Imagining the Future of Philanthropy Research in Europe : Paper prepared for the International Philanthropy Research Conference 22 and 23 September, Turin, IT

A conference paper by Rien Van Gendt, who argues for funding academic research in the field of philanthropy

SEMI-CenterNet: A Machine Learning Facilitated Approach for Semiconductor Defect Inspection

Continual shrinking of pattern dimensions in the semiconductor domain is making it increasingly difficult to inspect defects due to factors such as the presence of stochastic noise and the dynamic behavior of defect patterns and types. Conventional rule-based methods and non-parametric supervised machine learning algorithms like KNN mostly fail at the requirements of semiconductor defect inspection at these advanced nodes. Deep Learning (DL)-based methods have gained popularity in the semiconductor defect inspection domain because they have been proven robust towards these challenging scenarios. In this research work, we have presented an automated DL-based approach for efficient localization and classification of defects in SEM images. We have proposed SEMI-CenterNet (SEMI-CN), a customized CN architecture trained on SEM images of semiconductor wafer defects. The use of the proposed CN approach allows improved computational efficiency compared to previously studied DL models. SEMI-CN gets trained to output the center, class, size, and offset of a defect instance. This is different from the approach of most object detection models that use anchors for bounding box prediction. Previous methods predict redundant bounding boxes, most of which are discarded in postprocessing. CN mitigates this by only predicting boxes for likely defect center points. We train SEMI-CN on two datasets and benchmark two ResNet backbones for the framework. Initially, ResNet models pretrained on the COCO dataset undergo training using two datasets separately. Primarily, SEMI-CN shows significant improvement in inference time against previous research works. Finally, transfer learning (using weights of custom SEM dataset) is applied from ADI dataset to AEI dataset and vice-versa, which reduces the required training time for both backbones to reach the best mAP against conventional training method

Occurrence of testicular microlithiasis in androgen insensitive hypogonadal mice

<b>Background</b>: Testicular microliths are calcifications found within the seminiferous tubules. In humans, testicular microlithiasis (TM) has an unknown etiology but may be significantly associated with testicular germ cell tumors. Factors inducing microlith development may also, therefore, act as susceptibility factors for malignant testicular conditions. Studies to identify the mechanisms of microlith development have been hampered by the lack of suitable animal models for TM.<BR/> <b>Methods</b>: This was an observational study of the testicular phenotype of different mouse models. The mouse models were: cryptorchid mice, mice lacking androgen receptors (ARs) on the Sertoli cells (SCARKO), mice with a ubiquitous loss of androgen ARs (ARKO), hypogonadal (hpg) mice which lack circulating gonadotrophins, and hpg mice crossed with SCARKO (hpg.SCARKO) and ARKO (hpg.ARKO) mice.<BR/> <b>Results</b>: Microscopic TM was seen in 94% of hpg.ARKO mice (n=16) and the mean number of microliths per testis was 81 +/- 54. Occasional small microliths were seen in 36% (n=11) of hpg testes (mean 2 +/- 0.5 per testis) and 30% (n=10) of hpg.SCARKO testes (mean 8 +/- 6 per testis). No microliths were seen in cryptorchid, ARKO or SCARKO mice. There was no significant effect of FSH or androgen on TM in hpg.ARKO mice.<BR/> <b>Conclusions</b>: We have identified a mouse model of TM and show that lack of endocrine stimulation is a cause of TM. Importantly, this model will provide a means with which to identify the mechanisms of TM development and the underlying changes in protein and gene expression

Three cases of severe subfulminant hepatitis in heart-transplanted patients after nosocomial transmission of a mutant hepatitis B virus

Fulminant and severe viral hepatitis are frequently associated with mutant hepatitis B virus (HBV) strains. In this study, the genetic background of a viral strain causing severe subfulminant outcome in heart-transplanted patients was studied and compared with viral hepatitis B strains that were not linked to severe liver disease in the same setting. A total of 46 patients infected nosocomially with HBV genotype A were studied. Five different viral strains were detected, infecting 3, 9, 5, 24, and 5 patients, respectively. Only one viral strain was found to be associated with the subfulminant outcome and 3 patient deaths as a consequence of severe liver disease. The remaining 43 patients with posttransplantation HBV infection did not show this fatal outcome. Instead, symptoms of hepatitis were generally mild or clinically undiagnosed. Comparison of this virus genome with the four other strains showed an accumulation of mutations in the basic core promoter, a region that influences viral replication, but also in hepatitis B X protein (HBX) (7 mutant motifs), core (10 mutant motifs), the preS1 region (5 mutant motifs), and the HBpolymerase open reading frame (17 motifs). Some of these variations, such as those in the core region, were located on the tip of the protruding spike of the viral capsid (codons 60 to 90), also known in part as an important HLA class II-restricted epitope region. These mutations might therefore influence the immune-mediated response. The viral strain causing subfulminant hepatitis was, in addition, the only strain with a preCore stop codon mutation and, thus, hepatitis B e antigen (HBeAg) expression was never observed. The combination of these specific viral factors is thought to be responsible for the fatal outcome in these immune-suppressed heart-transplant recipients

Short and long-term adaptation in the auditory nerve stimulated with high-rate electrical pulse trains are better described by a power law

Despite the introduction of many new sound-coding strategies speech perception outcomes in cochlear implant listeners have leveled off. Computer models may help speed up the evaluation of new sound-coding strategies, but most existing models of auditory nerve responses to electrical stimulation include limited temporal detail, as the effects of longer stimulation, such as adaptation, are not well-studied. Measured neural responses to stimulation with both short (400 ms) and long (10 min) duration high-rate (5kpps) pulse trains were compared in terms of spike rate and vector strength (VS) with model outcomes obtained with different forms of adaptation. A previously published model combining biophysical and phenomenological approaches was adjusted with adaptation modeled as a single decaying exponent, multiple exponents and a power law. For long duration data, power law adaptation by far outperforms the single exponent model, especially when it is optimized per fiber. For short duration data, all tested models performed comparably well, with slightly better performance of the single exponent model for VS and of the power law model for the spike rates. The power law parameter sets obtained when fitted to the long duration data also yielded adequate predictions for short duration stimulation, and vice versa. The power law function can be approximated with multiple exponents, which is physiologically more viable. The number of required exponents depends on the duration of simulation; the 400 ms data was well-replicated by two exponents (23 and 212 ms), whereas the 10-minute data required at least seven exponents (ranging from 4 ms to 600 s). Adaptation of the auditory nerve to high-rate electrical stimulation can best be described by a power-law or a sum of exponents. This gives an adequate fit for both short and long duration stimuli, such as CI speech segments

The effect of a sertoli cell-selective knockout of the androgen receptor on testicular gene expression in prepubertal mice

To unravel the molecular mechanisms mediating the effects of androgens on spermatogenesis, testicular gene expression was compared in mice with Sertoli cell-selective androgen receptor knockout (SCARKO) and littermate controls on postnatal d 10. Microarray analysis identified 692 genes with significant differences in expression. Of these, 28 appeared to be down-regulated and 12 up-regulated at least 2-fold in SCARKOs compared with controls. For nine of the more than 2-fold down-regulated genes, androgen regulation was confirmed by treatment of wild-type mice with an antiandrogen ( flutamide). Some of them were previously described to be androgen regulated or essential for spermatogenesis. Serine-type protease inhibitors were markedly overrepresented in this down-regulated subgroup. A time study (d 8-20), followed by cluster analysis, allowed identification of distinct expression patterns of differentially expressed genes. Three genes with a pattern closely resembling that of Pem, a prototypical an-drogen-regulated gene expressed in Sertoli cells, were selected for confirmation by quantitative RTPCR and additional analysis. The data confirm that the SCARKO model allows identification of novel androgen-regulated genes in the testis. Moreover, they suggest that protease inhibitors and other proteins related to tubular restructuring and cell junction dynamics may be controlled in part by androgens