The aim of the present study was to induce chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) in rats by administering saturated salt and methyl-N’-nitro-N-nitrosoguanidine (MNNG) via oral gavage. Changes in gastric mucosal blood microcirculation and activation of the cyclo-oxygenase-2 (COX-2)/hypoxia inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway during CAG and IM development were investigated. After administering saturated salt and MNNG for 25 weeks, mild atrophy was detected in the stomach of model rats using hematoxylin and eosin staining. CAG with IM was successfully induced in the gastric mucosa of the model rats after 35 weeks. Gastric mucosal blood flow was decreased in comparison with controls as early as 15 weeks after treatment to induce CAG and the mRNA expression levels of COX-2, HIF-1α, vascular endothelial growth factor receptor (VEGFR)1 and VEGFR2 were increased in comparison with untreated rats as early as 25 weeks after treatment. HIF-1α, COX-2 and VEGFR2 expression levels were increased as early as 25 weeks after CAG induction treatment when compared to controls and HIF-1α, COX-2, VEGFR1 and VEGFR2 expression levels were significantly increased after 35 weeks. These findings indicated that administering saturated salt and MNNG by gavage for 35 weeks successfully induced CAG and IM in rats. Furthermore, the microcirculation was disturbed before activation of the COX-2/HIF-1α/VEGF signaling pathway.Conjunctival sac stenosis is the contraction of the conjunctival sac as a result of trauma or disease. The aim of the present study was to observe the clinical effects of low-level laser therapy (LLLT) combined with hydroxyapatite (HA) orbital implantation as a treatment strategy for conjunctival sac stenosis. A total of 10 patients with conjunctival sac stenosis were treated with scleral graft transplantation in conjunction with HA implantation and postoperative LLLT. In addition, a rabbit model was used to investigate the biological mechanism underlying the effects of LLLT with the aim of preventing and treating orbital implantation exposure. The right eyeball was removed, orbital implantation performed and LLLT applied to experimental groups. 99mTc-Methyl diphosphonate scanning methods were performed at different timepoints to compare the average radioactivity count of the region of interest between surgical (right) and control (left) eyes (R/L). L-NAME cost Histopathological examination was performed 8 weeks post-surgery, followed by analysis of fiber vascularization. Following LLLT, moderate conjunctival wounds were completely healed within 2 weeks and severe stenosis wounds healed within 3 weeks. Following prosthesis implantation in the rabbit model, a significantly elevated R/L ratio was observed after 4 weeks, whereas no significant difference was observed compared with the control group at 6 and 8 weeks postoperatively. Histopathological examination revealed that all implants were fibrotic. Overall, the present study demonstrated that LLLT promoted the survival of conjunctival grafts, stimulated conjunctival incision healing and promoted early vascularization of HA implants. Clinical trial registration no ChiCTR-DDT-12002660 (www.chictr.org/cn/).Tribbles pseudokinase 3 (TRIB3), a member of the tribbles-related family, has biological roles such as by acting as an oncogene or tumor suppressor gene, in various types of cancer, including colorectal cancer, breast cancer, lung cancer and renal cell carcinoma. However, the role of TRIB3 in oral squamous cell carcinoma (OSCC) is remains unclear. The current was aimed to determine the biological function of TRIB3 in OSCC progression. TRIB3 expression was examined in OSCC surgical specimens using reverse transcription-quantitative PCR and the role of TRIB3 in the proliferation capacities of OSCC cell lines was examined using crystal violet and MTT assays in vitro and tumorigenicity assays in vivo. The underlying mechanism by which TRIB3 exerts its function was investigated using western blotting. The results demonstrated that the mRNA and protein expression levels of TRIB3 were higher in human OSCC tissues compared with normal tissues. The role of TRIB3 in cell proliferation was also determined. TRIB3 overexpression significantly promoted OSCC cell proliferation, whereas TRIB3 knockdown inhibited OSCC cell proliferation compared with control cells. TRIB3 knockdown also suppressed tumor growth and decreased tumor volume in vivo compared with control cells. Moreover, the results suggested that TRIB3 overexpression increased the phosphorylation of protein kinase B (AKT) and mammalian target of rapamycin (mTOR), whereas TRIB3 knockdown decreased the phosphorylation of AKT and mTOR compared with control cells. To summarize, the present study indicated that TRIB3 promoted OSCC cell proliferation by activating the AKT signaling pathway; therefore, TRIB3 may serve as a potential target for the diagnosis and treatment of OSCC.Vitiligo is a skin disorder characterized by depigmentation of the skin due to a lack of melanin. This condition affects men and woman of all ages and its incidence is not restricted by ethnicity or region. Vitiligo is a multifactorial disease, in which melanocytes, which serve important functions in skin pigmentation and immune processes, are impaired. There is sufficient evidence that immunological and genetic factors are primarily responsible for the destruction and dysfunction of melanocytes. Therefore, genetic DNA sequence variants that participate in skin homeostasis, pigmentation and immune response regulation, as well as altered expression patterns, may contribute to the risk of developing vitiligo. The current review presented an overview of the mechanism of pigmentation and of currently known factors involved in depigmentation, as well as the classification, epidemiology, associated comorbidities, risk factors, immunopathogenesis and several genetic and molecular changes associated with vitiligo.Cranioectodermal dysplasia (CED) or Sensenbrenner syndrome is a very rare autosomal-recessive disease that is characterized by craniofacial, skeletal and ectodermal abnormalities. The proteins encoded by six CED-associated genes are members of the intraflagelline transport (IFT) system, which serves an essential role in the assembly, maintenance and function of primary cilia. The current study identified compound novel heterozygous IFT122 (NM_052985.3) variants in a male Chinese infant with CED. The latter variant changes the length of the protein and may result in the partial loss-of-function of IFT122. With the simultaneous presence of frameshift and stop-loss variants, the patient manifested typical CED with fine and sparse hair, macrocephaly, dysmorphic facial features and upper limb phocomelia. A number of unusual phenotypic characteristics were additionally observed and included postaxial polydactyly of both hands and feet. The molecular confirmation of CED in this patient expands the CED-associated variant spectrum of IFT122 in CED, while the manifestation of CED in this patient provides additional clinical information regarding this syndrome.