Munkriley1007

Haplochromis pharyngalis and Haplochromis petronius, two endemic cichlids from the Lake Edward system (Uganda, Democratic Republic of the Congo), are very similar in general morphology but have been reported to differ in pharyngeal jaw morphology and distribution. This study analysed 51 morphometrics and various qualitative characteristics of 48 specimens from different localities. The morphological traits of both species strongly overlap, and differences in the pharyngeal jaw morphology correspond to a geographic morphocline. We conclude that all specimens belong to one valid species, H. pharyngalis, and consider H. petronius to be a synonym.

Pulmonary fibrosis (PF) is a chronic lung disease with complex pathogenesis and poor prognosis. Studies had demonstrated that long non-coding RNAs (lncRNAs) play an important role in the development of fibrosis. We explored the roles of NEAT1 in PF progression in this study.

PF tissues and TGF-β1-induced cells were analyzed for the function of NEAT1 in PF progression. qRT-PCR or Western blot was applied to detect NEAT1, miR‑9-5p or protein expressions. PF mice model assay was used to detect the effects of NEAT1 on PF in vivo. Luciferase reporter assay was applied to confirm target relationship between NEAT1 and miR‑9-5p. Correlation of NEAT1 and miR-9-5p was analyzed by Spearman's method.

We observed that NEAT1 was significantly upregulated while miR-9-5p was downregulated in PF tissues and TGF-β1-induced cells. A negative correlation was exhibited of NEAT1 and miR-9-5p expression in PF tissues. Protein level of p-Smad2 was increased in TGF-β1 induced cells. Furthermore, NEAT1 knockdown increased E-cadherin expression, while decreased N-cadherin, Vimentin, Collagen I, Collagen III and α-smooth muscle actin (α-SMA) expressions in TGF-β1-induced cells. Moreover, NEAT1 could directly target miR-9-5p to regulate the PF induced by TGF-β1. The miR-9-5p overexpression inhibited TGF-β1 and p-Smad2 expression, while NEAT1 overexpression attenuated this effect. In addition, NEAT1 inhibition enhanced E-cadherin expression, and reduced TGF-β1, p-Smad2, N-cadherin, Collagen I, Collagen III, α-SMA and Vimentin expression after BLM treatment.

Taken together, our findings showed that NEAT1 knockdown attenuated PF via the regulatory of miR-9-5p and TGF-β signaling to repress EMT and might provide new therapeutic targets for PF patients.

Taken together, our findings showed that NEAT1 knockdown attenuated PF via the regulatory of miR-9-5p and TGF-β signaling to repress EMT and might provide new therapeutic targets for PF patients.

COVID-19 immune syndrome is a multi-systemic disorder induced by the COVID-19 infection. Pathobiological transitions and clinical stages of the COVID-19 syndrome following the attack of SARS-CoV-2 on the human body have not been fully explored. The aim of this review is to outline the three critical prominent phase regarding the clinicogenomics course of the COVID-19 immune syndrome.

In the clinical setting, the COVID-19 process presents as "asymptomatic/pre-symptomatic phase", "respiratory phase with mild/moderate/severe symptoms" and "multi-systemic clinical syndrome with impaired/disproportionate and/or defective immunity". The corresponding three genomic phases include the "ACE2, ANPEP transcripts in the initial phase", "EGFR and IGF2R transcripts in the propagating phase" and the "immune system related critical gene involvements of the complicating phase".

The separation of the phases is important since the genomic features of each phase are different from each other and these different mechanisms elopment of the vaccines and/or specific drugs targeting the COVID-19 processes. ANPEP gene pathway may have a potential for the vaccine development. Regarding the specific disease treatments, MAS agonists, TXA127, Angiotensin (1-7) and soluble ACE2 could have therapeutic potential for the COVID-19 course. Moreover, future CRISPR technology can be utilized for the genomic editing and future management of the clinical course of the syndrome.

Lopinavir/ritonavir has been used for the treatment of Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) coronavirus infections. It has been suggested that, based on this experience, this drug should also be studied in SARS-CoV2 infection.

We performed a systematic review of the literature regarding the use of lopinavir/ritonavir for the treatment of these three infections. We systematically searched the PubMed database from inception to April 30th, 2020, to identify in-vitro and animal studies and any reports of human use of lopinavir/ritonavir for the treatment of SARS, MERS and COVID-19. Tariquidar We also searched the Clinicatrial.gov to identify ongoing trials.

Five in-vitro studies evaluated the effect of lopinavir/ritonavir in SARS. Three additional in-vitro studies reported the EC50 of the antiviral activity of lopinavir/ritonavir in MERS. We identified no in vitro studies evaluating the effect of lopinavir/ritonavir on the novel coronavirus. Two retrospective matched-cohort studies reported the use of lopinavir/ritonavir in combination with ribavirin for SARS patients. Three case reports and one retrospective study described the use of lopinavir/ritonavir in MERS. Twenty-two papers describe the use of lopinavir/ritonavir in adult patients with COVID-19.

The existing literature does not suffice for assessing whether Lopinavir/ritonavir has any benefit in SARS, MERS or COVID-19.

The existing literature does not suffice for assessing whether Lopinavir/ritonavir has any benefit in SARS, MERS or COVID-19.Some surface proteins of the newly identified severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can bind to the hemoglobin molecule of an erythrocyte, which leads to the destruction of the structure of the heme and the release of harmful iron ions to the bloodstream. The degradation of hemoglobin results in the impairment of oxygen-carrying capacity of the blood, and the accumulation of free iron enhances the production of reactive oxygen species. Both events can lead to the development of oxidative stress. In this case, oxidative damage to the lungs leads then to the injuries of all other tissues and organs. The use of uridine, which preserves the structure of pulmonary alveoli and the air-blood barrier of the lungs in the course of experimental severe hypoxia, and dihydroquercetin, an effective free radical scavenger, is promising for the treatment of COVID-19. These drugs can also be used for the recovery of the body after the severe disease.