Evaluating Disaster Damages and Operational Status of Health-Care Facilities During the Emergency Response Phase of Hurricane Maria in Puerto Rico.

On September 20, 2017, Hurricane Maria made landfall on Puerto Rico as a category 4 storm, resulting in serious widespread impact across the island, including communication and power outages, water systems impairment, and damage to life-saving infrastructure. In collaboration with the Puerto Rico Department of Health, the Public Health Branch (PHB), operating under the Department of Health and Human Services Incident Response Coordination Team, was tasked with completing assessments of health-care facilities in Puerto Rico to determine infrastructure capabilities and post-hurricane capacity. Additionally, in response to significant data entry and presentation needs, the PHB leadership worked with the Puerto Rico Planning Board to develop and test a new app-based infrastructure capacity assessment tool. Assessments of hospitals were initiated September 28, 2017, and completed November 10, 2017 (n = 64 hospitals, 97%). Assessments of health-care centers were initiated on October 7, 2017, with 186 health-care centers (87%) assessed through November 18, 2017. All hospitals had working communications; however, 9% (n = 17) of health-care centers reported no communication capabilities. For the health-care centers, 114 (61%) reported they were operational but had sustainment needs. In conclusion, health-care facility assessments indicated structural damage issues and operational capacity decreases, while health-care centers reported loss of communication capabilities post-Hurricane Maria.

Structural processes at slow-spreading ridges.

Slow-spreading (<35 millimeters per year) mid-ocean ridges are dominated by segmented, asymmetric, rifted depressions like continental rifts. Fast-spreading ridges display symmetric, elevated volcanic edifices that vary in shape and size along axis. Deep earthquakes, major normal faults, and exposures of lower crustal rocks are common only along slow-spreading ridges. These contrasting features suggest that mechanical deformation is far more important in crustal formation at slow-spreading ridges than at fast-spreading ridges. New seismic images suggest that the nature and scale of segmentation of slow-spreading ridges is integral to the deformational process and not to magmatic processes that may control segmentation on fast-spreading ridges.

Seismic structure of the southern East pacific rise.

Seismic data from the ultrafast-spreading (150 to 162 millimeters per year) southern East Pacific Rise show that the rise axis is underlain by a thin (less than 200 meters thick) extrusive volcanic layer (seismic layer 2A) that thickens rapidly off axis. Also beneath the rise axis is a narrow (less than 1 kilometer wide) melt sill that is in some places less than 1000 meters below the sea floor. The small dimensions of this molten body indicate that magma chamber size does not depend strongly on spreading rate as predicted by many ridge-crest thermal models. However, the shallow depth of this body is consistent with an inverse correlation between magma chamber depth and spreading rate. These observations indicate that the paradigm of ridge crest magma chambers as small, sill-like, midcrustal bodies is applicable to a wide range of intermediate- and fast-spreading ridges.

Seismic Images of Active Magma Systems Beneath the East Pacific Rise Between 17{degrees}05' and 17{degrees}35'S.

Seismic reflection data from the East Pacific Rise between 17 degrees 05' and 17 degrees 35'S image a magma lens that varies regularly in depth and width as ridge morphology changes, confirming the notion that axial morphology can be used to infer ridge magmatic state. However, at 17 degrees 26'S, where the ridge is locally shallow and broad, the magma lens is markedly shallower and wider than predicted from regional trends. In this area, submersible dives reveal recent volcanic eruptions. These observations indicate that it is where the width and depth of the magma chamber differ from regional trends, indicating an enhanced magmatic budget, that is diagnostic of current magmatism.

Kawasaki's disease, acrodynia, and mercury.

A superantigen or autoimmunity has been hypothesized to be the main cause of the Kawasaki's Disease but the etiology is unknown. Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role. Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day. The presented pathogenetic model may lead to new preventive- and therapeutic strategies for Kawasaki's disease.

Nociceptin inhibits cough in the guinea-pig by activation of ORL(1) receptors.

We studied the central and peripheral antitussive effect of ORL(1) receptor activation with nociceptin/orphanin FQ in conscious guinea-pigs. In guinea-pig cough studies, nociceptin/orphanin FQ (10, 30, and 90 microg) given directly into the CNS by an intracerebroventricular (i.c.v.) route inhibited cough elicited by capsaicin exposure by approximately 23, 29 and 52%, respectively. The antitussive activity of nociceptin/orphanin FQ (90 microg, i.c.v.) was blocked by the selective ORL(1) antagonist [Phe(1)gamma(CH(2)-NH)Gly(2)]nociceptin-(1-13)-NH(2) (180 microg, i.c.v.) and J113397 (10 mg kg(-1), i.p.) but not by the opioid antagonist, naltrexone (3 mg kg(-1), i.p.). Furthermore, intravenous (i.v.) nociceptin/orphanin FQ (1.0 and 3.0 mg kg(-1)) also inhibited cough approximately by 25 and 42%, respectively. These findings indicate that selective ORL(1) agonists display the potential to inhibit cough by both a central and peripheral mechanism, and potentially represent a novel therapeutic approach for the treatment of cough.

Comparative in vitro activity of piperacillin, piperacillin-sulbactam and piperacillin-tazobactam against nosocomial pathogens isolated from intensive care patients.

We investigated the antimicrobial activity of piperacillin-tazobactam versus piperacillin-sulbactam against common nosocomial pathogens (n = 565) isolated from intensive care patients. For Gram-positive bacteria, antimicrobial susceptibilities to the two piperacillin-beta-lactamase inhibitor combinations were almost identical. For Gram-negative bacteria, piperacillin-tazobactam exhibited greater activity against Escherichia coli and Proteus vulgaris than piperacillin-sulbactam. Both combinations, however, were equally effective against the other Enterobacteriaceae and Pseudomonas aeruginosa isolates. Piperacillin-sulbactam exhibited better antimicrobial activity against Acinetobacter baumannii. Our findings might prove important for the appropriate choice of antibiotic therapy with beta-lactam-beta-lactamase inhibitor combinations.

Central angiotensin-induced water intake and salt appetite in the pig.

Single intracranial injections of the peptide analogues of angiotensin and the enzyme renin induced drinking of water and 1.8% NaCl solution in prepubertal female pigs maintained ad libitum on a sodium-free diet with unrestricted access to both fluids. Over the dose range 10(-12)-10(-9) mol angiotensin (AI), angiotensin II (AII), angiotensin III (AIII), and renin substrate (RS), the volumes of water and salt solution ingested were dose-dependent. As in other vertebrates, AII was the most potent and rapidly acting dipsogen. However, unlike in the rat, dog and pigeon, AIII was highly effective in stimulating both water intake and salt appetite, whereas AI and RS were relatively weak. Pretreatment of intracranial sites with 10(-9) mol of the AII competitive antagonist, Sar1-Ala8-angiotensin, had no effect on the volume of water or 1.8% NaCl ingested after 10(-10) mol AIII, suggesting that in the pig AIII can exert its dipsogenic effects without acting on central AII receptors. Single microinjections of 1 and 10 mU of renin also elicited dose-dependent drinking of water and 1.8% NaCl, but compared with the peptide analogues of angiotensin the responses had a longer latency and duration and were more variable between individual animals.

Amalgam studies: disregarding basic principles of mercury toxicity.

Dental amalgam, which has been used for over 150 years in dental practice, consists of about 50% metallic mercury. Studies on animal and humans show that mercury is continuously released from dental amalgam and absorbed by several body tissues. It is widely accepted that the main source of mercury vapor is dental amalgam and it contributes substantially to mercury load in human body tissues. There is still a controversy about the consequences of this additional mercury exposure from amalgam to human health. Many studies were performed to evaluate possible adverse effects. In this comment, these studies were analyzed with regard to their methodical quality by considering the newest findings on mercury toxicity and metabolism. In sum, a number of studies are methodically flawed drawing inaccurate conclusions as to the safety of dental amalgam.

Pharmacological characterization of alpha 2-adrenoceptor-mediated responses in pig nasal mucosa.

1. Pig nasal mucosal strips were incubated with alpha-adrenoceptor antagonists followed by alpha2-adrenoceptor agonist concentration-response curves. 2. Contractions elicited by the alpha2-adrenoceptor agonists BHT-920 (pD2 = 6.16 +/- 0.07), UK 14,304 (pD2 = 6.89 +/- 0.13) and PGE-6201204 (pD2 = 7.12 +/- 0.21) were blocked by the alpha2-adrenoceptor antagonist yohimbine (0.1 microm). In contrast, the alpha1-adrenoceptor antagonist prazosin (0.03 microm) had no effect on the BHT-920-, UK 14,304- and PGE-6201204-induced contractions, but blocked the contractile response to the alpha(1)-adrenoceptor agonist phenylephrine (pD2 = 5.38 +/- 0.04) and the mixed alpha1- and alpha2-adrenoceptor agonist oxymetazoline (pD(2) = 6.30 +/- 0.22). 3. The alpha2-adrenoceptor antagonist yohimbine (0.01-0.1 microm, pA2 = 8.04), alpha2B/C-adrenoceptor antagonist ARC 239 (10 microm, pK(b) = 6.33 +/- 0.21), alpha2A/C-adrenoceptor antagonist WB 4101 (0.3 microm, pK(b) = 8.01 +/- 0.24), alpha2A-adrenoceptor antagonists BRL44408 (0.1 microm, pK(b) = 6.82 +/- 0.34) and RX 821002 (0.1 microm, pKb = 8.31 +/- 0.35), alpha2C-adrenoceptor antagonists spiroxatrine (1 microm, pKb = 7.32 +/- 0.32), rauwolscine (0.1 microm, pKb = 8.16 +/- 0.14) and HV 723 (0.3 microm, pKb = 7.68 +/- 0.14) inhibited BHT-920-induced contractions in pig nasal mucosa. 4. The present antagonist potencies showed correlations with binding affinity estimates (pKi) obtained for these antagonists at the human recombinant alpha2A- and alpha2C-adrenoceptors (r = 0.78 and 0.83, respectively) and with binding affinity estimates (pKd) obtained in pig native alpha2A- and alpha2C-monoreceptor assays (r = 0.85 and 0.78, respectively). No correlation was observed for the alpha2B-subtype. 5. In conclusion, contractile responses to phenylephrine, BHT-920, UK 14,304, PGE-6201204 and oxymetazoline indicate that alpha1- and alpha2-adrenoceptors are present and mediate vasoconstriction in pig nasal mucosa. Furthermore, correlation analysis comparing antagonist potency in pig nasal mucosa with affinities for human recombinant alpha2-adrenoceptors and native pig alpha2-adrenoceptors suggest that alpha2A- and alpha2C-adrenoceptor subtypes constrict pig nasal mucosa vasculature.

[Mercury and Alzheimer's disease]. / Quecksilber und Alzheimer-Erkrankung.

Higher mercury concentrations were found in brain regions and blood of some patients with Alzheimer's disease (AD). Low levels of inorganic mercury were able to cause AD- typical nerve cell deteriorations in vitro and in animal experiments. Other metals like zinc, aluminum, copper, cadmium, manganese, iron, and chrome are not able to elicit all of these deteriorations in low levels, yet they aggravate the toxic effects of mercury (Hg). Main human sources for mercury are fish consumption (Methyl-Hg) and dental amalgam (Hg vapour). Regular fish consumption reduces the risk of development of AD. Amalgam consists of approx. 50 % of elementary mercury which is constantly being vaporized and absorbed by the organism. Mercury levels in brain tissues are 2 - 10 fold higher in individuals with dental amalgam. Persons showing a genetically determined subgroup of transportation protein for fats (apolipoprotein E4) have an increased AD risk. Apoliprotein E (APO E) is found in high concentrations in the central nervous system. The increased AD risk through APO E4 might be caused by its reduced ability to bind heavy metals. Latest therapeutic approaches to the treatment of Alzheimer disease embrace pharmaceuticals which remove or bind metals from the brain. Preliminary success has been documented with chelation of synergistic toxic metals (Fe, Al, Zn, Cu) and therefore also Hg. The available data does not answer the question, whether mercury is a relevant risk factor in AD distinctively. In sum, the findings from epidemiological and demographical studies, the frequency of amalgam application in industrialized countries, clinical studies, experimental studies and the dental state of Alzheimer patients in comparison to controls suggest a decisive role for inorganic mercury in the etiology of Alzheimer's disease. Other factors currently discussed as causes (e. g. other metals, inflammations, dietetic factors, vitamin deficiency, oxidative distress, and metabolic impairments) may act as co-factors.

alpha2-adrenoceptor agonists as nasal decongestants.

Nasal congestion, one of the major disease features of rhinitis, is induced by the filling of venous sinusoids causing mucosal engorgement with resultant obstruction of nasal airflow. The only available drugs that directly target the underlying vascular features driving nasal obstruction are the sympathomimetic alpha-adrenoceptor agonists due to their vasoconstrictor action. However, standard decongestants are nonselective alpha-adrenoceptor agonists, which have the potential for side-effects liabilities such as hypertension, stroke, insomnia and nervousness. In the present study, the effects of nonsubtype selective alpha(2)-adrenoceptor agonists BHT-920 and PGE-6201204 were evaluated in several isolated nasal mucosa contractile bioassays including dog, pig and monkey, and in a real-time tissue contractility assay using isolated pig nasal explants for BHT-920. The decongestant activity of PGE-6201204 was evaluated in vivo in a cat model of experimental congestion. Our results showed that alpha(2)-adrenoceptor agonists (1) contract nasal mucosa of different species, (2) exert a preferential vasoconstrictor effect on the capacitance vessels (veins and sinusoids), and (3) elicit decongestion. In conclusion, a selective alpha(2)-adrenoceptor agonist causing constriction preferentially in the large venous sinusoids and veins of nasal mucosa and producing nasal decongestion is expected to show efficacy in the treatment of nasal congestion without the characteristic arterio-constrictor action of the standard nonselective sympathomimetic decongestants.

[Amalgam risk assessment with coverage of references up to 2005]. / Amalgam: Eine Risikobewertung unter Berücksichtigung der neuen Literatur bis 2005.

Amalgam, which has been in use in dentistry for 150 years, consists of 50 % elemental mercury and a mixture of silver, tin, copper and zinc. Minute amounts of mercury vapour are released continuously from amalgam. Amalgam contributes substantially to human mercury load. Mercury accumulates in some organs, particularly in the brain, where it can bind to protein more tightly than other heavy metals (e. g. lead, cadmium). Therefore, the elimination half time is assumed to be up to 1 - 18 years in the brain and bones. Mercury is assumed to be one of the most toxic non-radioactive elements. There are pointers to show that mercury vapour is more neurotoxic than methyl-mercury in fish. Review of recent literature suggests that mercury from dental amalgam may lead to nephrotoxicity, neurobehavioural changes, autoimmunity, oxidative stress, autism, skin and mucosa alterations or non-specific symptoms and complaints. The development of Alzheimer's disease or multiple sclerosis has also been linked to low-dose mercury exposure. There may be individual genetical or acquired susceptibilities for negative effects from dental amalgam. Mercury levels in the blood, urine or other biomarkers do not reflect the mercury load in critical organs. Some studies regarding dental amalgam reveal substantial methodical flaws. Removal of dental amalgam leads to permanent improvement of various chronic complaints in a relevant number of patients in various trials. Summing up, available data suggests that dental amalgam is an unsuitable material for medical, occupational and ecological reasons.

Evidence for fault weakness and fluid flow within an active low-angle normal fault.

Determining the composition and physical properties of shallow-dipping, active normal faults (dips < 35 degrees with respect to the horizontal) is important for understanding how such faults slip under low resolved shear stress and accommodate significant extension of the crust and lithosphere. Seismic reflection images and earthquake source parameters show that a magnitude 6.2 earthquake occurred at about 5 km depth on or close to a normal fault with a dip of 25-30 degrees located ahead of a propagating spreading centre in the Woodlark basin. Here we present results from a genetic algorithm inversion of seismic reflection data, which shows that the fault at 4-5 km depth contains a 33-m-thick layer with seismic velocities of about 4.3 km s(-1), which we interpret to be composed of serpentinite fault gouge. Isolated zones exhibit velocities as low as approximately 1.7 km s(-1) with high porosities, which we suggest are maintained by high fluid pressures. We propose that hydrothermal fluid flow, possibly driven by a deep magmatic heat source, and high extensional stresses ahead of the ridge tip have created conditions for fault weakness and strain localization on the low-angle normal fault.

The initiation of smooth pursuit eye movements and saccades in normal subjects and in "express-saccade makers".

A vast knowledge exists about saccadic reaction times (RT) and their bi- or multimodal distributions with very fast (express) and regular RT. Recently, there has been some evidence that the smooth pursuit system may show a similar RT behavior. Since moving targets usually evoke a combined pursuit/saccade response, we asked which processes influence the initiation of pursuit and saccadic eye movements. Furthermore, we investigated whether and how the pursuit and saccadic system interact during the initiation of eye movements to moving targets. We measured the RT of the initial smooth pursuit (iSP) response and of the first corrective saccade and compared the RT behavior of both. Furthermore we compared the behavior of the corrective saccades to moving targets to that of saccades to stationary targets, known from the literature. The stimulus consisted of a target that moved suddenly at constant velocity (ramp). In addition, prior to the movement, a temporal gap, a position step or a combination of both could occur (gap-ramp, step-ramp, gap-step-ramp, respectively). Differently from most previous studies, we chose step and ramp with the same direction to provoke competition between the pursuit and saccade system. For the first time we investigated pursuit initiation in "express-saccade makers" (ES makers), a subject group known to produce an abnormally high percentage of short-latency saccades in saccade tasks. We compared their results with subject groups who were either naive or trained with respect to saccade tasks. The iSP started at approximately 100 ms, which corresponds to express saccade latencies. These short iSP-RT occurred reflex-like and almost independent of the experimental task. A bimodal frequency distribution of RT with a second peak of longer iSP-RT occurred exclusively in the ramp paradigm. The RT of the first corrective saccades in a pursuit task were comparable with that in a saccade task and depended on the stimulus. The ability of ES makers to produce a high number of express saccades was transferred to corrective saccades in the pursuit task, but not to pursuit initiation. In summary, short-latency pursuit responses differ from express saccades with respect to their independence of experiment and subject group. Therefore, a simple analogy to express saccades cannot be drawn, although some mechanisms seem to act similarly on both the pursuit and the saccade system (such as disengagement of attention with the gap effect). Furthermore, we found evidence that the initial pursuit response and the first corrective saccade are processed independently of each other. The first corrective saccades to moving targets behave like saccades to stationary targets. Normal pursuit but abnormal saccade RT of ES makers can be explained by recent theories of superior colliculus (SC) function in terms of retinal error handling.