Use of inhaled iloprost for the management of postoperative pulmonary hypertension in congenital heart surgery patients: review of a transition protocol.

Inhaled nitric oxide (iNO) is considered standard therapy for pediatric postcardiac surgical pulmonary hypertension (PH). Limited data suggest that inhaled iloprost (inIlo), an aerosolized prostacyclin, may be a feasible and more affordable therapeutic alternative. The goal of this study was to determine if significant hemodynamic change or adverse events would occur in postoperative congenital heart surgery (CHS) patients with PH after their transition from iNO to inIlo. This retrospective review investigated CHS patients with postoperative PH (mean pulmonary artery pressure [mPAP] >25 mmHg) between January 1, 2010 and December 31, 2011 who transitioned from iNO to inIlo. By protocol, CHS patients receiving stable doses of iNO were gradually transitioned to inIlo. After full transition, the patients received inIlo every 2 h, with a final dosing range of 1.25-5 µg/dose. Both PAP and systemic arterial pressure (SAP) were invasively measured during the transition period. Seven patients ages 10 days to 1.5 years completed the protocol. Measurements of mPAP (p = 0.27) and systolic PAP (p = 0.25) did not differ between iNO and inIlo therapy alone. No serious adverse events or complications (bleeding or thrombocytopenia) occurred. The ratio of systolic PAP to SAP decreased in all patients receiving inIlo alone (p = 0.03). Pulmonary hypertension in postoperative CHS patients can be managed successfully with inIlo, and the measured hemodynamics with this agent are similar to those observed with iNO. For the management of postoperative PH, inIlo may be a reasonable alternative, thus reducing the need for costly iNO. Larger confirmatory studies would more robustly facilitate its integration into standard care.

Is there an association between weight and dental caries among pediatric patients in an urban dental school? A correlation study.

Obesity in the young is a public health priority. The prevalence of overweight children in the United States has risen almost threefold in the last two decades. An association between weight and oral health has been suggested in adults, whereas evidence supporting this association in children is controversial at best. The aim of our study was to evaluate the association between weight and dental caries in a random prospective cohort of children at their initial visit at an urban dental school. One hundred and thirty-five children were recruited in a four-month period. The DS/ds index was used to assess caries, and BMI percentile was calculated based on age and gender-adjusted published scales. Correlation analyses, linear, and multivariate regression including age, gender, and BMI were calculated with a significance threshold of p>0.05. No correlation between dental decay in obese and non-obese children was detected (p=0.99). These findings support recent U.S. population-based literature that reports an inverse association between caries and weight in certain pediatric groups. Nevertheless, the impact of interventions to address the epidemic in the dental setting has not been investigated. As part of a health care team, dental students should be exposed to the changing demographics and sequelae of overweight in children.

Decreased expression of brain cAMP response element-binding protein gene following pentylenetetrazol seizure.

The present study investigated whether the expression of the cAMP response element-binding protein (CREB) in the rat brain is altered following an acute self-limited seizure induced by pentylenetetrazol (PTZ). Male rats were injected intraperitoneally with a single convulsive dose (45 mg/kg) of PTZ, and the matched controls were given saline. For immunohistochemistry, animals were perfused with 4% parafomaldehyde at 24 h following PTZ seizures, and CREB immunoreactivity was examined in rat brain. For real-time RT-PCR, animals were sacrificed at 2 and 24 h and 1 week following PTZ seizures. Tissues from different rat brain regions were micropunched and subjected to real-time RT-PCR using Taqman probe. The CREB immunoreactive profiles were significantly decreased in CA3 and dentate gyrus of hippocampal formation, sensory cerebral cortex and thalamus at 24 h after PTZ seizures. Consistent with changes in CREB immunoreactivity, levels of CREB mRNA were significantly decreased in the hippocampus, cerebral cortex, amygdala and thalamus at 24 h after PTZ seizures. No significant change was found for CREB mRNA expression in these regions at 2 h or 1 week following PTZ seizures. These results show that a brief seizure caused a decline in CREB expression up to 24 h later.

Brief seizure activity alters Ca2+/calmodulin dependent protein kinase II dephosphorylation and subcellular distribution in rat brain for several hours.

The effect of a brief pentylenetetrazol (PTZ) convulsive seizure on rat cerebral cortical Ca2+/calmodulin dependent protein kinase II (CaMKII) was investigated. By immunoblot, it was found that a single PTZ seizure, lasting less than a minute, caused translocation of CaMKII alpha-subunit (alpha-CaMKII) from the particulate to the soluble fraction for several hours, paralleled by a dramatic loss of alpha-CaMKII Thr286 phosphorylation. The reduced alpha-CaMKII Thr286 phosphorylation apparently resulted from enhanced phosphatase activity following PTZ seizure, especially in the particulate fraction. CaMKII translocation and phosphatase activation following a brief seizure episode can both contribute to long-lasting CaMKII regulation far outlasting the immediate effects of the seizure on neuronal function.

Prolonged changes in Ca2+/calmodulin-dependent protein kinase II after a brief pentylenetetrazol seizure; potential role in kindling.

This study evaluated the alteration of CaMKII autophosphorylation and distribution in rat brain following a single, brief pentylenetetrazol (PTZ) seizure and during PTZ kindling. Total CaMKII alpha subunit (alpha-CaMKII) and alpha-CaMKII phosphorylated at Thr(286) were detected by immunoblot. A large decrease in CaMKII Thr(286) phosphorylation, as well as CaMKII translocation from particulate to soluble fraction was observed in both cerebral cortex and hippocampus 0.5-4 h after the brief PTZ convulsion. These changes reverted to control values by 12 h. These long-lasting changes in CaMKII autophosphorylation and subcellular distribution after a brief seizure suggested that CaMKII could be involved in carrying forward the signal resulting from brief seizure activity, at least for a few hours, as would be required for kindling to occur. In PTZ kindled rats, convulsions produced changes in CaMKII Thr(286) phosphorylation and distribution in the same direction and of similar magnitude as after the acute convulsion, but lasting for a much longer time. In fact, reduced Thr(286) phosphorylation of alpha-CaMKII was observed up to 48 h, completely bridging the interval between PTZ injections. Similar, but intermediate changes were found in tissue from rats that were only partially kindled. These results implicate CaMKII as a molecular messenger in the acquisition of PTZ kindling.

Comparative healing of human cutaneous surgical incisions created by the PEAK PlasmaBlade, conventional electrosurgery, and a standard scalpel.

BACKGROUND: The authors investigated thermal injury depth, inflammation, and scarring in human abdominal skin by comparing the histology of incisions made with a standard "cold" scalpel blade, conventional electrosurgery, and the PEAK PlasmaBlade, a novel, low-thermal-injury electrosurgical instrument. METHODS: Approximately 6 and 3 weeks before abdominoplasty, full-thickness incisions were created in the abdominal pannus skin of 20 women, using a scalpel (scalpel), the PlasmaBlade, and a conventional electrosurgical instrument. Fresh (0-week) incisions were made immediately before surgery. After abdominoplasty, harvested incisions were analyzed for scar width, thermal injury depth, burst strength, and inflammatory response. RESULTS: Acute thermal injury depth was reduced 74 percent in PlasmaBlade incisions compared with conventional electrosurgical instrument (p < 0.001). Significant differences in inflammatory response were observed at 3 weeks, with mean CD3 response (T-lymphocytes) 40 percent (p = 0.01) and 21 percent (p ≈ 0.12) higher for the conventional electrosurgical instrument and PlasmaBlade, respectively, compared with the scalpel. CD68 response (monocytes/macrophages) was 52 percent (p = 0.05) and 16 percent (p ≈ 0.35) greater for a conventional electrosurgical instrument and the PlasmaBlade, respectively. PlasmaBlade incisions demonstrated 65 percent (p < 0.001) and 42 percent (p < 0.001) stronger burst strength than a conventional electrosurgical instrument, with equivalence to the scalpel at the 3- and 6-week time points, respectively. Scar width was equivalent for the PlasmaBlade and the scalpel at both time points, and 25 percent (p = 0.01) and 12 percent (p = 0.15) less than for electrosurgery, respectively. CONCLUSIONS: PlasmaBlade incisions demonstrated reduced thermal injury depth, inflammatory response, and scar width in healing skin compared with electrosurgery. These results suggest that the PlasmaBlade may provide clinically meaningful advantages over conventional electrosurgery during human cutaneous wound healing. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, II.(Figure is included in full-text article.).

Preventing heat-related illness among agricultural workers.

Hyperthermia from exertion and environmental conditions during agricultural work manifests itself by various symptoms and may lead to death. From 1992 through 2006, 68 workers employed in crop production and related services died from heat-related illness. The crop worker fatality rate averaged 4 heat-related deaths per one million workers per year-20 times higher than the 0.2 rate for US civilian workers overall. Many of the agricultural workers who died were foreign-born. Foreign-born workers tend to have limited English language skills and often are not acclimatized to exertion in hot weather when beginning seasonal jobs. Increased recognition of heat hazards to agricultural workers, in particular, has stimulated concern among employers, workers, and public policy makers. California and Washington have led the nation in adopting workplace safety standards designed to prevent heat-related illnesses. These state regulations include new specific requirements for employer provision of drinking water, shade for rest or other sufficient means to recover from heat, worker and supervisor training, and written heat safety plans. Agricultural employers face practical challenges in fulfilling the purpose and complying with these standards. By their very nature the standards impose generic requirements in a broad range of circumstances and may not be equally protective in all agricultural work settings. It is vital that employers and supervisors have a thorough knowledge of heat illness prevention to devise and implement safety measures that suit local conditions. Ongoing risk-based assessment of current heat conditions by employers is important to this safety effort. Workers need training to avoid heat illness and recognize the symptoms in themselves and coworkers. Innovative management practices are joining time-honored approaches to controlling heat stress and strain. Research targeted to answer questions about heat accumulation and dissipation during agricultural work and audience-sensitive education to promote understanding of basic physiology and recognition of hyperthermia symptoms can aid in heat illness prevention. This review was prepared for the Agricultural Safety and Health Council of America/ National Institute for Occupational Safety and Health conference, "Be Safe, Be Profitable: Protecting Workers in Agriculture," Dallas/Fort Worth, Texas, January 27-28, 2010.

Hepatic hydrothorax associated with vitamin a toxicity.

We report the first case of an adult presenting with respiratory symptoms caused by hepatic hydrothorax secondary to vitamin A intoxication. The patient was a 52-year-old woman who presented to the hospital with progressive dyspnea. Evaluation demonstrated mild elevation of her liver function tests, ascites, and a right pleural effusion. The patient consumed a variety of vitamins, including vitamin A. Her estimated vitamin A intake was at least 162,300,000 international units (IU) during 18 years. She dramatically escalated her dose the year before admission for a total acute dose of 98,550,000 IU, with a daily intake of 270,000 IU. The recommended daily allowance is 4,000 IU. A transjugular liver biopsy revealed histopathologic changes consistent with vitamin A toxicity: hypertrophy and hyperplasia of hepatic stellate cells, focal pericellular fibrosis, mild perivenular fibrosis, and minimal, predominantly microvesicular steatosis. Despite the absence of cirrhosis, pressure readings demonstrated portal hypertension. During her hospitalization, the patient's symptoms and biochemical profile improved. As the large and generally unregulated United States dietary supplement industry continues to grow, it is increasingly likely that individuals will present with the signs and symptoms of vitamin excess rather than vitamin deficiency. Physicians need to remain alert to the varied presentations and toxic manifestations of excessive vitamin use.