Lectin-like oxidized LDL receptor-1 is a cell-adhesion molecule involved in endotoxin-induced inflammation

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a major endothelial receptor for oxidized low-density lipoprotein, and is assumed to play a proatherogenic role in atherosclerosis. LOX-1 expression is induced by inflammatory cytokines as well as by proatherogenic stimuli. LOX-1 protein binds agedapoptotic cells, activated platelets, and bacteria, suggesting that it may have diverse activities in vivo. Here, we reveal a role for LOX-1 in endotoxin-induced inflammation. In a model of endotoxemia, injection of a high dose of endotoxin into rats induced leukopenia within 1 h and death of the animals within 24 h. Preadministration of anti-LOX-1 antibody reduced the degree of leukopenia and completely rescued the animals, whereas control IgG did not. In a model of low-dose endotoxin-induced uveitis, anti-LOX-1 antibody efficiently suppressed leukocyte infiltration and protein exudation. In situ videomicroscopic analyses of leukocyte interactions with retinal veins revealed that anti-LOX-1 antibody reduced the number of rolling leukocytes and increased the velocity of rolling, suggesting that LOX-1 functions as a vascular tethering ligand. The ability of LOX-1 to capture leukocytes under physiologic shear was confirmed in an in vitro flow model. Thus, LOX-1 is an adhesion molecule involved in leukocyte recruitment and may represent an attractive target for modulation of endotoxin-induced inflammation.     

Differentiation of a human eosinophilic leukemia cell line (EoL-1) by a human T-cell leukemia cell line (HIL-3)-derived factor.

Differentiation of a human eosinophilic leukemia cell line, EoL-1, induced by the culture supernatant of a human ATL cell line, HIL-3 (HIL-3 sup) was compared with differentiation induced by defined cytokines. HIL-3 sup induced EoL-1 cells to express eosinophilic granules and segmented nuclei after 6 to 9 days of incubation. HIL-3 sup also induced the expression of Fc epsilon receptor II (Fc epsilon RII/CD23) and an eosinophil differentiation antigen EO-1 mainly on eosinophilic granule (+) cells. Furthermore, HIL-3 sup induced EoL-1 cells to respond to an eosinophil chemotactic factor, platelet activating factor. HIL-3 cells express messenger RNA (mRNA) of interleukin-5 (IL-5), macrophage colony-stimulating factor (M-CSF), and IL-3 but not granulocyte CSF (G-CSF). Granulocyte-macrophage CSF (GM-CSF) and tumor necrosis factor-alpha (TNF-alpha) were detected in the HIL-3 sup. Recombinant IL-2 (rIL-2), rIL-3, rIL-4, rIL-5, rM-CSF, and rGM-CSF did not induce eosinophilic granules. rG-CSF induced a few eosinophilic granule (+) cells, and TNF-alpha, which did not induce eosinophilic granules by itself, enhanced the ability of G-CSF to induce them. However, G-CSF and TNF-alpha did not induce the expression of Fc epsilon RII and EO-1 antigen. Moreover, anti-G-CSF, anti-TNF-alpha, anti-GM-CSF, anti-IL-3, and anti-IL-5 antibodies did not suppress the effect of HIL-3 sup on the differentiation of EoL-1 cells. All the data suggest that HIL-3 sup contains an unidentified factor that induces differentiation of EoL-1 cells, and that EoL-1 cells and HIL-3 sup provide an important model for the examination of differentiation mechanisms and functions of eosinophils.     

Case report of perineal hernia after laparoscopic abdominoperineal resection

Perineal hernia (PH) is a rare complication following laparoscopic abdominoperineal resection (APR) for rectal cancer. We present a case report of perineal hernia after laparoscopic APR and discuss its management. The patient was a 77‐year‐old man who was diagnosed with lower rectal cancer. He underwent laparoscopic APR and bilateral lateral lymph node dissection. Two months after the surgery, pain and bulging in the perineal region developed, and PH was diagnosed by CT. Repair with a polypropylene mesh was performed using a combination of laparoscopic abdominal and transperineal approaches. Reportedly, the incidence of secondary PH after APR has increased along with the rate of laparoscopic surgery. Treatment of secondary PH with transperineal repair alone may cause injuries to other organs because of adhesion of the pelvic viscera. In the present case, we safely repaired the hernia repair using a laparoscopy‐assisted perineal approach.     

Case of idiopathic and complete appendiceal intussusception

Appendiceal intussusception is a rare disease in which the appendix invaginates into the cecum. It is often caused by organic diseases. The present case involved an appendiceal intussusception without an organic disease, and laparoscopic resection of part of the cecum was performed. Appendiceal intussusception has various causes, including malignant diseases. Therefore, diagnosis and selection of operative method are complex and could potentially lead to an excessively invasive option. By performing SILS with a multiuse single‐site port, we were able to provide an appropriate, non‐invasive treatment that had a good esthetic outcome.     

Conjugated oestrogen during the menstrual cycle measured by a direct radioimmunoassay with an antiserum prepared against oestradiol-17-glucosiduronate-[C-6]-BSA conjugate

Early morning and 24 h urine samples and serum were collected daily throughout the menstrual cycle in women. Urinary oestradiol-17-glucosiduronate (E2-17-G) was measured with a direct radioimmunoassay whose antiserum had been prepared against E2-17-G-[C-6]-bovine serum albumin conjugate and was very specific. On the average, E2-17-G in early morning and 24 h urine samples showed a prominent peak one day before the peak of urinary LH. The time relationship between these urinary E2-17-G and serum E2 levels and peaks was also investigated.     

Structures of defective P transposable elements prevalent in natural Q and Q-derived M strains of Drosophila melanogaster

Several DNA sequences with homology to the complete 2.9-kilobase (kb) P element from a P strain in the United States were isolated and characterized from two Drosophila melanogaster strains collected on Chichi Jima, an island 1000 km south of Tokyo. Except for a missing central region and trivial unsequenced regions of 38 base pairs, the 2.1-kb element isolated from a Q strain had the same DNA sequence as that of the complete P element. Seven other elements cloned from genomic DNAs of the Q strain and a Q-derived M strain all possessed the same restriction sites as those of the 2.9-kb P element except for one deleted region in each element. The finding of sequence conservation in P elements have had a common ancestor relatively recently. Thus, it is suggested that the P element family was a recent invader of the species. By contrast, no complete P element was found in these Japanese strains so far as surveyed, indicating the possibility that P elements in the Chichi Jima population are almost all defective. The implication of this possibility is discussed in relation to the uniqueness of the population on Chichi Jima where Q strains predominate and no P strains have yet been found.     

Dissociation of in vitro DNA deamination activity and physiological functions of AID mutants

Activation-induced cytidine deaminase (AID) is essential for the DNA cleavage that initiates both somatic hypermutation (SHM) and class switch recombination (CSR) of the Ig gene. Two alternative mechanisms of DNA cleavage by AID have been proposed: RNA editing and DNA deamination. In support of the latter, AID has DNA deamination activity in cell-free systems that is assumed to represent its physiological function. To test this hypothesis, we generated various mouse AID mutants and compared their DNA deamination, CSR, and SHM activities. Here, we compared DNA deamination, CSR, and SHM activities of various AID mutants and found that most of their CSR or SHM activities were disproportionate with their DNA deamination activities. Specifically, we identified a cluster of mutants (H48A, L49A, R50A, and N51A) with low DNA deamination activity but relatively intact CSR activity. Of note is an AID mutant (N51A) that retained CSR function but lost DNA deamination activity. In addition, an APOBEC1 mutation at N57, homologous to N51 of AID, also abolished DNA deamination activity but retained RNA editing activity. These results indicate that DNA deamination activity does not represent the physiological function of AID.     

Left ventricular retraining and anatomic correction in teenage patient with congenitally corrected transposition of the great arteries.

Left ventricular (LV) retraining followed by anatomical repair would be a superior alternative in patients with congenitally corrected transposition (ccTGA) having a deconditioned morphologically left ventricle (MLV); however, LV retraining in older children is a challenging task. A retraining process of the MLV in a teenage patient with ccTGA is reported here. Cardiac catheterization at 7 years of age revealed low pressure of the MLV (33/4 mm Hg) and a LV to right ventricular pressure ratio (LVp/RVp ratio) of 0.32. The first pulmonary artery banding (PAB) was performed at 10 years of age. Although the LVp/RVp ratio reached 0.68, there was no evidence of adequate LV hypertrophy. The second PAB was performed 2 years after the initial PAB, resulting in an increase in the LVp/RVp ratio to 0.93 and an adequate LV hypertrophy. The double switch procedure was successfully performed at 13 years of age. Although the ejection fraction of the MLV mildly decreased, the patient has been doing well during a follow-up period of 4 years. The MLV in the teenage patient with ccTGA was successfully trained using a retraining strategy and has sustained systemic circulation after anatomical repair.