Postoperative disappearance of leptomeningeal enhancement around the brainstem in glioblastoma.

PURPOSE: Leptomeningeal enhancement (LME) suggests leptomeningeal dissemination (LMD) of tumor cells, which is a complication of end-stage glioblastoma, and is associated with a poor prognosis. However, magnetic resonance imaging (MRI) occasionally indicates the disappearance of peri-brainstem LME after surgical resection of glioblastoma. Since preoperative LMD may affect treatment indications, we aimed to analyze the clinical significance of preoperative LME of the brainstem in glioblastoma. METHODS: We retrospectively collected clinical and radiological data from consecutive patients with glioblastoma and preoperative LME of the brainstem, who were treated at our hospital between 2017 and 2020. RESULTS: Among 112 patients with glioblastoma, nine (8%) showed preoperative LME of the brainstem. In comparison with tumors without LME, tumor size was significantly associated with the preoperative LME of the brainstem (p = 0.016). In addition, there was a trend toward significance for a relationship between deep tumor location and preoperative LME of the brainstem (p = 0.058). Notably, among six patients who underwent surgical resection for glioblastoma with LME of the brainstem, four showed significant radiological disappearance of the LME on postoperative MRI. This suggests that the LME did not result from LMD in these cases. Moreover, these four patients lived longer than would be expected from the presence of LMD. However, this LME disappearance was not observed after biopsy or chemoradiotherapy. CONCLUSIONS: These findings suggest that preoperative LME does not necessarily indicate the presence of untreatable LMD; moreover, LME may disappear after surgical tumor resection. Thus, transient preoperative LME could be attributed to other mechanisms, including impaired venous flow due to intratumoral arteriovenous shunts, which can be resolved by reducing the tumor burden.

One step fabrication of aligned carbon nanotubes using gas rectifier.

We report the one-step fabrication of aligned and high-quality carbon nanotubes (CNTs) using floating-catalyst chemical vapor deposition (FCCVD) with controlled fluidic properties assisted by a gas rectifier. The gas rectifier consists of one-dimensional straight channels for regulating the Reynolds number of the reaction gas. Our computational fluid dynamics simulation reveals that the narrow channels of the gas rectifier provide steady and accelerated laminar flow of the reaction gas. In addition, strong shear stress is induced near the side wall of the channels, resulting in the spontaneous formation of macroscopic CNT bundles aligned along the direction of the gas flow. After a wet-process using chlorosulfonic acid, the inter-tube voids inherently observed in as-grown CNT bundles are reduced from 16 to 0.3%. The resulting CNT fiber exhibits a tensile strength of 2.1 ± 0.1 N tex-1 with a Young's modulus of 39 ± 4 N tex-1 and an elongation of 6.3 ± 0.6%. FCCVD coupled with the strong shear stress of the reaction gas is an important pre-processing route for the fabrication of high-performance CNT fibers.

Hemichorea induced by a sphenoid ridge meningioma.

BACKGROUND: Movement disorders are rare in brain tumors. We describe a 45-year-old woman with hemichorea, a concomitant contralateral sphenoid ridge meningioma. CASE DESCRIPTION: The meningioma enlarged as her hemichorea worsened, and after meningioma resection, the hemichorea gradually subsided. N-isopropyl-p-[123I]-iodoamphetamine single-photon emission computed tomography performed preoperatively showed decreased regional cerebral blood flow (CBF) to the basal ganglia circuit ipsilateral to the tumor and, when repeated postoperatively, confirmed improved regional CBF. CONCLUSION: We propose that the enlarging sphenoid ridge meningioma had a remote effect on regional CBF and the thalamocortical motor center and that complex changes in the basal ganglia output may have caused the hemichorea.

Effects of 5-mg dose of olanzapine for breakthrough nausea and vomiting in patients receiving carboplatin-based chemotherapy: a prospective trial.

BACKGROUND: Olanzapine 10 mg is recommended for breakthrough chemotherapy-induced nausea and vomiting. However, there is a possibility that 5 mg can be expected to be sufficiently effective. We aimed to investigate the efficacy and safety of olanzapine 5 mg for breakthrough chemotherapy-induced nausea and vomiting. METHODS: A single-arm prospective trial of olanzapine 5 mg every 24 h for 72 h was conducted to treat breakthrough chemotherapy-induced nausea and vomiting in patients receiving carboplatinbased chemotherapy. The primary endpoint was total control (i.e., no emesis, no nausea, and no rescue medications) over 72 h. The secondary endpoints were early efficacy using the nausea scores at 30, 60, and 120 min after taking olanzapine from baseline and adverse events. RESULTS: Among 84 potentially eligible patients, 19 patients who took olanzapine for breakthrough chemotherapy-induced nausea and vomiting were examined. The total control rate was 32% (95% CI: 13- 57%), 65% (95% CI: 38-89%), 65% (95% CI: 38-89%), and 29% (95% CI: 10-56%) during 2-24, 24-48, 48-72 h, and overall period, respectively. The nausea scale significantly reduced after 30 min (P=0.0078), and the scale had been reduced by 67% from the baseline after 60 min. The adverse event of somnolence of any grade was observed in 13 (68%) patients, 6 (32%) of whom had grade 2 and 1 (5%) grade 3 somnolence. CONCLUSIONS: Olanzapine 5 mg did not show the expected effect on the complete disappearance of breakthrough chemotherapy-induced nausea and vomiting within 24 h.

Internal carotid artery aneurysms diagnosed after stereotactic radiosurgery for a growth hormone-secreting pituitary adenoma: a case report and literature review.

Radiation therapy is associated with the subsequent development of cerebral aneurysms; however, stereotactic radiosurgery (SRS)-associated aneurysm cases have not been well documented, with only 18 cases reported to date. We present a case of intracranial aneurysms with the rupture occurring 20 years after SRS for a growth hormone-producing pituitary adenoma. This is the first report of aneurysms diagnosed following transsphenoidal surgery and SRS for pituitary adenoma. We believe that the aneurysm reported here is a consequence of the SRS treatment, and thus this may be a very rare long-term complication following radiation treatments.

A Rare Case of Thyrotropin-Secreting Pituitary Adenoma Coexisting with Papillary Thyroid Carcinoma Presenting with Visual Disturbance without Hyperthyroidism.

BACKGROUND: Thyroid-stimulating hormone-secreting pituitary adenomas (TSHomas) are uncommon, and majority of the patients present with symptoms of hyperthyroidism. Herein, we report the first case of TSHoma with differentiated thyroid carcinoma (DTC) that presented with visual disturbance without any clinical feature of hyperthyroidism. CASE DESCRIPTION: A 57-year-old man presented with left temporal hemianopsia of his left eye without any sign of hyperthyroidism. A mass lesion in the sellar and suprasellar region compressing the optic nerves was identified via magnetic resonance imaging. Free thyroxine and free triiodothyronine levels were slightly elevated, whereas the serum level of thyroid-stimulating hormone remained within normal range. Further endocrinologic examination led to the preoperative diagnosis of TSHoma. Ultrasonography and 111In-octreotide scan showed a mass lesion in left lobe of the thyroid gland, and subsequent thyroid aspiration biopsy confirmed the diagnosis of papillary thyroid carcinoma. After administration of short-acting octreotide to prevent thyrotoxic crisis in the perioperative period, the tumor was removed via endoscopic transnasal-transsphenoidal surgery, and the pathologic diagnosis of TSHoma was made. His visual acuity improved, and free triiodothyronine and free thyroxine levels normalized. He underwent thyroidectomy 3 months later after endoscopic transnasal-transsphenoidal surgery. CONCLUSIONS: Herein, we report the first case of TSHoma with DTC that presented with visual disturbance without any clinical feature of hyperthyroidism and reviewed the 13 reported cases of TSHoma coexisting with DTC. The optimal treatment strategy in patients with TSHoma and coexistent DTC has not been established, and individualized therapeutic strategies are needed.

[Molecular mechanism of bone destruction].

In rheumatoid arthritis, T cells activation enhances osteoclast differentiation and bone destruction through receptor activator of NF-kappaB ligand (RANKL) . Recent study revealed the importance of interleukin-17 (IL-17) -producing helper T cell subset (Th17) in bone destruction. The emerging field of osteoimmunology will be of great importance not only to the better understanding of osteoclast differentiation and activation but also to the regulation of inflammation-associated bone destruction.

Significance of the N- and C-terminal regions of CAP-1, a cuticle calcification-associated peptide from the exoskeleton of the crayfish, for calcification.

Calcification-associated peptide (CAP)-1 is considered to play an important role in calcification of the exoskeleton of the crayfish, Procambarus clarkii. In this study, in order to clarify the molecular mechanism of calcification, we constructed expression systems of recombinant molecules of CAP-1 and its related peptides in Escherichia coli, and verified the structure-activity relationship of these peptides. The inhibitory assay on calcium carbonate precipitation and the calcium-binding assay showed that the C-terminal acidic region was most important for both activities. The CD spectra of these peptides varied depending on calcium concentration and showed that the N-terminal region is associated with the peptide conformation. These results indicate that the C-terminal part of CAP-1 may concentrate calcium ions for nucleation and/or interact with calcium carbonate precipitate to control the growth and that the N-terminal part contribute to maintaining the peptide conformation.

Histopathological study of time course changes in inter-renal aortic banding-induced left ventricular hypertrophy of mice.

The left ventricular hypertrophy (LVH) in response to pressure overload is an important risk factor in cardiac morbidity and mortality. To investigate the time course of histopathological alterations in the LVH in response to pressure overload, histopathological and immunohistochemical examination was performed using the aortic banding-induced mouse LVH model. Five-week-old male CD-1 mice were subjected to the inter-renal aortic banding. Major organs were sampled on 3, 10, 14, 21, 28 or 42 days after banding. Haematoxylin and eosin (H&E) staining, Masson's trichrome staining and immunohistochemistry for proliferating cell nuclear antigen (PCNA), alpha-smooth muscle actin (aSMA), ICAM-1, type I collagen and CD31 was performed and microscopically examined. Three days after aortic banding, acute inflammatory changes, such as macrophages/neutrophil infiltration and vascular wall injury were observed on/around the coronary arteries/arterioles of both ventricles. Intense ICAM-1 immunostaining was observed on the endothelium of the coronary arteries/arterioles. After day 10, vascular wall thickening and perivascular fibrosis was induced on the coronary arteries/arterioles. Immunohistochemistry for aSMA and PCNA demonstrated the proliferation of vascular smooth muscle cells in the media. After day 28, minimal cardiomyocyte hypertrophy was observed at the light microscope level. In the inter-renal aortic banding LVH model, histopathological alterations in early phase were mainly observed on coronary arteries/arterioles. These early phase alterations were thought to be hypertension-related changes in the coronary vasculatures. The cardiomyocyte hypertrophy observed in later phase was minimal at the light microscope level. These evidences would facilitate the understanding of pathophysiology of pressure overload LVH.

A novel calcium-binding peptide from the cuticle of the crayfish, Procambarus clarkii.

A novel peptide named calcification-associated peptide (CAP)-2 was isolated from the exoskeleton of the crayfish, Procambarus clarkii. CAP-2 consists of 65 amino acid residues and has a 44% sequence identity with CAP-1 characterized previously. It has a chitin-binding domain observed in many arthropod cuticle proteins. CAP-2 showed inhibitory activity on calcium carbonate precipitation and chitin-binding ability. A CAP-2 cDNA was cloned using RT-PCR and RACE and the open reading frame encoded a precursor peptide consisting of a signal peptide and CAP-2. RT-PCR revealed that CAP-2 mRNA was exclusively expressed in the epidermal tissue during the postmolt stage, the site and stage being associated with calcification. Calcium-binding assay using recombinant CAP-2 revealed that this peptide had affinity for calcium ions with a Kd value of about 1 mM. All these results suggest that CAP-2 serves as a nucleator or a regulator in the calcification of the exoskeleton.

Cloning and expression of a cDNA encoding a matrix peptide associated with calcification in the exoskeleton of the crayfish.

Calcification-associated peptide (CAP)-1 isolated from the exoskeleton of the crayfish, Procambarus clarkii, has anti-calcification activity and chitin-binding ability and is, therefore, considered to be associated with calcification. In this study, a cDNA encoding CAP-1 was cloned and characterized. An open reading frame encoded a pre-propeptide of 99 amino acid residues, which was composed of a signal peptide, a CAP-1 precursor and two-basic amino acid residues at the C-terminus. The dibasic residues were not observed in the natural CAP-1. Expression analyses using Northern blot and RT-PCR revealed that the mRNA encoding CAP-1 was strongly expressed in the epidermal tissue during the postmolt stage, where and when the calcification takes place. These results support that CAP-1 may play an important role in the calcification of the exoskeleton. Based on the nucleotide sequence of the cDNA encoding CAP-1, a recombinant CAP-1 and that carrying the basic residues at the C-terminus were expressed in Escherichia coli. Anti-calcification assay showed that these recombinant peptides were less active than natural CAP-1, indicating that the phosphate group at the 70th residue, Ser, in natural CAP-1 is important for inhibitory activity and that the paired basic residues have some contribution to the elevation of inhibitory activity.

Sildenafil and T-1032, phosphodiesterase type 5 inhibitors, showed a different vasorelaxant property in the isolated rat aorta.

The vasorelaxant effects of sildenafil and T-1032 [methyl-2-(4-aminophenyl)-1,2-dihydro-1-oxo-7-(2-pyridinylmethoxy)-4-(3,4,5-trimethoxyphenyl)-3-isoquinoline carboxylate sulfate], two phosphodiesterase type 5 inhibitors, were examined in the isolated rat aorta. Sildenafil and T-1032, both of which have almost the same potency and selectivity regarding phosphodiesterase type 5 inhibitory activity, produced a similar, moderate, relaxation at 10(-10) to 10(-7) M (sildenafil: 66.8 +/- 13.7%; T-1032: 77.9 +/- 10.8% at 10(-7) M). However, sildenafil, but not T-1032, produced further relaxation at the higher concentrations (sildenafil: 102.0 +/- 0.6%; T-1032: 81.0 +/- 7.2% at 10(-4) M, P < 0.05). Sildenafil also produced a more potent relaxation than did T-1032 at the high concentrations (10(-5) and 10(-4) M) in endothelium-denuded aortic rings and in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor (3 x 10(-4) M). Moreover, the high concentrations of sildenafil, but not of T-1032, caused a rightward shift of the concentration-response curve for calcium chloride in K(+)-depolarized endothelium-denuded preparations. In the ligand binding assay for the L-type Ca(2+) channels, the affinities of sildenafil at 10(-5) M for binding sites of nitrendipine and (--)-desmethoxyverapamil [(--)- D888] (35.2 +/- 3.3% and 35.8 +/- 1.9%, respectively) were higher than those of T-1032 (11.8 +/- 4.0% and -13.1 +/- 1.3%, respectively, P < 0.05). Regarding cyclic nucleotide levels, both phosphodiesterase type 5 inhibitors increased cGMP levels at 10(-6) M. However, sildenafil, but not T-1032, further increased cGMP levels at the higher concentrations (sildenafil: 15.7 +/- 2.7 pmol/mg protein; T-1032: 5.6 +/- 0.6 pmol/mg protein at 10(-4) M, P < 0.05). These results suggested that high concentrations of sildenafil had additional vasorelaxant properties through mechanisms other than phosphodiesterase type 5 inhibition. Sildenafil-induced relaxation appears to be due to inhibition of the external Ca(2+)-dependent cascade for contraction and/or to an increase in cGMP levels. In contrast, T-1032 only showed a vasorelaxant property due to phosphodiesterase type 5 inhibition. In conclusion, T-1032 appears to be a specific phosphodiesterase type 5 inhibitor compared with sildenafil and a useful compound to examine the physiological function of phosphodiesterase type 5.