Objective To evaluate the prognostic value of 18 F?FDG PET/CT in untreated small cell lung cancer ( SCLC) . Methods A total of 49 SCLC patients( 35 males, 14 females, median age 61 years) with pathologically confirmed SCLC had underwent 18 F?FDG PET/CT scan before treatment from January 2008 to December 2013 and were retrospectively analyzed in this study. Clinical staging were mainly deter?mined by 18 F?FDG PET/CT scan. Performance status ( PS) was acquired according to the clinical symptoms before PET examination. Patients were followed up for at least 6 months and the survival interval was recor?ded. Two?sample t test, Kaplan?Merier, log?rank and Cox regression analysis were used for statistical analy?sis. Results (1)Among 49 patients, 20 died during the follow?up, 1 patient was lost to follow?up, and 45 patients(91.84%) had metastasis. Patients with limited disease (LD) and extensive disease (ED) were 27 and 22 respectively according to 18F?FDG PET/CT imaging. (2)The median OS was 23.68 months and me?dian PFS was 19.93 months. LD patients had significantly longer OS and PFS than ED patients (35.30 months vs 12.57 months, 28.87 months vs 11.30 months;χ2=18.810, 13.647, both P<0.05). (3)SUVmax of primary tumor ranged from 1.97 to 21.50. The SUVmax of primary foci had no difference between LD(8.27± 3.14) and ED(9.68±5.36)patients(P>0.05). SUVmax of primary tumor showed no significant correlation with OS and PFS (both P>0.05).There were no significant differences in OS and PFS between low SUVmax group and high SUVmax group in both LD and ED patients (χ2=0.001-0.565, all P>0.05). (4) Staging based on 18 F?FDG PET/CT results and PS score were independent prognostic factors ( hazard ratios:3.93, 5?00, both P<0.05) , while SUVmax showed no significant prognostic value. Conclusions PS score before PET scan and imaging staging based on 18 F?FDG PET/CT results are independent prognostic factors. The predictive value of primary foci SUVmax needs further investigation.

Objective To assess the diagnosis safety by detecting the biological character of prenatal fetus rats’nervous tissue exposed to diagnostic ultrasound during earlier period. Methods Cell culture, morphology examining, cell proliferation curve measurement and flow cytometry detection were adopted. Results ①After morphology examining, there are no difference between the treated group and control group. ② We can see from the growth curve, the two groups has identical growth tendency. ③Through flow cytometry detection, results show that there are no significance between two groups. Conclusion Diagnostic ultrasound in early pregnancy have no significant effect on prenatal fetus rats’nervous tissue.

In this paper, the domestic and international demand and development trend of clinical diagnostic radionuclides are analyzed, and the medium and high-energy cyclotrons, adequate and systematic facilities, and preparation techniques required for the production of medical radionuclides based on solid targets are introduced. This paper focuses on the research and development carried out by some important medical institutions and scientific research institutes in China over the years in the aspects of medium and high-energy cyclotrons, beam transmission lines, high-power irradiation target stations and new medical isotope production processes etc. It also looks forward to some new directions for the development of medical radionuclides in China during the 14th Five-Year Plan period.

Cardiovascular System/pathology* ; Constriction, Pathologic/genetics* ; Point Mutation ; Neurofibromin 1/genetics* ; Animals ; Mice

The chronic use of morphine and other opioids is associated with opioid-induced hypersensitivity (OIH) and analgesic tolerance. Among the different forms of OIH and tolerance, the opioid receptors and cell types mediating opioid-induced mechanical allodynia and anti-allodynic tolerance remain unresolved. Here we demonstrated that the loss of peripheral μ-opioid receptors (MORs) or MOR-expressing neurons attenuated thermal tolerance, but did not affect the expression and maintenance of morphine-induced mechanical allodynia and anti-allodynic tolerance. To confirm this result, we made dorsal root ganglia-dorsal roots-sagittal spinal cord slice preparations and recorded low-threshold Aβ-fiber stimulation-evoked inputs and outputs in superficial dorsal horn neurons. Consistent with the behavioral results, peripheral MOR loss did not prevent the opening of Aβ mechanical allodynia pathways in the spinal dorsal horn. Therefore, the peripheral MOR signaling pathway may not be an optimal target for preventing mechanical OIH and analgesic tolerance. Future studies should focus more on central mechanisms.
Humans ; Morphine/pharmacology* ; Hyperalgesia/metabolism* ; Analgesics, Opioid/pharmacology* ; Neurons/metabolism* ; Signal Transduction

Mechanical allodynia (MA), including punctate and dynamic forms, is a common and debilitating symptom suffered by millions of chronic pain patients. Some peripheral injuries result in the development of bilateral MA, while most injuries usually led to unilateral MA. To date, the control of such laterality remains poorly understood. Here, to study the role of microglia in the control of MA laterality, we used genetic strategies to deplete microglia and tested both dynamic and punctate forms of MA in mice. Surprisingly, the depletion of central microglia did not prevent the induction of bilateral dynamic and punctate MA. Moreover, in dorsal root ganglion-dorsal root-sagittal spinal cord slice preparations we recorded the low-threshold Aβ-fiber stimulation-evoked inputs and outputs of superficial dorsal horn neurons. Consistent with behavioral results, microglial depletion did not prevent the opening of bilateral gates for Aβ pathways in the superficial dorsal horn. This study challenges the role of microglia in the control of MA laterality in mice. Future studies are needed to further understand whether the role of microglia in the control of MA laterality is etiology-or species-specific.
Mice ; Animals ; Hyperalgesia/metabolism* ; Microglia/metabolism* ; Disease Models, Animal ; Spinal Cord/metabolism* ; Spinal Cord Dorsal Horn/metabolism* ; Ganglia, Spinal/metabolism*