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The current global crisis facing the world is the COVID-19 pandemic. Infection from the SARS-CoV-2 virus leads to serious health complications and even death. As it turns out, COVID-19 not only physically assails the health of those infected, but also leads to serious mental illness regardless of the presence of the disease. Social isolation, fear, concern for oneself and one's loved ones, all of this occurs when a pandemic overloads people. People exhibit numerous neurological disorders that have never happened to them before. Patients are diagnosed with frequent panic attacks, the result of which can be seen in their Quantitative Electroencephalogram results. This test may be one of the main diagnostic tools of the COVID-19 pandemic. From the results obtained, it is possible to compare and draw conclusions. This method of testing effectively allows EEG biofeedback training and observes its effect on brain activity. The feedback received in this way gives us the opportunity to properly tailor a protocol for the patient and their conditions. Numerous studies support the effectiveness of EEG biofeedback for panic attacks and other psychiatric disorders. The purpose of our study was to show the effectiveness of EEG biofeedback with a Quantitative Electroencephalogram of the brainwave pattern after having COVID-19 and what symptoms may result.

Although a depressive state is known to occur following the resolution of an acute psychotic episode, little research has investigated its etiology, course, prognosis and treatment. Very often the depression is mistaken for an extrapyramidal-like syndrome--the secondary effect of antipsychotic medication--as a sense of inevitability assails both the patient and therapist. Post-psychotic depression, far from being an obscure and undefined clinical picture, has the characteristics of a clear-cut syndrome. Nevertheless, it was only recently referred to as a distinct entity in psychiatric classification systems. As a result, different researchers used varying criteria for the definition of the phenomenon, and the data collected in the different studies are therefore difficult to compare. We present a critical review of the data published to date, with emphasis on the importance of early recognition and treatment of post-psychotic depression.

Since 2002 we have been testing and refining a methodology for ontology development that is now being used by multiple groups of researchers in different life science domains. Gary Merrill, in a recent paper in this journal, describes some of the reasons why this methodology has been found attractive by researchers in the biological and biomedical sciences. At the same time he assails the methodology on philosophical grounds, focusing specifically on our recommendation that ontologies developed for scientific purposes should be constructed in such a way that their terms are seen as referring to what we call universals or types in reality. As we show, Merrill's critique is of little relevance to the success of our realist project, since it not only reveals no actual errors in our work but also criticizes views on universals that we do not in fact hold. However, it nonetheless provides us with a valuable opportunity to clarify the realist methodology, and to show how some of its principles are being applied, especially within the framework of the OBO (Open Biomedical Ontologies) Foundry initiative.

In a randomized single-blind trial 44 patients of the Unfallchir. Klinik of Wiesbaden with purulent exudates and/or necrotic substrates in wounds had been enzymatically debrided with preparation A or B (22 patients each group). The solutions had been applied topically in a wet-to-dry technique. Dressings were changed two times a day, until the area became clean and showed granulations. In the group treated with preparation A excellent and good results could be obtained in 16 patients, in the comparison group in 14 patients. Three patients in the group treated with preparation A remained unchanged; in the comparison group five patients remained unchanged or showed deterioration. Due to inefficiency or to side effects treatment was interrupted in four patients of the preparation A-group and in eight patients of the comparison group. The more satisfactory results with preparation A can be interpreted in regard to the action of the enzymes: Fibrinolysin immediately attacks the fibrin of blood clots and fibrinous exudates. Desoxyribonuclease assails desoxyribonucleic acid structures. Streptokinase and streptodornase however are needing plasminogen for transforming it into the effective enzyme of plasmin, as they themselves are uneffective. And the amounts of plasminogen in the treated wounds possibly are not sufficient.

The Argentine hemorrhagic fever (AHF) is an infectious disease, endemo-epidemical, of viral etiology, produced by the Junin virus and limited to the Buenos Aires Province, South of Córdoba, East of La Pampa, and South of Santa Fe. It generally assails rural workers at harvest-time, especially during corn-harvest. The incubation period of the disease does not exceed 12 days. A feverish syndrome with asthenia, adynamia, myalgias, migraine, photophobia, epigastralgia etc., appear. The patient has a facial erythema, petechias on the skin, enantema on the palate, conjunctive micropolyadenopaty injection. The laboratory shows a low erytro, leukopenia with aneosinophilia, thrombopenia and a urine with albuminuria and virous cells. After the fourth day, hemorrhage and a neurological case appears. The laboratory tends to normalize and cast appears in the urine. The most striking neurological signs are the following: muscular hypotonia, proprioceptive hyporreflexia or arreflexia, marinesco reflex, shakings, difficulty to stand and walk, oscillations in consciousness level, and ocular disturbances. The cytochemical test of the C.L. Rachis in the usual ways of the AHF is within its normal characteristics; on the other hand there are modifications in the nervous cases: the total proteins are nearly always increased and the cells augmented with a great predominance of mononuclear cells. The electroencephalogrammes were always abnormal, varying from a brief disorganization up to a diffusive and permanent slowness. The half of which additionally presented paroxisms generalized by slow waves. The pathological anatomy over the central nervous system makes us think that the lesion would not primitively neuronal but that the action of the virus would be indirectly done through the capillar wall. This capillar lesion is produced by multiple focuses. The neuronal destruction with necrosis by microinfarcts is minimum. The symptoms and neurological signs are present in 10% of the clinical cases; the death-rate in the nervous clinical cases having reached 50% of them. The premature treatment allows the death-rate to diminish and the cases that survive have not many after effects.