A Deep Learning-Based Phenotypic Analysis of Rice Root Distribution from Field Images.

Root distribution in the soil determines plants' nutrient and water uptake capacity. Therefore, root distribution is one of the most important factors in crop production. The trench profile method is used to observe the root distribution underground by making a rectangular hole close to the crop, providing informative images of the root distribution compared to other root phenotyping methods. However, much effort is required to segment the root area for quantification. In this study, we present a promising approach employing a convolutional neural network for root segmentation in trench profile images. We defined two parameters, Depth50 and Width50, representing the vertical and horizontal centroid of root distribution, respectively. Quantified parameters for root distribution in rice (Oryza sativa L.) predicted by the trained model were highly correlated with parameters calculated by manual tracing. These results indicated that this approach is useful for rapid quantification of the root distribution from the trench profile images. Using the trained model, we quantified the root distribution parameters among 60 rice accessions, revealing the phenotypic diversity of root distributions. We conclude that employing the trench profile method and a convolutional neural network is reliable for root phenotyping and it will furthermore facilitate the study of crop roots in the field.

Prematurely ruptured dominant follicles often retain competent oocytes in infertile women.

Ovulation consists of a follicle's rupture and subsequent oocyte extrusion, although there is a paucity of evidence regarding whether every follicle's rupture is associated with extrusion of its oocyte. We examined this issue in a large-scale window-of-opportunity study by attempting aspiration of single dominant follicles that were found to have ruptured before a scheduled oocyte retrieval during in vitro fertilisation and embryo transfer treatment of infertile women. We were able to aspirate 587 of 1,071 ultrasonographically confirmed post-rupture dominant follicles from 1,071 women (i.e. one dominant follicle per woman) and retrieved 225 oocytes (oocyte recovery ratio: 43.4% of aspirated follicles), which yielded 28 live births (live birth ratio: 11.0% of retrieved oocytes). Interestingly, the live birth ratio for post-rupture dominant follicles was not statistically different from that achieved using regular pre-rupture aspiration of dominant follicles (1,085/8,977, 12.1%). These findings suggest that oocyte extrusion frequently does not occur after follicle rupture in infertile women undergoing in vitro fertilisation treatment, although the oocyte retained in the follicle can remain competent for use during that treatment.

Randomized study of orally administered fluorinated pyrimidines (capecitabine versus S-1) in women with metastatic or recurrent breast cancer: Japan Breast Cancer Research Network 05 Trial.

PURPOSE: Capecitabine and S-1 are orally administered fluorinated pyrimidines with high-level activity against metastatic breast cancer (MBC). This randomized, multicenter, phase II study compared the activities and safeties of the oral fluoropyrimidines, capecitabine and S-1, in breast cancer patients. METHODS: Patients with MBC were randomly assigned to receive capecitabine 825 g/m(2) twice daily on days 1-21 every 4 weeks or S-1 40-60 mg twice daily, according to body surface area, on days 1-28 every 6 weeks. The primary endpoint was progression-free survival (PFS). RESULTS: A total of 142 patients were enrolled and randomized to either capecitabine (N = 73) or S-1 (N = 69). Median PFS (progression-free survival) was 1.2 years for capecitabine and 1.3 years for S-1, with a hazard ratio (S-1/capecitabine) of 0.85 (95 % confidence interval [CI] 0.52-1.38) (P = 0.48 by log-rank). The confirmed objective response rates were 24.0 % for capecitabine and 23.1 % for S-1 (P = 0.938). The most common treatment-related adverse events were grade 1-2 in intensity. Thrombocytopenia (S-1: 9.2 %, capecitabine: 1.4 %; P = 0.040) and nausea (S-1: 26.2 %, capecitabine: 14.1 %; P = 0.079) were more frequent in the S-1 group, while hand-foot syndrome occurred more often in the capecitabine group (S-1: 10.8 %, capecitabine: 25.4 %; P = 0.029). CONCLUSIONS: The results of the current study demonstrate that both S-1 and capecitabine are effective and well-tolerated treatments in patients with MBC, while their adverse events were different. They are both convenient, orally administered drugs, making them attractive agents for use in outpatient treatment.

Phase II trial of preoperative chemotherapy for breast cancer: Japan Breast Cancer Research Network (JBCRN)-02 trial.

BACKGROUND: Neoadjuvant chemotherapy (NAC) is one of the main strategies for patients with locally advanced breast cancer. In our previous study, biological markers such as estrogen receptor (ER), progesterone receptor (PgR), and HER2 were essential predictors of the effectiveness of NAC to help individualize treatment. This study examined the effect of NAC on the disease-free survival (DFS) of breast cancer patients. Furthermore, the study was expanded by adding Ki-67 as a biological marker, and examined the correlation between Ki-67 and the prognosis. PATIENTS AND METHODS: Between September 2005 and September 2007, 43 patients with breast cancer received NAC and surgery. Four cycles of DC (doxorubicin: 60 mg/m(2) and cyclophosphamide: 500 mg/m(2)) were administered intravenously (i.v.) on day 1 every 21 days, followed by 12 cycles of paclitaxel i.v. (80 mg/m(2)) every 7 days, prior to surgery. The primary endpoint was the pathological complete response (pCR) rate and the secondary endpoint was DFS; the pCR rate was estimated for each groups stratified by the presence or absence of different factors (PcR, ER/PgR, and Ki-67). RESULTS: The clinical response (cCR+cPR) rate was 81.0%, and the pCR rate was 25.6%. The pCR rate was 75, 50, 9 and 0% in HER2(+)/ER(-), HER2(+)/ER(+), HER2(-)/ER(-), and HER2(-)/ER(+) patients, respectively. The 4-year DFS rate was estimated at 78% for all patients. The HER2 status was an independent predictor of pathological complete response (pCR). The DFS rate of patients with lower Ki-67 values (<15%) was higher than that of patients with higher Ki-67 values (≥15%). The treatment-related adverse events were manageable: the majority were mild, but five patients experienced grade 3 (neutropenia and sensory neuropathy) adverse events. CONCLUSION: DC followed by weekly paclitaxel is an active and manageable preoperative regimen for breast cancer patients. HER2 overexpression may be a good predictive marker of pCR, and the Ki-67 value after NAC may be a prognostic factor for DFS.

Effects of p27Kip1 on cell cycle status and viability in A549 lung adenocarcinoma cells.

p27Kip1 is a cyclin-dependent kinase inhibitor, it negatively regulates G1 progression and is reported to modulate apoptosis. Phosphorylation of this protein is thought to regulate its intracellular localisation and affect its stability. The aim of this study was to regulate p27Kip1 expression levels, and to examine how this protein affects cell cycle status and modulates viability in A549 lung adenocarcinoma cells. In addition, the association between phosphorylation status of p27Kip1 and its intracellular localisation was investigated, using expression vectors with cDNA of p27Kip1 or mutants in which the phosphorylation sites had been mutated. Although overexpression of p27Kip1 reduced cell cycle progression, its removal did not change cell cycle status. Modest induction of p27Kip1 rescued adenovector-induced apoptosis and its removal with short interfering RNA increased spontaneous cell death. It was also observed that p27Kip1 localised mainly in the cytoplasm, and forced expression of p27Kip1 cDNA with the substitution of serine (S) 10, threonine (T) 157 and T198 to glutamate (phosphor-mimetic) induced its cytoplasmic localisation. In conclusion, p27Kip1, when expressed physiologically, exists mainly in the cytoplasm, has little effect on cell cycle status and contributes viability in A549 lung adenocarcinoma cells. It was also surmised that intracellular localisation of p27Kip1 dominates its function and that its localisation was partly determined by its phosphorylation.

An in vitro screening system for characterizing the cleft palate-inducing potential of chemicals and underlying mechanisms.

An in vitro organ culture system with developing mouse palates was improved to characterize the cleft palate (CP)-inducing potential of chemicals and underlying mechanisms. Palatal explants collected from gestation day 12 mouse fetuses were cultured with various concentrations of teratogens and examined for palatal development after 48 and 72 h of culture to assess effects of the chemicals on growth and/or fusion of palatal shelves. When the explants were exposed to diphenylhydantoin or 5-fluorouracil, palatal growth was inhibited in a concentration-dependent manner at 48 h. Suppression of the expression of proliferative cell nuclear antigen revealed poor cell proliferation. At 72 h, the incidence of explants with CP was significantly increased in the high-dose groups, suggesting that CP induction is mainly attributable to inhibition of palatal growth. By contrast, retinoic acid and hydrocortisone significantly lowered the rates of fused palates at 72 h in all treated groups, while they exhibited no effects on palatal growth at 48 h even at the highest concentration. Because no apoptosis was found in the epithelial cells at the tip of these palates, these chemicals are suggested to inhibit palatal fusion process by preventing apoptosis.

[A case of endobronchial tuberculosis associated with bronchial asthma treated with high doses of inhaled corticosteroid].

A 46-year-old woman had been treated with 1,600-2,000 micrograms/day of beclomethasone dipropionate (BDP) and oral theophylline on the basis of a diagnosis of bronchial asthma in 1993. Eosinophilic pneumonia was diagnosed in June 1999, and she was then treated with 40 mg/day of oral prednisolone (PSL), which was gradually tapered off, and then stopped in October 1999. She was referred to our hospital because acid-fast bacilli were found in the sputum on January 18, 2000. Her chest radiographs and CT scans showed partial atelectasis of the right upper lobe, and fiberoptic bronchoscopy revealed bronchial inflammatory changes and whitish mucosal nodular lesions in the walls of the lower trachea, the right main bronchus and the orifice of the right upper lobe bronchus. She was found to have endobronchial tuberculosis. Anti-tuberculosis treatment with isoniazid, rifampicin, streptomycin and pyrazinamide was started. Serum levels of interferon-gamma were markedly elevated on admission. Asthma symptoms improved for a period of one month after the beginning of anti-tuberculosis treatment, despite the termination of inhaled corticosteroid. However, as the tuberculosis improved, the frequency and severity of the asthma increased and so corticosteroid inhalation was started again. Four months after administration of the anti-tuberculosis drug, fiberoptic bronchoscopy revealed that the endobronchial lesions had improved without any stenosis or constrictive changes. It was speculated that high doses of inhaled corticosteroid may have the potential to cause endobronchial tuberculosis whilst, ironically, at the same time preventing bronchial stenosis by endobronchial tuberculosis. This is an interesting case in which the asthma symptoms first decreased during the acute phase of endobronchial tuberculosis and then increased again after the tuberculosis improved.

Relationship between swallowing function and gas exchange during day and night in patients with obstructive sleep apnea syndrome.

Patients with obstructive sleep apnea syndrome (OSAS) are likely to exhibit an impaired swallowing reflex. However, mechanisms of disturbed swallowing reflex have not been determined. Because the upper-airway function is inhibited by hypoxia and hypercapnia, we examined the relationship between the swallowing function and gas exchange during day and night in patients with OSAS. Twenty-four patients with OSAS and 24 age-matched controls were studied. OSAS was diagnosed from overnight polysomnography. The swallowing reflex was judged by the latent time (LT) for swallowing following bolus injection of distilled water at the suprapharynx, the inspiratory suppression time (IST) from swallowing termination to the next onset of inspiration, and the threshold for evoking the swallowing response in terms of a volume of water (TV). Whereas the LT values are positively correlated with PaCO2 but not with PaO2 during the day, the values of IST and TV were not associated with daytime PaCO2 or PaO2. Nocturnal nadir SaO2 was correlated with LT, IST, and TV. These results indicate that oxyhemoglobin desaturation and hypercapnia may be associated with one of the mechanisms of the impaired swallowing function in patients with OSAS.

Extinction of expression of the genes encoding haematopoietic cell-restricted transcription factors in T-lymphoma x fibroblast cell hybrids.

We previously reported that expression of the T-cell receptor (TCR) alpha and lck genes is extinguished in hybrids between mouse T-lymphoma EL4 cells and mouse fibroblast B82 cells. In the present study, we found that the activities of the TCRalpha minimum enhancer and the lck promoter monitored by the luciferase or chloramphenicol acetyltransferase (CAT) assays were markedly inhibited in the hybrids. Expression of the TCF-1, LEF-1, GATA-3, Ikaros, c-myb and Fli-1 genes, which encode the haematopoietic cell-restricted transcription factors that appear to be responsible for the activities of the enhancer and the promoter, was fully extinguished or markedly suppressed in the hybrids. On the other hand, expression of the transcription factor genes observed in both parental cells, such as the AML1 and c-ets-1 genes, and that of the genes encoding ubiquitously expressed transcription factors, such as the E2A, CREB and c-ets-2 genes, was not significantly suppressed in the hybrids. These results suggest that the genes encoding haematopoietic cell-restricted transcription factors are targets for negative regulation in fibroblastic background and that the repression of these genes may consequently lead to suppression of the promoter and/or enhancer activities of several T-cell-specific structural genes in T-lymphoma x fibroblast cell hybrids.