Cognitive Deficits: Verbal and Semantic Fluency in People Living with HIV and AIDS.

BACKGROUND: Since the beginning of the HIV epidemic, the virus has taken millions of lives worldwide. The United Nations AIDS Fund's statistics reported that deaths caused by HIVrelated conditions and AIDS were about 39 million from the beginning of the epidemic to 2015. The united global efforts to fight the virus are considerably changing the indicators, such as mortality and morbidity, but the challenges remain. The total number of people living with HIV in Bulgaria as of 12th May, 2015, was 2,121. As of 30th November, 2016, the official data reported 2 460 people living with HIV. As of 13th February, 2017, 2 487 individuals were HIV-seropositive. Approximately 60% of people with HIV are prone to developing cognitive impairment due to the infection. OBJECTIVE: This study aimed to know the level of cognitive deficiency, in particular, the verbal and semantic fluency of people living with HIV and AIDS. METHODS: In this study, a comparative analysis was carried out. The Stewart test was used to compare the average independent samples. For clarity, the average values, the test statistics, and the estimated significance levels are presented in the tables. Additionally, a statistical mechanism of factor selection was used by the forward stepwise method. The Wilks' Lambda statistic reported values between 0 and 1, with values close to zero indicating good discrimination of the model. RESULTS: According to this research, the HIV positives participants generated fewer verbs than the ones from the control group. The data were partially confirmed by the present study. There were differences in terms of both adjectives and nouns among people living with HIV and AIDS. CONCLUSION: The study data proves that language deficits are detectable in neurocognitive testing of HIV. The overall hypothesis of the study has been confirmed. The language impairments are primarily qualitative and can be used as a marker for the initial and subsequent therapy assessment.

Duration of the patient interval in breast cancer and factors associated with longer delays in low-and middle-income countries: A systematic review with meta-analysis.

OBJECTIVE: Breast cancer survival is lower in low- and middle-income countries (LMICs) partially due to many women being diagnosed with late-stage disease. The patient interval refers to the time elapsed between the detection of symptoms and the first consultation with a healthcare provider and is considered one of the core indicators for early diagnosis and treatment. The goal of the current research was to conduct a meta-analysis of the duration of the patient interval in LMICs and investigate the socio-demographic and socio-cultural factors related to longer delays in presentation. METHODS: We conducted a systematic review with meta-analysis (pre-registered protocol CRD42020200752). We searched seven information sources (2009-2022) and included 50 articles reporting the duration of patient intervals for 18,014 breast cancer patients residing in LMICs. RESULTS: The longest patient intervals were reported in studies from the Middle East (3-4 months), followed by South-East Asia (2 months), Africa (1-2 months), Latin America (1 month), and Eastern Europe (1 month). Older age, not being married, lower socio-economic status, illiteracy, low knowledge about cancer, disregarding symptoms or not attributing them to cancer, fear, negative beliefs about cancer, and low social support were related to longer delays across most regions. Longer delays were also related to use of alternative medicine in the Middle East, South-East Asia, and Africa and distrust in the healthcare system in Eastern Europe. CONCLUSIONS: There is large variation in the duration of patient intervals across LMICs in different geographical regions. Patient intervals should be reduced and, for this purpose, it is important to explore their determinants taking into account the social, cultural, and economic context.

Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes.

The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and although rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism and insulin signalling is delayed in circadian mutant mice, and both Clock and Bmal1 (also called Arntl) mutants show impaired glucose tolerance, reduced insulin secretion and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival and synaptic vesicle assembly. Notably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective beta-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the beta-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger the onset of diabetes mellitus.

Obesity and metabolic syndrome in circadian Clock mutant mice.

The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.