identified as a precancerous lesion for colorectal cancer. Up-to-date genomic research revealed the value of many
noncoding RNAs (ncRNAs) in UC pathogenesis, diagnosis, and prognosis.
Aim: The present study was aimed at measuring both MALAT-1 and CCAT-1 in the sera of UC patients as
diagnostic and prognostic biomarkers and correlating them with the Mayo score which is a novel predictive
indicator of malignant transformation as well as with clinicopathological characteristics of the disease.
Patients and methods: Sixty-six UC patients and 80 healthy individuals participated in this study, the serum fold
changes of MALAT-1 and CCAT-1 were measured by using quantitative real-time PCR (qRT-PCR).
Results: The current study findings include overexpressed lncRNAs MALAT-1 and CCAT-1 in the sera of ulcerative
colitis patients [(median (IQR) = 2.290 (0.16–9.36), mean ± SD = 3.37 ± 3.904 for MALAT-1, and median
(IQR) = 7.305 (0.57–16.96), mean ± SD = 6.81 ± 4.002 for CCAT-1 than controls, ROC curve analysis reported
that these genes could predict UC. Both genes were positively correlated with each other which enforces their
synergistic effects. Both genes are diagnostic for UC patients.
We related studied genes to the severity of the disease. In addition to a significant positive correlation between
each gene with ESR and Mayo score, we further classified the patients according to severity (according to Mayo
score to remission, mild, moderate, and severe groups) with the following results; lower levels of MALAT-1 and
CCAT-1 were significantly associated with mild disease and increased gradually with more severe forms of the
disease (p < 0.05). Linear regression analysis with Mayo Score as a dependent variable revealed that only the
predictive power of CCAT-1 and ESR are significant. Moreover, ROC curve analysis when compared to that of the
Mayo score revealed that CCAT-1 reached 99 % accuracy. In summary, both genes are prognostic factors for UC
patients.
Conclusion: MALAT-1 and CCAT-1 are diagnostic and prognostic serum biomarkers of ulcerative colitis.

Abstract: Metabolic myopathies are a group of inherited illnesses affecting skeletal muscle metabolism due to enzymatic deficiencies in glycogen breakdown, fatty acid oxidation, or mitochondrial energy production. These disorders result in exercise intolerance, muscle weakness, & rhabdomyolysis (muscle breakdown resulting in the release of toxic cellular components into the bloodstream), which may progress to chronic muscle degeneration and functional impairment. Diagnosis relies on clinical symptoms, biochemical markers, genetic testing, and muscle biopsy. Common disorders include glycogen storage diseases like McArdle illness, which impairs glycogen breakdown, fatty a` oxidation disorders like carnitine palmitoyl transferase II deficiency that disrupts lipid metabolism, and mitochondrial myopathies, which affect cellular energy production. Management strategies focus on dietary modifications, including tailored carbohydrate or fat intake, controlled exercise programs to prevent muscle damage, and novel therapies like enzyme replacement treatment and gene therapy. Supportive treatments, including symptom management and physical therapy, also play a crucial role in improving mobility & overall well-being. Early diagnosis and individualized interventions are essential for optimizing patient outcomes, minimizing complications, and enhancing quality of life. Continued research into the molecular mechanisms of these disorders is vital for developing more effective therapies and improving longterm prognosisAbstract: Metabolic myopathies are a group of inherited illnesses affecting skeletal muscle metabolism due to enzymatic deficiencies in glycogen breakdown, fatty acid oxidation, or mitochondrial energy production. These disorders result in exercise intolerance, muscle weakness, & rhabdomyolysis (muscle breakdown resulting in the release of toxic cellular components into the bloodstream), which may progress to chronic muscle degeneration and functional impairment. Diagnosis relies on clinical symptoms, biochemical markers, genetic testing, and muscle biopsy. Common disorders include glycogen storage diseases like McArdle illness, which impairs glycogen breakdown, fatty a` oxidation disorders like carnitine palmitoyl transferase II deficiency that disrupts lipid metabolism, and mitochondrial myopathies, which affect cellular energy production. Management strategies focus on dietary modifications, including tailored carbohydrate or fat intake, controlled exercise programs to prevent muscle damage, and novel therapies like enzyme replacement treatment and gene therapy. Supportive treatments, including symptom management and physical therapy, also play a crucial role in improving mobility & overall well-being. Early diagnosis and individualized interventions are essential for optimizing patient outcomes, minimizing complications, and enhancing quality of life. Continued research into the molecular mechanisms of these disorders is vital for developing more effective therapies and improving longterm prognosis

 Splenic artery ligation was not inferior to splenectomy as a method to perform portal inflow modulation to alleviate graft dysfunction in living donor liver transplant with portal hypertension.