Streptodornase and Streptokinase
Tissue Plasminogen Activator
Laundry Service, Hospital
Purification and cloning of a streptokinase from Streptococcus uberis. (1/634)A bovine plasminogen activator was purified from the culture supernatant of the bovine pathogen Streptococcus uberis NCTC 3858. After the final reverse-phase high-performance liquid chromatography step a single protein with a molecular mass of 32 kDa was detected in the active fraction. A partial peptide map was established, and degenerate primers were designed and used for amplification of fragments of the gene encoding the activator. Inverse PCR was subsequently used for obtaining the full-length gene. The S. uberis plasminogen activator gene (skc) encodes a protein consisting of 286 amino acids including a signal peptide of 25 amino acids. In an amino acid sequence comparison the cloned activator showed an identity of approximately 26% to the streptokinases isolated from Streptococcus equisimilis and Streptococcus pyogenes. Interestingly, the activator from S. uberis was found to lack the C-terminal domain possessed by the streptokinase from S. equisimilis. This is apparently a general feature of the streptokinases of this species; biochemical and genetic analysis of 10 additional strains of S. uberis revealed that 9 of these were highly similar to strain NCTC 3858. Sequencing of the skc gene from three of these strains indicated that the amino acid sequence of the protein is highly conserved within the species. (+info)
Expression and characterization of the intact N-terminal domain of streptokinase. (2/634)Proteolytic studies have enabled two of the three putative domains of the fibrinolytic protein streptokinase to be isolated and characterized (Conejero-Lara F et al., 1996, Protein Sci 5:2583-2591). The N-terminal domain, however, could not be isolated in these experiments because of its susceptibility to proteolytic cleavage. To complete the biophysical characterization of the domain structure of streptokinase we have overexpressed, purified, and characterized the N-terminal region of the protein, residues 1-146. The results show this is cooperatively folded with secondary structure content and overall stability closely similar to those of the equivalent region in the intact protein. (+info)
Low molecular weight heparin (dalteparin) as adjuvant treatment of thrombolysis in acute myocardial infarction--a pilot study: biochemical markers in acute coronary syndromes (BIOMACS II). (3/634)OBJECTIVES: This randomized, double blind, placebo-controlled pilot trial evaluated the effect of dalteparin as an adjuvant to thrombolysis in patients with acute myocardial infarction regarding early reperfusion, recurrent ischemia and patency at 24 h. BACKGROUND: Low-molecular-weight heparin, given subcutaneously twice daily without monitoring, might be an attractive alternative to conventional intravenous heparin in the treatment of acute myocardial infarction. METHODS: In 101 patients dalteparin/placebo 100 IU/kg was given just before streptokinase and a second injection 120 IU/kg after 12 h. Monitoring with continuous vector-ECG was done to obtain signs of early reperfusion and later ischemic episodes. Blood samples for myoglobin were obtained at start and after 90 min to evaluate signs of reperfusion. Coronary angiography was performed after 20-28 h to evaluate TIMI-flow in the infarct-related artery. RESULTS: Dalteparin added to streptokinase tended to provide a higher rate of TIMI grade 3 flow in infarct-related artery compared to placebo, 68% versus 51% (p = 0.10). Dalteparin had no effects on noninvasive signs of early reperfusion. In patients with signs of early reperfusion, there seemed to be a higher rate of TIMI grade 3 flow, 74% versus 46% (myoglobin) (p = 0.04) and 73% versus 52% (vector-ECG) (p = 0.11). Ischemic episodes 6-24 h. after start of treatment were fewer in the dalteparin group, 16% versus 38% (p = 0.04). CONCLUSIONS: When dalteparin was added as an adjuvant to streptokinase and aspirin, there were tendencies for less ECG monitoring evidence of recurrent ischemia and better patency at 24 h, warranting further study. (+info)
The rgg gene of Streptococcus pyogenes NZ131 positively influences extracellular SPE B production. (4/634)Streptococcus pyogenes produces several extracellular proteins, including streptococcal erythrogenic toxin B (SPE B), also known as streptococcal pyrogenic exotoxin B and streptococcal proteinase. Several reports suggest that SPE B contributes to the virulence associated with S. pyogenes; however, little is known about its regulation. Nucleotide sequence data revealed the presence, upstream of the speB gene, of a gene, designated rgg, that was predicted to encode a polypeptide similar to previously described positive regulatory factors. The putative Rgg polypeptide of S. pyogenes NZ131 consisted of 280 amino acids and had a predicted molecular weight of 33,246. To assess the potential role of Rgg in the production of SPE B, the rgg gene was insertionally inactivated in S. pyogenes NZ131, which resulted in markedly decreased SPE B production, as determined both by immunoblotting and caseinolytic activity on agar plates. However, the production of other extracellular products, including streptolysin O, streptokinase, and DNase, was not affected. Complementation of the rgg mutant with an intact rgg gene copy in S. pyogenes NZ131 could restore SPE B production and confirmed that the rgg gene product is involved in the production of SPE B. (+info)
Use of fibrinolytic agents in the management of complicated parapneumonic effusions and empyemas. (5/634)BACKGROUND: Standard treatment for pleural infection includes catheter drainage and antibiotics. Tube drainage often fails if the fluid is loculated by fibrinous adhesions when surgical drainage is needed. Streptokinase may aid the process of pleural drainage, but there have been no controlled trials to assess its efficacy. METHODS: Twenty four patients with infected community acquired parapneumonic effusions were studied. All had either frankly purulent/culture or Gram stain positive pleural fluid (13 cases; 54%) or fluid which fulfilled the biochemical criteria for pleural infection. Fluid was drained with a 14F catheter. The antibiotics used were cefuroxime and metronidazole or were guided by culture. Subjects were randomly assigned to receive intrapleural streptokinase, 250,000 IU daily, or control saline flushes for three days. The primary end points related to the efficacy of pleural drainage--namely, the volume of pleural fluid drained and the chest radiographic response to treatment. Other end points were the number of pleural procedures needed and blood indices of inflammation. RESULTS: The streptokinase group drained more pleural fluid both during the days of streptokinase/control treatment (mean (SD) 391 (200) ml versus 124 (44) ml; difference 267 ml, 95% confidence interval (CI) 144 to 390; p < 0.001) and overall (2564 (1663) ml versus 1059 (502) ml; difference 1505 ml, 95% CI 465 to 2545; p < 0.01). They showed greater improvement on the chest radiograph at discharge, measured as the fall in the maximum dimension of the pleural collection (6.0 (2.7) cm versus 3.4 (2.7) cm; difference 2.9 cm, 95% CI 0.3 to 4.4; p < 0.05) and the overall reduction in pleural fluid collection size (p < 0.05, two tailed Fisher's exact test). Systemic fibrinolysis and bleeding complications did not occur. Surgery was required by three control patients but none in the streptokinase group. CONCLUSIONS: Intrapleural streptokinase probably aids the treatment of pleural infections by improving pleural drainage without causing systemic fibrinolysis or local haemorrhage. (+info)
Empirical treatment with fibrinolysis and early surgery reduces the duration of hospitalization in pleural sepsis. (6/634)The efficacy of three different treatment protocols was compared: 1) simple chest tube drainage (Drain); 2) adjunctive intrapleural streptokinase (IP-SK); and 3) an aggressive empirical approach incorporating SK and early surgical drainage (SK+early OP) in patients with pleural empyema and high-risk parapneumonic effusions. This was a nonrandomized, prospective, controlled time series study of 82 consecutive patients with community-acquired empyema (n=68) and high-risk parapneumonic effusions (n=14). The following three treatment protocols were administered in sequence over 6 years: 1) Drain (n=29, chest catheter drainage); 2) IP-SK (n=23, adjunctive intrapleural fibrinolysis with 250,000 U x day(-1) SK); and 3) SK+early OP (n=30, early surgical drainage was offered to patients who failed to respond promptly following initial drainage plus SK). The average duration of hospital stay in the SK+early OP group was significantly shorter than in the Drain and IP-SK groups. The mortality rate was also significantly lower in the SK+early OP than the Drain groups (3 versus 24%). It was concluded that an empirical treatment strategy which combines adjunctive intrapleural fibrinolysis with early surgical intervention results in shorter hospital stays and may reduce mortality in patients with pleural sepsis. (+info)
Intrapericardial streptokinase in purulent pericarditis. (7/634)Six consecutive children with proven purulent pericarditis were treated with pericardial irrigation with streptokinase. Mean (SD) 861 (678) ml (range 240-2000) of thick purulent fluid was drained, and five children had complete clearance of the pus within 3-8 days. One child developed intrapericardial haemorrhage with a submitral pseudoaneurysm and underwent patch closure of the neck of the aneurysm as well as anterior pericardiectomy. Follow up of 13 to 30 months revealed no pericardial constriction. (+info)
Sustained benefit at 10-14 years follow-up after thrombolytic therapy in myocardial infarction. (8/634)AIMS: To investigate whether the benefit of thrombolytic therapy was sustained beyond the first decade. We report the 10-14 year outcome of 533 patients who were randomized to treatment with intracoronary streptokinase or to conventional therapy during the years 1980-1985. METHODS AND RESULTS: Details of survival and cardiac events were obtained from the civil registry, from medical records or from the patient's physician. At follow-up, 158 patients (59%) of the 269 patients allocated to thrombolytic treatment and only 129 patients (49%) of the 264 conventionally treated patients were alive. The cumulative 1-, 5- and 10-year survival rates were 91%, 81% and 69% in patients treated with streptokinase and 84%, 71% and 59% in the control group, respectively (P=0.02). Reinfarction during 10-years of follow-up was more frequent after thrombolytic therapy, particularly during the first year. Coronary bypass surgery and coronary angioplasty were more frequently performed after thrombolytic therapy. At 10 years approximately 30% of the patients were free from subsequent cardiac events. Independent determinants of mortality were elderly age, indicators of impaired residual left ventricular function, multivessel disease and an inability to perform an exercise test at the time of hospital discharge. CONCLUSION: Improved survival after thrombolytic therapy is maintained beyond the first decade. Age, left ventricular function, multivessel disease and an inability to perform an exercise test were independent predictors for long-term mortality, as they are predictors for early mortality. (+info)
There are different types of myocardial infarctions, including:
1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.
Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.
Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.
Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.
Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.
A condition characterized by the accumulation of pus in the pleural space between the lungs and chest wall, caused by bacterial infection or other inflammatory conditions. Symptoms include fever, chest pain, coughing, and difficulty breathing. Treatment involves antibiotics, drainage of pus, and supportive care.
From the Greek words "empyema" meaning "into the pleura" and "pleural" referring to the space between the lungs and chest wall.
There are several types of empyema, including:
1. Pyogenic empyema: caused by bacterial infection, most commonly with Staphylococcus aureus.
2. Tubercular empyema: caused by tuberculosis infection.
3. Cat-scratch empyema: caused by bacteria entering the pleural space through a scratch or wound.
4. Hemorrhagic empyema: caused by bleeding into the pleural space.
Symptoms of empyema may include:
2. Chest pain that worsens with deep breathing or coughing
3. Coughing up pus or blood
4. Difficulty breathing
6. Loss of appetite
Empyema is diagnosed through a combination of physical examination, chest x-ray, and pleural fluid analysis. A chest x-ray can confirm the presence of pus in the pleural space, while pleural fluid analysis can identify the type of bacteria or other infectious agents present.
Treatment of empyema typically involves antibiotics to eradicate the underlying infection and drainage of the pleural fluid. In some cases, surgical intervention may be necessary to remove infected tissue or repair damaged lung tissue.
The prognosis for empyema depends on the severity of the infection and the promptness and effectiveness of treatment. With prompt and appropriate treatment, the majority of patients with empyema can recover fully. However, delays in diagnosis and treatment can lead to serious complications, including respiratory failure, sepsis, and death.
Preventing the development of empyema requires prompt and effective management of underlying conditions such as pneumonia, tuberculosis, or other respiratory infections. Vaccination against Streptococcus pneumoniae and other bacteria that can cause empyema may also be recommended.
Empyema is a potentially life-threatening condition that requires prompt and appropriate treatment to prevent serious complications and improve outcomes. Awareness of the risk factors, symptoms, diagnosis, and treatment options for empyema can help healthcare providers provide effective care for patients with this condition.
Some common types of streptococcal infections include:
1. Strep throat (pharyngitis): an infection of the throat and tonsils that can cause fever, sore throat, and swollen lymph nodes.
2. Sinusitis: an infection of the sinuses (air-filled cavities in the skull) that can cause headache, facial pain, and nasal congestion.
3. Pneumonia: an infection of the lungs that can cause cough, fever, chills, and shortness of breath.
4. Cellulitis: an infection of the skin and underlying tissue that can cause redness, swelling, and warmth over the affected area.
5. Endocarditis: an infection of the heart valves, which can cause fever, fatigue, and swelling in the legs and abdomen.
6. Meningitis: an infection of the membranes covering the brain and spinal cord that can cause fever, headache, stiff neck, and confusion.
7. Septicemia (blood poisoning): an infection of the bloodstream that can cause fever, chills, rapid heart rate, and low blood pressure.
Streptococcal infections are usually treated with antibiotics, which can help clear the infection and prevent complications. In some cases, hospitalization may be necessary to monitor and treat the infection.
Prevention measures for streptococcal infections include:
1. Good hygiene practices, such as washing hands frequently, especially after contact with someone who is sick.
2. Avoiding close contact with people who have streptococcal infections.
3. Keeping wounds and cuts clean and covered to prevent bacterial entry.
4. Practicing safe sex to prevent the spread of streptococcal infections through sexual contact.
5. Getting vaccinated against streptococcus pneumoniae, which can help prevent pneumonia and other infections caused by this bacterium.
It is important to seek medical attention if you suspect you or someone else may have a streptococcal infection, as early diagnosis and treatment can help prevent complications and improve outcomes.
The symptoms of pulmonary embolism can vary, but may include shortness of breath, chest pain, coughing up blood, rapid heart rate, and fever. In some cases, the clot may be large enough to cause a pulmonary infarction (a " lung injury" caused by lack of oxygen), which can lead to respiratory failure and death.
Pulmonary embolism can be diagnosed with imaging tests such as chest X-rays, CT scans, and ultrasound. Treatment typically involves medications to dissolve the clot or prevent new ones from forming, and in some cases, surgery may be necessary to remove the clot.
Preventive measures include:
* Avoiding prolonged periods of immobility, such as during long-distance travel
* Exercising regularly to improve circulation
* Managing chronic conditions such as high blood pressure and cancer
* Taking blood-thinning medications to prevent clot formation
Early recognition and treatment of pulmonary embolism are critical to reduce the risk of complications and death.
History of invasive and interventional cardiology
Acute limb ischaemia
Institute of Microbial Technology
New York University Grossman School of Medicine
FasX small RNA
William S. Tillett
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- Liver injury was abolished by the anticoagulant heparin and was significantly attenuated by the fibrinolytic agent streptokinase. (nih.gov)
- Patients undergoing invasive procedures or having signs/symptoms of underlying coagulopathy or other increased risk of bleeding (due to other therapies such as coumarin anticoagulants, heparin, tPA, streptokinase, high dose aspirin, or nonsteroidal anti-inflammatory drugs) should be evaluated for hemorrhage. (medscape.com)
- Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. (ox.ac.uk)
- Urokinase, tissue-type plasminogen activator (tPA), and streptokinase have all been used. (medscape.com)
- Urokinase is nonantigenic but more expensive than streptokinase, which limits its use. (medscape.com)
- Early agents included the bacterial enzyme streptokinase and urokinase, an enzyme produced in the kidneys. (nih.gov)
- Interaction of streptokinase and plasminogen. (nih.gov)
- The interaction of streptokinase (SK) with human plasminogen (HPlg) was investigated using truncated SK peptides prepared by gene cloning techniques. (nih.gov)
- Streptokinase acts with plasminogen to convert plasminogen to plasmin. (medscape.com)
- 13. Delivery of tissue plasminogen activator and streptokinase magnetic nanoparticles to target vascular diseases. (nih.gov)
- Activities of aminotransferases after treatment with streptokinase for acute myocardial infarction. (nih.gov)