The coronavirus COVID-19 has recently started to spread rapidly in Malaysia. The number of total infected cases has increased to 3662 on 05 April 2020, leading to the country being placed under lockdown. As the main public concern is whether the current situation will continue for the next few months, this study aims to predict the epidemic peak using the Susceptible-Exposed-Infectious-Recovered (SEIR) model, with incorporation of the mortality cases. The infection rate was estimated using the Genetic Algorithm (GA), while the Adaptive Neuro-Fuzzy Inference System (ANFIS) model was used to provide short-time forecasting of the number of infected cases. The results show that the estimated infection rate is 0.228 ± 0.013, while the basic reproductive number is 2.28 ± 0.13. The epidemic peak of COVID-19 in Malaysia could be reached on 26 July 2020, with an uncertain period of 30 days (12 July-11 August). Possible interventions by the government to reduce the infection rate by 25% over two or three months would delay the epidemic peak by 30 and 46 days, respectively. The forecasting results using the ANFIS model show a low Normalized Root Mean Square Error (NRMSE) of 0.041; a low Mean Absolute Percentage Error (MAPE) of 2.45%; and a high coefficient of determination (R2) of 0.9964. The results also show that an intervention has a great effect on delaying the epidemic peak and a longer intervention period would reduce the epidemic size at the peak. The study provides important information for public health providers and the government to control the COVID-19 epidemic.
Leigh syndrome (LS) is one of the most puzzling mitochondrial disorders, which is also known as subacute necrotizing encephalopathy. It has an incidence of 1 in 77,000 live births worldwide with poor prognosis. Currently, there is a poor understanding of the underlying pathophysiological mechanisms of the disease without any available effective treatment. Hence, the inevitability for developing suitable animal and cellular models needed for the development of successful new therapeutic modalities. In this short report, we blocked FOXRED1 gene with small interfering RNA (siRNA) using C57bl/6 mice. Results showed neurobehavioral changes in the injected mice along with parallel degeneration in corpus striatum and sparing of the substantia nigra similar to what happen in Leigh syndrome cases. FOXRED1 blockage could serve as a new animal model for Leigh syndrome due to defective CI, which echoes damage to corpus striatum and affection of the central dopaminergic system in this disease. Further preclinical studies are required to validate this model.
Tauopathy comprises a group of disorders caused by abnormal aggregates of tau protein. In these disorders phosphorylated tau protein tends to accumulate inside neuronal cells (soma) instead of the normal axonal distribution of tau. A suggested therapeutic strategy for tauopathy is to induce autophagy to increase the ability to get rid of the unwanted tau aggregates. One of the key controllers of autophagy is mTOR. Blocking mTOR leads to stimulation of autophagy. Recently, unravelling molecular structure of mTOR showed that it is formed of two subunits: mTORC1/C2. So, blocking both subunits of mTOR seems more attractive as it will explore all abilities of mTOR molecule. In the present study, we report using pp242 which is a dual mTORC1/C2 blocker in cellular model of tauopathy using LUHMES cell line. Adding fenazaquin to LUHMES cells induced tauopathy in the form of increased phospho tau aggregates. Moreover, fenazaquin treated cells showed the characteristic somatic redistribution of tau. PP242 use in the present tauopathy model reversed the pathology significantly without observable cellular toxicity for the used dosage of 1000 nM. The present study suggests the possible use of pp242 as a dual mTOR blocker to treat tauopathy.
(1) Background. Dental implant placement in the anterior region requires extreme precision due to relatively high aesthetic demand. This narrative review aimed to analyse some of the available clinical studies of the socket-shield technique and determine its viability for dental implant survival/success and complication rates. (2) Methods. An electronic search for publications was performed using the Cochrane, PubMed-MEDLINE, Web of Science, and Google Scholar databases. All electronic searches included human clinical and animal studies and were performed by three independent examiners. (3) Results. A total of 1383 records were identified with the initial search strategies, but only 25 full texts + five abstracts clinical studies were kept after the recruitment criteria screening. The technical details, advantages, and limitations of the techniques were illustrated. (4) Conclusion. Within the limitations of the present review, it would be merely justified that immediate dental implant placement in conjunction with the socket-shield technique can be a promising strategy for dental implant therapy.
Tauopathy is a pathological hallmark of many neurodegenerative diseases. It is characterized by abnormal aggregates of pathological phosphotau and somatodendritic redistribution. One suggested strategy for treating tauopathy is to stimulate autophagy, hence, getting rid of these pathological protein aggregates. One key controller of autophagy is mTOR. Since stimulation of mTOR leads to inhibition of autophagy, inhibitors of mTOR will cause stimulation of autophagy process. In this report, tauopathy was induced in mice using annonacin. Blocking of mTOR was achieved through stereotaxic injection of siRNA against mTOR. The behavioral and immunohistochemical evaluation revealed the development of tauopathy model as proven by deterioration of behavioral performance in open field test and significant tau aggregates in annonacin-treated mice. Blocking of mTOR revealed significant clearance of tau aggregates in the injected side; however, tau expression was not affected by mTOR blockage.