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Nicotine, the main component of cigarette smoke, affects white/brown adipocytes. Few studies have concentrated on beige adipocytes. In this study, 3T3-L1 cells were differentiated in the presence of nicotine (25, 50 and 100 μmol/L) during early differentiation and maintenance stages. Cell viability and the state of lipid droplets were assessed by the MTT assay and Oil Red O, respectively, and the expression of beige-related genes and proteins was examined by RT-qPCR, Western blotting and flow cytometry. Nicotine did not alter adipocyte differentiation; however, it increased the expression of peroxisome proliferator- activated receptor gamma (PPARγ) protein during early differentiation and maintenance. Nicotine treatment during early differentiation downregulated gene and protein expression of PPARγ coactivator 1-alpha (PGC-1α), uncoupling protein 1 (UCP1) and cluster of differentiation 137 (CD137), and gene expression of Cbp/p300 interacting transactivator with Glu/ Asp rich carboxy-terminal domain 1 (Cited1), transmembrane protein 26 (Tmem26), and short stature homeobox 2 (Shox2). Nicotine treatment during the maintenance stage upregulated these beige-related genes/proteins. Nicotine treatment of immature adipocytes damaged beige function through a decrease in PGC-1α/UCP1 expression, but nicotine treatment of mature adipocytes or both immature and mature cells enhanced beige functioning. Nicotine induced beige-like phenotype dysfunction in 3T3-L1 adipocytes. This process may affect thermogenesis in adipose tissue and cause a dysfunction in fat metabolism.

Summary Background & aims The effect of maternal omega-3 fatty acids intake on the body composition of the offspring is unclear. The aim of this study was to conduct a systematic review and meta-analysis to confirm the effects of omega-3 fatty acids supplementation during pregnancy and/or lactation on body weight, body length, body mass index (BMI), waist circumference, fat mass and sum of skinfold thicknesses of offspring. Methods Human intervention studies were selected by a systematic search of PubMed, Web of Science, the Cochrane Library and references of related reviews and studies. Randomized controlled trials of maternal omega-3 fatty acids intake during pregnancy or lactation for offspring's growth were included. The data were analyzed with RevMan 5.3 and Stata 12.0. Effect sizes were presented as weighted mean differences (WMD) or standardized mean difference (SMD) with 95% confidence intervals (95% CI). Results Twenty-six studies comprising 10,970 participants were included. Significant increases were found in birth weight (WMD = 42.55 g, 95% CI: 21.25, 63.85) and waist circumference (WMD = 0.35 cm, 95% CI: 0.04, 0.67) in the omega-3 fatty acids group. There were no effects on birth length (WMD = 0.09 cm, 95% CI: −0.03, 0.21), postnatal length (WMD = 0.13 cm, 95% CI: −0.11, 0.36), postnatal weight (WMD = 0.04 kg, 95% CI: −0.07, 0.14), BMI (WMD = 0.09, 95% CI: −0.05, 0.23), the sum of skinfold thicknesses (WMD = 0.45 mm, 95% CI: −0.30, 1.20), fat mass (WMD = 0.05 kg, 95% CI: −0.01, 0.11) and the percentage of body fat (WMD = 0.04%, 95% CI: −0.38, 0.46). Conclusions This meta-analysis showed that maternal omega-3 fatty acids supplementation can increase offspring's birth weight and postnatal waist circumference. However, it did not appear to influence children's birth length, postnatal weight/length, BMI, sum of skinfold thicknesses, fat mass and the percentage of body fat during postnatal period. Larger, well-designed studies are recommended to confirm this conclusion. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of prenatal and lactation nicotine exposure on the morphology and function of brown adipose tissue (BAT) in male rat offspring. We conducted a morphological assay and gene expression study of interscapular BAT (iBAT) in male rat offspring. The male offspring from nicotine-exposed dams exhibited higher body weight and iBAT weight. Hematoxylin and eosin staining and transmission electron microscopy showed that iBAT from nicotine-exposed male offspring presented a “whitening” phenotype characterized by lipid droplet accumulation and impaired mitochondria with a randomly oriented and fractured cristae. The expression of the iBAT structure and function-related genes all decreased in nicotine-exposed male offspring. These data indicate that prenatal and lactation nicotine exposure affects morphology and function of iBAT in male rat offspring. [ABSTRACT FROM PUBLISHER]

There is increasing evidence suggesting that maternal nicotine (NIC) exposure alone can lead to many deleterious consequences in the fetus. In this study, we aimed to evaluate the effects of prenatal and lactation NIC exposure on glucose homeostasis, lipogenesis and lipid metabolism in mothers and pups. After maternal NIC exposure (from gestational day 9 to weaning), NIC mothers showed lower body weight, decreased parametrial white adipose tissue (pWAT) and inguinal WAT weights, lower homeostasis model assessment of beta cell function, higher serum total cholesterol (TC) and low-density lipoprotein cholesterol levels, higher Castelli index values, lower hepatic mRNA levels of sterol regulatory element binding protein-1c (SREBP1c), lipoprotein lipase, acetyl-CoA carboxylase, fatty acid synthase (FAS) and glucose transporters 4 (GLUT4), as well as lower SREBP1c, FAS, leptin and GLUT4 mRNA levels in pWAT. However, female NIC pups presented higher body weights and serum TC levels, and increased trends for high density lipoprotein-cholesterol and Castelli index I. Male NIC pups had higher body weight, serum TC levels and Castelli index I values, and lower glycemia levels. Additionally, hepatic and adipose FAS gene expression from the female NIC pups presented a decreasing trend, while the male NIC pups had lower hepatic FAS expression and higher adipose FAS expression. In conclusion, prenatal and lactation NIC exposure induced deleterious effects on the glucose homeostasis, lipogenesis and lipid metabolism in both mothers and pups, which may promote several important metabolic disorders in the progeny. Additionally, there are gender-specific effects on pups. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that China is one of the domestication centres of Asian cultivated rice ( Oryza sativa), and common wild rice ( O. rufipogon) is the progenitor of O. sativa. However, the number of domestication times and the geographic origin of Asian cultivated rice in China are still under debate. In this study, 100 accessions of Asian cultivated rice and 111 accessions of common wild rice in China were selected to examine the relationship between O. sativa and O. rufipogon and thereby infer the domestication and evolution of O. sativa in China through sequence analyses of six gene regions, trn C-ycf6 in chloroplast genomes, cox3 in mitochondrial genomes and ITS, Ehd1, Waxy, Hd1 in nuclear genomes. The results indicated that the two subspecies of O. sativa (indica and japonica) were domesticated independently from different populations of O. rufipogon with gene flow occurring later from japonica to indica; Southern China was the genetic diversity centre of O. rufipogon, and the Pearl River basin near the Tropic of Cancer was the domestication centre of O. sativa in China. [ABSTRACT FROM AUTHOR]

The waxy protein primarily controls the synthesis of amylose, which is a key determinant of rice (Oryza sativa L.) cooking and processing qualities. Knowledge of the diversity of waxy gene in Chinese rice is essential to validate molecular markers for marker-assisted selection and to trace the origin of Chinese glutinous rice. The waxy (Wx) gene in the wild rice has rarely been studied, and the origin of Chinese glutinous rice is not well understood. The objectives of our investigation were (i) to identify the diversity of Wx and molecular markers for marker-assisted breeding and (ii) trace the origin of Chinese glutinous rice. We examined the sequence variations for the waxy gene of 98 accessions of cultivated rice and 134 accessions of wild rice from a previously established microcore collection of Chinese rice germplasm. A total of 51 and 226 single nucleotide polymorphisms (SNPs) or insertions or deletions were found in the cultivated rice and the wild rice, respectively. Wild rice accessions had much higher diversity than cultivated rice and nonglutinous rice had much higher diversity than glutinous rice whereas the genetic diversity of indica rice was similar to that of japonica rice. Polymorphisms of CTn microsatellite, G/T SNP, and 23-bp insertion in the waxy gene and their relationship to amylose content were explored using cultivated rice. The G/T allele and 23-bp insertion were better associated with amylose content than with the CTn alleles, and they were validated as molecular markers for markerassisted selection. All the wild rice accessions with 23-bp insertion or Τ allele came from South China and the glutinous rice originated from wild rice of South China parallel with indica and japonica differentiation. [ABSTRACT FROM AUTHOR]

Maternal nicotine exposure during pregnancy and lactation is associated with obesity in female offspring. Brown adipose tissue (BAT) is related to energy metabolism and obesity. In this study, we explored the mechanism of maternal nicotine exposure on BAT "whitening" in female offspring. Pregnant rats were randomly assigned to nicotine (1.0 mg/kg twice per day, subcutaneous administration) or control groups. The weight, structure, and microvascular density of interscapular BAT (iBAT) and the expression of PGC-1α UCP1 signals, mitochondrial biogenesis-related genes and angiogenesis-related genes were tested in 4- and 26-week-aged female offspring. In vitro, C3H10T1/2 cells were induced to differentiate into mature brown adipocytes, and 0–50 μM nicotine was treated on cells during the differentiation process. Nicotine-exposed females had higher iBAT weight, white-like adipocytes and abnormal mitochondrial structure in iBAT at 26 weeks rather than 4 weeks. The PGC-1α UCP1 signals and brown-like genes were down-regulated at 26 weeks, but the microvascular density and the expression of pro-angiogenic factors reduced more at 4 weeks in the nicotine group. In vitro, 50 μM nicotine significantly decreased the expression of PGC-1α UCP1 signals and angiogenesis-related genes. In conclusion, maternal nicotine exposure during pregnancy and lactation led to the "whitening" of BAT in adult female offspring: nicotine decreased BAT angiogenesis in the early development stage, and then, the impairment of blood vessels programed for the reduction of BAT phenotype through down-regulating the PGC-1α UCP1 signals in adulthood. This impairment of BAT may be a potential mechanism of nicotine-induced obesity in female offspring. Unlabelled Image • Maternal nicotine exposure led to the whitening of brown adipose tissue. • Nicotine exposure decreased the angiogenesis of brown adipose tissue at weaning. • Nicotine reduced brown phenotype in adulthood via decreasing PGC-1α UCP1 signals. [ABSTRACT FROM AUTHOR]

Maternal nicotine exposure during pregnancy and lactation is associated with obesity in offspring. Brown adipose tissue (BAT) is correlated with energy metabolism and obesity. In this study, we explored the mechanism of maternal nicotine exposure on BAT changes in male offspring. Pregnant rats were randomly assigned to nicotine (1.0 mg/kg twice per day, subcutaneous administration) or control groups. In vitro, C3H10T1/2 cells were induced to differentiate into mature brown adipocytes, and 0–50 μM nicotine was given to C3H10T1/2 cells during the differentiation process. Nicotine-exposed males had white-like adipocytes and abnormal mitochondria structure in iBAT at 26 weeks. The expression of mitochondrial genes, UCP1 and AMPK-SIRT1-PGC-1α pathway were downregulated in the nicotine group at 26 weeks rather than 4 weeks. In vitro, 50 μM nicotine decreased the expression of mitochondrial genes, UCP1 and AMPK-SIRT1-PGC-1α pathway in brown adipocytes. Maternal nicotine exposure showed the "programming" effect on the decreased brown-like phenotype in BAT of adult male offspring via downregulating AMPK-SIRT1-PGC-1α pathway. This impairment of BAT may be a potential mechanism of nicotine-induced obesity in male offspring. • Maternal nicotine exposure led to the impairment of brown adipose tissue. • Nicotine exposure down-regulated the AMPK SIRT1 PGC-1α signals. • Nicotine showed the programming effect in regulating brown adipose tissue. [ABSTRACT FROM AUTHOR]

Tendon-bone insertion injuries such as rotator cuff and anterior cruciate ligament injuries are currently highly common and severe. The key method of treating this kind of injury is the reconstruction operation. The success of this reconstructive process depends on the ability of the graft to incorporate into the bone. Recently, there has been substantial discussion about how to enhance the integration of tendon and bone through biological methods. Stem cells like bone marrow mesenchymal stem cells (MSCs), tendon stem/progenitor cells, synovium-derived MSCs, adipose-derived stem cells, or periosteum-derived periosteal stem cells can self-regenerate and potentially differentiate into different cell types, which have been widely used in tissue repair and regeneration. Thus, we concentrate in this review on the current circumstances of tendon-bone healing using stem cell therapy., Competing Interests: Conflict-of-interest statement: The authors declare no conflict of interests for this article., (©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.)

Concurrent hearing and genetic screening of newborns is expected to play important roles not only in early detection and diagnosis of congenital deafness, which triggers intervention, but also in predicting late-onset and progressive hearing loss and identifying individuals who are at risk of drug-induced HL. Concurrent hearing and genetic screening in the whole newborn population in Beijing was launched in January 2012. This study included 180,469 infants born in Beijing between April 2013 and March 2014, with last follow-up on February 24, 2018. Hearing screening was performed using transiently evoked otoacoustic emission (TEOAE) and automated auditory brainstem response (AABR). For genetic testing, dried blood spots were collected and nine variants in four genes, GJB2, SLC26A4, mtDNA 12S rRNA, and GJB3, were screened using a DNA microarray platform. Of the 180,469 infants, 1,915 (1.061%) were referred bilaterally or unilaterally for hearing screening; 8,136 (4.508%) were positive for genetic screening (heterozygote, homozygote, or compound heterozygote and mtDNA homoplasmy or heteroplasmy), among whom 7,896 (4.375%) passed hearing screening. Forty (0.022%) infants carried two variants in GJB2 or SLC26A4 (homozygote or compound heterozygote) and 10 of those infants passed newborn hearing screening. In total, 409 (0.227%) infants carried the mtDNA 12S rRNA variant (m.1555A>G or m.1494C>T), and 405 of them passed newborn hearing screening. In this cohort study, 25% of infants with pathogenic combinations of GJB2 or SLC26A4 variants and 99% of infants with an m.1555A>G or m.1494C>T variant passed routine newborn hearing screening, indicating that concurrent screening provides a more comprehensive approach for management of congenital deafness and prevention of ototoxicity., (Copyright © 2019 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.)

The present study aims to evaluate whether perinatal nicotine (NIC) exposure increases obesity susceptibility in adult male rat offspring by altering early adipogenesis. NIC was sc administered (2.0 mg/kg per day) to pregnant rats from gestational day 9 to the time of weaning (postnatal day 28). At weaning, NIC-exposed male pups had an increased body weight and inguinal sc fat mass and a decreased average cell area of adipocyte, which was accompanied by an overexpression of adipogenic and lipogenic genes in the epididymal white adipose tissue. Additionally, the hepatic lipogenic gene levels from NIC-exposed male pups were also affected. At 12 and 26 weeks of age, body weight and fat mass were increased, whereas there was no change in food intake in NIC-exposed male offspring. Adipogenic and lipogenic genes, glucose transporter 4, and leptin mRNA levels were increased, whereas adiponectin mRNA levels were decreased in the epididymal white adipose tissue of NIC-exposed males. The hepatic lipogenic gene expression of NIC-exposed males was increased. NIC-exposed male offspring showed normal glycemia and a higher serum insulin level, homeostasis model assessment of insulin resistance, and homeostasis model assessment of β-cell function. Furthermore, the NIC-exposed male offspring showed higher serum lipids and Castelli index I and lower nonesterified fatty acid. At 26 weeks, in the ip glucose and insulin tolerance tests, the glucose clearance was delayed, and the area under the curve was higher in the NIC-exposed male offspring. In conclusion, perinatal NIC exposure increased obesity susceptibility in adult male rat offspring by altering early adipogenesis.

Quantitative real-time PCR (qRT-PCR) is the most classical technique in the field of gene expression study. This method requires an appropriate reference gene to normalize mRNA levels. In this study, the expression stability of four frequently-used reference genes in epididymal white adipose tissue (eWAT), inguinal beige adipose tissue (iBeAT) and brown adipose tissue (BAT) from obese and lean rats were evaluated by geNorm, NormFinder and BestKeeper. Based on the Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) guidelines, the two most stable reference genes were recommended in each type of adipose tissue. Two target genes were applied to test the stability of the reference genes. The geNorm and NormFinder results revealed that GAPDH and 36B4 exhibited the highest expression stabilities in eWAT, while 36B4 and β-actin had the highest expression stabilities in iBeAT and BAT. According to the results of the BestKeeper analysis, 36B4 was the most stable gene in eWAT, iBeAT and BAT, in terms of the coefficient of variance. In terms of the coefficient of correlation, GAPDH, 36B4 and β-actin were the most stable genes in eWAT, iBeAT and BAT, respectively. Additionally, expected results and statistical significance were obtained using a combination of two suitable reference genes for data normalization. In conclusion, 36B4 and GAPDH, in combination, are the best reference genes for eWAT, while 36B4 and β-actin are two most suitable reference genes for both iBeAT and BAT. We recommend using these reference genes accordingly.