Malignant transformation of pulmonary bronchiolar adenoma into mucinous adenocarcinoma: A case report.

BACKGROUND: Bronchiolar adenoma (BA) and ciliated muconodular papillary tumor are rare tumors that have bilayered cell proliferation and continuous expression of p40 and CK5/6 in the basal cell layer. Diagnosis is difficult because of the limited knowledge of these tumors and their morphological similarities to malignant tumors, including invasive mucinous adenocarcinoma, especially based on the histopathology of intraoperative frozen sections. These tumors are now considered to be benign neoplasms, with malignant transformation reported in only a few cases. CASE SUMMARY: A 57-year-old woman presented with a 17.0 mm × 7.0 mm nodule in the lower lobe of the left lung. Hematoxylin-eosin staining and immunohistochemistry of a surgical specimen were performed. The tumor consisted of a BA area and a mucinous adenocarcinoma (MA) area. In the BA area, the tumor had a bilayered structure of luminal cells and basal cells. The basal cells were positive for CK5/6 and p40, but the MA area was negative for these biomarkers. The Ki-67 proliferation index was low (1%-2%). The patient was diagnosed with BA accompanied by MA, and had a favorable outcome. CONCLUSION: The present study indicated that BA may be carcinogenic, and suggests that clinicians should be aware of its potential for malignant transformation.

Status of maternal serum B vitamins and pregnancy outcomes: New insights from in vitro fertilization and embryo transfer (IVF-ET) treatment.

The influence of B vitamins on human fertility and infertility treatments remains elusive. Therefore, this study investigated the association of most B vitamins with IVF-ET outcomes. A total of 216 subjects aged <35 year in their first oocyte retrieval cycle were recruited. Blood samples from the participants were collected before the oocyte pick-up procedure, and serum levels of riboflavin, niacin, pantothenic acid, vitamin B6 (including PA and PLP), folate, and methylmalonic acid (MMA) were detected using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Endpoints were classified into three groups according to tertiles (lower, middle, and upper) of each vitamin index, and the association of the serum vitamin status with intermediate and clinical outcomes was analyzed using a generalized estimating equation model. Higher riboflavin levels were associated with elevated probabilities of high-quality embryos, as well as clinical pregnancy after embryo transfer. A greater likelihood of transferable embryos was found in the middle tertile of serum folate. Similarly, a negative correlation of serum MMA, a marker of vitamin B12 deficiency, with high-quality embryos was identified. No significance was observed for other vitamins in terms of all endpoints. Therefore, sufficient levels of pre-conception riboflavin, folate, and vitamin B12 are recommended for successful infertility treatment and pregnancy planning; further evidence is needed to confirm our conclusion.

Neurotrophic factors stimulate the activation of hepatic stellate cells in liver fibrosis.

BACKGROUND AND AIMS: Patients with liver fibrosis who have pain in the liver region may have changed nerve factors. The expression of neurokines and hepatic nerves in liver fibrosis, however, was little understood. In order to better understand how liver fibrosis develops, we plan to look into the hepatic nerve and neurokine changes and how they relate to hepatic stellate cells (HSCs). METHODS: The expression of neurokines in liver samples from 55 chronic hepatitis B patients and the carbon tetrachloride (CCl4) animal model were studied. The co-staining of Nissl and α-SMA allowed us to investigate the neurons and their interaction with α-SMA in fibrotic livers, as well as the expression of the glial cell marker glial fibrillary acidic protein (GFAP) and its relationship with α-SMA, a marker of HSCs. SH-SY5Y cells were treated with a fibrotic serum to imitate the hepatic microenvironment on neuronal cells. We also used brain-derived neurotrophic factor (BDNF) to stimulate mouse primary HSCs and LX2. RESULTS: The levels of mRNA for neurokines such as BDNF, GFAP, and growth-associated protein (GAP43) are significantly increased in both human and animal liver fibrosis. As liver fibrosis advances, we found that Nissl bodies and α-SMA may co-localize, suggesting a connection between hepatic nerves and HSCs. Human fibrotic serum may increase neurkines, notably BDNF, in SH-SY5Y cells. We also found that BDNF increased pro-inflammatory cytokines and fibrogenic markers in hHSCs. CONCLUSIONS: Patients with hepatic fibrosis had significantly higher levels of BDNF, GFAP, GAP43, and nerve fibers. HSC and nerve fibers interact, and nerves also create neurogenic substances that promote liver fibrosis and HSC activation.

[Three-dimensional morphology of C6/36 cells infected by dengue virus: a study based on digital holographic microscopy].

OBJECTIVE: To monitor the 3-dimensional (3D) morphological changes of C6/36 cells during dengue virus (DENV) infection using a live-cell imaging technique based on digital holographic microscopy and provide clues for better understanding the mechanisms of DENV infection. METHODS: C6/36 cells were seeded in 6-well plates to determine the optimal imaging density under a holographic cell imager, and the morphological changes of the cells were recorded in response to a culture temperature change from 28 degrees celsius; to 37 degrees celsius; C6/36 cells were infected with 4 DENV strains with different serotypes at 28 degrees celsius; and incubated at 37 degrees celsius; for 24 h, and the 3D holograms and relevant morphological parameters were recorded at different time points using HoloMonitor M4 holographic cell imaging and analysis system. RESULTS: The holograms of C6/36 cells inoculated at the optimal density for imaging (4×105 per well) showed unified 3D morphologies of the single cells with minimal dispersions in the cell area, thickness and volume (P<0.05), which did not undergo obvious changes when the cells were incubated at 37 degrees celsius; for 24 h (P>0.05). The cell area and volume of the cells infected with the 4 DENV strains all increased and the cell thickness was reduced during incubation. Among the 4 strains, DENV-1 and DENV-2 caused reduced cell thickness while DENV-3 and DENV-4 increased the cell thickness, and the pattern and degree of such changes differ among the 4 strains. CONCLUSIONS: Digital holographic microscopy allows monitoring of the complex morphological changes of cells during DENV infection. The 4 DENV strains with different serotypes causes characteristic cell damages during infection.

[Effect of ginsenoside Rb1 on cerebral infarction volume and IL-1 beta in the brain tissue and sera of focal cerebral ischemia/reperfusion injury model rats].

OBJECTIVE: To investigate the effect of ginsenoside Rb1 on cerebral infarction volume as well as IL-1 beta in the brain tissue and sera of focal cerebral ischemia/reperfusion (I/R) injury model rats. METHODS: The I/R rat model was established by using thread according to Zea-Longa. SD rats were randomly divided into five groups, i.e., the sham-operation group, the model group, the low dose ginsenoside Rb1 (20 mg/kg) group, the medium dose ginsenoside Rb1 group (40 mg/kg), and the high dose ginsenoside Rb1 group (80 mg/kg), 12 in each group. Rats in the sham-operation group only received middle cerebral artery occlusion (MCAO) but without thread insertion. The MCAO model was prepared in the rest 4 groups, followed by MCAO2 h later. Ginsenoside Rb1 at each dose was peritoneally administrated to rats in corresponding groups immediately after cerebral ischemia. Equal volume of normal saline was administered to rats in the sham-operation group. Rats' cerebral infarction volume, integrals of neurologic defect degree, expression of IL-1 beta content in the brain tissue and sera were observed 24 h after 2-h cerebral I/R. RESULTS: In the model group, integrals of neurologic defect degree were improved (P < 0.01), IL-1 beta positive cells in the brain tissue increased and serum IL-1 beta content elevated (P < 0.05), when compared with the sham-operation group. In comparison of the model group, integrals of neurologic defect degree were lowered in the medium dose and high dose ginsenoside Rb1 groups (P < 0.05, P < 0.01). The cerebral infarction volume was all shrunken in each ginsenoside Rb1 group, IL-1 beta positive cells in the brain tissue decreased, and IL-1 beta content in serum reduced (P < 0.01, P < 0.05). Compared with the low dose ginsenoside Rb1 group, integrals of neurologic defect degree decreased, the cerebral infarction volume shrunken, and IL-1 beta content in serum reduced in the high dose ginsenoside Rb1 group (P < 0.01, P < 0.05). CONCLUSION: Ginsenoside Rb1 (20, 40, 80 mg/kg) might effectively release local cerebral ischemia by down-regulating the IL-1 beta expression.