UNASSIGNED: Waiting time is an important indicator of the quality of healthcare services in public and private health facilities. This study compared the waiting time at the general outpatient clinics (GOPC) in a private and public hospital in Rivers State.
UNASSIGNED: A comparative cross-sectional survey using a multi-stage sampling technique was used to select a total of 299 ambulatory adult patients attending the GOPC in a public and a private hospital. Time spent at service stations was obtained using a record sheet. SPSS version 23 was used to analyze data and p-values ≤0.05 were considered significant.
UNASSIGNED: Ambulatory patients on average spend 122.6 minutes for GOPC encounters in the public hospital and 44.9 minutes in the private hospital. This difference of 77.8 (95%CI: 66.6, 89.0) minutes was statistically significant (p = 0.001).
UNASSIGNED: The duration of time spent to access GOPC services underscores the need for system redesign to reduce the time spent and improve the satisfaction of patients attending the GOPC.

Globozoospermia is a type of teratozoospermia characterized by round morphology of the sperm head. Gopc-/- infertile globozoospermic murine model has failures during spermiogenesis, such as the incorrect biogenesis of the acrosome, disorganized acroplaxome and manchette, round nuclei and spiral flagella. In this study, Western blot, RT-PCR, immunohistochemistry and immunogold were done for the localization of the acrosome protein Zona Pellucida sperm-binding protein 3 receptor (ZP3R), also called sp56, in wild type and Gopc-/- mice testis. The ZP3R protein was located in the acrosome and pseudo-acrosome vesicles of wild type and Gopc-/- mice, respectively. Also, it is distributed through the cytoplasm of the haploid spermatids only. The incorrect spermiogenesis of Gopc-/- mice causes a deregulation in the expression of ZP3R in the globozoospermic spermatids. Our results suggest that although the lack of GOPC causes a failure during the transport of the pre-acrosomal vesicles, the acrosome protein ZP3R is localized in the acrosome and is distributed through the cytoplasm only during spermiogenesis. Furthermore, the failure in spermiogenesis does not impair the synthesis of ZP3R and its localization in the pre-acrosomal vesicles.

COVID 19 viral infection is a rapidly spreading droplets infection that has a global impact. Kaduna is one of the states in Nigeria with a high number of COVID-19 infected individuals. Some staff of Barau Dikko Teaching Hospital, Kaduna (BDTH) were infected with COVID-19 during the initial period of the pandemic. Most of the infected staff were from the General Out-Patient Clinic (GOPC), as it was the only Department with up to 11 staff infected during this initial period of the COVID-19 pandemic. This had led to the temporary closure of the Department. The aim of this paper is to characterize the GOPC Staff that tested positive to COVID-19 following previous contact with COVID-19 patients that were seen at the GOPC during the first wave of the pandemic. This is with the view to consider GOPC staff as high risk and frontline health workers for COVID 19. It was a retrospective study, and data were collected from the record of all the staff of the GOPC who were traced to have had contact with the COVID-19 positive patients and were also tested positive. Eleven (34%) out of the 32 staff were infected with COVID-19 at the GOPC. Only 1 staff was above 50 years. Most of them had mild symptoms and had side effects from the antiviral drugs. Staff of the GOPC are at risk of COVID-19 infection and should be considered frontline workers for COVID-19.
L’infection virale COVID 19 est une infection par gouttelettes à propagation rapide qui a un impact mondial. Kaduna est l’un des États du Nigéria comptant un nombre élevé de personnes infectées par le COVID-19. Certains membres du personnel de l’hôpital universitaire Barau Dikko de Kaduna (BDTH) ont été infectés par le COVID-19 au cours de la période initiale de la pandémie. La plupart du personnel infecté provenait de la Clinique générale de consultation externe (GOPC), car c’était le seul département avec jusqu’à 11 membres du personnel infectés au cours de cette période initiale de la pandémie de COVID-19. Cela a conduit à la fermeture temporaire du département. Le but de cet article est de caractériser le personnel du GOPC qui a été testé positif au COVID-19 à la suite de contacts antérieurs avec des patients COVID-19 qui ont été vus au GOPC pendant la première vague de la pandémie. Ceci dans le but de considérer le personnel du GOPC comme des agents de santé à haut risque et de première ligne pour COVID 19. Il s’agissait d’une étude rétrospective, et les données ont été collectées à partir du dossier de tout le personnel du GOPC qui a été identifié comme ayant été en contact avec le COVID -19 patients positifs et ont également été testés positifs. Onze (34%) des 32 employés ont été infectés par COVID-19 au GOPC. Seul 1 membre du personnel avait plus de 50 ans. La plupart d’entre eux présentaient des symptômes bénins et des effets secondaires des médicaments antiviraux. Le personnel du GOPC est à risque d’infection au COVID-19 et doit être considéré comme un travailleur de première ligne pour le COVID-19 Mots-clés: Covid 19, Personnels, GOPC.

Spitz tumors are genetically associated with activating HRAS point mutations or fusions of either ALK, ROS1, NTRK1, NTRK3, RET, MET, MERTK, LCK, BRAF, MAP3K8, or MAP3K3. All these driver gene alterations are mutually exclusive. We report two cases of agminated Spitz naevi with a GOPC-ROS1 fusion. Both cases occurred on the lower limb of young adults. Since adolescence, pigmented or pink-colored papules have been periodically arising in a limited area of skin. In one case, an ill-defined hyperpigmented macule known since childhood was present in the background. Morphologically, at least five lesions were analyzed from each patient. In one case, all were predominantly junctional pigmented Spitz naevi, and in the other case, all were compound unpigmented Spitz naevi. No atypical features were present. RNA-sequencing revealed a GOPC-ROS1 gene translocation in both cases. Split signals of ROS1 gene in fluorescence in situ hybridization were observed not only in the nests of spitzoid melanocytes but also in the bland basal melanocytes surrounding the proliferations. These findings suggest the presence of a GOPC-ROS1 mosaicism in melanocytes with further emergence of agminated Spitz naevi potentially triggered by other genetic alterations. This expands the spectrum of genetic anomalies described in agminated Spitz naevi and our understanding of the mechanisms involved in their emergence.

ROS1 is a transmembrane receptor tyrosine kinase proto-oncogene that has been shown to have rearrangements with several genes in glioblastoma and other neoplasms, including intrachromosomal fusion with GOPC due to microdeletions at 6q22.1. ROS1 fusion events are important findings in these tumors, as they are potentially targetable alterations with newer tyrosine kinase inhibitors; however, whether these tumors represent a distinct entity remains unknown. In this report, we identify 3 cases of unusual pediatric glioma with GOPC-ROS1 fusion. We reviewed the clinical history, radiologic and histologic features, performed methylation analysis, whole genome copy number profiling, and next generation sequencing analysis for the detection of oncogenic mutation and fusion events to fully characterize the genetic and epigenetic alterations present in these tumors. Two of 3 tumors showed pilocytic features with focal expression of synaptophysin staining and variable high-grade histologic features; the third tumor aligned best with glioblastoma and showed no evidence of neuronal differentiation. Copy number profiling revealed chromosome 6q22 microdeletions corresponding to the GOPC-ROS1 fusion in all 3 cases and methylation profiling showed that the tumors did not cluster together as a single entity or within known methylation classes by t-Distributed Stochastic Neighbor Embedding.

Hepatic angiosarcoma (HAS) is a rare and highly lethal malignancy with few effective systemic treatments. Relatively little is known about the genetic abnormalities that drive this disease. As a result, there has been minimal progress towards applying targeted therapies to the treatment of HAS. We describe the first reported case of a patient with HAS that harbored a fusion of ROS1 with GOPC/FIG. Similar to other rearrangements involving ROS1, the resulting fusion protein is believed to act as a major driver of carcinogenesis and may be subject to inhibition by drugs that target ROS1 such as crizotinib. We then queried the MSK-IMPACT clinical sequencing cohort and cBioportal datasets, demonstrating the previously unknown prevalence of ROS1-GOPC fusions in soft tissue sarcomas and hepatobiliary cancers. Amplification of these genes was also found to correlate with reduced overall survival. This is followed by a review of the role played by ROS1 rearrangements in cancer, as well as the evidence supporting the use of targeted therapies against the resulting fusion protein. We suggest that testing for ROS1 fusion and, if positive, treatment with a targeted therapy could be considered at the time of diagnosis for patients with angiosarcoma. This report also highlights the need for further investigation into the molecular pathophysiology of this deadly disease.

Pediatric high-grade glioma is a rare tumor characterized by high mortality. The authors report the first case of a high-grade glioma associated with a GOPC(FIG)-ROS1 fusion in a pediatric patient. The patient underwent gross-total resection at the age of 4 years, followed by adjuvant high-dose chemotherapy and autologous hematopoietic stem cell rescue. At 30 months after transplantation, she remains disease free.

Complement is undeniably quintessential for innate immunity by detecting and eliminating infectious microorganisms. Recent work, however, highlights an equally profound impact of complement on the induction and regulation of a wide range of immune cells. In particular, the complement regulator CD46 emerges as a key sensor of immune activation and a vital modulator of adaptive immunity. In this review, we summarize the current knowledge of CD46-mediated signalling events and their functional consequences on immune-competent cells with a specific focus on those in CD4(+) T cells. We will also discuss the promises and challenges that potential therapeutic modulation of CD46 may hold and pose.

Although crucial for their correct function, the mechanisms controlling surface expression of ion channels are poorly understood. In the case of the voltage-gated potassium channel KV10.1, this is determinant not only for its physiological function in brain, but also for its pathophysiology in tumors and possible use as a therapeutic target. The Golgi resident protein PIST binds several membrane proteins, thereby modulating their expression. Here we describe a PDZ domain-mediated interaction of KV10.1 and PIST, which enhances surface levels of KV10.1. The functional, but not the physical interaction of both proteins is dependent on the coiled-coil and PDZ domains of PIST; insertion of eight amino acids in the coiled-coil domain to render the neural form of PIST (nPIST) and the corresponding short isoform in an as-of-yet unknown form abolishes the effect. In addition, two new isoforms of PIST (sPIST and nsPIST) lacking nearly the complete PDZ domain were cloned and shown to be ubiquitously expressed. PIST and KV10.1 co-precipitate from native and expression systems. nPIST also showed interaction, but did not alter the functional expression of the channel. We could not document physical interaction between KV10.1 and sPIST, but it reduced KV10.1 functional expression in a dominant-negative manner. nsPIST showed weak physical interaction and no functional effect on KV10.1. We propose these isoforms to work as modulators of PIST function via regulating the binding on interaction partners.

The accumulation of amyloid-β-containing neuritic plaques and intracellular tau protein tangles are key histopathological hallmarks of Alzheimer\'s disease (AD). This type of pathology clearly indicates that the mechanisms of neuronal housekeeping and protein quality control are compromised in AD. There is mounting evidence that the autophagosome-lysosomal degradation is impaired, which could disturb the processing of APP and provoke AD pathology. Beclin 1 is a molecular platform assembling an interactome with stimulating and suppressive components which regulate the initiation of the autophagosome formation. Recent studies have indicated that the expression Beclin 1 is reduced in AD brain. Moreover, the deficiency of Beclin 1 in cultured neurons and transgenic mice provokes the deposition of amyloid-β peptides whereas its overexpression reduces the accumulation of amyloid-β. There are several potential mechanisms, which could inhibit the function of Beclin 1 interactome and thus impair autophagy and promote AD pathology. The mechanisms include (i) reduction of Beclin 1 expression or its increased proteolytic cleavage by caspases, (ii) sequestration of Beclin 1 to non-functional locations, such as tau tangles, (iii) formation of inhibitory complexes between Beclin 1 and antiapoptotic Bcl-2 proteins or inflammasomes, (iv) interaction of Beclin 1 with inhibitory neurovirulent proteins, e.g. herpex simplex ICP34.5, or (v) inhibition of the Beclin 1/Vps34 complex through the activation of CDK1 and CDK5. We will shortly introduce the function of Beclin 1 interactome in autophagy and phagocytosis, review the recent evidence indicating that Beclin 1 regulates autophagy and APP processing in AD, and finally examine the potential mechanisms through which Beclin 1 dysfunction could be involved in the pathogenesis of AD.