Recurrent cervical cancer is a clinically complex disease that is difficult to treat. There are numerous treatment options, but the results achieved by each are poor. External-beam radiation therapy of the pelvic lymph drainage area, in combination with intracavitary afterloading or the interstitial implantation of a radiation source (i.e., brachytherapy), are the current standard radiotherapy regimens used in high-risk clinical targets. However, there are few reports concerning the use of iodine-125 (125I) seed implantation brachytherapy in recurrent cervical cancer, and the effects of treatment and adverse reactions have not yet been systematically evaluated. In the present study one such case is reported, in which the patient was successfully treated with intensity-modulated radiotherapy (IMRT) in combination with 125I seed implantation. The patient, a 47-year-old woman, was initially diagnosed with International Federation of Gynecology and Obstetrics stage IB1 cervical cancer, and received a radical hysterectomy, left lateral adnexectomy and pelvic lymph node dissection. A follow-up examination 23 months later revealed vaginal invasion and a solitary lump in the cervical stump with a maximum diameter of 38 mm. The patient was subsequently diagnosed with recurrent cervical cancer and was treated with six cycles of docetaxel and nedaplatin chemotherapy, alongside IMRT and interstitial 125I seed implantation. At the point of manuscript submission, the patient's progression-free survival time was 33 months and long-term adverse reactions were acceptable. The response of this patient indicates that 125I seed implantation could be used as a complementary treatment for recurrent cervical cancer and may also prove to be a reliable means for the comprehensive treatment of primary cervical cancer, as the patient had characteristics similar to primary cervical cancer, although this hypothesis could not be confirmed in the present study.
Diabetes mellitus (DM) and Parkinson’s disease (PD) have been and will continue to be two common chronic diseases globally that are difficult to diagnose during the prodromal phase. Current molecular genetics, cell biological, and epidemiological evidences have shown the correlation between PD and DM. PD shares the same pathogenesis pathways and pathological factors with DM. In addition, β-cell reduction, which can cause hyperglycemia, is a striking feature of DM. Recent studies indicated that hyperglycemia is highly relevant to the pathologic changes in PD. However, further correlation between DM and PD remains to be investigated. Intriguingly, polycystic monoamine transporter 2 (VMAT2), which is co-expressed in dopaminergic neurons and β cells, is responsible for taking up dopamine into the presynaptic vesicles and can specifically bind to the β cells. Furthermore, we have summarized the specific molecular and diagnostic functions of VMAT2 for the two diseases reported in this review. Therefore, VMAT2 can be applied as a target probe for positron emission tomography (PET) imaging to detect β-cell and dopamine level changes, which can contribute to the diagnosis of DM and PD during the prodromal phase. Targeting VMAT2 with the molecular probe 18 F-FP-(+)-DTBZ can be an entry point for the β cell mass (BCM) changes in DM at the molecular level, to clarify the potential relationship between DM and PD. VMAT2 has promising clinical significance in investigating the pathogenesis, early diagnosis, and treatment evaluation of the two diseases.
Parkinson's disease (PD) is a common neurodegenerative disease in elderly people, which is characterized by motor disabilities in PD patients. Nav1.6 is the most abundant subtype of voltage‐gated sodium channels (VGSCs) in the brain of adult mammals and rodents. Here we investigated the role of Nav1.6 in the external globus pallidus (GP) involved in the pathogenesis of motor deficits in unilateral 6‐OHDA(6‐hydroxydopamine)lesioned rats. The results show that Nav1.6 is dramatically increased in reactive astrocytes of the ipsilateral GP in the middle stage, but not different from the control rats in the later stage of the pathological process in 6‐OHDA lesioned rats. Furthermore, the down‐regulation of Nav1.6 expression in the ipsilateral GP can significantly improve motor deficits in 6‐OHDA lesioned rats in the middle stage of the pathological process. The electrophysiological experiments show that the down‐regulation of Nav1.6 expression in the ipsilateral GP significantly decreases the abnormal high synchronization between the ipsilateral M1 (the primary motor cortex) and GP in 6‐OHDA lesioned rats. Ca2+ imaging reveals that the down‐regulation of Nav1.6 expression reduces the intracellular concentration of Ca2+ ([Ca2+]i) in primary cultured astrocytes. These findings suggest that the increased Nav1.6 expression of reactive astrocytes in the GP play an important role in the pathogenesis of motor dysfunction in the middle stage in 6‐OHDA lesioned rats, which may participate in astrocyte‐neuron communication by regulating [Ca2+]i of astrocytes, thereby contributing to the formation of abnormal electrical signals of the basal ganglia (BG) in 6‐OHDA lesioned rats.
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