35 research outputs found
Similarity-based Classification: Connecting Similarity Learning to Binary Classification
In real-world classification problems, pairwise supervision (i.e., a pair of
patterns with a binary label indicating whether they belong to the same class
or not) can often be obtained at a lower cost than ordinary class labels.
Similarity learning is a general framework to utilize such pairwise supervision
to elicit useful representations by inferring the relationship between two data
points, which encompasses various important preprocessing tasks such as metric
learning, kernel learning, graph embedding, and contrastive representation
learning. Although elicited representations are expected to perform well in
downstream tasks such as classification, little theoretical insight has been
given in the literature so far. In this paper, we reveal that a specific
formulation of similarity learning is strongly related to the objective of
binary classification, which spurs us to learn a binary classifier without
ordinary class labels---by fitting the product of real-valued prediction
functions of pairwise patterns to their similarity. Our formulation of
similarity learning does not only generalize many existing ones, but also
admits an excess risk bound showing an explicit connection to classification.
Finally, we empirically demonstrate the practical usefulness of the proposed
method on benchmark datasets.Comment: 22 page
The first Japanese MDPL case
Mandibular hypoplasia, deafness, progeroid features and lipodystrophy (MDPL) syndrome is a rare autosomal dominant disorder caused by heterozygous POLD1 mutations. To date, 13 patients affected by POLD1 mutation-caused MDPL have been described. We report a clinically undiagnosed 11-year-old male who noted joint contractures at 6 years of age. Targeted exome sequencing identified a known POLD1 mutation [NM_002691.3:c.1812_1814del, p.(Ser605del)] that diagnosed him as the first Japanese/East Asian MDPL case
A Cluster of Respiratory Syncytial Virus Infections in a Hospital Ward for Adult Immunocompromised Patients
Four male patients admitted to the same ward in the first half of September 201Y were identified to have respiratory syncytial virus(RSV)infection. Their ages ranged from 49 to 85 years(median 72.5). One patient was infected with human immunodeficiency virus and three patients had hematological malignancies. Following immuno-chromatological testing with a nasal cavity swab, RSV infection was diagnosed. Although blood and sputum cultures were performed in three patients, no significant bacteria were detected. Two cases responded to supportive therapy. However, one patient died secondary to multiple myeloma, and another patient developed pneumonia and died with an exacerbation of leukemia. RSV infections in immunocompromised hosts are associated with a poor prognosis. Early diagnosis will facilitate isolation of infected individuals to prevent hospital outbreaks
Brugada-like Precordial ST Elevation on ECG by Anterior Mediastinal Infective Mass Lesion
Several causes are known to induce the right precordial ST elevation mimicking Brugada syndrome. Right ventricular outflow area is assumed to be responsible for such ECG changes. We experienced a case of anterior mediastinal infective mass lesion with a Brugada-like ECG.
A 52-year-old female, who has pulmonary stenosis and recurrent episodes of right ventricular heart failure, complained of high fever, abdominal discomfort, and edema. On physical examination, jugular vein dilation, hepatomegaly, and facial and leg edema were noted. Leucocytosis was also noted on blood examination. An ECG showed right ventricular hypertrophy, incomplete right bundle branch block pattern and marked ST elevation on precordial leads mimicking Brugada syndrome. Magnetic resonance imaging revealed an abnormal mass shadow located on the anterior mediastinum and compressing the right ventricle (Figure 1A). Trans-thoracic echocardiography also showed the high echogenic mass lesion at the anterior side of right ventricle and the vicinity of pulmonary valve. After treatment with antibiotics, the mass lesion gradually shrunk. Concomitantly, the ST elevation disappeared with improvement of inflammatory markers (Figure 1B). The symptoms suggesting right ventricular failure were also ameliorated. The mechanism of Brugada-like ST elevation in this patient was considered to be compression, by the abnormal infective mass, of the right ventricular outflow tract with/without focal pericardial inflammation
Differential patterns of Fos induction in the hypothalamus of the rat following central injections of galanin-like peptide and galanin
Galanin and its newly discovered relative galanin-like peptide (GALP) are
neuropeptides that are implicated in the neuroendocrine regulation of body
weight and reproduction. GALP has been shown to bind in vitro to galanin
receptor subtypes 1 and 2, but whether it has its own specific receptor(s)
is unknown. We reasoned that if GALP acts through a receptor that is
distinct from galanin receptors, then GALP should activate central
pathways that are different from those activated by galanin. The purpose
of this study was to determine whether galanin and GALP produce different
patterns of neuronal activation within the hypothalamus. Quantitative
analysis of Fos immunoreactivity showed that galanin induced a
significantly greater number of Fos-positive nuclei in the paraventricular
nucleus compared with GALP (P < 0.001); however, compared with galanin,
GALP induced significantly more Fos-positive cells in the horizontal limb
of the diagonal band of Broca, caudal preoptic area, arcuate nucleus, and
median eminence (P < 0.05). These observations suggest that GALP and
galanin act through different receptor-mediated pathways to exert their
effects on the regulation of body weight and reproduction and identify
target cells for GALP's specific actions in the hypothalamus, including
the preoptic area, paraventricular and arcuate nuclei, and the median
eminence
SDF-1α Secreted by Human CD133-Derived Multipotent Stromal Cells Promotes Neural Progenitor Cell Survival Through CXCR7
We recently reported that concentrated conditioned medium (CdM) from human CD133-derived bone marrow progenitor cells (CD133 CdM) was neuroprotective after stroke. Here we identify stromal-derived factor 1 alpha (SDF-1) as a potential neuroprotective candidate in CD133 CdM by interrogating the transcriptional responses of CD133-derived multipotent stromal cells (CD133dMSCs) after cell injection into the ischemic brain. Human SDF-1 mRNA was upregulated 79-fold by CD133dMSCs when injected into the stroke peri-infarct area compared with cells injected into the uninjured parenchyma of sham-operated animals. In cell protection assays, we replaced the typical growth medium in mouse neural progenitor cell (mNPC) cultures with serum-free CD133 CdM immediately before exposure to hypoxia (1% oxygen) for 48 h. CD133 CdM significantly increased the survival of mNPCs during hypoxia exposure and growth factor withdrawal. To determine whether MSC-secreted SDF-1 influenced mNPC survival, we used lentiviral short hairpin RNA against SDF1 (shSDF-1) to knockdown SDF-1 expression in CD133dMSCs. The CdM generated from shSDF-1-treated cells had a 94% decrease in secreted SDF-1 and was significantly less protective for mNPCs when compared with control CdM from CD133dMSCs transduced with scrambled short hairpin RNA. Pharmacological inhibition of the 2 known SDF-1 receptors, CXCR4 and CXCR7, revealed that only CXCR7 activity was functionally linked to survival signaling in mNPCs during hypoxia exposure. Treatment of mNPCs with CD133 CdM and CXCR7 inhibitor decreased mNPC viability by 36.5% ± 12.8% and decreased cell number by 21% ± 6.7% compared with dimethyl sulfoxide treated controls. These data indicate that SDF-1 is a key neuroprotective cytokine secreted by CD133dMSCs that protects mNPCs through CXCR7
A Rare Case of Coronary Involvement in IgG4-Related Disease
Although cardiovascular involvement in immunoglobulin G4–related disease is uncommon, it can lead to life-threatening events. We report a patient with multiple coronary aneurysms that were diagnosed by multimodal imaging. The patient had been treated with prednisolone for more than 15 years for immunoglobulin G4–related disease