Histomorphometry aspect of thyroid gland and biochemical profile in pregnant and non-pregnant dromedary camels

Modulation of body physiology and metabolism is a prerequisite for successful pregnancy in camels, which is about a year and few months. The present study was carried out to verify the effect of pregnancy on histomorphometry and functional traits of thyroid gland, as well as some biochemical indices of liver and kidney functions and mineral profile in one humped camels, under Egyptian climatic conditions or desert conditions. The thyroid tissues were fixed in 10% formalin solution and processed following routine histological techniques after gross examination and biometric assessment. Serum levels of thyroid hormones (triiodothyronine, thyroxineand thyroid stimulating hormone), serum blood metabolites (total bilirubin, blood urea nitrogen and creatinine), liver enzymatic activity (aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP)), and minerals (sodium, potassium, calcium and phosphorus) were estimated in pregnant (n=30) and non-pregnant (n=30) camels. There were no significant differences between the right and left thyroid lobes between pregnant and non-pregnant camel. Pregnant status in camels had insignificant influence on histological and functional traits of thyroid as well as serum blood metabolites, liver enzymes and minerals levels, as compared with non-pregnant animals during the first six months of pregnancy. Therefore, reproductive status (during early pregnancy) has no substantial effect on camel physiological mechanisms or metabolic activity.Key words: Biochemical, dromedary, histology, thyroid gland, thyroid hormones

Molecular Characterization of Chromosome 7 in AML and MDS Patients

Myelodysplastic syndromes (MDS) share many features with acute myeloid leukemias (AML) and in fact 20 - 40% of the patients eventually develop a picture of full blown AML. Chromosome 7 has been a focus of attention as a site harboring tumor suppressor genes whose loss of function contributes to leukemia transformation or tumor progression. Abnormalities of chromosome 7 are frequently encountered in AML and MDS. The aim of the present study was to detect the molecular abnormalities of chromosome 7 in Egyptian AML and MDS patients using the FISH technique and whether the abnormality has an implication on the prognosis of the disease after a period of one year follow up. Fluorescence in-situ hybridization (FISH) was performed for chromosome 7 using a locus specific probe for 7q31 and a centromeric probe from 7p11.1-q11.1 in a series of 30 patients diagnosed as: AML (20 patients) and MDS (10 patients) according to the FAB criteria. Aberrations of Chromosome 7 were found in 36.6% of AML patients: 3 cases showing monosomy with a mean positivity of 17.3%, 2 cases showing 7q deletion with a mean positivity of 11%. While both monosomy and deletion were detected in 3 cases. However, in MDS patients; monosomy for chromosome 7 was the only abnormality detected and was found in 30% of cases. Genetic abnormality of chromosome 7 showed a significant association with poor prognostic criteria. Patients who had normal FISH results showed a higher percentage (31.6%) of complete remission (CR) versus 0% in patients with monosomy or deletion who showed a higher percentage (100%) of death or poor response to therapy (NR). Although AML patients had a worse prognosis when compared to MDS patients, patients with genetic abnormalities showed the worst outcome

FRUCTO SYRUP FROM WHEY MILK VIA BIOTECHNOLOGY

The present study deal with hydrolysis of lactose by kluyveromyces fragilis that grown in Whey and synthetic mediumandthe effect of incubated temperature and pH on enzyme activity Lactase (ß- galactosidase) that hydrolyze lactose in whey milk and synthetic medium .Also the conversion of glucose that released from lactose hydrolysis by kluyveromyces fragilis into fructose via addition of glucose isomerase. The present work showed that the optimum pH and incubated temperature were (4,35°C) respectively to optimum enzyme activity Lactase with total glucose reached 60.21 mg/ 100ml in whey medium and 58.61 mg/100ml in synthetic medium after 24 hours. In addition fructose content was 48.15 mg/100ml from released glucose in whey milk that confirmed due to the highest sweet syrup. In conclusion, this study indicated that ability of kluyveromyces fragilis to hydrolyze lactose in natural whey milk higher than synthetic medium

A Systematic Design of a Compact Wideband Hybrid Directional Coupler Based on Printed RGW Technology

Printed ridge gap waveguide (PRGW) is considered among the state of art guiding technologies due to its low signal distortion and low loss at Millimeter Wave (mmWave) spectrum, which motivates the research community to use this guiding structure as a host technology for various passive microwave and mmWave components. One of the most important passive components used in antenna beam-switching networks is the quadrature hybrid directional coupler providing signal power division with 90° phase shift. A featured design of a broadband and compact PRGW hybrid coupler is propose in this paper. A novel design methodology, based on mode analysis, is introduced to design the objective coupler. The proposed design is suitable for mmWave applications with small electrical dimensions ( 1.2λo×1.2λo ), low loss, and wide bandwidth. The proposed hybrid coupler is fabricated on Roger/RT 6002 substrate material of thickness 0.762 mm. The measured results highlight that the coupler can provide a good return loss with a bandwidth of 26.5% at 30 GHz and isolation beyond 15 dB. The measured phase difference between the coupler output ports is equal 90∘± 5∘ through the interested operating bandwidth. A clear agreement between the simulated and the measured results over the assigned operating bandwidth has been illustrated

Fabrication and Characterization of a W-Band Cylindrical Dielectric Resonator Antenna-Coupled Niobium Microbolometer

We report on the fabrication and characterization of a novel antenna-coupled detector configuration for detection at 94 GHz, a coplanar waveguide- (CPW-) fed, slot-excited twin dielectric resonator antenna- (DRA-) coupled niobium (Nb) microbolometer. The antenna is based on two low permittivity cylindrical dielectric resonators (CDRs) excited by rectangular slots placed below the CDRs. The antenna resonant currents are fed to an Nb microbolometer by the means of a CPW feed. The ceramic DRA structure is manufactured using a novel fabrication process that enables patterning an SU-8–Alumina (Al2O3) nanopowder composite using conventional photolithography. The detector measured a voltage responsivity of 0.181 V/W at a modulation frequency of 150 Hz. The detector measured a time constant of 1.94 μs. The antenna radiation pattern of the developed detector configuration was measured and shows a good agreement with the simulation

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 hospitalization2–4 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

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

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

Numerical methods for the design and description of in vitro expansion processes of human mesenchymal stem cells

Human mesenchymal stem cells (hMSCs) are a valuable source of cells for clinical applications (e.g., treatment of acute myocardial infarction or inflammatory diseases), especially in the field of regenerative medicine. However, for autologous (patient-specific) and allogeneic (off-the-shelf) hMSC-based therapies, in vitro expansion is necessary prior to the clinical application in order to achieve the required cell numbers. Safe, reproducible, and economic in vitro expansion of hMSCs for autologous and allogeneic therapies can be problematic because the cell material is restricted and the cells are sensitive to environmental changes. It is beneficial to collect detailed information on the hydrodynamic conditions and cell growth behavior in a bioreactor system, in order to develop a so called “Digital Twin” of the cultivation system and expansion process. Numerical methods, such as Computational Fluid Dynamics (CFD) which has become widely used in the biotech industry for studying local characteristics within bioreactors or kinetic growth modelling, provide possible solutions for such tasks. In this review, we will present the current state-of-the-art for the in vitro expansion of hMSCs. Different numerical tools, including numerical fluid flow simulations and cell growth modelling approaches for hMSCs, will be presented. In addition, a case study demonstrating the applicability of CFD and kinetic growth modelling for the development of an microcarrier-based hMSC process will be shown