Hasil untuk "Biochemistry"

E. King

R. D. Murray, J. Méndez, Stewart A. Brown

E. Newsholme, A. Leech

W. Lennarz

H. Van den bosch, R. Schutgens, R. Wanders et al.

Mercedes Martínez, J. Whitaker

G. Dormán, Glenn D. Prestwich

F. Peypoux, J. Bonmatin, J. Wallach

B. Teusink, J. Passarge, C. A. Reijenga et al.

E. Pichersky, David R. Gang

I. Roberts

A. Bones, J. Rossiter

S. Burley, R. Roeder

N. Dudareva, E. Pichersky, J. Gershenzon

D. White

Agung Riyanto Budi Santoso, Respati Suryanto Dradjat, Edi Mustamsir et al.

Aim Orthopedic implants must meet specific criteria, including mechanical strength, durability, and biocompatibility. This study compares the immune response of zirconia, polyether ether ketone (PEEK), and stainless-steel implants in vivo, focusing on lymphocyte and fibroblast infiltration as indicators of immune activation. Methods A total of 27 New Zealand white rabbits were used, with nine animals in each group. Implants of zirconia, PEEK, or stainless steel were surgically placed in the thigh and observed for 4 weeks. Histological analysis measured lymphocyte and fibroblast infiltration at the implant site using a microscope at 400x magnification. Statistical analysis included the Kruskal-Wallis test for group comparisons, followed by Mann-Whitney and Bonferroni correction for pairwise comparisons. Results The Kruskal-Wallis test showed significant differences in lymphocyte (p=0.002) and fibroblast (p=0.003) counts among the groups. Zirconia exhibited significantly lower lymphocyte (median=0.5) and fibroblast (median=1.0) infiltration compared to stainless steel (lymphocytes: median=3.0, fibroblasts: median=2.0), and PEEK (lymphocytes: median=2.0, fibroblasts: median=3.0). Bonferroni correction confirmed zirconia showed the least immune activation (p<0.0167). Conclusion Zirconia offers superior biocompatibility with minimal immune response, making it an ideal material for orthopedic implants, particularly for patients with metal sensitivities. PEEK showed moderate immune activation but is helpful for non-load-bearing applications. Stainless Steel induced the highest immune response due to the release of metal ions and corrosion. Zirconia is the most biocompatible material tested, making it a promising choice for orthopedic implants.

Saranya Prashath

Abstract L-arginine (L-Arg) is metabolised in the cell to generate nitric oxide (NO) and citrulline via nitric oxide synthase (NOS). NO is an important cellular signalling molecule that regulates lipid and glucose metabolism. The biological availability of NO is affected by the NOS inhibitor; NG-nitro-L-Arg methyl ester (L-NAME) and the external NO donor; S-nitroso-N-acetyl-D, L-penicillamine (SNAP). Mouse adipocyte 3T3 L1 cells were cultured with 0, 400 and 800 µM L-Arg or control complete DMEM media. The impact of L-NAME (4 mM), and SNAP (100 µM) was also analysed. The cell fitness was similar and the mRNA levels of AMPK was increased and ACC-1 was decreased, whilst the activation of AMPK and ACC-1 was decreased upon the addition of exogenous L-Arg. Transcript and protein levels of AMPK and ACC-1 were regulated by addition of L-NAME and SNAP, however the impact of these targets was related to the concentration of L-Arg added to the cells and the culture time point of analysis. NO in the form of NO2 − in cell culture supernatant was elevated in 400 and 800 µM L-Arg cultures. L-NAME significantly inhibited NO production from adipose cells in a time-dependent manner and subsequently impacted AMPK and ACC expression. Associated with these changes were changed in the concentration of L-Arg, L-Cit and L-Orn in the culture media. Collectively, these results show that excess L-Arg is sensed by the cell which then regulates AMPK and ACC-1 expression in response. The findings could have implications in modulation of signalling pathways for treating obesity and obesity induced diabetic mellitus.

Atefeh Ansarin, Dariush Shanehbandi, Habib Zarredar et al.

Introduction: Given the well-established association between metabolic syndrome (MetS) and obesity, this study elucidates the influences of sleep duration and weight on MetS risk and explores the potential role of miRNAs as underlying mechanisms. Methods: According to sleep logs and biochemistry tests, this study investigated the association between MetS and its components, sleep duration, and weight in four subgroups: A: normal sleepers with normal weight (N = 145), B: normal sleepers with obesity (N = 140), C: short sleepers with normal weight (N = 130), and D: short sleepers with obesity (N = 142). Chi-square, one-way ANOVA, and Tukey’s post hoc tests were used for statistical analysis. Furthermore, following total RNA isolation by TRIzol from blood samples, cDNA was synthesized using stem-loop technique. Quantitative real-time polymerase chain reaction (qRT-PCR) was then employed to evaluate the expression levels of miR-33a, miR-378a, miR-132-3p, and miR-181d. The data were analyzed using one-way ANOVA. Results: Our findings revealed the strongest association between MetS prevalence and individuals in group D (short sleepers with obesity; Cramer's V = 0.649, P < 0.001). This observation underscores the synergistic effect of short sleep and obesity on MetS risk. Furthermore, there was an independent association between short sleep duration and elevated triglyceride levels (P < 0.05). MicroRNA expression analysis revealed downregulation of miR-33a and miR-181d in B, C, and D groups compared to the normal group. Conversely, miR-132-3p expression was upregulated in the B, C, and D groups. Conclusion: Short sleep and obesity synergistically elevate MetS risk, potentially via miR-33a and miR-181d downregulation and miR-132-3p upregulation, impacting triglyceride metabolism.

Judith Owokuhaisa, Eleanor Turyakira, Frank Ssedyabane et al.

Abstract Background Cervical cancer continues to threaten women’s health, especially in low-resource settings. Regular follow-up after screening and treatment is an effective strategy for monitoring treatment outcomes. Consequently, understanding the factors contributing to patient non-attendance of scheduled follow-up visits is vital to providing high-quality care, reducing morbidity and mortality, and unnecessary healthcare costs in low-resource settings. Methods A descriptive qualitative study was done among healthcare providers and patients who attended the cervical cancer screening clinic at Mbarara Regional Referral Hospital in southwestern Uganda. In-depth interviews were conducted using a semi-structured interview guide. Interviews were audio-recorded, transcribed verbatim, and thematically analysed in line with the social-ecological model to identify barriers and facilitators. Results We conducted 23 in-depth interviews with 5 healthcare providers and 18 patients. Health system barriers included long waiting time at the facility, long turnaround time for laboratory results, congestion and lack of privacy affecting counselling, and healthcare provider training gaps. The most important interpersonal barrier among married women was lacking support from male partners. Individual-level barriers were lack of money for transport, fear of painful procedures, emotional distress, and illiteracy. Inadequate and inaccurate information was a cross-cutting barrier across the individual, interpersonal, and community levels of the socio-ecological model. The facilitators were social support, positive self-perception, and patient counselling. Conclusions Our study revealed barriers to retention in care after cervical cancer screening, including lack of partner support, financial and educational constraints, and inadequate information. It also found facilitators that included social support, positive self-perception, and effective counselling.

María J. Esteban-Amo, Patricia Jiménez-Cuadrado, Pablo Serrano-Lorenzo et al.

Succinate dehydrogenase (also known as complex II) plays a dual role in respiration by catalyzing the oxidation of succinate to fumarate in the tricarboxylic acid (TCA) cycle and transferring electrons from succinate to ubiquinone in the mitochondrial electron transport chain (ETC). Owing to the privileged position of SDH/CII, its dysfunction leads to TCA cycle arrest and altered respiration. This review aims to elucidate the widely documented profound metabolic effects of SDH/CII deficiency, along with the newly unveiled survival mechanisms in SDH/CII-deficient cells. Such an understanding reveals exploitable vulnerabilities for strategic targeting, which is crucial for the development of novel and more precise therapies for primary mitochondrial diseases, as well as for familial and sporadic cancers associated with SDH/CII mutations.