Perioperative care of nipple-areola complex-sparing mastectomy and one-stage breast reconstruction via endoscopic axillary approach for ductal carcinoma in situ: A case report.

RATIONALE: Breast cancer represents a prevalent malignancy that primarily impacts women, with pronounced consequences on their overarching health. The major therapeutic approach, encompassing surgical procedures, can often culminate in mastectomy, potentially inciting psychological turmoil and disorders. PATIENT CONCERNS: A patient was admitted to our facility on May 5, 2023, precipitated by the discovery of bilateral breast masses during a routine physical examination conducted 3 days before admission. DIAGNOSIS: The breasts were symmetric, with the right nipple inverted and a palpable mass in the upper outer quadrant of the right breast, measuring approximately 5 cm × 4 cm. The mass was firm with indistinct borders, relatively regular morphology, poor mobility, and no tenderness. Outpatient color Doppler ultrasound revealed heterogeneous echogenicity in the right breast, classified as Breast Imaging Reporting and Data System (BI-RADS) category 0, along with multiple ductal dilatations. The left breast exhibited a hypoechoic area (BI-RADS 3), indicative of proliferative changes. Radiographic mammography confirmed diffuse changes in the right breast (BI-RADS 0) and proliferative signs in the left breast (BI-RADS 2). Biopsy results reveal significant atypical ductal hyperplasia consistent with intermediate-grade ductal carcinoma in situ. This patient was diagnosed as ductal carcinoma in situ of the right breast (cTisN0M0 and Stage 0), accompanied by a left breast mass. INTERVENTIONS: On May 15, 2023, the patient was readmitted for further surgical intervention. Following relevant auxiliary examinations, the patient underwent nipple-areola complex-sparing radical mastectomy for the right breast, sentinel lymph node biopsy in the right axillary area, prosthesis-based breast reconstruction for the right breast, and microrotatotomy of the left breast mass on the left side on May 17. OUTCOMES: The patient made a successful recovery under scrupulous perioperative supervision and was discharged 7 days post-surgery. LESSONS: The axillary approach for endoscopic mammary gland excision and immediate implant reconstruction permits patients to preserve the esthetics of the female form while undergoing conventional medical treatment. This methodology considerably enhances the psychophysical health of the patients, thereby marking it as an advantageous practice worthy of broad dissemination in the medical community.

Attenuation of histone H4 lysine 16 acetylation (H4K16ac) elicits a neuroprotection against ischemic stroke by alleviating the autophagic/lysosomal dysfunction in neurons at the penumbra.

A modest autophagy benefits neuroprotection while an excessive autophagy leads to neuronal death after cerebral ischemia, but what governs an appropriate autophagy remains to be understood. Studies indicated that acetylation of histone H4 at lysine16 (H4K16ac) strongly modulated autophagic/lysosomal signaling pathway. Thus, this study was to investigate whether the autophagic neuronal injury could be alleviated by amending H4K16ac level after ischemic stroke. A rat model of middle cerebral artery occlusion (MCAO)/reperfusion was prepared to investigate dynamic variations between H4K16ac and autophagy at the penumbra. The results illustrated that the significantly elevated H4K16ac was coupled with dramatically promoted autophagic activity at 4 h after the insult, suggesting H4K16ac tightly controlled autophagic signaling. After that, H4K16ac level was altered by pretreatment with trichostatin A (TSA, a H4K16ac facilitator) and MG149 (a H4K16ac inhibitor), respectively. Four hours after MCAO/reperfusion, the penumbral tissues were obtained to detect the key proteins in autophagic/lysosomal pathway by western blot and immunofluorescence, respectively. Meanwhile, the infarct volume, neurological deficits, and neuron survival were assessed to evaluate the neurological outcomes. The results showed that TSA-promoted H4K16ac led to an excessively up-regulated autophagy resulting in autophagic/lysosomal dysfunction, as indicated by the accumulated autophagic substrates and exacerbated lysosomal inefficiency in neurons. By contrast, MG149-depressed H4K16ac significantly down-regulated autophagic activity and thereby restored the impaired autophagic flux. Consequently, the neurological injury was markedly alleviated in MCAO + MG149 group, compared with that in MCAO group. Our study suggests that the H4K16ac attenuation elicits neuroprotection against ischemic stroke by ameliorating autophagic/lysosomal dysfunction in neurons.

Ginkgo biloba leaf extract (EGb-761) elicits neuroprotection against cerebral ischemia/reperfusion injury by enhancement of autophagy flux in neurons in the penumbra.

OBJECTIVES: Ginkgo biloba leaf extract (EGb-761) injection has been widely used as adjuvant therapy for cerebral stroke in China. However, its underlying pharmacological mechanism is not completely understood. The present study aimed to investigate whether the therapeutic effects of EGb-761 are exerted by modulating autophagy flux. MATERIALS AND METHODS: Ischemic cerebral stroke was prepared in male Sprague-Dawley rats by middle cerebral artery occlusion (MCAO) followed by reperfusion. The MCAO/reperfusion rats were then treated with EGb-761 injection once daily for 7 days. Thereafter, the brain tissues in the ischemic penumbra were obtained to detect the key proteins in the autophagic/lysosomal pathway with Beclin1, LC3, (SQSTM1)/p62, ubiquitin, LAMP-1, cathepsin B, and cathepsin D antibodies by western blot and immunofluorescence. Meanwhile, the infarct volume, neurological deficits, and neuronal apoptosis were assessed to evaluate the therapeutic outcomes. RESULTS: The results illustrated that EGb-761 treatment was not only able to promote the autophagic activities of Beclin1 and LC3-II in neurons, but also could enhance the autophagic clearance, as indicated by reinforced lysosomal activities of LAMP-1, cathepsin B, and cathepsin D, as well as alleviating autophagic accumulation of ubiquitin and insoluble p62 in the MCAO+EGb-761 group, compared with those in the MCAO+saline group. Meanwhile, cerebral ischemia-induced neurological deficits, infarct volume, and neuronal apoptosis were significantly attenuated by 7 days of EGb-761 therapy. CONCLUSION: Our data suggest that EGb-761 injection can elicit a neuroprotective efficacy against MCAO/reperfusion injury, and this neuroprotection may be exerted by enhancement of autophagy flux in neurons in the ischemic penumbra.