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You Name It: Interpersonal Impact Brands Diminishes Problems throughout Passionate Partners.
To evaluate resilience in severe mental disorders and correlate it with clinical measures and quality of life.

Resilience (Resilience Scale, RS) and quality of life (WHOQOL-BREF questionnaire) were prospectively evaluated in a sample of 384 hospitalized patients diagnosed with severe mental disorders (depression, bipolar disorder and schizophrenia). Clinical outcomes were measured using the Global Assessment of Functioning Scale (GAF), Clinical Global Impression (CGI), Cumulative Illness Rating Scale (CIRS), Hamilton Scale-Depression (HAM-D), Young Mania Rating Scale (YMRS), and Brief Psychiatric Rating Scale (BPRS).

Resilience measure showed a difference between the three clinical groups analyzed in the study, with lower scores in depressed patients than in bipolar disorder or schizophrenia patients. There was a trend toward a correlation between resilience and depressive symptoms (Hamilton Scale-Depression; P = 0.052; r
 = - 0.163). The scores in the resilience scale's personal competence domain presented a tendency of association with general psychiatric symptoms (Brief Psychiatric Rating Scale; P = 0.058; r = - 0.138). There was a significantly positive association between resilience and all domains of quality of life (r = 0.306-0.545; P < 0.05). Sociodemographic data like age, education, intelligence quotient, sex, and marital status were associated with resilience.

Depressive patients had low scores on the resilience scale compared to patients with other disorders. Resilience was positively associated with quality of life. Therefore, it deserves special attention, as it promotes more positive outcomes and improves patients' quality of life with severe mental disorders.
Depressive patients had low scores on the resilience scale compared to patients with other disorders. Resilience was positively associated with quality of life. Therefore, it deserves special attention, as it promotes more positive outcomes and improves patients' quality of life with severe mental disorders.Glutamate delta-1 receptor (GluD1) is a member of the ionotropic glutamate receptor family expressed at excitatory synapses and functions as a synaptogenic protein by interacting with presynaptic neurexin. We have previously shown that GluD1 plays a role in the maintenance of excitatory synapses in a region-specific manner. Loss of GluD1 leads to reduced excitatory neurotransmission in medium spiny neurons (MSNs) in the dorsal striatum, but not in the ventral striatum (both core and shell of the nucleus accumbens (NAc)). Here, we found that GluD1 loss leads to reduced inhibitory neurotransmission in MSNs of the NAc core as evidenced by a reduction in the miniature inhibitory postsynaptic current frequency and amplitude. Presynaptic effect of GluD1 loss was further supported by an increase in paired pulse ratio of evoked inhibitory responses indicating reduced release probability. Furthermore, analysis of GAD67 puncta indicated a reduction in the number of putative inhibitory terminals. The changes in mIPSC were independent of cannabinoid or dopamine signaling. A role of feed-forward inhibition was tested by selective ablation of GluD1 from PV neurons which produced modest reduction in mIPSCs. Behaviorally, local ablation of GluD1 from NAc led to hypolocomotion and affected anxiety- and depression-like behaviors. When GluD1 was ablated from the dorsal striatum, several behavioral phenotypes were altered in opposite manner compared to GluD1 ablation from NAc. Our findings demonstrate that GluD1 regulates inhibitory neurotransmission in the NAc by a combination of pre- and postsynaptic mechanisms which is critical for motor control and behaviors relevant to neuropsychiatric disorders.Owing to its lipophilic nature, cypermethrin makes entry into the brain through the blood-brain barrier and causes severe damage to the nigrostriatal dopaminergic neurons after prolonged exposure. Following substantial accrual in the brain, cypermethrin induces the abnormal expression and accumulation of α-synuclein. Besides, cytochrome P450 2E1 (CYP2E1) causes free radical generation leading to lipid peroxidation in toxicant-induced parkinsonism. Conversely, 4-hydroxynonenal (4-HNE), a byproduct of lipid peroxidation, is known to contribute to neuronal damage. The current investigation aimed to explicate the participation of endogenous redox-sensitive proteins in cypermethrin-induced cellular and animal models of parkinsonism. The qualitative and quantitative expressions of selected redox-sensitive proteins were evaluated employing the standard procedures. Cypermethrin reduced the expression of peroxiredoxin 3 (Prx3), thioredoxin 2 (Trx2), and protein deglycase-1 (DJ-1). Knocking down of Prx3, Trx2, or DJ-1 further reduced the level of expression in the cypermethrin-treated group. Reduction in the expression of Prx3, Trx2, or DJ-1 was found to be associated with overexpression of α-synuclein and 4-HNE modification of proteins. Besides, cypermethrin increased the expression of CYP2E1, which was not altered after Prx3 or Trx2 knockdown. Sulfopin However, knocking down the DJ-1 augmented the level of CYP2E1 both in the cypermethrin-treated group and its respective control. The outcomes of the study demonstrate that cypermethrin reduces the level of Prx3, Trx2, and DJ-1 proteins. While the reduction in the expression of selected redox-sensitive proteins leads to α-synuclein overexpression and 4-HNE modification of proteins, DJ-1 attenuation is also linked with increased CYP2E1 expression, which in turn could lead to oxidative stress-mediated neuronal damage.The optimal thromboprophylactic strategy for patients affected by Coronavirus disease 2019 (COVID-19) has been debated among experts. This study evaluated the safety and efficacy of a thromboprophylaxis algorithm. This was a retrospective, single-center study in critically ill patients admitted to the intensive care unit (University affiliated Hospital) for acute respiratory failure due to Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2). From March 16 to April 9, 2020, thromboprophylaxis was adjusted according to weight (control group, n = 19) and after this date, thromboprophylaxis depended on an algorithm based on thrombotic and hemorrhagic risk factors (protocol group, n = 13). With regard to safety (number of major bleeding events and blood transfusions), the groups were not significantly different. With regard to efficacy, the number of thrombotic events decreased from 37 to 0%, p = 0.025 after implementation of the algorithm. Also, peak fibrinogen dropped from 8.6 (7.2-9.3) to 6.5 (4.6-8.4) g/L, p = 0.
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