1.A single center retrospective analysis of absolute and pseudo-incidental prostate cancer
Yue ZHANG ; Yang YU ; Hang LYU ; Wei WANG ; Chen SHEN ; Lijie WEN ; Yi HE ; Bo YANG
Chinese Journal of Urology 2020;41(9):651-655
Objective:To analyze the clinical features of absolute incidental prostate cancer (AIPCa) and pseudo-incidental prostate cancer (PIPCa).Methods:Between January 2013 and October 2019, 52 male patients who were diagnosed as incidental prostate cancer (IPCa) with their postoperative pathological examination in our center were included. None of them had any evidence of prostate cancer before. Their median age was 77.5(ranging 55-93) years old. 48 cases underwent PSA examination. The median tPSA was 6.7 (ranging 1-46) ng/ml, except 1 case tPAS>100ng/ml. The median IPSS score was 27.7(ranging 12-35). 48 cases accepted prostatic ultrasound examination. The median prostate volume was 38.6 (ranging 2.3-130.2)ml. Among them, 13 patients underwent transurethral resection of the prostate (TURP), 24 patients underwent transurethral enucleation and resection of the prostate(TUERP), 15 patients underwent radical cystoprostatectomy(RCP). According to the patients′ preoperative examination, AIPCa and PIPCa were redefined. Clinical characteristics, postoperative pathology and follow-up of the two groups were compared and analyzed.Results:There was no significant difference in age, IPSS score, tPSA, T stage and Gleason score between the operation methods groups except for prostate volume and resection ration of prostate ( P>0.05). Among those group, the sequence of prostatic resection ration was RCP>TUERP>TURP( P<0.001). There was no significant difference in age, IPSS score, prostate volume, proportion of T 1b and Gleason score between AIPCa and PIPCa groups. However, the analysis showed higher tPSA(14.68 ng/ml vs. 3.14 ng/ml) in PIPCa ( P<0.001). With a mean follow-up of 33 months(ranging 6-78 months), 23.8%(5/21) patients in AIPCa group and 45.2%(14/31) patients in PIPCa group were found to have increased PSA and underwent radical prostatectomy or androgen deprivation therapy in the follow-up. There was no metastasis or death in AIPCa group, while 2 patients had bone metastasis and 1 patient died of prostate cancer in PIPCa group. Conclusions:According to the indication of prostate biopsy, PIPCa and AIPCa were defined. PIPCa has a relatively poor prognosis, some of them may be missed diagnosis and clinical underestimation. In order to avoid missed diagnosis before operation, we should strictly define IPCa and follow the indications of biopsy, emphasize the reference value of PSA in tumor screening and biopsy, and careful handle the negative results of biopsy when PSA is abnormal.
2.Treadmill exercise alleviates neuropathic pain by regulating mitophagy of the anterior cingulate cortex in rats.
Cui LI ; Xiao-Ge WANG ; Shuai YANG ; Yi-Hang LYU ; Xiao-Juan GAO ; Jing CAO ; Wei-Dong ZANG
Acta Physiologica Sinica 2023;75(2):160-170
This study aimed to investigate the effect of treadmill exercise on neuropathic pain and to determine whether mitophagy of the anterior cingulate cortex (ACC) contributes to exercise-mediated amelioration of neuropathic pain. Chronic constriction injury of the sciatic nerve (CCI) was used to establish a neuropathic pain model in Sprague-Dawley (SD) rats. Von-Frey filaments were used to assess the mechanical paw withdrawal threshold (PWT), and a thermal radiation meter was used to assess the thermal paw withdrawal latency (PWL) in rats. qPCR was used to evaluate the mRNA levels of Pink1, Parkin, Fundc1, and Bnip3. Western blot was used to evaluate the protein levels of PINK1 and PARKIN. To determine the impact of the mitophagy inducer carbonyl cyanide m-chlorophenylhydrazone (CCCP) on pain behaviors in CCI rats, 24 SD rats were randomly divided into CCI drug control group (CCI+Veh group), CCI+CCCP low-dose group (CCI+CCCP0.25), CCI+CCCP medium-dose group (CCI+CCCP2.5), and CCI+CCCP high-dose group (CCI+CCCP5). Pain behaviors were assessed on 0, 1, 3, 5, and 7 days after modeling. To explore whether exercise regulates pain through mitophagy, 24 SD rats were divided into sham, CCI, and CCI+Exercise (CCI+Exe) groups. The rats in the CCI+Exe group underwent 4-week low-moderate treadmill training one week after modeling. The mechanical pain and thermal pain behaviors of the rats in each group were assessed on 0, 7, 14, 21, and 35 days after modeling. Western blot was used to detect the levels of the mitophagy-related proteins PINK1, PARKIN, LC3 II/LC3 I, and P62 in ACC tissues. Transmission electron microscopy was used to observe the ultrastructure of mitochondrial morphology in the ACC. The results showed that: (1) Compared with the sham group, the pain thresholds of the ipsilateral side of the CCI group decreased significantly (P < 0.001). Meanwhile, the mRNA and protein levels of Pink1 were significantly higher, and those of Parkin were lower in the CCI group (P < 0.05). (2) Compared with the CCI+Veh group, each CCCP-dose group showed higher mechanical and thermal pain thresholds, and the levels of PINK1 and LC3 II/LC3 I were elevated significantly (P < 0.05, P < 0.01). (3) The pain thresholds of the CCI+Exe group increased significantly compared with those of the CCI group after treadmill intervention (P < 0.001, P < 0.01). Compared with the CCI group, the protein levels of PINK1 and P62 were decreased (P < 0.001, P < 0.01), and the protein levels of PARKIN and LC3 II/LC3 I were increased in the CCI+Exe group (P < 0.01, P < 0.05). Rod-shaped mitochondria were observed in the ACC of CCI+Exe group, and there were little mitochondrial fragmentation, swelling, or vacuoles. The results suggest that the mitochondrial PINK1/PARKIN autophagy pathway is blocked in the ACC of neuropathic pain model rats. Treadmill exercise could restore mitochondrial homeostasis and relieve neuropathic pain via the PINK1/PARKIN pathway.
Rats
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Animals
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Mitophagy/physiology*
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Rats, Sprague-Dawley
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Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology*
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Gyrus Cinguli
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Neuralgia
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Ubiquitin-Protein Ligases/metabolism*
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Protein Kinases
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Membrane Proteins/metabolism*
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Mitochondrial Proteins/metabolism*