Clinical field studies were conducted in 297 dogs of different breeds undergoing orthopedic or soft tissue surgery. Dogs were administered 2 mg/lb of carprofen two hours prior to surgery then once daily, as needed for 2 days (soft tissue surgery) or 3 days (orthopedic surgery). Carprofen was well tolerated when used in conjunction with a variety of anesthetic-related drugs. The type and severity of abnormal health observations in carprofen-and placebo-treated animals were approximately equal and few in number (see Adverse Reactions ). The most frequent abnormal health observation was vomiting and was observed at approximately the same frequency in carprofen- and placebo- treated animals. Changes in clinicopathologic indices of hematopoetic, renal, hepatic, and clotting function were not clinically significant. The mean post-treatment serum ALT values were IU and IU less than pre-treatment values for dogs receiving carprofen and placebo, respectively. The mean post-treatment AST values were IU less for dogs receiving carprofen and IU greater for dogs receiving placebo.
Patients with a history of drug and/or alcohol abuse are believed to have an increased risk of abusing delorazepam (as well as all other benzodiazepines), this must be considered when a physician prescribes delorazepam to such patients. Although all patients being treated with delorazepam should be routinely monitored for signs of abuse and diversion of medication, increased monitoring of patients with a history of drug and/or alcohol abuse is always warranted. Benzodiazepine abuse in patients taking them as prescribed on an as-needed basis for chronic/refractory anxiety, insomnia, and intermittent muscle spasms has occurred and generally occurs very slowly, becoming evident only after months or years since the initiation of therapy. Monitoring of patients actively using delorazepam should never be discontinued even if the patients has been stable on the medication for many months or years.
It should be noted that in theory if one was to consistently suppress your natural estrogen levels for a long period of time, this would negatively impact your health, including your cholesterol. Due to the ability of Letrozole- to inhibit estrogen so much, this should definitely be a concern to most users. However the research that has focused on the relationship between use of letrozole and cholesterol levels is rather inconsistent in it's findings. Many studies have concluded that the compound is detrimental to both a user's HDL and LDL cholesterol levels, while other research has found no link. Obviously individuals are best served to monitor their cholesterol while using any compound via blood tests however barring that, letrozole should simply not be run for extended periods of time if at all possible. Doing so could cause serious medical complications.
Along with the issues related to blood lipids is the fact that many users complain that their libido is dramatically reduced when using the compound. This is related to the fact that estrogen is partly responsible for the regulation of an individual's sex drive. Since Letrozole- is so potent it can often drive estrogen levels too low and this inhibits a user's libido. To avoid this users can lower dosages, but some anecdotally report that even extremely low doses of the drug can cause problems. If this is the case a less potent compound such as exemestane or anastrozole may be a more appropriate option.
In normal tissue, DIM (300nM) can activate the ATM genetic repair pathway in response to irradiation damage in a manner dependent on BRCA1 (one of its targets  ) without increasing survival of breast cancer cells (MDA-MB-231  ); there are known alterations in this pathway in some breast cancers where BRCA1 is reduced while ATM itself seems to be hyperactive, and oral supplementation of 300mg DIM has been noted to increase BRCA1 mRNA levels after 4-6 weeks supplementation (measured in white blood cells) in women who had a low activity mutation. 
In normal tissue, DIM (300nM) can activate the ATM genetic repair pathway in response to irradiation damage in a manner dependent on BRCA1 (one of its targets  ) without increasing survival of breast cancer cells (MDA-MB-231  ); there are known alterations in this pathway in some breast cancers where BRCA1 is reduced while ATM itself seems to be hyperactive, and oral supplementation of 300mg DIM has been noted to increase BRCA1 mRNA levels after 4-6 weeks supplementation (measured in white blood cells) in women who had a low activity mutation.