Frequency and erroneous usage of temporary medical exemptions and knowledge of immunization guidelines among some Miami-Dade County Florida providers

Objective

We assessed knowledge and practices regarding immunization guidelines and the Florida Certificate of Immunization (DH-680) based on FL-DOH and CDC recommendations, to identify the cause of the increasing number of erroneously issued temporary medical exemptions (TME) among selected health care providers in Miami-Dade County Florida.

Methodology

After reviewing immunization certificates from all public schools, a list of physicians who improperly issued 3 or more TMEs, defined as one given to a child who was up to date for their kindergarten and seventh grade requirements, was compiled. The DOH-Miami-Dade developed educational materials and questionnaires, and conducted face-to-face interviews and interventions during site visits to these providers (n = 134). Data was analyzed using SAS 9.2.

Results

Of the 104 questionnaires completed, 4 (3.85%) had correct answers to all 10 vaccine knowledge and practice related questions, while 10 (9.62%) had 7 or more incorrect answers. Frequently missed questions included: the required doses of varicella vaccine for seventh grade students entering the 2011–12 school year (86, 82.7%) and the proper scenario for issuing a TME (57, 54.8%).

Conclusions

In order to eliminate the improper use of TMEs, long-term efforts are needed to provide immunization-related educational materials and trainings to the medical community regarding vaccinations. These findings also suggest a need for enhanced explanation in multiple languages on the current Florida Immunization Certificate. Due to enhanced surveillance and education, the number of TMEs for kindergarten and seventh grade students was reduced by 12% and 4.9%, respectively, during the 2011 and 2012 school year.     

Systemic and ocular manifestations of a patient with mosaic ARID1A‐associated Coffin‐Siris syndrome and review of select mosaic conditions with ophthalmic manifestations

Mosaic genetic mutations may be somatic, germline, or “gonosomal” and have the potential to cause genetic syndromes, disorders, or malformations. Mutations can occur at any point in embryonic development and the timing determines the extent of distribution of the mutation throughout the body and different tissue types. The eye and visual pathway offer a unique opportunity to study somatic and gonosomal mosaic mutations as the eye consists of tissues derived from all three germ layers allowing disease pathology to be assessed with noninvasive imaging. In this review, we describe systemic and ocular manifestations in a child with mosaic Coffin‐Siris syndrome. The patient presented with a significant medical history of accommodative esotropia and hyperopia, macrocephaly, polydactyly, global developmental delay, hypotonia, ureteropelvic junction (UPJ) obstruction, and brain MRI abnormalities. The ophthalmic findings in this patient were nonspecific, however, they are consistent with ocular manifestations reported in other patients with Coffin‐Siris syndrome. We also review ophthalmic findings of select mosaic chromosomal and single‐gene disorders. Ophthalmic assessment alongside clinical genetic testing may play an important role in diagnosis of genetic syndromes as well as understanding disease pathology, particularly when mosaicism plays a role.     

Modified C-Reactive Protein Is Expressed by Stroke Neovessels and Is a Potent Activator of Angiogenesis In Vitro

Native C-reactive protein (nCRP) is a pentameric oligo-protein and an acute phase reactant whose serum expression is increased in patients with inflammatory disease. We have identified by immunohistochemistry, significant expression of a tissue-binding insoluble modified version or monomeric form of CRP (mCRP) associated with angiogenic microvessels in peri-infarcted regions of patients studied with acute ischaemic stroke. mCRP, but not nCRP was expressed in the cytoplasm and nucleus of damaged neurons. mCRP co-localized with CD105, a marker of angiogenesis in regions of revascularisation. In vitro investigations demonstrated that mCRP was preferentially expressed in human brain microvessel endothelial cells following oxygen-glucose deprivation and mCRP (but not column purified nCRP) associated with the endothelial cell surface, and was angiogenic to vascular endothelial cells, stimulating migration and tube formation in matrigel more strongly than fibroblast growth factor-2. The mechanism of signal transduction was not through the CD16 receptor. Western blotting showed that mCRP stimulated phosphorylation of the key down-stream mitogenic signalling protein ERK1/2. Pharmacological inhibition of ERK1/2 phosphorylation blocked the angiogenic effects of mCRP. We propose that mCRP may contribute to the neovascularization process and because of its abundant presence, be important in modulating angiogenesis in both acute stroke and later during neuro-recovery.     

Surgical site infections at the National Cancer Institute in Mexico: a case-control study

OBJECTIVES: To quantify the surgical infection rate and to identify risk factors associated with surgical site infection. METHODS: We conducted a case-control study of all surgical patients between January 1, 1993, and June 30, 1994. The frequency of surgical site infection per 100 surgeries was calculated. The odds ratio (OR) was estimated by using logistic regression analysis. SETTING: A 130-bed tertiary-care teaching hospital for adult patients with cancer. RESULTS: The study followed 3372 surgeries. Three hundred thirteen patients had a surgical site infection (rate per 100 surgeries: 9. 30). The risk factors associated with surgical site infection were diabetes mellitus (OR = 2.5, 95% confidence interval [CI] = 1.27-4. 91), obesity (OR = 1.76, 95% CI = 1.14-2.7), presence of surgical drains for >5 and <16 days (OR = 1.84, 95% CI = 1.02-3.31), and presence of surgical drains for >/=16 days (OR = 2.14, 95% CI = 1. 0-4.6). The bacteria most frequently isolated were Escherichia coli 38 (21.8% of the total of microorganisms found), Pseudomonas sp 22 (12.6%), Staphylococcus aureus 16 (9.2%), and coagulase-negative Staphylococcus 25 (13.6%). The coexistence of other nosocomial infections was greater among the cases (OR = 1.8, 95% CI = 1.1-3.1) than in the control group. CONCLUSIONS: The surgical site infection rate in our hospital is slightly higher than the rates reported for general hospitals. The risk factors associated with surgical site infection are similar to those previously reported. Diabetes mellitus, obesity, and prolonged presence of a surgical drain increased the risk of infection.     

Expression of protectin (CD59) in human melanoma and its functional role in cell- and complement-mediated cytotoxicity

Immunohistochemical and/or indirect immunofluorescence analysis with monoclonal antibody (MAb) H19 demonstrated the expression of protectin (CD59) in 54 surgically removed metastatic melanoma lesions and on 8 out of 12 melanoma cell lines. CD59 expression had a low degree of intra- and intertumor heterogeneity. SDS-PAGE analysis showed that the molecular weight of CD59 expressed on melanoma cells is about 20 kDa. Treatment of melanoma cells with 5 U/ml of phosphatidylinositol-specific phospholipase C completely abolished cell-surface expression of CD59. Interferon-γ and/or tumor necrosis factor-α or phorbol 12-myristate 13-acetate neither modulated the expression of CD59 by melanoma cells nor influenced the amounts of CD59-specific mRNA. F(ab')₂ fragments of anti-CD59 MAb YTH53.1 did not inhibit the lysis of melanoma cells by allogeneic natural killer (NK) cells or lymphokine-activated killer (LAK) cells. In contrast, the whole lg molecule of MAb H19 or YTH53. I significantly (p < 0.05) enhanced NK-cell-mediated lysis of melanoma cells, suggesting the induction of antibody-dependent cell-mediated cytotoxicity. Lastly, masking of CD59 by MAb YTH53. I or its F(ab')₂ fragments significantly (p < 0.05) enhanced, in a dose-dependent fashion, the lysis of anti-GD3-sensitized melanoma cells by homologous complement. These data demonstrate that CD59 expressed by human melanoma cells might regulate host-tumor interaction by protecting neoplastic cells from complement-mediated lysis. © 1995 Wiley-Liss, Inc.     

An aflatoxin-associated mutational hotspot at codon 249 in the p53 tumor suppressor gene occurs in hepatocellular carcinomas from Mexico

The p53 tumor suppressor gene is commonly mutated in human hepatocellularcarcinoma (HCC). The most frequent mutation in HCC in populationsexposed to a high dietary intake of aflatoxin Bl (AFB1) is anAGG^arg