SARS-CoV-2 Prediction Strategy Based on Classification Algorithms from a Full Blood Examination.

A fast and efficient diagnosis of serious infectious diseases, such as the recent SARS-CoV-2, is necessary in order to curb both the spread of existing variants and the emergence of new ones. In this regard and recognizing the shortcomings of the reverse transcription-polymerase chain reaction (RT-PCR) and rapid diagnostic test (RDT), strategic planning in the public health system is required. In particular, helping researchers develop a more accurate diagnosis means to distinguish patients with symptoms with COVID-19 from other common infections is what is needed.

The effect of prolactin on casein kinase II, MAP kinase and PKC in rabbit mammary cells and Nb2 rat lymphoid cells.

Prolactin induces milk protein gene expression in rabbit primary mammary cells without any concomitant cell multiplication. Prolactin or other lactogenic hormones is the major inducer of cell division in the rat lymphoid Nb2 cells. In Nb2 cells, prolactin also rapidly induces the expression of the c-myc gene, and beta-actin and stathmin gene expression is induced more slowly.

CFTR gene transfer corrects defective glycoconjugate secretion in human CF epithelial tracheal cells.

We demonstrate that in immortalized normal human tracheal epithelial cells (NT-1 and 56FHTE8o-) 14C-labeled glycoconjugate secretion may be regulated independently by agonists of the protein kinase A (PKA) and protein kinase C (PKC) signaling pathways. In contrast, in immortalized cystic fibrosis (CF) human tracheal epithelial cells (CFT-1 and CFT-2), regulation is defective for agonists specific for the PKA but not for the PKC pathway. To characterize the involvement of the cystic fibrosis transmembrane conductance regulator (CFTR) in regulated glycoconjugate secretion, we examined the effect of adenovirus-mediated gene transfer of CFTR to CF and control cells.

Overexpression of annexin V in cystic fibrosis epithelial cells from fetal trachea.

In this report, we investigated the expression of annexins I, II, V, and VI by Northern and Western blot analysis in four cell lines isolated from human fetal tracheae. Two cell lines were obtained from normal fetuses and the two others from fetuses with cystic fibrosis (CF). One CF fetus was heterozygous for the S549N and N1303K substitutions, whereas the other was homozygous for the delta F508 deletion.

Stathmin gene expression in mammary gland and in Nb2 cells.

Mammary gland growth occurs essentially during pregnancy and induction of milk synthesis is triggered at parturition. Prolactin is mammogenic in vivo but only marginally in vitro. Prolactin induces milk synthesis in vivo and in cultured mammary cells.

Protein kinase C is not necessary for beta-casein gene induction by prolactin in HC11 mouse mammary cells.

HC11 mouse mammary cells cultured in the presence of insulin, cortisol and prolactin for 24 h accumulated beta-casein mRNA. When the specific inhibitor of protein kinase C, GF 109203 X, was added to the medium with the hormones, the accumulation of beta-casein mRNA was unaltered, although the protein kinase C activity was almost completely suppressed. This suggests that protein kinase C is not strictly necessary for prolactin to induce milk protein gene expression.

Increase of bradykinin-stimulated arachidonic acid release in a delta F508 cystic fibrosis epithelial cell line.

Modification of chloride conductance by bradykinin in epithelial cells has been attributed to an activation of protein kinase A resulting from adenylcyclase stimulation by arachidonic acid cyclooxygenase products. The results presented here compare tracheal epithelial cell lines from one control and two cystic fibrosis patients which were immortalized by transfection with the SV40 large T oncogene. The three cell lines presented the same arachidonic acid content, turnover and mobilisation under basal conditions.

[Cellular expression of CFTR in cystic fibrosis: defective cyclic AMP-dependent regulation of glycoconjugate secretion in cystic fibrosis fetal tracheal epithelial cells transfected by SV40 large T oncogene].

Epithelial tracheal cells isolated from two fetuses with cystic fibrosis (CF) and non-CF fetus (control) were transfected with a plasmid vector recombined with the large T oncogene of SV40. All transfected cells expressed SV40 antigen and exhibited an epithelial morphology (junctional complex, cytokeratins). CFT cells retained the mutations of the CF gene, one heterozygous for the S549N/N1303K substitutions (CFT-1 cells), the other homozygous for the deletion delta F508 (CFT-2 cells).

Oncogene-mediated propagation of tracheal epithelial cells from two cystic fibrosis fetuses with different mutations. Characterization of CFT-1 and CFT-2 cells in culture.

Primary tracheal epithelial cells obtained from two fetuses with cystic fibrosis (CF) were successfully transfected with a plasmid vector recombined with the large T oncogene of SV40. The resulting tracheal cells were propagated in culture for up to 25 passages and retained the mutations of the CF genes carried by the two fetuses, one heterozygous for the S549N and N1303K substitutions (CFT-1 cells), and the other homozygous for the most common deletion delta F508 (CFT-2 cells). The transfected cells: (a) expressed the SV40 large T oncogene, as determined by immunofluorescence and Northern blot analysis; (b) retained typical epithelial morphology, as assessed by the presence of microvilli, desmosomes, gap junctions, and cytokeratin expression; (c) were fully responsive to the cAMP-stimulating agents isoproterenol, forskolin and vasoactive intestinal peptide for cAMP production and PKA activation; (d) do not produce any tumour in the athymic nude mice; (e) were diploid and tetraploid with a normal chromosomal complement at early passages, and (f) exhibited the abnormal regulation of chloride conductance characteristic of CF.