somatic embryo maturation, mycorrhization of regenerated plantlets and its resistance to .

Pine wilt disease, caused by the pine wood nematode (PWN, ), is a major quarantine forest disease that poses a threat to various pine species, including (masson pine), worldwide. Breeding of PWN-resistant pine trees is an important approach to prevent the disease. To expedite the production of PWN-resistant accessions, we investigated the effects of maturation medium treatments on somatic embryo development, germination, survival, and rooting.

Identification of nine novel variants across PAX3, SOX10, EDNRB, and MITF genes in Waardenburg syndrome with next-generation sequencing.

Background: Waardenburg syndrome (WS) is a hereditary, genetically heterogeneous disorder characterized by variable presentations of sensorineural hearing impairment and pigmentation anomalies. This study aimed to investigate the clinical features of WS in detail and determine the genetic causes of patients with clinically suspected WS.

Methods: A total of 24 patients from 21 Han-Taiwanese families were enrolled and underwent comprehensive physical and audiological examinations.

[Surveillance results of national monitoring sites for soil-transmitted nematode infections in Xinchang County from 2009 to 2017].

Objective: To understand the infection status of soil-transmitted nematodes in Xinchang County, so as to offer the evidence for the formulation of control measures.

Methods: The infection of soiltransmitted nematodes in residents was investigated by using the Kato-Katz method and cellophane anal swab.

Results: A total of 3 069 people were examined in 2009, 2012 and 2017, of which 1 520 people were male and 61 people were infected, with the infection rate of 4.

Identification of Glucose-responsive and Insulin-responsive Elements in Promoter of Mouse ob Gene.

Glucose and insulin stimulate leptin gene expression in vitro and in vivo. To identify cis-elements that are responsible for the glucose and insulin effects, mouse 3T3-L1 adipocytes were transiently transfected with reporter constructs with serial deletions in mouse ob gene promoter. The cis-elements were identified with Gel mobility shift assays (GMSA), DNase I footprint assays and PCR mediated site-directed mutation assays.