Homotopy Theoretic Models of Type Theory

We introduce the notion of a logical model category which is a Quillen model category satisfying some additional conditions. Those conditions provide enough expressive power that one can soundly interpret dependent products and sums in it. On the other hand, those conditions are easy to check and provide a wide class of models some of which are listed in the paper.Comment: Corrected version of the published articl

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Impact of GnRH Analogues and Exogenous Progesterone Supplementation in Treatment of Ovarian Inactivity for Primiparous and Multiparous Dromedary She-Camels in Egypt

The present investigations were designed to deal with the problem of ovarian inactivity of Dromedary camel. Twenty she-camels were divided into two equal groups as primiparous or multiparous. The same protocol was applied on both groups which was two doses of Receptal® (10μg GnRH analogue) with 10 days apart and exogenous progesterone (PRID) insertion at day zero and was removed at day 10. Blood samples were taken several days for analysing Follicle-stimulating hormone (FSH), Progesterone (P4) and Estradiol (E2). Also, Follicular Size was measured using ultrasound. Significant differences were obtained in FSH, P4 and E2 along days of treatment. Moreover, multiparous had higher levels of FSH and E2 than primiparous. On the other hand, no significant difference in P4 level was recorded between groups. In general, treatment induced significantly a new follicular wave and stimulates follicle growth from 8.406 mm (day13) up to 12.791 mm (day 15 of PRID insertion), nevertheless, no significance in follicular size between groups was observed. She-camels in both groups revealed a noticed response to treatment protocol which was observed via estrous signs. Pregnancy rate doesn't reveal a significant difference between groups. We can conclude that, a combination of 1.55gm of exogenous P4 and two doses of 10µg GnRH analogues can enhance emergence of follicular development up to pre ovulatory size and significantly alter hormonal profile of primiparous and multiparous she camels with inactive ovaries

Heritability of cold tolerance in Nile tilapia, Oreochromis niloticus, juveniles

The inability of tilapia to tolerate low temperatures is of major economic concern as it reduces their growing season and leads to over winter mortality. In this study, cold tolerance of juvenile Nile tilapia, Oreochromis niloticus, was investigated and heritability estimates obtained. A total of 80 maternal full-sib families were produced by mating each sire with two dams. Fry were grown in hapas suspended in earthen ponds fertilized with chicken manure, and were 41¿91 days post-hatch at the start of the experiment (mean standard length 50.6 mm; mean body weight 5.1 g). Fry were tagged and exposed to low temperature in an indoor facility. Temperature was lowered from 16 °C to 11 °C in 48 h and from 11 °C to 8 °C at the rate of 1 °C/day. Cold tolerance was expressed as temperature at death (TAD) and cooling degree hours (CDH). Fish mortality started at 13.6 °C and total mortality occurred at 8.6 °C. Mean TAD and CDH were 10.1 °C and 298.07 respectively. Fish body weight (BW) had a highly significant effect on cold tolerance (P <0.0001). Smaller fish (<5g) were more susceptible to lower temperature than larger fish. The heritability of cold tolerance was 0.08 ± 0.17 for CDH and 0.09 ± 0.19 for TAD, estimated with an animal model. There was a considerable common environmental/full-sib effect for this trait (0.33 ± 0.10 for CDH and 0.27 ± 0.09 for TAD). These values indicate that estimation of genetic parameters for cold tolerance in tilapia should include both direct additive and common environmental effects. Based on the results of this study, we conclude that the most appropriate way of enhancing cold tolerance of tilapia juveniles is by husbandry practices that increase pre-winter body weight