The aim of the current study is to investigate programmed death-1 (PD-1) and programmed death ligand-1 (PD-L1) expressions and to analyze the relationship between the expression of PD-L1 and PD-1 proteins and the molecular type, clinicopathological factors, and prognosis of invasive ductal carcinoma. We enrolled 136 patients with invasive ductal carcinoma of the breast. The expression of PD-L1 in tumor cells and that of PD-1 on paratumor-infiltrating immune cells was detected by immunohistochemistry, and the data were analyzed using SPSS software. The positive expression rates of PD-L1 and PD-1 in triple-negative breast cancer (TNBC) were 47.8 and 43.5%, which were higher than those of other subtypes (P<0.05). The expression of PD-L1 in tumor cells was correlated with the expression of estrogen receptor, progesterone receptor, and Ki-67 (P<0.05). The expression of PD-1 in the tumor-infiltrating immune cells was correlated with the expression of estrogen receptor, progesterone receptor, and Ki-67 and the histological grade (P<0.05). The expression of PD-L1 in tumor cells was correlated with the expression of PD-1 in paratumor-infiltrating immune cells (P<0.001). The expression of PD-L1 in tumor cells was found to be an independent prognostic risk factor with the progression-free survival rate for breast invasive ductal carcinoma (P=0.003). These results indicate that PD-L1 and PD-1 were highly expressed in TNBC which suggests that patients with TNBC may benefit from targeted immune therapies to a greater degree than patients with other subtypes. PD-L1 expression is an independent risk factor for breast invasive ductal carcinoma and expression of PD-L1 is expected to be a prognostic factor for breast cancer.
A 66-year-old woman with a history of hypertension was examined for recurrent chest discomfort and palpitations at our hospital. A dual-chamber pacemaker (Abbott/SJM) was implanted due to sick sinus syndrome 1 year ago. The Holter monitor test recorded recurrent episodes of a sudden change in pacing rate, starting with an intrinsic P wave (Figure 1a). In total, 25 episodes were recorded, of which, the longest episode lasted for 3 min.Most episodes corresponded to the patient's symptoms of recurrent chest discomfort and palpitations. Notably, Figure 1b shows pacing pulses in two opposite directions: an upward pulse (Up), followed by a positive P wave, and a downward pulse (Dp), followed by a negative P wave.The patient offered following information about the last interrogation: DDD mode, base rate 60 bpm, auto-mode switch base rate (AMSBR) 80 bpm, PAV/SAV interval 300/250 ms, and activity sensor off.What accounts for the sudden change in pacing rate?
| COMMENTARYThe following reasons may be attributed for the sudden change in pacing rate: an auto-mode switch (AMS) (Sharma et al., 2016), atrial overdrive pacing function (Hohnloser et al., 2012), and sensor rate.Every episode started with an intrinsic P wave, which is consistent with the startup characteristics of AMS in the SJM (Barold, 2017). However, no atrial tachycardia was observed before any episode. This suggested that the AMS might be due to atrial oversensing. In contrast, the atrial pacing rate (105 bpm, AP-AP interval 570 ms) did not correspond with AMSBR (80 bpm). The atrial pacing rate to
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