Idiopathic myointimal hyperplasia of mesenteric veins: Rare case of ischemic colitis mimicking inflammatory bowel disease

Idiopathic myointimal hyperplasia of mesenteric veins (IMHMV) is a rare and poorly understood ischemic colitis that occurs in the rectosigmoid colon of predominantly young, previously healthy, male patients. A 76‐year‐old Japanese man presented to our hospital with a 1‐year history of worsening diarrhea, lower abdominal pain, and weight loss (−6 kg). Laboratory evaluation revealed white blood cell count of 13 200/μL, C‐reactive protein level of 2.0 mg/dL (normal range, 0.0–0.3), and negative results for stool culture (including Clostridium difficile). Colonoscopy showed circumferential and edematous narrowing of the sigmoid colon with deep longitude ulceration. Biopsy was done and examination of the specimen demonstrated no specific ischemia. The patient was treated with bowel rest, antibiotics, and i.v. fluids; however, his symptoms worsened. Finally, sigmoidectomy was carried out. Histological examination demonstrated significant myointimal hyperplasia of mesenteric veins leading to thickening and stenosis of the venous lumen. Therefore, the final diagnosis was IMHMV. Three months following sigmoidectomy, he was asymptomatic.     

Polymer conformation and NMR chemical shifts, 9. Poly(α-methylene-γ-butyrolactone)

The conformational energies of poly(α-methylene-γ-butyrolactone) are calculated and compared with those of poly(methyl methacrylate). In spite of the structural resemblance of these two polymers, the patterns of the energy contour maps are clearly distinguishable from each other; the energy barriers between rotational isomeric states are appreciably higher in the former than in the latter polymer. The calculation indicates large non-bonded interactions between the protons in one lactone ring and those in the adjacent lactone rings. The broad NMR spectrum of poly(α-methylene-γ-butyrolactone) apparently reflects its rigid conformational structure. ¹H and ¹³C NMR chemical shifts are calculated by theoretical shielding calculations based on conformational analysis. Much lower magnetic field resonances of the O? CH₂ and α-CH₂ carbons in poly(α-methylene-γ-butyrolactone) as compared with those of the O? CH₃ and α-CH₃ carbons in poly(methyl methacrylate) are well reproduced by the calculation. The shift to lower magnetic field is mainly attributed to paramagnetic shielding derived from the interaction between O? CH₂ carbon and α-CH₂ carbon. Tacticity- and conformation-dependent ¹H and ¹³C NMR chemical shifts of poly(α-methylene-γ-butyrolactone) are well interpreted on the basis of the conformational analysis.     

Polymer conformation and NMR chemical shifts, 6. Alternating copolymer of α-methylene-γ-butyrolactone with styrene

In view of the structural resemblance of α-methylene-γ-butyrolactone to methyl methacrylate, conformation and NMR chemical shifts of poly(α-methylene-γ-butyrolactone-alt-styrene). are calculated and compared with those of poly(methyl methacrylate-alt-styrene). The conformational energy surfaces for the dyad sequence models of the both copolymers are analogous to each other, as is expected from the similarity in the constituting monomeric units. Agreement of calculation with observation is satisfactory with respect to the cotacticity-dependent splittings in the ¹³C NMR spectra and is improved by the fixation of a substituent in poly(α-methylene-γ-butyrolactone-alt-styrene). Calculation of ¹H chemical shifts gives an alignment of NMR signals which is in accordance with the observation.     

Biochemical, histological and echocardiographic changes during experimental cardiomyopathy in STZ-induced diabetic rats.

Diabetes mellitus is associated with an increased susceptibility to cardiovascular disease and it has been suggested that alterations in myocardial function may contribute to the development of diabetic cardiovascular complications. The objective of the present study is to examine the left ventricular (LV) function in streptozotocin (STZ)-induced diabetic rats in a definite course of time by non-invasive methods, i.e. M-mode and Doppler echocardiography. From the results, it was found that treatment of animals with STZ resulted in increase in blood glucose, triglycerides, cholesterol, low density lipoproteins (LDL) and decrease in serum total protein levels.Echocardiographic studies revealed that LV internal dimension (mm) during systole was significantly increased after 12 weeks of diabetes when compared to base line data of the same animals and with control animals 6.50+/-0.13 versus 4.25+/-0.17, versus 4.34+/-0.25 (P<0.05), however there was no significant change after 4-8 weeks of diabetes. Also LV internal dimension (mm) during end diastole increased significantly only after 12 weeks of diabetes than to base line data of the same animals and with control animals 7.71+/-0.34 versus 6.18+/-0.25, versus 6.25+/-0.18 (P<0.05). Fractional shortening (%), 15.69+/-5.1 versus 31.22+/-1.7, versus 30.56+/-2.1 (P<0.05), and ejection fraction (%) 37+/-2.31 versus 68.18+/-2.8, versus 60.32+/-3.5 (P<0.05), differ significantly after 12 weeks of diabetes when compared to base line data of the same animals and with control animals. E-wave (cm/s) was significantly decreased after 12 weeks of diabetes 21.11+/-1.5 versus 35.19+/-4.5, versus 32.75+/-3.0 (P<0.05), and A-wave (cm/s) was significantly increased after 12 weeks of diabetes 34.88+/-4.2 versus 19.21+/-2.8, versus 20.59+/-2.1 (P<0.05); thus, diabetic animals after 12 weeks had an inversed E/A ratio. Histological studies revealed that after 8 weeks of diabetes, necrosis was minimal, but after 12 weeks of diabetes extensive focal endomyocardial necrosis was observed. From this study, we conclude that overt LV systolic and diastolic dysfunction was fully visible at 12 weeks of diabetes on echocardiography and this non-invasive technique of echocardiography is useful in diagnosing LV dysfunction in diabetic rats without the need of invasive histopathological procedures.     

The influence of androgen deprivation therapy on dihydrotestosterone levels in the prostatic tissue of patients with prostate cancer.

PURPOSE: The influence of androgen deprivation therapy on dihydrotestosterone levels in the prostatic tissue is not clearly known. Changes in dihydrotestosterone levels in the prostatic tissue during androgen deprivation therapy in the same patients have not been reported. We analyzed dihydrotestosterone levels in prostatic tissue before and after androgen deprivation therapy. EXPERIMENTAL DESIGN: A total of 103 patients who were suspected of having prostate cancer underwent prostatic biopsy. Sixty-nine patients were diagnosed as having prostate cancer whereas the remaining 34 were negative. Serum samples were collected before biopsy or prostatectomy. Dihydrotestosterone levels in prostatic tissue and serum were analyzed using liquid chromatography/electrospray ionization-mass spectrometry after polar derivatization. In 30 of the patients with prostate cancer, dihydrotestosterone levels in prostatic tissue were determined by performing rebiopsy or with prostate tissues excised after 6 months on androgen deprivation therapy with castration and flutamide. RESULTS: Dihydrotestosterone levels in prostate tissue after androgen deprivation therapy remained at approximately 25% of the amount measured before androgen deprivation therapy. Dihydrotestosterone levels in serum decreased to approximately 7.5% after androgen deprivation therapy. The level of dihydrotestosterone in prostatic tissue before androgen deprivation therapy was not correlated with the serum level of testosterone. Serum levels of adrenal androgens were reduced to approximately 60% after androgen deprivation therapy. CONCLUSIONS: The source of dihydrotestosterone in prostatic tissue after androgen deprivation therapy involves intracrine production within the prostate, converting adrenal androgens to dihydrotestosterone. Dihydrotestosterone still remaining in prostate tissue after androgen deprivation therapy may require new therapies such as treatment with a combination of 5alpha-reductase inhibitors and antiandrogens, as well as castration.     

Diagnostic and prognostic role of urinary collagens in primary human bladder cancer

Collagen type 4 alpha 1 (COL4A1) and collagen type 13 alpha 1 (COL13A1) produced by urothelial cancer cells support the vital oncogenic property of tumor invasion. We investigated the diagnostic and prognostic capability of COL4A1 and COL13A1 in voided urine and compared the observed values with those of fragments of cytokeratin‐19 (CYFRA21‐1), nuclear matrix protein 22 (NMP‐22), and voided urine cytology in bladder cancer (BCa). We collected voided urine samples from 154 patients newly diagnosed with BCa, before surgery and from 61 control subjects. Protein levels of COL4A1, COL13A1, CYFRA21‐1, and NMP‐22 in urine supernatants were measured using enzyme‐linked immunosorbent assays. Diagnostic performance and optimal cut‐off values were determined by receiver operating characteristic analysis. Urine levels of COL4A1, COL13A1, the combined values of COL4A1 and COL13A1 (COL4A1 + COL13A1), and CYFRA21‐1 were significantly elevated in urine from patients with BCa compared to the controls. Among these biomarkers, the optimal cut‐off value of COL4A1 + COL13A1 at 1.33 ng/mL resulted in 57.4%, 83.7%, 56.1%, 80.7%, and 91.7% sensitivity for low‐grade tumors, high‐grade tumors, Ta, T1, and muscle invasive disease, respectively. We evaluated the prognostic value of preoperative urine levels in 130 non‐muscle invasive BCa samples after the initial transurethral surgery. A high urinary COL4A1 + COL13A1 was found to be an independent risk factor for intravesical recurrence. Although these data need to be externally validated, urinary COL4A1 and COL13A1 could be a potential diagnostic and prognostic biomarker for BCa. This easy‐to‐use urinary signature identifies a subgroup of patients with a high probability of recurrence and progression in non‐muscle invasive and muscle invasive BCa.     

Altered gene expression due to aberrant DNA methylation correlates with responsiveness to anti‐EGFR antibody treatment

The cetuximab gene expression signature and DNA methylation status of colorectal cancer (CRC) are predictive of the therapeutic effects of anti‐epidermal growth factor receptor (EGFR) antibody therapy. As DNA methylation is a means of regulating gene expression, it may play an important role in the expression of cetuximab signature genes. This study aims to determine the effects of aberrant DNA methylation on the regulation of cetuximab signature gene expression. Comprehensive DNA methylation and gene expression data were retrieved from CRC patients in three tumor tissue (TT) cohorts and three normal colorectal mucosa/tumor tissue paired (NCM‐TT) cohorts. Of the 231 cetuximab signature genes, 57 exhibited an inverse correlation between the methylation of promoter CpG sites and gene expression level in multiple cohorts. About two‐thirds of the promoter CpG sites associated with the 57 genes exhibited this correlation. In all 57 gene promoter regions, the methylation levels in NCMs did not differ according to comparisons based on cetuximab signature or DNA methylation status classification of matched TTs. Thus, the altered expression of 57 genes was caused by aberrant DNA methylation during carcinogenesis. Analysis of the association between cetuximab signature or DNA methylation status and progression‐free survival (PFS) of anti‐EGFR antibody agents in the same cohort showed that DNA methylation status was most associated with PFS. In conclusion, we found that aberrant DNA methylation regulates specific gene expression in cetuximab signature during carcinogenesis, suggesting that it is one of the important determinants of sensitivity to anti‐EGFR antibody agents.     

Clinical evaluations of pituitary apoplexy in incidental nonfunctional pituitary adenomas

Pituitary apoplexy is an uncommon syndrome that often results in spontaneous hemorrhage or infarction of pituitary tumors or glands. We previously reported pituitary apoplexy occurred most frequently in nonfunctional pituitary adenomas among all types of pituitary incidentalomas. In the present study, we aimed to investigate the characteristics of pituitary apoplexy in patients with incidental nonfunctional pituitary adenomas. 65 patients with pituitary incidentaloma were enrolled. All patients underwent clinical/endocrinological/pathological investigations. As a result, 33 patients were diagnosed with nonfunctional pituitary adenomas. Of these, 12.1% of patients had pituitary apoplexy. There was no difference in tumor diameter, age, or sex between the apoplexy and the non-apoplexy groups. However, the liver enzymes aspartate transaminase and alanine aminotransferase were significantly higher, and plasma sodium and chloride levels were significantly lower in the apoplexy group than in the non-apoplexy group (each P < .05). In addition, low-density lipoprotein-cholesterol was significantly higher in the apoplexy group than in the non-apoplexy group (P < .05). Besides, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and prolactin deficiencies were significantly more frequent in the apoplexy group than in the non-apoplexy group (each P < .05), and growth hormone and adrenocorticotropic hormone deficiencies were more frequent in the apoplexy group than in the non-apoplexy group (P = .09 and.08, respectively). Furthermore, tumor diameter was not associated with pituitary apoplexy, whereas thyroid-stimulating hormone, luteinizing hormone, and follicle-stimulating hormone deficiencies were significantly associated with the apoplexy group (each P < .05). Hence, the present study indicated that pituitary apoplexy could not be related to tumor diameter. Moreover, hormonal deficiencies, hepatic dysfunction, hyponatremia or hypochloremia, and dyslipidemia might be indicators of pituitary apoplexy. There could be the possibility the treatment for dyslipidemia prevents pituitary apoplexy.     

Efficacy of sitting balance training with delayed visual feedback among patients with stroke: a randomized crossover clinical trial

[Purpose] This study aimed to determine the effect of delayed visual feedback on the center of pressure and sitting balance in patients with stroke. [Participants and Methods] This was a single-blinded, randomized crossover trial. The duration of each intervention in real-time visual feedback and delayed visual feedback conditions while sitting on the platform was five days. We measured the center of pressure, function in sitting test, and functional independence measure for physiotherapy assessment. [Results] Twenty patients with stroke were included in this study. The delayed visual feedback condition improved the center of pressure for lateral distance, function in sitting test, and functional independence measure. The lateral center of pressure deviation increased significantly after 500 ms of intervention. The function in sitting test evaluated the interaction between pre- and post-training, and these conditions revealed that timing and condition factors contributed to the improvement. Sitting balance training affected the functional independence measure. [Conclusion] Sensory-motor and cognitive learning was facilitated through balance training with delayed visual feedback, and the internal model was updated with the efference copy of error correction. Sensory-motor feedback to visual stimulation can improve postural control, balance, and activities of daily living.