Temperature is a critical environmental stimulus that has a strong impact on an organism’s biochemistry. Animals can respond to changes in ambient temperature through behaviour or altered physiology. However, how animals habituate to temperature is poorly understood. The nematode C. elegans stores temperature experiences and can induce temperature habituation-linked cold tolerance. Here we show that light and pheromone-sensing neurons (ASJ) regulate cold habituation through insulin signalling. Calcium imaging reveals that ASJ neurons respond to temperature. Cold habituation is abnormal in a mutant with impaired cGMP signalling in ASJ neurons. Insulin released from ASJ neurons is received by the intestine and neurons regulating gene expression for cold habituation. Thus, temperature sensation in a light and pheromone-sensing neuron produces a robust effect on insulin signalling that controls experience-dependent temperature habituation.
Tolerance to environmental temperature change is essential for the survival and proliferation of animals. The process is controlled by various body tissues, but the orchestration of activity within the tissue network has not been elucidated in detail. Here, we show that sperm affects the activity of temperature-sensing neurons (ASJ) that control cold tolerance in Caenorhabditis elegans. Genetic impairment of sperm caused abnormal cold tolerance, which was unexpectedly restored by impairment of temperature signaling in ASJ neurons. Calcium imaging revealed that ASJ neuronal activity in response to temperature was decreased in sperm mutant gsp-4 with impaired protein phosphatase 1 and rescued by expressing gsp-4 in sperm. Genetic analysis revealed a feedback network in which ASJ neuronal activity regulates the intestine through insulin and a steroid hormone, which then affects sperm and, in turn, controls ASJ neuronal activity. Thus, we propose that feedback between sperm and a sensory neuron mediating temperature tolerance.
The glandular odontogenic cyst (GOC) is a rare odontogenic cyst which is still controversial in regard to classification, terminology, and origin. The first Japanese case of GOC is reported. Immunohistochemical examination for expression of cytokeratins and epithelial membrane antigen by monoclonal antibodies suggested that the lining epithelium was of odontogenic origin with metaplastic mucus-laden cells. We have reviewed the literature and compared the clinicopathological findings of the reported case of GOC with those of botryoid odontogenic cysts (BOC). The anatomical location, age range, and sex of GOC cases were very similar to those of BOC. GOC appears to be a multiocular and mucoepidermoid variant of non-keratinizing odontogenic cysts, which also includes BOC. GOC should be separated from the other types of odontogenic cyst and central mucoepidermoid tumours of salivary gland origin.
These results suggest an association between a decrease in contrast enhancement of the posterior disk attachment and resolution or reduction in joint pain. This association was much stronger than the association between the clinical findings and the anatomy of the disk.
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