The rice ethylene response factor OsERF83 positively regulates disease resistance to Magnaporthe oryzae.

Rice blast caused by Magnaporthe oryzae is one of the most destructive diseases of rice (Oryza sativa) worldwide. Here, we report the identification and functional characterization of a novel ethylene response factor (ERF) gene, OsERF83, which was expressed in rice leaves in response to rice blast fungus infection. OsERF83 expression was also induced by treatments with methyl jasmonate, ethephon, and salicylic acid, indicating that multiple phytohormones could be involved in the regulation of OsERF83 expression under biotic stress.

Does a Vascularized Fibula Free Bone Grafted Immediately After Hemimandibulectomy in a Child Grow or Relapse During Adolescence?

For young growing children before the end of skeletal maturity, the growth activity of the grafted bone after hemimandibulectomy is not well-known. After an adolescence, such a patient may have facial deformity because the anterior growth point of the mandible is in the condylar neck. A 13-year-old boy was performed hemimandibulectomy with immediate mandibular reconstruction by fibula free flap (FFF) because of a huge ameloblastic fibroma.

Clinical Study of 597 Oral Squamous Cell Carcinomas in Our Department - Especially about 318 Tongue Carcinoma.

This clinico-statistical study includes 597 cases of oral squamous cell carcinoma treated at the Maxillofacial Surgery Section of Tokyo Medical and Dental University between January 2002 and December 2011. There were 373 male and 224 female patients (male to female ratio, 1.7 : 1), and the median age was 67 years.

[Clinicopathological study of calcifying cystic odontogenic tumors].

Calcifying cystic odontogenic tumors are benign tumors, characterized by the presence of ghost cells and calcified materials. We evaluated clinical characteristics of calcifying cystic odontogenic tumors in 21 cases at the Maxillofacial Surgery, Tokyo Medical and Dental University Hospital, between January 1979 and December 2006. Of the 21 lesions that were studied, 12 were observed in male patients, and 9 in female patients.

Type VI collagen deficiency induces osteopenia with distortion of osteoblastic cell morphology.

Bone consists of type I collagen as a major protein with minor various matrix proteins. Type VI collagen is one of bone matrix proteins but its function is not known. We therefore examined the effects of type VI collagen deficiency on bone.

Dok-1 and Dok-2 deficiency induces osteopenia via activation of osteoclasts.

Osteoporosis causes fractures that lead to reduction in the quality of life and it is one of the most prevalent diseases as it affects approximately 10% of the population. One of the important features of osteoporosis is osteopenia. However, its etiology is not fully elucidated.

Nanogel-based scaffold delivery of prostaglandin E(2) receptor-specific agonist in combination with a low dose of growth factor heals critical-size bone defects in mice.

Objective: Regeneration of bone requires the combination of appropriate drugs and an appropriate delivery system to control cell behavior. However, the delivery of multiple drugs to heal bone is complicated by the availability of carriers. The aim of this study was to explore a new system for delivery of a selective EP4 receptor agonist (EP4A) in combination with low-dose bone morphogenetic protein 2 (BMP-2).

Angiotensin II type 2 receptor blockade increases bone mass.

Renin angiotensin system (RAS) regulates circulating blood volume and blood pressure systemically, whereas RAS also plays a role in the local milieu. Previous in vitro studies suggested that RAS may be involved in the regulation of bone cells. However, it was not known whether molecules involved in RAS are present in bone in vivo.

JunD suppresses bone formation and contributes to low bone mass induced by estrogen depletion.

JunD is an activator protein-1 (AP-1) component though its function in skeletal system is still not fully understood. To elucidate the role of JunD in the regulation of bone metabolism, we analyzed JunD-deficient mice. JunD deficiency significantly increased bone mass and trabecular number.