Ultrasound Diagnosis and Treatment of Breast Lumps after Breast Augmentation with Autologous Fat Grafting.

BACKGROUND: Breast augmentation with autologous fat has been performed in Japan for over 30 years. However, complications include breast lumps and oil cysts. Such breast lumps greatly reduce patient satisfaction, and are currently difficult to diagnose and treat for many cosmetic surgery clinics. This study aimed to elucidate the effectiveness of ultrasound diagnosis and treatment of patients with breast lumps after breast augmentation with autologous fat grafting. METHODS: We used diagnostic and therapeutic ultrasound to examine 256 patients with breast lumps between April 2012 and April 2017. We determined the nature, size, and location of the maximal lump. Breast lumps were classified into five types: cystic, complex, solid, calcification, and unclassifiable. The method of treatment (including fine-needle aspiration, VASER liposuction, lumpectomy, and extended lumpectomy) was selected according to the lump type, and the efficacy of treatment was determined by postoperative palpation and ultrasound. RESULTS: A total of 198 patients (198/256, 77%) requested treatment. Cystic lumps (79/256, 31%) were treated by fine-needle aspiration. VASER liposuction was used to treat complex (64/256, 25%) and solid lumps (50/256, 19%). Calcification (58/256, 23%) and unclassifiable lumps (5/256, 2%) were removed via periareolar incision. There were no serious complications. In all cases, the lumps were no longer palpable after treatment, and ultrasound showed that they had either contracted or disappeared. CONCLUSIONS: The appropriate treatment for breast lumps after breast augmentation with autologous fat grafting must be selected according to the nature of the lumps. Ultrasound is essential for diagnosing the breast lump type and determining the best treatment.

A case of abdominal compartment syndrome derived from simple elongated sigmoid colon in an elderly man.

INTRODUCTION: Abdominal compartment syndrome or intra-abdominal hypertension may occur after intra-abdominal events, but their etiology and clinical signs remain unclear. We report a case of abdominal compartment syndrome in an elderly patient without other risk factors. PRESENTATION OF CASE: An 86-year-old man had been admitted to our hospital several times for a dilated sigmoid colon with elongation, and had complained about abdominal pain and abdominal fullness. At every admission we decompressed the sigmoid colon gas by colonoscopy, resulting in early discharge the following day. Recently, the patient developed dementia and experienced reduced activities of daily living that are common with aging. He frequently complained of severe abdominal distension with hypotension, tachycardia and tachypnea, and finally entered hospital twice a week. We decided to perform elective surgery, which showed abdominal compartment syndrome caused by elongated sigmoid colon without volvulus (the first reported case). DISCUSSION AND CONCLUSION: Considering the increase in the aging population, we must bear in mind that abdominal compartment syndrome may occur in simple elongated sigmoid colon without other risk factors.

Impaired mitophagy activates mtROS/HIF-1α interplay and increases cancer aggressiveness in gastric cancer cells under hypoxia.

Mitochondrial autophagy (mitophagy) is a selective form of autophagy and a critical step in excluding mitochondria damaged by stress, including hypoxia. This study aimed to determine whether the integrity of mitophagy affected production of the mitochondrial reactive oxygen species (mtROS), hypoxia inducible factor (HIF)-1α expression and aggressive characteristics in GC cells under hypoxia. Three GC cell lines, 44As3, 58As9 and MKN45, were investigated in this study. HIF-1α expression was induced in the three GC cell lines under hypoxia, with higher expression observed in 44As3 and 58As9 cells compared with MKN45 cells. Cell survival and invasion abilities under hypoxia were significantly stronger in 44As3 and 58As9 cells than MKN45 cells. Moreover, mtROS accumulated in a time-dependent manner in 44As3 and 58As9 cells, but not in MKN45 cells. ROS scavenger N-acetyl-L-cysteine (NAC) treatment resulted in strong attenuation of HIF-1α expression, whereas HIF-1α knockdown increased ROS production in the three GC cell lines under hypoxia. These results suggested that the mtROS/HIF-1α interplay affected the hypoxia-induced cancer aggressiveness. Assessment of mitophagy by LC3-I/II conversion, SQSTM1/p62 degradation and specific fluorescence markers demonstrated that hypoxia-induced mitophagy was observed only in MKN45 cells, while the process was impaired in the other two cell lines. Treatment with the autophagy inhibitor chloroquine conversely increased HIF-1α expression, mtROS generation, cell survival and invasion in hypoxic MKN45 cells. The present study revealed a novel mechanism in which the integrity of mitophagy might determine cancer aggressiveness via mtROS/HIF-1α interplay in GC cells under hypoxic conditions.

Regulation and clinical significance of the hypoxia-induced expression of ANGPTL4 in gastric cancer.

Solid tumors are often exposed to hypoxia. Hypoxia inducible factor (HIF)-1α upregulates numerous target genes associated with the malignant behavior of hypoxic cancer cells. A member of the angiopoietin family, angiopoietin-like protein 4 (ANGPTL4) is a hypoxia-inducible gene. The present study aimed to clarify whether ANGPTL4 is regulated by HIF-1α in gastric cancer cells. The study also assessed whether ANGPTL4 expression is associated with clinicopathological factors or HIF-1α expression in gastric cancer tissues. Hypoxia-induced ANGPTL4 expression was quantitatively analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in 10 gastric cancer cell lines. RT-qPCR was further employed to investigate the HIF-1α dependency of ANGPTL4 expression using HIF-1α-knockdown transfectant 58As9-KD and control 58As9-SC gastric cancer cells. The HIF-1α and ANGPTL4 expression levels were immunohistochemically analyzed in 170 gastric cancer tissue specimens and were assessed for any correlations with the clinicopathological factors and/or patient survival. Subsequently, hypoxia-induced ANGPTL4 expression was observed in 7 out of 10 gastric cancer cell lines. The hypoxic induction of ANGPTL4 was almost preserved in the 58As9-KD cells compared with that observed in the 58As9-SC cells, while the induction of known HIF-1α target gene, carbonic anhydrase 9, was completely suppressed in the 58As9-KD cells. In the gastric cancer tissues, ANGPTL4 expression was inversely correlated with the tumor depth, whereas HIF-1α expression was positively correlated with venous invasion. A survival analysis revealed that the expression of ANGPTL4 was significantly correlated with a longer survival time, whereas that of HIF-1α was correlated with a shorter survival time. In conclusion, the present findings indicate that hypoxia-induced ANGPTL4 expression is independent of HIF-1α in hypoxic gastric cancer cells. ANGPTL4 may be a favorable marker for predicting a long survival time, whereas HIF-1α predicts a poor prognosis, in gastric cancer patients. The hypoxic environment independently induces ANGPTL4 and HIF-1α, which are believed to exhibit adverse effects on tumor progression.

The Apoptotic Effect of HIF-1α Inhibition Combined with Glucose plus Insulin Treatment on Gastric Cancer under Hypoxic Conditions.

Gastric cancer grows under a hypoxic environment. HIF-1α is known to play an important role in controlling the production of reactive oxygen species (ROS) in the mitochondria under hypoxic conditions. We previously established HIF-1α knockdown (KD) cells and control (SC) cells in the 58As9 gastric cancer cell line. In this study, we revealed that KD cells, but not SC cells, induced apoptosis under conditions of hypoxia (1% O2) due to excessive production of ROS. A quantitative RT-PCR analysis demonstrated that the expressions of ten genes, which are involved in the control mechanisms of ROS (including the Warburg effect, mitophagy, electron transport chain [ETC] modification and ROS scavenging), were regulated by HIF-1α. Moreover, the promotion of glucose uptake by glucose plus insulin (GI) treatment enhanced the apoptotic effect, which was accompanied by further ROS production in hypoxic KD cells. A Western blot analysis showed that the membranous expression of GLUT1 in KD cells was elevated by glucose and/or insulin treatments, indicating that the GI-induced glucose uptake is mediated by the increased translocation of GLUT1 on the cell membrane. Finally, the anti-tumor effect of HIF-1α knockdown (KD) plus GI was evaluated using a tumor xenograft model, where a hypoxic environment naturally exists. As a result, the GI treatment strongly inhibited the growth of the KD tumors whereby cell apoptosis was highly induced in comparison to the control treatment. In contrast, the growth of the SC tumors expressing HIF-1α was not affected by the GI treatment. Taken together, the results suggest that HIF-1α inhibition plus GI may be an ideal therapy, because the apoptosis due to the destruction of ROS homeostasis is specifically induced in gastric cancer that grows under a hypoxic environment, but not in the normal tissue under the aerobic conditions.