A Basis for New Testament Chronology

Novozavjetni kronološki problemi su ili unutarnji, te se bave tumačenjem samog teksta, ili vanjski, te se bave odnosom novozavjetnih događaja i svjetovne kronologije. Namjera ovog članka je iznijeti činjenice koje mogu biti poznate, te ukazati na zaključke do kojih se može racionalno doći u vezi s najvažnijim vanjskim kronološkim problemima: datiranje (1) Kristova rođenja, (2) njegova krštenja, i prema tome početka njegova djelovanja i (3) njegova raspeća i uskrsnuća. Kao predgovor tome, potrebno je objasniti više starih kronoloških era i metoda računanja godina.New Testament chronological problems are either internal, concerned with the interpretation of the text itself, or external, concerned with the relation between New Testament events and secular chronology. The purpose of this article is to present the facts that can be known, and to point to the conclusions that may reasonably be reached, on the most important external chronological problems in dating (1) The birth of Christ, (2) His baptism, and thus the beginning of His ministry, and (3) His crucifixion and resurrection. As a preface to this, it is necessary to explain various ancient chronological eras and methods of reckoning years

AN INVESTIGATION OF PROVIDER SELF-INSIGHT INTO THEIR CHRON-IC PAIN MANAGEMENT

poster abstractResearch indicates pain management varies across patient sex, race, and mental health status; however, little is known about the ex-tent to which providers are aware of these influences on their clinical decisions. This preliminary study examines the correspondence be-tween providers’ actual and self-reported use of these variables when making pain-related treatment decisions. We also examined the rela-tionship between providers’ self-awareness and their attitudes about sex, race, and depression. Forty-four participants (24 providers, 20 trainees) made pain treatment decisions for sixteen computer-simulated patients presenting with chronic back pain. Patient sex, race, and depression status were manipulated across vignettes. At study conclusion, participants rated the extent to which nine factors influenced their treatment decisions and completed measures as-sessing their attitudes about sex, race, and depression. Approximately 68% and 91% of participants reported using patient demographic characteristics and mental health symptoms, respectively, to make pain treatment decisions. Participants demonstrated some self-awareness for the influence of patient sex, but not race or depression, on their treatment decisions. Participants’ attitudes about sex and race were not significantly associated with their self-reported or actual use of patient demographic information when making treatment decisions. Of the participants who reportedly used mental health symptoms, higher negative attitudes about depression were significantly associat-ed with greater self-reported influence of mental health symptoms on pain treatment decisions (r=-0.42, p<0.01). However, there was no significant association between depression attitudes and actual use of depression symptoms. These findings suggest that (1) providers’ have some awareness of the influence of patient sex, but not race or de-pression, on their treatment decisions, and (2) providers’ attitudes about sex, race, and depression do not sufficiently explain this general lack of awareness. These findings have important clinical implications and may inform interventions to improve pain management and re-duce pain disparities

Methods for preventing or treating insulin resistance

The invention provides methods of preventing or treating insulin resistance in a mammalian subject. The methods comprise administering to the subject an effective amount of an aromatic-cationic peptide having at least one net positive charge; a minimum of four amino acids; a maximum of about twenty amino acids; a relationship between the minimum number of net positive charges (pm) and the total number of amino acid residues (r) wherein 3pm is the largest number that is less than or equal to r + 1; and a relationship between the minimum number of aromatic groups (a) and the total number of net positive charges (pt) wherein 2a is the largest number that is less than or equal to pt + 1, except that when a is 1, pt may also be 1

Overexpression of Long-Chain Acyl-CoA Synthetase 5 Increases Fatty Acid Oxidation and Free Radical Formation While Attenuating Insulin Signaling in Primary Human Skeletal Myotubes

In rodent skeletal muscle, acyl-coenzyme A (CoA) synthetase 5 (ACSL-5) is suggested to localize to the mitochondria but its precise function in human skeletal muscle is unknown. The purpose of these studies was to define the role of ACSL-5 in mitochondrial fatty acid metabolism and the potential effects on insulin action in human skeletal muscle cells (HSKMC). Primary myoblasts isolated from vastus lateralis (obese women (body mass index (BMI) = 34.7 ± 3.1 kg/m2)) were transfected with ACSL-5 plasmid DNA or green fluorescent protein (GFP) vector (control), differentiated into myotubes, and harvested (7 days). HSKMC were assayed for complete and incomplete fatty acid oxidation ([1-14C] palmitate) or permeabilized to determine mitochondrial respiratory capacity (basal (non-ADP stimulated state 4), maximal uncoupled (carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP)-linked) respiration, and free radical (superoxide) emitting potential). Protein levels of ACSL-5 were 2-fold higher in ACSL-5 overexpressed HSKMC. Both complete and incomplete fatty acid oxidation increased by 2-fold (p < 0.05). In permeabilized HSKMC, ACSL-5 overexpression significantly increased basal and maximal uncoupled respiration (p < 0.05). Unexpectedly, however, elevated ACSL-5 expression increased mitochondrial superoxide production (+30%), which was associated with a significant reduction (p < 0.05) in insulin-stimulated p-Akt and p-AS160 protein levels. We concluded that ACSL-5 in human skeletal muscle functions to increase mitochondrial fatty acid oxidation, but contrary to conventional wisdom, is associated with increased free radical production and reduced insulin signaling

Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle

Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all as- sociated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dy- namic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochon- dria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in O2 respiration and increase in oxidative stress) in skeletal muscle. The bal- ance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mito- chondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal mus- cle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle

Metformin Improves Insulin Signaling in Obese Rats via Reduced IKK Action in a Fiber-Type Specific Manner

Metformin is a widely used insulin-sensitizing drug, though its mechanisms are not fully understood. Metformin has been shown to activate AMPK in skeletal muscle; however, its effects on the inhibitor of κB kinaseβ (IKKβ) in this same tissue are unknown. The aim of this study was to (1) determine the ability of metformin to attenuate IKKβ action, (2) determine whether changes in AMPK activity are associated with changes in IKKβ action in skeletal muscle, and (3) examine whether changes in AMPK and IKKβ function are consistent with improved insulin signaling. Lean and obese male Zuckers received either vehicle or metformin by oral gavage daily for four weeks (four groups of eight). Proteins were measured in white gastrocnemius (WG), red gastrocnemius (RG), and soleus. AMPK phosphorylation increased (P < .05) in WG in both lean (57%) and obese (106%), and this was supported by an increase in phospho-ACC in WG. Further, metformin increased IκBα levels in both WG (150%) and RG (67%) of obese rats, indicative of reduced IKKβ activity (P < .05), and was associated with reduced IRS1-pSer307 (30%) in the WG of obese rats (P < .02). From these data we conclude that metformin treatment appears to exert an inhibitory influence on skeletal muscle IKKβ activity, as evidenced by elevated IκBα levels and reduced IRS1-Ser307 phosphorylation in a fiber-type specific manner