Chronic pain is often accompanied by anxiety and depression disorders. Amygdala nuclei play important roles in emotional responses, fear, depression, anxiety and pain modulation. The exact mechanism of how amygdala neurons are involved in pain and anxiety is not completely understood. The central nucleus of the amygdala (CeA) contains two major subpopulations of GABAergic neurons that express somatostatin (SOM+) or protein kinase Cδ (PKCδ+). In this study, we found about 70% of pERK-positive neurons colocalized with PKCδ+ neurons in the formalin-induced pain model in mice. Optogenetic activation of PKCδ+ neurons was sufficient to induce mechanical hyperalgesia without changing anxiety-like behavior in naïve mice.  https://www.selleckchem.com/products/icfsp1.html  Conversely, chemogenetic inhibition of PKCδ+ neurons significantly reduced the mechanical hyperalgesia in the pain model. In contrast, optogenetic inhibition of SOM+ neurons induced mechanical hyperalgesia in naïve mice and increased pERK-positive neurons mainly in PKCδ+ neurons. Optogenetic activaike behavior in naïve mice. Conversely, chemogenetic inhibition of PKCδ+ neurons significantly reduced the mechanical hyperalgesia in the pain model. In contrast, optogenetic inhibition of SOM+ neurons induced mechanical hyperalgesia in naïve mice and increased pERK-positive neurons mainly in PKCδ+ neurons. Optogenetic activation of SOM+ neurons slightly reduced the mechanical hyperalgesia in the pain model but did not change the mechanical sensitivity in naïve mice. Instead, it induced anxiety-like behavior. Our results suggest that the PKCδ+ and SOM+ neurons in CeA exert different functions in regulating pain- and anxiety-like behaviors in mice.
  Driving is a complex task that requires both the ability to rapidly identify potential hazards and respond appropriately to driving situations to avoid crashing. A great deal of research has sought to increase road safety by focusing on risky behaviours, very few of which have explored the effects of chronic pain (CP) on driving behaviour. This systematic review aimed to assess driving behaviour and motor vehicle crash risk in drivers with CP. Four databases (Embase, PubMed, Scopus, and PsycINFO) were searched using relevant search terms. From 8543 studies, 22 studies met the eligibility criteria for inclusion in this review. A driving behaviour framework, based on the Michon model of driving behaviour, is proposed to map the effect of CP on driving behaviour. Findings suggest that drivers with CP engage in risk-compensatory strategies that are positive from a precautionary perspective. However, there is considerable variability in the use of such strategies across different samples, suggesting that there a8543 studies, 22 studies met the eligibility criteria for inclusion in this review. A driving behaviour framework, based on the Michon model of driving behaviour, is proposed to map the effect of CP on driving behaviour. Findings suggest that drivers with CP engage in risk-compensatory strategies that are positive from a precautionary perspective. However, there is considerable variability in the use of such strategies across different samples, suggesting that there are significant barriers and facilitators involved in these decisions. Moreover, our findings provide some evidence that CP could increase crash risk and change driving behaviour. Evidence-based recommendations for practitioners and policymakers are proposed regarding the risks of driving in individuals experiencing CP. Future research into CP in driving could benefit from having a unified evidence-based approach to determine behaviour at all levels of the driving task.
  Sexually transmitted infection (STI) testing is not routinely offered in many countries and management is symptoms-based. Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG) are associated with increased risk of HIV transmission. We assess the feasibility and acceptability of integrating CT/NG testing into routine HIV care in Botswana, as well as the prevalence and correlates of CT/NG infections.
 
  A prospective study was conducted at an HIV clinic in Gaborone between February and October 2019. Eligibility criteria included ≥ 18 years, HIV-infected, and not treated for CT/NG in past month. Participants self-collected samples and responded to a questionnaire on sociodemographic and health characteristics. Samples were processed using the GeneXpert®. Patients were offered same-day results in person or by telephone. Those who tested positive were treated.
 
  Of 806 patients informed of the study, 526 (65%) expressed interest and 451 (60%) were enrolled. The median age was 48 years, and 66% were women. Alltive patients, younger patients and women.The management of multidrug-resistant (MDR) and extensively drug-resistant tuberculosis (XDR-TB) presents a main challenge and the drug options for treating these infections are very limited. Linezolid (LNZ) has recently been approved for the treatment of MDR and XDR-TB. But, there are narrow data on genotypic and phenotypic LNZ resistance in clinical isolates. So, we aimed to determine the prevalence of LNZ resistance and to identify the mutations associated with LNZ resistance among clinical MDR-TB isolates. The minimum inhibitory concentration (MIC) values of LNZ for 22 MDR-TB isolates were determined by broth microdilution method. All MDR-TB isolates were sequenced in the rrl and rplC genes conferring LNZ resistance. LNZ resistance was found in 3 (13.6%) of 22 MDR-TB isolates. The MICs of LNZ were 8 μg/mL for two isolates and 16 μg/mL for one isolate. The 421 (A/G) and 449 (T/A) mutations in rplC gene were detected in one of the LNZ-resistant isolates. There was no mutation in rrl gene. The results reveal that the prevalence of LNZ-resistant isolates is 13.6% among MDR-TB isolates and drug susceptibility testing (DST) against LNZ is useful in the management of complicated and drug-resistant cases. However, further studies could identify other possible genetic mechanism of resistance in TB.
  The Apolipoprotein 1 (APOL1) protein is a product of the human APOL1 gene located on chromosome 22q13.1 and performs functions including lipid transport and metabolism, programmed cell death, autophagy and innate immunity against intracellular pathogens. It is unique among its gene family in its possession of a signal peptide that confers on it the ability for export out of the cell and into the blood stream. The aim of this review is to explore the genetic epidemiology and biology of the APOL1 gene, describe its association with different renal and extra-renal disorders and highlight the timelines of the discoveries of the various associations.
 
  A literature search was carried out using combination of terms including "apolipoproteins", "apolipoprotein L", "APOL1", "genetics of APOL1", "Chronic Kidney Disease (CKD) and APOL1"," APOL1 and associated diseases" covering the period January 1990 to April 2020.
 
  High frequency of the APOL1 gene arose as a result of natural selection in East and West Africa, regions endemic for Trypanosoma brucei infection.