Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The information submitted is knowledge accumulated over years of experience teaching dentists how to bill medical insurance. This is supplemented with a good number of personal expert witness testimonies in criminal and malpractice insurance cases. The objective is to prevent problems before they start with the prudent use of information. My experience in court testimony on these issues has shown me that there is an army of lawyers, insurance company fraud examiners, and dentists working for the aforementioned, just waiting for you to improperly use this method of insurance reimbursement. Use this only if you understand the nuances of what it is you are doing! For example, any procedure you bill to dental insurance using CDT-2 codes can be billed to medical insurance using medical insurance CPT-95 codes. The difference is that if the procedure is not a covered medical expense, it will not be paid by the medical insurance carrier. I strongly suggest that you do not fall into the trap of obfuscating these codes. There are a number of so-called insurance "gurus" teaching dentists how to write confusing and misleading operative reports so as to obtain reimbursement for procedures that normally would not be covered. I beseech you--please do not do it! The penalties are severe. You will experience a significant increase in payments from the medical insurance when procedures are submitted in the proper manner. More and more computerized dental insurance management programs are offering their clients the ability to automatically cross-code and submit dental/medical insurance claims. It is a recognized ability of dentists to do such. Billing responsibly is of the utmost importance.
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PMID:How to complete a medical insurance form. 961 Feb 82

Our aim was to assess thermal sensitivity in both trigeminal and extra-trigeminal regions in patients with myofascial temporomandibular disorder (TMD) but without comorbid conditions as compared to age-matched controls. Twenty women (age 24 +/- 3 years) diagnosed with myofascial TMD according to the research diagnostic criteria for TMD and 20 healthy women (age 24 +/- 4 years) were included. Warm and cold detection thresholds (WDT and CDT, respectively) and heat and cold pain thresholds (HPT and CPT, respectively) were bilaterally assessed over the masseter and frontalis muscles (trigeminal regions) and the wrist (extra-trigeminal region). The mean of three determinations at each site was calculated and used for analysis. The order of the test sites was randomized. A two-way ANOVA was used to test for differences between groups and sides (most painful/contra-lateral side; dominant/non-dominant). No significant differences between groups for WDT or CDT in trigeminal and extra-trigeminal regions (ANOVA, P > 0.389) were found. There were significant differences between groups, but not between sides, for HPT and CPT in both trigeminal and extra-trigeminal areas (ANOVA, P < 0.001). CPT (P < 0.001) over the trigeminal area was positively correlated with both pain intensity and duration of pain symptoms: the longer the history of pain or the greater the pain intensity, the higher the CPT (i.e., the greater cold hyperalgesia) over the trigeminal region. Our findings revealed bilateral thermal hyperalgesia (lower HPT and higher CPT) but normal WDT and CDT in trigeminal and extra-trigeminal regions in women with myofascial TMD as compared to healthy controls. Bilateral heat/cold hyperalgesia in trigeminal and extra-trigeminal areas may reflect a dysfunction of thermal channels in myofascial TMD patients as result of some combination of peripheral sensitization, facilitation of central nociceptive processing and/or decreased descending inhibition.
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PMID:Bilateral thermal hyperalgesia in trigeminal and extra-trigeminal regions in patients with myofascial temporomandibular disorders. 2001 56

Tuberous sclerosis complex 1 (TSC1) inhibits mammalian target of rapamycin (mTOR), a central promotor of cell growth and proliferation. The protein product of the TSC1 gene, hamartin (referred to as TSC1) is known to interact with Polo-like kinase 1 (Plk1) in a cell cycle regulated, phosphorylation-dependent manner. We hypothesized that the p53 target gene, Plk2, is a tumor suppressor, mediating its tumor suppressor function through interactions with TSC1 that facilitate TSC1/2 restraint of mTOR under hypoxic stress. We found that human lung tumor cells deficient in Plk2 grew larger than control tumors, and that Plk2 interacts with endogenous TSC1 protein. Additionally, C-terminal Plk2-GST fusion protein bound both TSC1 and TSC2 proteins. TSC1 levels were elevated in response to Adriamycin and cells transiently overexpressing Plk2 demonstrated decreased phosphorylation of the downstream target of mTOR, ribosomal protein p70S6 kinase during hypoxia. Plk2 levels were inversely correlated with cytoplasmic p70S6K phosphorylation. Plk2 levels did not increase in response to DNA damage (Adriamycin, CPT -11) when HCT 116 and H460 cells were exposed to hypoxia. TSC1-deficient mouse embryonic fibroblasts with TSC1 added back demonstrated decreased S6K phosphorylation, which was further decreased when Plk2 was transiently overexpressed. Interestingly, under normoxia, Plk2 deficient tumor cells demonstrated increased apoptosis in response to various chemotherapeutic agents including CPT -11 but increased resistance to apoptotic death after CPT-11 treatment under hypoxia, and tumor xenografts comprised of these Plk2-deficient cells were resistant to CPT -11. Our results point to a novel Plk2-TSC1 interaction with effects on mTOR signaling during hypoxia, and tumor growth that may enable targeting Plk2 signaling in cancer therapy.
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PMID:The p53 target Plk2 interacts with TSC proteins impacting mTOR signaling, tumor growth and chemosensitivity under hypoxic conditions. 2005 36