Assisting components within a resistance reflex of the stick insect, Cuniculina impigra

ABSTRACT. Rapid relaxation (shortening) of the femoral chordotonal organ in Cuniculina impigra Redtenbacher induces a depolarization followed by hyperpolarization of the fast and slow extensor tibiae motor neurons (FETi and SETi). The initial depolarization is caused by acceleration-sensitive units of the chordotonal organ. The reverse sequence of responses is induced in flexor motor neurons. The common inhibitor neuron (CI) is depolarized by both lengthening (stretch) and relaxation of the chordotonal organ.
The initial depolarization of FETi and SETi and the initial hyperpolarization of flexor motor neurons produced by rapid relaxation of the chordotonal organ and the depolarization of CI produced by lengthening of the chordotonal organ all oppose the resistance reflex response. However, these assisting components are weak compared to the resisting ones.     

Haplotype-based analysis resolves missing heritability in oculocutaneous albinism type 1B

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Enamel hypoplasias as indicators of developmental stress in pongids and hominids

This paper reports the results from a study of enamel hypoplasia in the deciduous dentition of free-living Liberian chimpanzees (Pan troglodytes verus). The entire study collection includes 280 specimens (278 skulls plus two unassociated mandibles), of which 70 are young enough to retain some decidous teeth. Among the subsample of infants, the total frequency of hypoplasia summed over all teeth in any individual reaches 80%, being expressed in the form of pits rather than transverse lines. Hypoplasia of a linear form was common in the permanent dentition, attaining a frequency of 46.7% on maxillary central incisors and 69.7% on mandibular canines.     

Simple recessive mutation in ENAM is associated with amelogenesis imperfecta in Italian Greyhounds

We report a familial enamel hypoplasia in Italian Greyhounds resembling non‐syndromic autosomal recessive amelogenesis imperfecta (AI) of humans. The condition uniformly affects deciduous and permanent teeth and is manifested by enamel roughening/thinning and brownish mottling. Affected teeth are often small and pointed with increased gaps. However, basic tooth structure is usually maintained throughout life, and fractures and dental cavities are not a serious problem as in humans. No tissues or organs other than teeth were affected by this mutation, and there was no relationship between enamel hypoplasia and either autoimmunity or periodontal disease, which also are prevalent in the breed. The enamel hypoplasia was associated with a 5‐bp deletion in exon 10 of the enamelin (ENAM) gene. The prevalence of the enamel defect in Italian Greyhounds was 14%, and 30% of dogs with normal teeth were carriers. Genome analyses suggest that the trait is under inadvertent positive selection. Based on the deletion detected in the ENAM gene, a genetic test was developed for identifying mutation carriers, which would enable breeders to manage the trait.     

The role of biomechanical forces and MALAT1/miR-329-5p/PRIP signalling on glucocorticoid-induced osteonecrosis of the femoral head

Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is a common orthopaedic disease. GIONFH primarily manifests clinically as hip pain in the early stages, followed by the collapse of the femoral head, narrowing of the hip joint space and damage to the acetabulum, resulting in severely impaired mobility. However, the pathogenesis of GIONFH is not clearly understood. Recently, biomechanical forces and non-coding RNAs have been suggested to play important roles in the pathogenesis of GIONFH. This study aimed to evaluate the role of biomechanical forced and non-coding RNAs in GIONFH. We utilized an in vivo, rat model of GIONFH and used MRI, μCT, GIONFH-TST (tail suspension test), GIONFH-treadmill, haematoxylin and eosin staining, qRT-PCR and Western blot analysis to analyse the roles of biomechanical forces and non-coding RNAs in GIONFH. We used RAW264.7 cells and MC3T3E1 cells to verify the role of MALAT1/miR-329-5p/PRIP signalling using a dual luciferase reporter assay, qRT-PCR and Western blot analysis. The results demonstrated that MALAT1 and PRIP were up-regulated in the femoral head tissues of GIONFH rats, RAW264.7 cells, and MC3T3E1 cells exposed to dexamethasone (Dex). Knockdown of MALAT1 decreased PRIP expression in rats and cultured cells and rescued glucocorticoid-induced osteonecrosis of femoral head in rats. The dual luciferase reporter gene assay revealed a targeting relationship for MALAT1/miR-329-5p and miR-329-5p/PRIP in MC3T3E1 and RAW264.7 cells. In conclusion, MALAT1 played a vital role in the pathogenesis of GIONFH by binding to (‘sponging’) miR-329-5p to up-regulate PRIP. Also, biomechanical forces aggravated the pathogenesis of GIONFH through MALAT1/miR-329-5p/PRIP signalling.