To be one of the programs of medical foreign aid for Africa as Sent Successfully, Standing Firmly, Being Popular, and Needed Forever, rehabilitation medicine should be based on the core idea, identify the commencement, focus on key points and cultivate the turning points.

In Africa about 133 million people lived with disabilities which were mainly the sequelae of infectious disease, war or trauma accidents, single organ dysfunction, refractive error and some others. Medical rehabilitation and community-based rehabilitation could only meet 5%~55% of their rehabilitation needs. Weak infrastructure, poverty and lack of funds, negative attitudes and the monotonous human and culture environments restricted the development of rehabilitation medicine in Africa. Chinese model of rehabilitation medicine seemed to be suitable for Africa. Chinese medical teams in Africa could do a lot in admissions of the disabled, improving hardware conditions,training of professionals, developing new technology and expanding the prestige of rehabilitation medicine.

The hypoxanthine-guanine phosphoribosyl transferase (HGPRT) gene mutation is responsible for gouty arthritis, kidney stone, and Lesch-Nyhan Syndrome (LNS). It has been reported that the expression of HGPRT is decreased or even absent in these diseases. Rabbits are an ideal model for studying the pathology of these diseases. Therefore, the development of an HGPRT-knockdown rabbit model will be highly beneficial m such studies. Stable HGPRT-knoekdown transgenie fibroblast lines were generated by transfecting rabbit fibroblasts with RNA interference (RNAi) plasmids. Polymerase chain reaction (PCR) analyses indicated that the average positive rate was 83.3%. The mRNA and protein levels of HGPRT in the transgenic fibroblast lines were significantly lower than that in the control. Transgenic rabbit blastocysts were derived after performing nuclear transfer. The results show that RNAi can be used to stably knock down expression of the HGPRT in rabbit fibroblasts and further improvements in related technologies will facilitate the use of this method for the generation of HGPRT-knockdown rabbits.

OBJECTIVETo study the correlation between the MRI apparent diffusion coefficient (ADC) value and histological grade and molecular biology of breast invasive ductal carcinoma (IDC).

METHODSThis retrospective study included 125 patients with IDC verified by pathology from February 2010 to February 2013. Conventional MRI and diffusion-weighted imaging (DWI) examination were performed using a 3.0T scanner with diffusion factor of 0 and 800 s/mm(2). The region of interest (ROI) was drawn on the largest lesion and/or its two adjacent slices. The ADC value of the whole tumor was calculated as the mean ADC value. The correlation between mean ADCs and histological grade and biological factors was analyzed.

RESULTSThe mean ADC of pathological grade I, II and III IDC was (1.152 ± 0.072)×10(-3) mm(2)/s, (1.102 ± 0.101)×10(-3) mm(2)/s, and (1.035 ± 0.107)×10(-3) mm(2)/s, respectively. There was a statistically significant difference among them (P = 0.003). Statistically a significant difference was observed between grade III and I (P = 0.034), grade III and II (P = 0.006), but not between grade I and II (P = 0.741). A significant correlation was observed between ADC value and pathological grade (r = -0.342, P < 0.001). The median ADC values were significantly higher in the ER-negative than in the ER-positive cases [(1.130 ± 0.115)×10(-3) mm(2)/s vs. (1.060 ± 0.089) ×10(-3) mm(2)/s, P < 0.001)], in PR-negative than in PR-positive cases [(1.121 ± 0.106)×10(-3) mm(2)/s vs. (1.055 ± 0.096) ×10(-3) mm(2)/s, P < 0.001)], and in Ki-67-negative than in Ki-67-positive cases [(1.153 ± 0.090)×10(-3) mm(2)/s vs. (1.063 ± 0.101) ×10(-3) mm(2)/s, P < 0.001]. A statistically significant correlation was observed between ADC value and expressions of ER, PR, and Ki-67 (r = -0.311, r = -0.317, r = -0.414, P < 0.001).

CONCLUSIONADC value of breast invasive ductal carcinoma is correlated with histological grade, and expression of ER, PR and Ki-67.

Breast Neoplasms ; diagnosis ; Carcinoma, Ductal ; diagnosis ; Diffusion Magnetic Resonance Imaging ; Humans ; Magnetic Resonance Imaging ; Retrospective Studies

Despite the large number of genomic and transcriptomic resources in maize, there is still much to learn about the function of genes in developmental and biochemical processes. Some maize mutants that were generated by gamma-irradiation showed clear segregation for the kernel phenotypes in B73 × Mo17 F2 ears. To better understand the functional genomics of kernel development, we developed a mapping and gene identification pipeline, bulked segregant exome sequencing (BSEx-seq), to map mutants with kernel phenotypes including opaque endosperm and reduced kernel size. BSEx-seq generates and compares the sequence of the exon fraction from mutant and normal plant F2 DNA pools. The comparison can derive mapping peaks, identify deletions within the mapping peak, and suggest candidate genes within the deleted regions. We then used the public kernel-specific expression data to narrow down the list of candidate genes/mutations and identified deletions ranging from several kb to more than 1 Mb. A full deletion allele of the Opaque-2 gene was identified in mutant 531, which occurs within a ∼200-kb deletion. Opaque mutant 1486 has a 6248-bp deletion in the mapping interval containing two candidate genes encoding RNA-directed DNA methylation 4 (RdDM4) and AMP-binding protein, respectively. This study demonstrates the efficiency and cost-effectiveness of BSEx-seq for causal mutation mapping and candidate gene selection, providing a new option in mapping-by-sequencing for maize functional genomics studies.
Chromosome Mapping ; methods ; DNA, Plant ; genetics ; DNA-Binding Proteins ; genetics ; Endosperm ; Exome ; genetics ; Exons ; genetics ; Gene Deletion ; Genomics ; Phenotype ; Plant Proteins ; genetics ; Sequence Analysis, DNA ; methods ; Transcription Factors ; genetics ; Zea mays ; genetics

The generation of a tau-V337M point mutation mouse model using gene editing technology can provide an animal model with fast disease progression and more severe symptoms, which facilitate the study of pathogenesis and treatment of Alzheimer's disease (AD). In this study, single guide RNAs (sgRNA) and single-stranded oligonucleotides (ssODN) were designed and synthesized in vitro. The mixture of sgRNA, Cas9 protein and ssODN was microinjected into the zygotes of C57BL/6J mice. After DNA cutting and recombination, the site homologous to human 337 valine (GTG) in exon 11 was mutated into methionine (ATG). In order to improve the efficiency of recombination, a Rad51 protein was added. The female mice mated with the nonvasectomy male mice were used as the surrogates. Subsequently, the 2-cell stage gene edited embryos were transferred into the unilateral oviduct, and the F0 tau-V337M mutation mice were obtained. Higher mutation efficiency could be obtained by adding Rad51 protein. The F0 tau-V337M point mutation mice can pass the mutation on to the F1 generation mice. In conclusion, this study successfully established the first tau-V337M mutation mouse by using Cas9, ssODN and Rad51. These results provide a new method for developing AD mice model which can be used in further research on the pathogenesis and treatment of AD.
Animals ; Male ; Female ; Mice ; Humans ; CRISPR-Cas Systems/genetics* ; RNA, Guide, CRISPR-Cas Systems ; Rad51 Recombinase/genetics* ; Mice, Inbred C57BL ; Disease Models, Animal ; Recombination, Genetic

Adipose tissue is a promising target for treating obesity and metabolic diseases. However, pharmacological agents usually fail to effectively engage adipocytes due to their extraordinarily large size and insufficient vascularization, especially in obese subjects. We have previously shown that during cold exposure, connexin43 (Cx43) gap junctions are induced and activated to connect neighboring adipocytes to share limited sympathetic neuronal input amongst multiple cells. We reason the same mechanism may be leveraged to improve the efficacy of various pharmacological agents that target adipose tissue. Using an adipose tissue-specific Cx43 overexpression mouse model, we demonstrate effectiveness in connecting adipocytes to augment metabolic efficacy of the β ₃-adrenergic receptor agonist Mirabegron and FGF21. Additionally, combing those molecules with the Cx43 gap junction channel activator danegaptide shows a similar enhanced efficacy. In light of these findings, we propose a model in which connecting adipocytes via Cx43 gap junction channels primes adipose tissue to pharmacological agents designed to engage it. Thus, Cx43 gap junction activators hold great potential for combination with additional agents targeting adipose tissue.