Single-photon 3D imaging with a multi-stage network.

Active single-photon 3D imaging technology has been applied to 3D imaging of complex scenes in many frontier fields such as biomedicine, remote sensing mapping, etc. However, single-photon 3D imaging with strong background noise is still a major challenge. Several classical algorithms and machine learning methods have been proposed to solve the problem. In this paper, we propose a novel multi-stage synergistic recovery network to reconstruct an accurate depth map. In the model, we first extract multi-scale feature information using encoder and decoder architectures, then combine them with an original resolution network that retains complete spatial location information. Through this way, we can compensate the deficiencies of the original resolution network for multi-scale local feature extraction. Moreover, a self-supervised attention module (SAM) is constructed to weight local features between different stages, optimizing the feature exchange between different stages of the multi-stage architecture network. Our method currently performs the best of all the tested methods.

Acute Transverse Myelitis after COVID-19 Vaccination.

The adverse effects of the COVID-19 vaccine have been discovered as the rapid application of the vaccines continues. Neurological complications such as transverse myelitis raise concerns as cases were observed in clinical trials. Transverse myelitis is a rare immune-mediated disease with spinal cord neural injury, resulting in neurological deficits in the motor, sensory, and autonomic system. Vaccine-related transverse myelitis is even rarer. We present a case of acute transverse myelitis after vaccination against COVID-19 with the ChAdOx1 nCOV-19 vaccine (AZD1222), which was the first case reported in Taiwan. Although it rarely occurs, post-vaccination neurological complications should not be ignored. As the pandemic of SARS-CoV-2 continues to spread and concern about vaccination efficacy and safety rises, heterologous vaccination were implemented in health public policy in several countries. A literature review of several clinical trials shows promising effects of mix-and-match vaccination. Further study on different combinations of vaccines can be expected.

Molecular characterization and pathogenicity of Francisella noatunensis subsp. orientalis isolated from cultured tilapia (Oreochromis sp.) in Taiwan.

Francisella noatunensis subsp. orientalis is a causative agent of systemic granulomatous disease in tilapia. The present study was designed to understand the genetic and phenotypic diversities among Taiwanese Fno isolates obtained from tilapia (n = 17) and green Texas cichlid (Herichthys cyanoguttatus) (n = 1). The enzymatic profiles of the isolates were studied using the API ZYM system. Phylogenetic tree analysis of the 16S rRNA and housekeeping gene and pulsed-field gel electrophoresis (PFGE) were carried out to determine the genotypic characters of all isolates. The phylogenetic tree showed similarity of 99%-100% nucleotide sequences of 16S rRNA and housekeeping genes compared to the Fno references genes from GenBank database. Comparatively, the results revealed an identical profile of enzymatic and PFGE pattern which was distincted from that of F. philomiragia. To understand the pathogenicity, the isolates were intraperitoneal injected to tilapia the gross lesions were observed concomitant with natural outbreak. Median lethal dose upon Nile tilapia and red tilapia were 9.06 × 103 CFU/fish and 2.08 × 102 CFU/fish, respectively. Thus, our data provide understanding the epidemiology of Taiwanese Fno isolates, and help in development of future control and prevention.

[Meiotic analysis of spermatogenic cells in severe oligoasthenoteratozoospermia with chromosome 13 rearrangement].

OBJECTIVE: To explore the possible mechanisms of spermatogenic arrest in severe oligoasthenoteratozoospermia induced by supernumerary, ring-neocentric 13q12.3 --> 13q22 chromosome and reciprocal deletion. METHODS: We performed a genomic-wide high-density oaCGH analysis for a case of oligoasthenoteratozoospermia with abnormal chromosome 13 to characterize the breakpoints of the chromosome involved or the gene deletion caused by the rearrangement. We also conducted a fluorescence in situ hybridization analysis on the germ cells using probes of 13q14/13qter to observe the pairing condition of homologous chromosome 13. RESULTS: We identified by oaCGH analysis a microdeletion of 4 consecutive probes (A_16_P19757882, A_16_P02744617, A_14_ P108858 and A_16_P02744687 at chr13q12.3: 27979261 --> 28039191) with 59.93 kb between the FLT1 and POMP genes, with no annotated genes in the deleted region. The signals of 13q14 and 13qter were separated from each other in 90% of all the primary spermatocytes examined, indicating the unpairing of homologous chromosome 13 or synapse failure. CONCLUSION: Chromosomal rearrangement-induced spermatogenesis failure is caused by the unpairing of the homologous chromosomes involved in the first meiotic division of germ cells.

Rac1 and Akt Exhibit Distinct Roles in Mediating Aß-Induced Memory Damage and Learning Impairment.

Accumulated beta-amyloid (Aß) in the brain is the hallmark of Alzheimer's disease (AD). Despite Aß accumulation is known to trigger cellular dysfunctions and learning and memory damage, the detailed molecular mechanism remains elusive. Recent studies have shown that the onset of memory impairment and learning damage in the AD animal is different, suggesting that the underlying mechanism of the development of memory impairment and learning damage may not be the same. In the current study, with the use of Aß42 transgenic flies as models, we found that Aß induces memory damage and learning impairment via differential molecular signaling pathways. In early stage, Aß activates both Ras and PI3K to regulate Rac1 activity, which affects mostly on memory performance. In later stage, PI3K-Akt is strongly activated by Aß, which leads to learning damage. Moreover, reduced Akt, but not Rac1, activity promotes cell viability in the Aß42 transgenic flies, indicating that Akt and Rac1 exhibit differential roles in Aß regulating toxicity. Taken together, different molecular and cellular mechanisms are involved in Aß-induced learning damage and memory decline; thus, caution should be taken during the development of therapeutic intervention in the future.

Investigating ABCD1 mutations in a Taiwanese cohort with hereditary spastic paraplegia phenotype.

BACKGROUND: Adrenoleukodystrophy (ALD) is an X-linked peroxisomal disorder caused by mutations in the ABCD1 gene. The clinical manifestations of ALD vary widely with some patients presenting with adrenomyeloneuropathy (AMN) that resembles the phenotype of hereditary spastic paraplegia (HSP). The aim of this study is to investigate the frequency, spectrum, and clinical features of ABCD1 mutations in Taiwanese patients with HSP phenotype. METHODS: Mutational analysis of the ABCD1 gene was performed in 230 unrelated Taiwanese patients with clinically suspected HSP by targeted resequencing. Clinical, electrophysiological, and neuroimaging features of the patients carrying an ABCD1 pathogenic mutation were characterized. RESULTS: Ten different ABCD1 mutations were identified in eleven patients, including two novel mutations (p.Q177Pfs*17 and p.Y357*) and eight ever reported in ALD cases of other ethnicities. All patients were male and exhibited slowly progressive spastic paraparesis with onset ages ranging from 21 to 50 years. Most of them had additional non-motor symptoms, including autonomic dysfunction in nine patients, sensory deficits in seven, premature baldness in seven, skin hyperpigmentation in five, psychiatric symptoms in one and cerebellar ataxia in one. Seven of the ten patients who ever received nerve conduction studies showed axonal polyneuropathy. Magnetic resonance imaging (MRI) revealed diffuse spinal cord atrophy in seven patients, cerebral white matter hyperintensity in one patient, and cerebellar involvement in one patient. CONCLUSIONS: ABCD1 mutations account for 4.8% (11/230) of the cases with HSP phenotype in Taiwan. This study highlights the importance to consider ABCD1 mutations in patients with clinically suspected HSP of unknown genetic causes.

Stromal cell-derived factor-1/CXCR4 enhanced motility of human osteosarcoma cells involves MEK1/2, ERK and NF-kappaB-dependent pathways.

Osteosarcoma is characterized by a high malignant and metastatic potential. The chemokine stromal-derived factor-1alpha (SDF-1alpha) and its receptor, CXCR4, play a crucial role in adhesion and migration of human cancer cells. Integrins are the major adhesive molecules in mammalian cells, and has been associated with metastasis of cancer cells. Here, we found that human osteosarcoma cell lines had significant expression of SDF-1 and CXCR4 (SDF-1 receptor). Treatment of osteosarcoma cells with SDF-1alpha increased the migration and cell surface expression of alphavbeta3 integrin. CXCR4-neutralizing antibody, CXCR4 specific inhibitor (AMD3100) or small interfering RNA against CXCR4 inhibited the SDF-1alpha-induced increase the migration and integrin expression of osteosarcoma cells. Pretreated of osteosarcoma cells with MAPK kinase (MEK) inhibitor PD98059 inhibited the SDF-1alpha-mediated migration and integrin expression. Stimulation of cells with SDF-1alpha increased the phosphorylation of MEK and extracellular signal-regulating kinase (ERK). In addition, NF-kappaB inhibitor (PDTC) or IkappaB protease inhibitor (TPCK) also inhibited SDF-1alpha-mediated cell migration and integrin up-regulation. Stimulation of cells with SDF-1alpha induced IkappaB kinase (IKKalpha/beta) phosphorylation, IkappaB phosphorylation, p65 Ser(536) phosphorylation, and kappaB-luciferase activity. Furthermore, the SDF-1alpha-mediated increasing kappaB-luciferase activity was inhibited by AMD3100, PD98059, PDTC and TPCK or MEK1, ERK2, IKKalpha and IKKbeta mutants. Taken together, these results suggest that the SDF-1alpha acts through CXCR4 to activate MEK and ERK, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of alphavbeta3 integrins and contributing the migration of human osteosarcoma cells.

The epidemiology of traumatic humeral shaft fractures in Taiwan.

We retrospectively analysed 106 consecutive traumatic humeral shaft fractures over a five-year period. The mechanism of injury, age, gender, fracture types, associated injury and the presence of injury to the radial nerve were reviewed. The incidence was about 10 per 100,000 per year; most were closed fractures in young males which had been sustained as a result of traffic accidents. The age-gender distribution was characterised by gradually increased incidence from the fifth decade in women, while it reached a peak at the third decade and decreased after the fifth decade in men. The results revealed different epidemiological features from previous studies. The epidemiology differs between ethnicity and country, and updating the epidemiological features of humeral shaft fractures may provide information for appropriate treatment programmes. This study documents the epidemiology of humeral shaft fracture in Taiwan, probably for the first time in this Asian community.

Investigating CCNF mutations in a Taiwanese cohort with amyotrophic lateral sclerosis.

Mutations in the cyclin F gene (CCNF) have been recently identified in a small number of patients with amyotrophic lateral sclerosis (ALS) and/or frontotemporal dementia, and their role in patients with ALS in Taiwan remains elusive. The aim of this study was to elucidate the frequency and spectrum of CCNF mutations in a Taiwanese ALS cohort of Han Chinese origin. Mutational analyses of the CCNF gene were performed using Sanger sequencing in a cohort of 255 unrelated patients with ALS. Among these patients, the genetic diagnoses of 204 patients remained unclear after mutations in SOD1, C9ORF72, TARDBP, FUS, ATXN2, OPTN, VCP, UBQLN2, SQSTM1, PFN1, HNRNPA1, HNRNPA2B1, MATR3, CHCHD10, TUBA4A, and TKB1 had been investigated. Two novel heterozygous missense mutations in CCNF, p.S222P (c.664T>C) and p.S532R (c.1596C>T), were identified; 1 in each patient with apparently sporadic ALS. In vitro functional study demonstrated that both mutations result in a general and cyclin F-mediated ubiquitin-proteasome pathway dysfunction. The frequency of CCNF mutations in ALS patients in Taiwan is, therefore, approximately 0.8% (2/255). These findings expand the mutational spectrum of CCNF and also emphasize the pathogenic role of CCNF mutations in ALS.

Exciplex-Forming Cohost for High Efficiency and High Stability Phosphorescent Organic Light-Emitting Diodes.

An exciplex forming cohost system is employed to achieve a highly efficient organic light-emitting diode (OLED) with good electroluminescent lifetime. The exciplex is formed at the interfacial contact of a conventional star-shaped carbazole hole-transporting material, 4,4',4″-tris(N-carbazolyl)-triphenylamine (TCTA), and a triazine electron-transporting material, 2,4,6-tris[3-(1H-pyrazol-1-yl)phenyl]-1,3,5-triazine (3P-T2T). The excellent combination of TCTA and 3P-T2T is applied as the cohost of a common green phosphorescent emitter with almost zero energy loss. When Ir(ppy)2(acac) is dispersed in such exciplex cohost system, OLED device with maximum external quantum efficiency of 29.6%, the ultrahigh power efficiency of 147.3 lm/W, and current efficiency of 107 cd/A were successfully achieved. More importantly, the OLED device showed a low-efficiency roll-off and an operational lifetime (τ80) of ∼1020 min with the initial brightness of 2000 cd/m2, which is 56 times longer than the reference device. The significant difference of device stability was attributed to the degradation of exciplex system for energy transfer process, which was investigated by the photoluminescence aging measurement at room temperature and 100 K, respectively.

Unmasking adrenoleukodystrophy in a cohort of cerebellar ataxia.

Adrenoleukodystrophy (ALD) is a rare and progressive neurogenetic disease that may manifest disparate symptoms. The present study aims at investigating the role of ataxic variant of ALD (AVALD) in patients with adult-onset cerebellar ataxia, as well as characterizing their clinical features that distinguish AVALD from other cerebellar ataxias. Mutations in the ATP binding cassette subfamily D member 1 gene (ABCD1) were ascertained in 516 unrelated patients with ataxia. The patients were categorized into three groups: molecularly unassigned hereditary ataxia (n = 118), sporadic ataxia with autonomic dysfunctions (n = 296), and sporadic ataxia without autonomic dysfunctions (n = 102). Brain MRIs were scrutinized for white matter hyperintensity (WMH) in the parieto-occipital lobes, frontal lobes, corticospinal tracts, pons, middle cerebellar peduncles and cerebellar hemispheres. Two ABCD1 mutations (p.S108L and p.P623fs) previously linked to cerebral ALD and adrenomyeloneuropathy but not AVALD were identified. ALD accounts for 0.85% (1/118) of the patients with molecularly unassigned hereditary ataxia and 0.34% (1/296) of the patients with sporadic ataxia with autonomic dysfunctions. WMH in the corticospinal tracts and WMH in the cerebellar hemispheres were strongly associated with AVALD rather than other ataxias. To conclude, ALD accounts for approximately 0.39% (2/516) of adult-onset cerebellar ataxias. This study expands the mutational spectrum of AVALD and underscores the importance of considering ALD as a potential etiology of cerebellar ataxia.

Molecular Basis Underlying Leaf Variegation of a Moth Orchid Mutant (Phalaenopsis aphrodite subsp. formosana).

Leaf variegation is often the focus of plant breeding. Here, we studied a variegated mutant of Phalaenopsis aphrodite subsp. formosana, which is usually used as a parent of horticultural breeding, to understand its anatomic and genetic regulatory mechanisms in variegation. Chloroplasts with well-organized thylakoids and starch grains were found only in the mesophyll cells of green sectors but not of yellow sectors, confirming that the variegation belongs to the chlorophyll type. The two-dimensional electrophoresis and LC/MS/MS also reveal differential expressions of PsbP and PsbO between the green and yellow leaf sectors. Full-length cDNA sequencing revealed that mutant transcripts were caused by intron retention. When conditioning on the total RNA expression, we found that the functional transcript of PsbO and mutant transcript of PsbP are higher expressed in the yellow sector than in the green sector, suggesting that the post-transcriptional regulation of PsbO and PsbP differentiates the performance between green and yellow sectors. Because PsbP plays an important role in the stability of thylakoid folding, we suggest that the negative regulation of PsbP may inhibit thylakoid development in the yellow sectors. This causes chlorophyll deficiency in the yellow sectors and results in leaf variegation. We also provide evidence of the link of virus CymMV and the formation of variegation according to the differential expression of CymMV between green and yellow sectors.

Fat embolism syndrome in long bone fracture--clinical experience in a tertiary referral center in Taiwan.

BACKGROUND: Fat embolism syndrome (FES) is a potentially fatal complication of long bone fractures. There have been no reports of FES in long bone fractures in this decade in Taiwan. The purpose of this study was to review the FES experiences in a tertiary referral center between January 1997 and February 2008. METHODS: Between January 1997 and February 2008, 13 patients with long bone fractures with documented FES in our institution were reviewed. FES was diagnosed clinically by at least 2 major criteria or 1 major with at least 4 minor signs of Gurd's criteria. RESULTS: The incidences of FES, less than those reported in the literature, were 0.15% in fracture of the tibia, 0.78% in fracture of the femur and 2.4% in multiple fractures. The mortality rate of FES, similar to other available results, was about 7.7%. All cases were less than 35 years old, except for 1 70-year-old male. Fat embolism occurred within an average of 48.5 hours after long bone fracture. Eleven presented with sudden drop in hemoglobin level, dropping 4.2 g/dL on average. Nine presented with thrombocytopenia, and 10 presented with sudden drop in platelet count, dropping 140,000/dL on average. Two had cerebral sequelae without recovery at the last 48-month follow-up. CONCLUSION: This 12-year interval retrospective study revealed modern epidemiologic results for FES in long bone fracture. Compared with the available literature in the recent decade, the incidence of FES in long bone fracture in our institution is less and the mortality rate is similar.

Collaborative cell-resistant properties of polyelectrolyte multilayer films and surface PEGylation on reducing cell adhesion to cytophilic surfaces.

Both poly(ethylene glycol) (PEG) grafting and layer-by-layer polyelectrolyte multilayer (PEM) deposition for surface modification of biomaterials have been shown to decrease cell adhesion. The aim of this study was to investigate the synergic efficacy of PEGylated PEM films on reducing cell adhesion. PEG grafted to poly(ethylene imine) (PEI) was deposited onto the top of PEI/PAA (poly(acrylic acid)) multilayer films which were deposited onto cytophilic substrates, including tissue culture polystyrene and collagen-based substrate. The efficacy of the PEGylated PEM films in blocking adhesion of L929 cells was investigated by varying the amount of conjugated PEG and the layer numbers of PEM films. We found that cell adhesion was reduced on the swollen PEM films and further decreased by deposition of PEI-g-PEG as the topmost layer. The ability in cell resistance was enhanced with increasing PEG contents of PEGylated PEM films. PEGylated PEM films were stable for long-term incubation in phosphate-buffered saline. We demonstrated that cell affinity of cytophilic surfaces could be depressed by deposition of PEGylated PEM films.

Treatment for ipsilateral fractures of femoral neck and shaft.

BACKGROUND: Concomitant ipsilateral femoral shaft and neck fractures present a challenge to the orthopaedic surgeon, and no consensus has yet emerged on the optimal treatment method. We report the results of a retrospective study of 43 patients with these complex fractures who were treated at a single Level 1 trauma centre. PATIENTS AND METHODS: The study participants consisted of 28 males and 15 females with a mean age of 43 years. The mean follow-up period was 48 months. Four different treatment methods were used: (1) antegrade reamed intramedullary nailing of the shaft with cancellous screw fixation of the neck, (2) dynamic hip screw (DHS) fixation of the neck and low-contact dynamic compression plate (LCDCP) fixation of the shaft, (3) cancellous screw fixation of the neck and LCDCP fixation of the shaft, and (4) reconstruction nailing of both shaft and neck. RESULTS: No statistically significant differences in amount of blood loss, duration of surgery, total complication rate, nor clinical results were found among the four treatment methods. For femoral neck fracture, however, the complication rate of cannulated screw with antegrade intramedullary nailing fixation was 11 times that of DHS with LCDCP fixation. CONCLUSIONS: Antegrade nail with screw fixation is not a recommended treatment method in patients with ipsilateral femoral shaft and neck fractures.