Background: As we enter the year 2000, it is worth looking at whether primary care practices are reaching the goals established in Healthy People 2000 for breast, cervical, colorectal, and prostatic cancer screening. The objectives of this study were (1) to determine the current rates of cancer screening; and (2) to determine which factors predict completion of a single screening test, of all tests for each cancer, and of all procedures for age and sex. Methods: Medical records of 200 eligible patients (100 men and 100 women) from each of 24 community-based primary care practices were abstracted for cancer-screening events. Results: We audited 5125 charts. A Papanicolaou smear was documented for 63.8% of women with an intact cervix within 3 years of the audit .. We found that 46.8% of women had documentation of ever having a discussion of breast self-examination. For breast cancer screening, 41.8% of the women had a clinical breast examination within 1 year, 48.2% aged 40 to 49 years had a mammogram within 2 years, and 38.5% aged 50 years and older had a mammogram within 1 year. Only 29% of women aged 40 to 49 years and 17% of women 50 years and older were current for all breast cancer-screening tests. Among patients 50 years and older, 33% of men and 38% of women had a digital rectal examination within 1 year, 26% of men and 28% of women had a fecal occult blood test within 1 year, and 22% of men and 16.8% of women had a Oexible sigmoidoscopy within 5 years. Of all men 28.7% had a prostate-specific antigen test within 1 year. Completion of all tests relevant for age and sex were documented for 8.6% of women aged 40 to 49 years, 3% of women 50 years and older, and 5% of men 50 years and older. The single most Significant predictor of documented cancer screening was a health maintenance visit. Conclusions: This sample of primary care clinicians has not reached the goals set in Healthy People 2000 for cancer screening. Interventions aimed at increasing the percentage of patients who schedule a health maintenance visit could serve to increase cancer screening and help us reach goals set for the year 2010.

Human T-cell leukemia virus type 1 (HTLV-1) infects target cells primarily through cell-to-cell routes. Here, we provide evidence that cellular protein M-Sec plays a critical role in this process. When purified and briefly cultured, CD4⁺ T cells of HTLV-1 carriers, but not of HTLV-1^- individuals, expressed M-Sec. The viral protein Tax was revealed to mediate M-Sec induction. Knockdown or pharmacological inhibition of M-Sec reduced viral infection in multiple co-culture conditions. Furthermore, M-Sec knockdown reduced the number of proviral copies in the tissues of a mouse model of HTLV-1 infection. Phenotypically, M-Sec knockdown or inhibition reduced not only plasma membrane protrusions and migratory activity of cells, but also large clusters of Gag, a viral structural protein required for the formation of viral particles. Taken together, these results suggest that M-Sec induced by Tax mediates an efficient cell-to-cell viral infection, which is likely due to enhanced membrane protrusions, cell migration, and the clustering of Gag.

The receptor of CSF-1 (CSF1R) encoding tyrosine kinase is essential for tissue macrophage development, and the therapeutic target for many tumors. However, it is not completely understood how CSF1R activation is regulated. Here, we identify the cellular protein TNF-α–induced protein 2 (TNFAIP2) as a unique regulator of CSF1R. CSF1R forms large aggregates in macrophages via unknown mechanisms. The inhibition or knockdown of TNFAIP2 reduced CSF1R aggregate formation and functional response of macrophages to CSF-1, which was consistent with reduced CSF1R activation after CSF-1 stimulation. When expressed in 293 cells, TNFAIP2 augmented CSF1R aggregate formation and CSF-1–induced CSF1R activation. CSF1R and TNFAIP2 bind the cellular phosphatidylinositol 4,5-bisphosphate (PIP2). The removal of the PIP2-binding motif of CSF1R or TNFAIP2, or the depletion of cellular PIP2 reduced CSF1R aggregate formation. Moreover, TNFAIP2 altered the cellular distribution of PIP2. Because CSF-1–induced dimerization of CSF1R is critical for its activation, our findings suggest that TNFAIP2 augments CSF1R aggregate formation via PIP2, which brings CSF1R monomers close to each other and enables the efficient dimerization and activation of CSF1R in response to CSF-1.

Respiratory infections have a significant impact on health worldwide. Viruses are major causes of acute respiratory infections among children. Limited information regarding its prevalence in Egypt is available. This study investigated prevalence of 10 respiratory viruses; Adenovirus, influenza A, B, respiratory syncytial virus (RSV), Parainfluenza virus (PIV)type 1-4, enterovirus, and human coronavirus OC43 (HCoV-OC43) among children in Alexandria, Egypt presenting with acute lower respiratory tract infections.The study was conducted on children <14 years of age selected from ElShatby Pediatric Hospital, Alexandria University, Egypt. One hundred children presenting during winter season with influenza-like illness were eligible for the study. Oropharyngeal swabs were collected and subjected to viral RNA and DNA extraction followed by polymerase chain reaction.Viral infections were detected in 44% of cases. Adenovirus was the most common, it was found in 19% of the patients. Prevalence of PIV (3 and 4) and enterovirus was 7% each. Prevalence of RSV and HCoV-OC43 was 5% and 3% respectively. Two percentage were Influenza A positive and 1% positive for influenza B. Mixed viral infection was observed in 7%.To the best of our knowledge, this is the first report of the isolation of HCoV-OC43 from respiratory infections in Alexandria, Egypt.

Since 1958 witnessed the detection of Monkeypox virus in monkeys, no human infection was encountered until 1970. Afterwards, zoonotic transmission was the rule near African rainforests, mainly in DRC. Most cases occurred in children who weren’t immunized against smallpox. Since 2003 and the first human infection in the USA, research was accelerated. Two clades were identified with different virulence, demographic distribution and transmissibility. The mean age of infection increased with waning smallpox vaccine immunity. Mild febrile prodrome can precede lymphadenopathy, which doesn’t occur in smallpox. Homogenous crops of lesions appear in stages until scabs fall and contagiosity ends. However, since May outbreak, cases started to appear in non-endemic areas, human transmission increased and was linked to close sexual contact especially in MSM community. Lesions were found mainly perioral, at genitals and perianal. Newer system for nomenclature was suggested in which there are 3 viral clades and the responsible clade for the outbreak is clade 3 (lineage B.1). About 50 mutations were detected compared with the strains isolated 4 years ago. Gene loss and APOBEC3 may be related to accelerated mutation rate which may accelerate human transmission. Previous mistakes in failure to allocate available vaccines to control the disease in previously endemic areas should be avoided and rapid ring vaccination of potential contacts and those at risk should be a priority. Case isolation, contact isolation or tracing for an incubation period, standard measures for airborne infections and safe sex should be implanted in the light of the current uncertainty.