new bone, PTH can improve the bone's microstructure, increase bone mass, and increase bone strength, thereby reducing the risk of fractures. Although many factors are involved in the process of bone formation, the selective down-regulation of osteoclast differentiation factor (RANKL) and the stimulation of osteoblasts secreting osteoprotegerin (OPG) seem to play a key role. On the contrary, endogenous PTH is persistently excessive, such as severe hyperparathyroidism, which is harmful to the bone because the stimulation of bone resorption is greater than the stimulation of bone formation.
Clinical studies Teriparatide 20 μg was treated in a study involving 1326 patients who had similar baseline factors and 25-hydroxyvitamin D values ​​associated with new vertebral fractures compared with placebo. The relative risk of ≥ 1 new vertebral fracture in the group and the 40 μg treatment group was reduced by 65% ​​and 69%, respectively.
In another fracture prevention trial involving 1637 postmenopausal women (1326 patients had an appraisal baseline X-ray and X-rays reviewed, 55 of them had at least one new moderate or severe vertebrae Fractures. Baseline factors associated with new vertebral fractures and blood 25-hydroxyvitamin D values ​​were similar.) Compared to the placebo group, there was at least 1 new occurrence of teriparatide in the 20 μg and 40 μg treatment groups. The relative risk of moderate or severe vertebral fractures was reduced by 90% and 78%, respectively; the relative risk of ≥ 2 new non-vertebral fragility fractures was reduced by 53% and 54%, respectively.
In the fracture prevention trial, the overall difference in adverse events between treatment groups was not statistically significant (P = 0.098). Compared with the placebo group, the total incidence of adverse events during the treatment period was significantly lower in the teriparatide 20 μg/d treatment group (P=0.047).
There was no statistically significant difference in the incidence of dizziness in each treatment group. Dizziness was the most commonly reported adverse neurological event. Dizziness was reported in 33 patients (6.1%) in the placebo group, 50 (9.2%) in the 20 μg group, and 44 (8.0%) in the 40 μg group (P=0.144). .
The incidence of nausea and headache in the 20 μg group was similar to that in the placebo group, with 3% of patients reporting leg cramps. The 40 μg group reported significantly more nausea and headache than the placebo group (P<0.001). The incidence of leg paralysis in the 40 μg group was similar to that in the placebo group.
126 patients (7.7%) withdrew due to adverse events: 32 patients (5.9%/544 patients) in the placebo group, 30 patients (6.5%/541 patients) with teriparatide 20 μg, and 40 μg of teriparatide There were 59 cases (10.7%/552 cases) in the group.
Studies and discussions of preclinical studies have shown that as a synthetic drug, intermittent use of PTH may stimulate the reconstruction of osteoblasts and bone. Clinical trials have demonstrated that intermittent use of PTH can rapidly and dramatically increase bone mineral density (BMD) and prevent new fractures.
PTH is effective for both men and women and is effective for both primary osteoporosis and glucocorticoid-induced osteoporosis.
In summary, PTH can improve the microstructure of cortical bone and trabecular bone, thereby improving the biomechanical properties of bone and reducing the risk of new fractures.
Related Links Treatment and prevention of osteoporosis drugs are divided into two major categories based on their mechanism of action: one is bone resorption inhibitors, and the other is drugs that stimulate bone formation. Drugs that inhibit bone resorption include: estrogens and estrogens + progestogens, selective estrogen receptor modulators (eg, raloxifene, Evita), calcitonin, and bisphosphonates (alendronate phosphate, and risperidone Salts, zoledronic acid, etc.); drugs that stimulate bone formation include fluoride (which can significantly increase bone density, but at the same time increase bone density, its brittleness also increases significantly, resulting in a decrease in bone strength, which is not currently used), Parathyroid hormone. Others include drugs that have a combination of action mechanisms: active vitamins and lanthanum levulinate. At the same time, calcium and vitamin D are recommended for all women at risk of osteoporosis.
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