Fmoc-L-Cysteinol(Acm)
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Fmoc-L-Cysteinol(Acm)

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Category
Amino Alcohol
Catalog number
BAT-000630
CAS number
198543-46-3
Molecular Formula
C21H24N2O4S
Molecular Weight
400.5
Fmoc-L-Cysteinol(Acm)
IUPAC Name
9H-fluoren-9-ylmethyl N-[(2R)-1-(acetamidomethylsulfanyl)-3-hydroxypropan-2-yl]carbamate
Synonyms
Fmoc-S-acetamidomethyl-L-cysteinol; Fmoc-L-Cys(Acm)-ol
Purity
≥ 98% (HPLC)
Melting Point
135-137 °C
Storage
Store at 2-8 °C
InChI
InChI=1S/C21H24N2O4S/c1-14(25)22-13-28-12-15(10-24)23-21(26)27-11-20-18-8-4-2-6-16(18)17-7-3-5-9-19(17)20/h2-9,15,20,24H,10-13H2,1H3,(H,22,25)(H,23,26)/t15-/m1/s1
InChI Key
ILFFSHOJZXAWJQ-OAHLLOKOSA-N
Canonical SMILES
CC(=O)NCSCC(CO)NC(=O)OCC1C2=CC=CC=C2C3=CC=CC=C13
1. Arnold-Chiari Malformation: Core Concepts
Kristina Fons, Amy J Jnah Neonatal Netw. 2021 Aug 1;40(5):313-320. doi: 10.1891/11-T-704.
Arnold-Chiari malformation (ACM), a defect that involves downward displacement of the hindbrain and herniation of the cerebellar vermis, tonsils, pons, medulla, and fourth ventricle through the foramen magnum, is the most complex of the 4 types of Chiari malformations. Unique to the other types of Chiari malformations, approximately 95 percent of infants with ACM also present with an associated myelomeningocele (MMC), the most severe form of spina bifida. Among affected infants, those with symptomatic comorbidities incur a significantly higher morbidity and mortality risk. Prompt identification and diagnosis of ACM, as well as evidence-based postnatal and postsurgical nursing and medical care, is critical. Early surgical intervention can repair an existing MMC and restore proper cerebrospinal fluid circulation, which can dramatically improve patient outcomes and quality of life, and reduce disease and health care burden.
2. The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy
Joaquim Fernández-Solà Nutrients. 2020 Feb 22;12(2):572. doi: 10.3390/nu12020572.
Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.
3. A Non-Linear Association of Triglyceride Glycemic Index With Cardiovascular and All-Cause Mortality Among Patients With Hypertension
Dan Zhou, Xiao-Cong Liu, Lo Kenneth, Yu-Qing Huang, Ying-Qing Feng Front Cardiovasc Med. 2022 Jan 27;8:778038. doi: 10.3389/fcvm.2021.778038. eCollection 2021.
Background: To investigate the association between insulin resistance (IR), quantified by triglyceride glycemic index (TyG index), cardiovascular mortality (CVM), and all-cause mortality (ACM) in hypertension patients. Methods: We included 8,554 patients with hypertension aged ≥18 years old from the 1999-2014 National Health and Nutrition Examination Surveys (NHANES). The status of CVM and ACM of participants were followed through December 31, 2015. Cox proportional hazards models and Kaplan-Meier survival curves were used to evaluate the relationship between TyG index, CVM, and ACM. Results: During a median of 82 months follow-up, 1,882 mortality cases had occurred, 434 of which were due to cardiovascular disease. The patients with hypertension with TyG ≥ 10 were older, had a higher chance of being smokers, were obese, had higher blood pressure, and had risk or had cardiovascular disease. In Cox proportional hazards models, compared with the patients with TyG <8, those with TyG ≥ 10 had 56% increased risk for ACM. On the other hand, no significant difference for CVM between the four groups were observed. In the restricted cubic spline regression models, the relationship between TyG index and ACM was non-linear. Subgroup analysis showed non-linear relationship between TyG index and ACM in elderly patients aged ≥60 years. The cut-off value of TyG for ACM was 9.45, and those with higher or lower than 9.45 had more risk of ACM. When TyG index was more than 9.52, the risk for CVM would increase among the whole group. Kaplan-Meier survival curves showed patients with TyG ≥ 10 had higher risk of ACM and CVM (Log rank P < 0.05). Conclusions: We demonstrated that the association between ACM and TyG index in elderly patients with hypertension aged ≥60 years was non-linear. However, TyG index was only more than 9.52, hence, the risk for CVM would increase among the whole hypertension group.
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