Nicotinamide N-methyltransferase in non-alcoholic fatty liver disease: Mechanistic insights and emerging therapeutic strategies.

Non-alcoholic fatty liver disease (NAFLD), characterized by abnormal lipid accumulation in hepatocytes, is a prevalent metabolic disorder strongly linked to insulin resistance and obesity. Emerging evidence highlights the central role of nicotinamide N-methyltransferase (NNMT) in NAFLD pathogenesis through its regulation of nicotinamide adenine dinucleotide (NAD) metabolism, the methionine cycle, epigenetic modifications, and gut microbiota. NNMT methylates NAM to methylnicotinamide (MNAM), consuming SAM, raising SAH/Hcy, depleting NAD and worsening oxidative stress.

Nicotinamide N-Methyltransferase (NNMT) and Liver Cancer: From Metabolic Networks to Therapeutic Targets.

Hepatocellular carcinoma (HCC), the predominant form of primary liver cancer, remains a global health challenge with limited therapeutic options and high mortality rates. Despite advances in understanding its molecular pathogenesis, the role of metabolic reprogramming in HCC progression and therapy resistance demands further exploration. Nicotinamide N-methyltransferase (NNMT), a metabolic enzyme central to NAD and methionine cycles, has emerged as a critical regulator of tumorigenesis across cancers.

Nicotinamide N-methyltransferase in cardiovascular Diseases: Mechanistic insights and therapeutic potential.

Cardiovascular diseases (CVDs), including conditions like ischemic heart disease, heart failure (HF), and atherosclerosis (AS), have complex pathogenesis that involves both behavioral and metabolic factors. Nicotinamide N-methyltransferase (NNMT) is an enzyme involved in the methylation of nicotinamide (NAM), and its increased activity is associated with disruptions in the NAD and methionine cycles. These disruptions are considered significant risk factors for cardiovascular diseases, though the specific mechanisms of NNMT remain unclear.

Nicotinamide N-methyltransferase as a potential therapeutic target for neurodegenerative disorders: Mechanisms, challenges, and future directions.

Neurodegenerative diseases (NDs), including Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD), are characterized by progressive neuronal loss and functional decline, posing significant global health challenges. Emerging evidence highlights nicotinamide N-methyltransferase (NNMT), a cytosolic enzyme regulating nicotinamide (NAM) methylation, as a pivotal player in NDs through its dual impact on epigenetic regulation and metabolic homeostasis. This review synthesizes current knowledge on NNMT's role in disease pathogenesis, focusing on its epigenetic modulation via DNA hypomethylation and histone modifications, alongside its disruption of NAD synthesis and homocysteine (Hcy) metabolism.

Orrella daihaiensis sp. nov., a bacterium isolated from Daihai Lake in Inner Mongolia.

A novel aerobic, Gram-staining-negative, non-motile, short-rod-shaped strain, designated f23, was obtained from Daihai Lake, Inner Mongolia, Republic of China. 16S rRNA gene sequences analysis showed that f23 belongs to the genus Orrella and is most closely related to Orrella marina H-Z20 with 98.35% sequence similarity.

Mongoliitalea daihaiensis sp. nov., isolated from Daihai Lake in Inner Mongolia.

A novel Gram-negative strain, designated X100-76, was isolated from Daihai Lake in Inner Mongolia, Republic of China. The strain was non-motile, non-spore-forming, long-rod-shaped, oxidase positive and catalase positive. Colonies incubated at 33 °C on 2216 marine agar medium for 3 days were circular, smooth, transparent, convex with clear edges, orange-red in colour and approximately 1.

Effect of glucocorticoids on mortality in patients with acute respiratory distress syndrome: A meta-analysis.

To date, the efficacy of glucocorticoid therapy to reduce mortality in patients with acute respiratory distress syndrome (ARDS) has remained controversial among the studies available. The present meta-analysis study aimed to further clarify the impact of glucocorticoid therapy on mortality in patients with ARDS by performing a pooled analysis of the previous data. The PubMed, Chinese Knowledge Infrastructure, Wanfang and Cochrane trials databases were searched for relevant studies published between 1966 and 2016.

Effects of Premature Delivery and Birth Weight on Eruption Pattern of Primary Dentition among Beijing Children.

Objective: To evaluate the effect of premature delivery and birth weight (BW) on primary tooth eruption.

Methods: A total of 2,230 children aged 3 to 36 months from urban and rural areas in Beijing, China, were classified for analysis by gestational age at delivery (89 preterm and 2,141 full term) and BW (low, normal and high). The tooth eruption status of these children was examined and recorded every 3 months.

Evaluation of the Effect of the Closed-eruption Technique on Impacted Immature Maxillary Incisors.

Objective: To investigate the effects of the closed-eruption technique on impacted immature maxillary incisors.

Methods: The contour and position of the gingival margin, root development, and pulp status were evaluated in 50 impacted immature maxillary incisors immediately after treatment and 2 years later.

Results: Chronic periapical periodontitis and trauma of the primary teeth were the main causes of impacted immature maxillary incisors.

Early dental treatments for patients with cleidocranial dysplasia.

Objective: To explore the early dental interventional strategies for adolescent patients and a child patient with cleidocranial dysplasia (CCD).

Methods: Surgical exposure using the apically repositioned flap technique combined with orthodontic traction was used in the adolescent patients whose ideal treatment time for initiating treatment was missed. For the child patient whose ideal treatment time for initiating treatment was not missed, the simple surgical exposure method was carried out in order to promote the eruption of the impacted incisors.

Gain-of-function ADCY5 mutations in familial dyskinesia with facial myokymia.

Objective: To identify the cause of childhood onset involuntary paroxysmal choreiform and dystonic movements in 2 unrelated sporadic cases and to investigate the functional effect of missense mutations in adenylyl cyclase 5 (ADCY5) in sporadic and inherited cases of autosomal dominant familial dyskinesia with facial myokymia (FDFM).

Methods: Whole exome sequencing was performed on 2 parent-child trios. The effect of mutations in ADCY5 was studied by measurement of cyclic adenosine monophosphate (cAMP) accumulation under stimulatory and inhibitory conditions.

Autosomal dominant familial dyskinesia and facial myokymia: single exome sequencing identifies a mutation in adenylyl cyclase 5.

Background: Familial dyskinesia with facial myokymia (FDFM) is an autosomal dominant disorder that is exacerbated by anxiety. In a 5-generation family of German ancestry, we previously mapped FDFM to chromosome band 3p21-3q21. The 72.

Evidence for involvement of GNB1L in autism.

Structural variations in the chromosome 22q11.2 region mediated by nonallelic homologous recombination result in 22q11.2 deletion (del22q11.

[Analysis of root resorption and dental structure in patients with cleidocranial dysplasia].

Objective: To observe the morphologic characteristic of root resorption surfaces and the histological structure of primary teeth in patients with cleidocranial dysplasia (CCD).

Methods: The primary teeth of CCD patients were collected, the resorption lacunae of which were analyzed by scanning electron microscope and the histological structure was analyzed by the polarized light microscope.

Results: Comparing with the normal teeth, the patients have typically clinical characteristics of CCD.

Senataxin, the yeast Sen1p orthologue: characterization of a unique protein in which recessive mutations cause ataxia and dominant mutations cause motor neuron disease.

A severe recessive cerebellar ataxia, Ataxia-Oculomotor Apraxia 2 (AOA2) and a juvenile onset form of dominant amyotrophic lateral sclerosis (ALS4) result from mutations of the Senataxin (SETX) gene. To begin characterization this disease protein, we developed a specific antibody to the DNA/RNA helicase domain of SETX. In murine brain, SETX concentrates in several regions, including cerebellum, hippocampus and olfactory bulb with a general neuronal expression profile, colocalizing with NeuN.

DNA/RNA helicase gene mutations in a form of juvenile amyotrophic lateral sclerosis (ALS4).

Juvenile amyotrophic lateral sclerosis (ALS4) is a rare autosomal dominant form of juvenile amyotrophic lateral sclerosis (ALS) characterized by distal muscle weakness and atrophy, normal sensation, and pyramidal signs. Individuals affected with ALS4 usually have an onset of symptoms at age <25 years, a slow rate of progression, and a normal life span. The ALS4 locus maps to a 1.

Genomic structure and mutational analysis of the human KIF1Balpha gene located at 1p36.2 in neuroblastoma.

KIF1a is a member of the kinesin superfamily proteins that are microtubule-dependent molecular motors involved in important intracellular functions such as organelle transport and cell division. We previously determined the structure of the human KIF1Bbeta gene, which was found to be a homologue of the murine Kif1bbeta, and demonstrated that the human KIF1Bbeta is a causative gene of Charcot-Marie-Tooth disease type 2A although we did not prove that it is a tumor suppressor gene of neuroblastoma. Here, we identified another isoform of the human KIF1B gene, KIF1Balpha.

Breakpoints at 1p36.3 in three MDS/AML(M4) patients with t(1;3)(p36;q21) occur in the first intron and in the 5' region of MEL1.

The recurrent translocation t(1;3)(p36;q21) is associated with myelodysplastic syndrome (MDS)/acute myelogenous leukemia (AML) characterized by trilineage dysplasia, especially dysmegakaryopoiesis and a poor prognosis. Recently, the two genes involved in this translocation have been identified: the MEL1 gene at 1p36.3, and the RPN1 gene at 3q21.