1.Effects of vitamin A deficiency on infectious diseases in children
Qizhi WANG ; Jiangying ZHOU ; Qunbo GE ; Jiena SHEN ; Xiaoyan FANG
Chinese Journal of Biochemical Pharmaceutics 2017;37(5):85-86,89
Objective To investigate the relationship between serum vitamin A deficiency (vitam in A deficiency, VAD) and infectious diseases in children.MethodsAdopt the method of random sampling, sample of Cixi City prevention center with a total of 5000 children under the age of 6, according to the age groups were divided into 6 groups, the detection of vitamin A in children refers to the blood, separation of serum collected in dark conditions, with strict quality control, detection of serum vitamin A by fluorescence method (vitamin A the concentration of VA.).ResultsIn the two weeks, the incidence of VA in children with fever and acute respiratory infection (ARI) increased.ConclusionOur children's serum VA content is low, the lack of the high rate of children regardless of individuals or groups are prone to acute infection, VAD is the cause of children prone to acute infectious diseases is one of the important reasons.To strengthen health education, improve parents' feeding knowledge, proper oral Cod Liver Oil drops and reasonable feeding, is conducive to the healthy growth of children.
2.Semaphorins play an important role in bone homeostasis and metabolic bone disease
Yu CONG ; Ting GUO ; Jianning ZHAO ; Jiangying RU ; Liwu ZHOU ; Nirong BAO
Chinese Journal of Tissue Engineering Research 2015;(11):1761-1767
BACKGROUND:Bone formation is a dynamic process, and osteoclasts and osteoblasts are involved in this dynamic process. Semaphorins were found first as axonal growth cone guidance molecules, which express in many different tissues and regulate many physiological processes. Recently, Semaphorins are confirmed to play an important role in the regulation of osteoclasts and osteoblasts. OBJECTIVE:To summarize the role of Semaphorins in bone homeostasis. METHODS: A computer-based search of PubMed and Web of Science was performed for articles related to the effect of Semaphorins in regulation of bone metabolism published from June 1993 to January 2014 using the keywords of “semaphorin, sema”. Irrelevant articles or duplicate content articles were excluded, and finaly 48 articles were reviewed. RESULTS AND CONCLUSION:Semaphorins act as a new class of regulatory molecules in the aspect of bone cytobiology. Studies have show semaphorins are actively involved in bone remodeling through some special mechanisms, and semaphorin proteins are crucial for bone homeostasis, which provides a new method and therapeutic target for the treatment of osteoporosis, bone sclerosis, osteolysis adjacent to joint prosthesis and other bone diseases.
3.Ca2+/calmodulin-dependent protein kinase Ⅱ inhibitor K N-93 aggravates the calcium paradox-induced heart injury
Lingheng KONG ; Xiaoming GU ; Ying NAN ; Jiangying ZHANG ; Na SUN ; Juanxia ZHU ; Jingjun ZHOU
Chinese Pharmacological Bulletin 2016;32(6):832-835,836
Aim ToinvestigatetheeffectsofCa2+/calmodulin-dependent protein kinase Ⅱ inhibitor KN-93 on calcium overload-induced heart injury.Methods Thirty-twoisolatedratheartswererandomlydivided into the control group,KN-93 control group,calcium paradox group,and calcium paradox with KN-93 treat-ment group.Left ventricular pressure were recorded, and the heart function was evaluated by the left ventric-ular end-diastolic pressure (LVEDP ) and developed pressure (LVDP).Coronary flow (CF)were collect-ed,and lactate dehydrogenase (LDH)content was de-termined.Triphenyltetrazolium chloride staining was usedtomeasuretheinfarctsize.Results Compared with the control group,KN-93 at 2. 5 μmol·L-1 had no effects on coronary flow,cardiac performance and cell death at the end of perfusion in normal rats (P>0. 05 );The hearts of calcium paradox exhibited a de-crease in LVDP and CF,meanwhile an increase in LV-EDP,LDH,and infarct size of 18 ±7. 2% (P <0. 01).2. 5 μmol·L-1 KN-93 further increased the levels of LVEDP,LDH and infarct size (P<0. 01)in Ca2+paradoxical hearts,while it provoked the decline intheCFandLVDP(P<0.01).Conclusion The data demonstrates that KN-93 aggravates heart injury in calcium paradox,it also suggests that CaMKⅡ is in-volved in the Ca2+overload-induced heart injury.