Increased GS-II lectin binding and SATB2 downregulation are biological features for sessile serrated lesions and microvesicular hyperplastic polyps.

Sessile serrated lesions (SSLs) and microvesicular hyperplastic polyps (MVHPs) are colorectal lesions displaying gastric differentiation. Griffonia simplicifolia-II (GS-II) is a lectin specific to terminal α/ßGlcNAc residues. Here, we assessed GS-II binding and performed immunostaining for HIK1083 (specific to terminal αGlcNAc residues), MUC5AC, MUC6, and special AT-rich sequence binding protein 2 (SATB2) in SSLs, MVHPs, and tubular adenomas (TAs). We observed MUC5AC positivity in 28 of 30 SSLs, but in only three of 23 TAs. Moreover, 24 of 30 SSLs were MUC6-positive, while none of the 23 TAs were MUC6-positive. None of the 30 SSLs or 23 TAs showed HIK1083 positivity. All 30 SSLs and 26 MVHPs were GS-II-positive, while only seven of 23 were in TAs. GS-II staining was mainly distributed in the Golgi region, but SSLs and MVHPs showed goblet cell distribution, in 20 of 30 and 19 of 26 cases, respectively. All SSLs, MVHPs, and TAs were SATB2-positive, but 21 of 30 SSLs and 12 of 26 MVHPs showed decreased staining intensity relative to adjacent mucosa, a decrease seen in only two of 23 in TAs. These results indicate overall that increased terminal ßGlcNAc and decreased SATB2 expression are characteristics of SSLs and MVHPs.

Mucin distribution in bronchiolar adenoma/ciliated muconodular papillary tumor reveals organoid differentiation simulating the normal lung.

Bronchiolar adenoma/ciliated muconodular papillary tumor is a lung neoplasm exhibiting various degrees of proximal and distal bronchiolar differentiation. Here, we evaluated distribution of MUC5AC and MUC5B in bronchiolar adenoma/ciliated muconodular papillary tumor for comparison with that seen in normal respiratory tract. In normal respiratory tract, MUC5AC was mainly distributed in large bronchi, while MUC5B was distributed in bronchi, bronchioles, and submucosal glands. In bronchiolar adenoma/ciliated muconodular papillary tumor, MUC5AC was primarily distributed in luminal cells of large airspaces, and MUC5B was distributed in luminal cells of small airspaces and mucinous glands, in addition to large airspaces, regardless of distal or proximal differentiation. In particular, MUC5B was distributed in non-mucinous club and ciliated cells in both the normal respiratory tract and bronchiolar adenoma/ciliated muconodular papillary tumor. These results indicate that MUC5AC and MUC5B distribution in bronchiolar adenoma/ciliated muconodular papillary tumor is similar to that seen in normal respiratory tract, suggestive of organoid differentiation simulating the normal lung.

[Inverted Variant of Urothelial Carcinoma of the Urinary Bladder : A Case Report].

A 69-year-old male complained of gross hematuria. Cystoscopy revealed a papillary pedunculated tumor. The tumor was approximately 4 cm in length, and mimicked an inverted papilloma with a small stalk and smooth surface, located on the bladder trigone. Transurethral resection of the bladder tumor was performed, and the tumor was resected en bloc. Histopathological examination revealed thick and irregular epithelial cords. Immunohistochemically, Ki-67 labeling index was 5%, p40 and CK7 were positive, and CK20 was negative. Then, this tumor was diagnosed as inverted variant of urothelial carcinoma. Even when gross appearance is compatible with inverted papilloma, pathological and immunohistochemical examinations are essential for accurate diagnosis of inverted bladder tumor. No recurrence was observed by cystoscopy 13 months after the resection.

Left ventricular outflow tract obstruction caused by massive mitral annular calcification in a patient with hypertensive heart disease.

Mitral annular calcification (MAC) is frequently observed, but it rarely causes left ventricular outflow tract (LVOT) obstruction (LVOTO). An 83-year-old woman with hypertension, diabetes, and dyslipidemia was admitted to our hospital because of exertional dyspnea. She was diagnosed with hypertensive heart disease. Her symptoms were exacerbated by exertion, and she had no symptoms at rest. Transthoracic echocardiography showed massive posterior MAC, a sigmoid septum, and LVOTO, with a peak gradient of 15.4 mmHg at rest. Systolic anterior motion of the anterior mitral leaflet was not found. Moreover, the LVOT gradient in the stress condition was evaluated, and an increased LVOT gradient (47.3 mmHg) and chest discomfort was noted after 20 µg/kg/min of dobutamine was administered and the Valsalva maneuver was used. Hence, the patient was diagnosed with latent LVOTO. Interestingly, the distance between the septal wall, which was protruding into the left ventricular cavity, and the mitral valve coaptation, which was pushed up by the posterior MAC, had become closer, causing dynamic LVOTO. Since it is difficult to treat LVOTO with medication, ultimately, septal myectomy and mitral valve replacement were performed, which improved her symptoms. Evaluating the LVOT pressure gradient in stress condition is important in patients with MAC. .

Evaluation of platelet reactivity using P2Y12 reaction units in acute coronary syndrome with essential thrombocythemia: A case report.

Essential thrombocythemia (ET) has been reported to cause acute coronary disease. However, the efficacy of anti-platelet therapy for ET is unclear since there are individual differences in the platelet function of ET patients. Here we report a case of a 62-year-old man with ET who was admitted to our hospital because of acute coronary syndrome. He underwent coronary angioplasty. Dual anti-platelet therapy with aspirin (81 mg/day) and clopidogrel (75 mg/day) was subsequently initiated. We evaluated platelet reactivity in P2Y12 reaction units, and subsequently determined anti-platelet drugs and corresponding doses. .

T-138C polymorphism of matrix gla protein promoter alters its expression but is not directly associated with atherosclerotic vascular calcification.

Matrix Gla protein (MGP) is a crucial inhibitor of vessel and cartilage calcification. We investigated the association of T-138C MGP promoter polymorphism with the degree of atherosclerosis, vascular calcification and patients' clinical background including calcification of the trachea and costal cartilage. Analysis of 108 autopsy cases was carried out by polymorphism-specific PCR on formalin-fixed paraffin-embedded samples. Statistical correlations among eight risk factors and five markers related to atherosclerosis and extra-bone tissue calcification were multivariantly analyzed. We found very high canonical correlations between the factors and the markers, and Pearson's correlation analysis revealed six significant correlations between age and the Gore index; age and costal cartilage calcification; sex and costal cartilage calcification; hypertension and the Gore index; hypertension and the calcification factor of the Gore index; and hyperlipidemia and costal cartilage calcification. The promoter activity of the -138T allele was significantly higher than that of the -138C allele; treatment with 12-O-tetradecanonylphorbol 13-acetate (TPA) significantly activated the former, but had almost no effect on the latter. The C genotype was significantly common among Japanese subjects, (TT 45.5%, TC 37.6% and CC 16.8%) compared with that reported in the Netherlands, Northern Ireland and France. No significant correlation was observed, however, between T-138C MGP promoter polymorphism and the markers. Although the C genotype (TC+CC) tended to show a higher calcification factor than the TT genotype, no significant difference was observed among the genotypes in the Gore index or in the calcification factor. Although MGP promoter activity and the binding of the AP-1 transcription factor were clearly different between T-138 and C-138 MGP promoter polymorphism in vitro, T-138C polymorphism was, statistically, not an independent factor of atherosclerosis or atherosclerotic vascular calcification in the abdominal aorta.