Objective To investigate the protective effect of meglumine adenosine cyclosphosp (MAC) on the cerebral ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty four healthy rabbits were randomly divided into control group (n =6),I/R group (n =6),MAC pretreated group (n =6),and MAC treated group (n =6).Cerebral ischemia-reperfusion injury model was made by separating and electrocoagulating vertebral arteries and clipping common carotid arteries in the latter 3 groups after anesthesia.The sham-operated group underwent vessel separation without clipping.L/R group was administered with nothing,while MAC pretreated group with MAC before ischemia,and MAC treated group with MAC just after ischemia.Blood was gathered from jugular vein before ischemia,and 30 min,1 h,and 2 h after reperfusion for testing IL-8,superoxide dismutase (SOD) and malondialdehyde (MDA).The brain tissue slice was observed by optical microscope.Results Compared to control group and before ischemia,the levels of IL-8 and SOD in serum were significantly increased and decreased,and the levels of MDA was significantly increased at 30 min after reperfusion in I/R group; the levels of IL-8 and MDA in serum were significantly increased,and the levels of SOD in serum was significantly decreased at 1 h and 2 h after reperfusion in I/R group.The levels of IL-8 in serum was less at 30 min and 1 h and 2 h after reperfusion in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of MDA in serum was less and the levels of SOD in serum was higher in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of IL-8 in serum were less and the levels of SOD in serum were higher in MAC treated group than in I/R group.The levels of MDA in serum were less at 2 h after reperfusion in MAC treated group than in I/R group.Compared to I/R group,pathological change was lighter in the MAC pretreated and MAC treated group.Conclusions MAC has a fine cerebral-protective effect and has no side effect.

OBJECTIVETo explore the experimental method of obtaining position emission tonogiaphy (PET) imaging evidence of changes in cerebral function by puncturing the Stomach 36 (ST36, Zusanli) acupoint.

METHODSData on changes of cerebral glycometabolism were obtained from six healthy male volunteers with positron emission tomography. Visual experimental evidence, as well as statistical parametric mapping (SPM), was gathered while puncturing the ST36 (Zusanli, right leg) acupoint.

RESULTSThere was increased glycometabolism in the hypothalamus, head of the caudate nucleus, temporal lobe, the sinistral cerebellum, postcentral gyrus, and brain stem while the acupoint ST36 was being punctured.

CONCLUSIONSAcupuncture on ST36 can lead to increase in glycometabolism in the vegetative nerve centers, which is correlated with gastric function. Visual experimental evidence of ST36 acupuncturing on functional gastrointestinal disorder was obtained in our study.

Acupuncture ; Acupuncture Points ; Adult ; Brain ; diagnostic imaging ; physiology ; Glucose ; metabolism ; Humans ; Male ; Tomography, Emission-Computed

OBJECTIVETo explore the genetic etiology for 11 sporadic patients with neurofibromatosis type 1.

METHODSChip targeting capture and high-throughput sequencing were employed to detect potential mutations of NF1 and NF2 genes among the 11 patients. The data was filtered through multiple mutational databases and in-house whole exome sequence database. Sanger sequencing was used for analysis of family members of the patients.

RESULTSEleven pathogenic variants were found among the 11 patients, which included two splicing mutations, one missense mutation, two nonsense mutations, and six frame-shifting mutations. None of the mutations was recorded by the public database or the in-house database generated from 1775 samples through whole exome sequencing. None of the unaffected parents carried the same mutation. Seven mutations were associated with neurofibromatosis type 1 previously, while the remaining four were discovered for the first time. Prenatal diagnosis of two high-risk pregnancies suggested that neither fetus has inherited the NF1 mutation from their affected parents.

CONCLUSIONIdentification of causative mutations in patients with sporadic-type neurofibromatosis type 1 has provided a basis for genetic counseling. The four novel mutations have enriched the spectrum of NF1 gene mutations.