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Bs En 933 Pdf 40
l - length of boltd - the nominal diameter of the threadk - head heightr - radiuse - the diameter of the circumscribed circle (not less than)s - size hex head turnkeyc - thickness of the mounting collara - length undercut
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Data extraction and synthesis: Two reviewers independently extracted data on populations, interventions, outcomes, risk of bias, and quality of evidence. A Bayesian framework was used to perform a series of random-effects network meta-analyses with meta-regression to estimate the relative effectiveness of diet classes and programs for change in weight and body mass index from baseline. Our analyses adjusted for behavioral support and exercise.
Results: Among 59 eligible articles reporting 48 unique randomized trials (including 7286 individuals) and compared with no diet, the largest weight loss was associated with low-carbohydrate diets (8.73 kg [95% credible interval CI, 7.27 to 10.20 kg] at 6-month follow-up and 7.25 kg [95% CI, 5.33 to 9.25 kg] at 12-month follow-up) and low-fat diets (7.99 kg [95% CI, 6.01 to 9.92 kg] at 6-month follow-up and 7.27 kg [95% CI, 5.26 to 9.34 kg] at 12-month follow-up). Weight loss differences between individual diets were minimal. For example, the Atkins diet resulted in a 1.71 kg greater weight loss than the Zone diet at 6-month follow-up. Between 6- and 12-month follow-up, the influence of behavioral support (3.23 kg [95% CI, 2.23 to 4.23 kg] at 6-month follow-up vs 1.08 kg [95% CI, -1.82 to 3.96 kg] at 12-month follow-up) and exercise (0.64 kg [95% CI, -0.35 to 1.66 kg] vs 2.13 kg [95% CI, 0.43 to 3.85 kg], respectively) on weight loss differed.
Conclusions and relevance: Significant weight loss was observed with any low-carbohydrate or low-fat diet. Weight loss differences between individual named diets were small. This supports the practice of recommending any diet that a patient will adhere to in order to lose weight.
Major risk factors include alcohol consumption and tobacco use. Most studies have shown that alcohol is the primary risk factor but smoking in combination with alcohol consumption may have a synergistic effect and increase the relative risk. The relative risk in men who used both heavy tobacco and alcohol was 35.4 in white males and 149.2 in black males compared to men of the same race and region who were non-smokers or drinkers[12]. The mechanism of how tobacco and alcohol in combination lead to increased risk of esophageal cancer has been extensively studied. Alcohol can damage the cellular DNA by decreasing metabolic activity within the cell and therefore reduce detoxification function while promoting oxidation[13]. Alcohol is a solvent, specifically of fat-soluble compounds. Therefore, the hazardous carcinogens within tobacco are able to penetrate the esophageal epithelium easier[14]. Some of the carcinogens in tobacco include aromatic amines, nitrosamines, polycyclic aromatic hydrocarbons, aldehydes and phenols.
Some studies have shown that the risk of adenocarcinoma of the esophagus may be affected by the extent of esophagus lined by esophageal metaplasia[18]. The longer the segment of esophagus affected the higher the risk of adenocarcinoma. However, given the fact that short segment esophageal metaplasia is more common in the general population, many cases of adenocarcinoma occur in patients with short-segment metaplasia. Less than five percent of patients diagnosed with adenocarcinoma of the esophagus had a prior diagnosis of BE[19]. The risk of developing esophageal cancer is 50-100 times more likely in those patients with BE[15]. However, a majority of patients with BE will not develop EAC, the annual risk in patients with BE has been reported as 0.12%[20].
Another risk factor for EAC is obesity, specifically in those individuals with predominately abdominal centered fat distribution. Hypertrophied adipocytes and inflammatory cells within fat deposits create an environment of low-grade inflammation and promote tumor development through the release of adipokines and cytokines[23]. Adipocytes in the tumor microenvironment supply energy production and support tumor growth and progression[22].
EUS has been shown to be more accurate in determining nodal involvement in esophageal cancer, with an accuracy of 72%-80%[44]. Accuracy has increased greatly with the use of EUS in combination with United States guided fine-needle aspiration to evaluate for lymph node metastasis.
In the classification system of metastasis set forth by the AJCC, distant metastasis can be subdivided into M1a and M1b. Each of these classifications is crucial in determining possible treatment options. M1a includes metastasis to celiac and cervical lymph node groups. This classification is associated with a better prognosis compared to M1b. Patients classified as M1a often times complete a course of neoadjuvant therapy followed by surgical resection. Patients with M1b include those with distant site metastasis. This classification usually carries a worse prognosis given that surgical resection with curative intent is not indicated in these cases[46].
Cancer causes a hypercoagulable state and this environment encourages tumors to grow and produce more pro-coagulants. D-dimers are the end product of fibrin and fibrinolysis and have been reported to be associated with tumor prognosis, tumor stage, lymph node involvement, and overall survival. One study looked at the plasma D-dimer levels in patients with esophageal cancer before and after surgery as well as patients without cancer. Their research showed that high levels of D-dimers in the pre-operative state correlated with a higher tumor stage and surgery caused more patients to have a hypercoagulable state which shortened their survival time[56].
An article from Cancer Control found that in the United States, neoadjuvant chemoradiotherapy followed by esophagectomy for resectable esophageal cancer, had a better survival rate than those patients treated with surgery alone[72]. A meta-analysis comparing neoadjuvant chemotherapy with surgery vs surgery alone showed a survival increase for those patients who underwent neoadjuvant chemotherapy vs surgery alone[73]. 2ff7e9595c
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