Influence of meteorological variables and air pollutants on measurements from automatic pollen sampling devices.

This study examines the influence of meteorological factors and air pollutants on the performance of automatic pollen monitoring devices, as part of the EUMETNET Autopollen COST ADOPT-intercomparison campaign held in Munich, Germany, during the 2021 pollen season. The campaign offered a unique opportunity to compare all automatic monitors available at the time, a Plair Rapid-E, a Hund-Wetzlar BAA500, an OPC Alphasense, a KH-3000 Yamatronics, three Swisens Polenos, a PollenSense APS, a FLIR IBAC2, a DMT WIBS-5, an Aerotape Sextant, to the average of four manual Hirst traps, under the same environmental conditions. The investigation aimed to elucidate how meteorological factors and air pollution impact particle capture and identification efficiency. The analysis showed coherent results for most devices regarding the correlation between environmental conditions and pollen concentrations. This reflects on one hand, a significant correlation between weather and airborne pollen concentration, and on the other hand the capability of devices to provide meaningful data under the conditions under which measurements were taken. However, correlation strength varied among devices, reflecting differences in design, algorithms, or sensors used. Additionally, it was observed that different algorithms applied to the same dataset resulted in different concentration outputs, highlighting the role of algorithm design in these systems (monitor + algorithm). Notably, no significant influence from air pollutants on the pollen concentrations was observed, suggesting that any potential difference in effect on the systems might require higher air pollution concentrations or more complex interactions. However, results from some monitors were affected to a minor degree by specific weather variables. Our findings suggest that the application of real-time devices in urban environments should focus on the associated algorithm that classifies pollen taxa. The impact of air pollution, although not to be excluded, is of secondary concern as long as the pollution levels are similar to a large European city like Munich.

Higher probability of compound flooding from precipitation and storm surge in Europe under anthropogenic climate change.

In low-lying coastal areas, the co-occurrence of high sea level and precipitation resulting in large runoff may cause compound flooding (CF). When the two hazards interact, the resulting impact can be worse than when they occur individually. Both storm surges and heavy precipitation, as well as their interplay, are likely to change in response to global warming. Despite the CF relevance, a comprehensive hazard assessment beyond individual locations is missing, and no studies have examined CF in the future. Analyzing co-occurring high sea level and heavy precipitation in Europe, we show that the Mediterranean coasts are experiencing the highest CF probability in the present. However, future climate projections show emerging high CF probability along parts of the northern European coast. In several European regions, CF should be considered as a potential hazard aggravating the risk caused by mean sea level rise in the future.

Transmission parameters of Mycobacterium avium subspecies paratuberculosis infections in a dairy herd going through a control program.

A Johne's disease control program, including stringent management practices and a test-and-cull program (whole-herd fecal-samples taken twice a year), was implemented on a medium-sized Pennsylvania dairy farm that was suffering losses from clinical Johne's disease. The data that emerged from the control program, combined with birthdates, culling dates, lactation information and pedigrees, yielded an extensive longitudinal dataset. The dataset was processed through SAS 9.1 for statistical analysis; herd-level disease dynamics and dam-to-daughter transmission parameters were calculated. After the implementation of the program in 1984, prevalence dropped dramatically from 60% to less than 20% in 1989. After an apparent prevalence peak (25%) in 1991 due to improved test sensitivity, prevalence maintained a plateau of 10% from 1996 to 2000. After the implementation of the program, 9.5% of the offspring from test-negative dams and 26.8% of the offspring from known-infected dams became infected with Mycobacterium avium subspecies paratuberculosis (Map) (chi(2)=14.7; p=0.0001). Calves born shortly following the calving of an infected dam and calves growing up with a future high shedder were more likely to be infected compared to calves without this risk profile. It was concluded that, after the implementation of the control program, the most important causes of infections of susceptible calves were their own dams or infected animals which had calved recently.

Complete video-assisted resection of trilobar mucormycosis.

A case of trilobar pulmonary mucormycosis in a diabetic patient with severe obstructive pulmonary disease, successfully treated with systemic antifungal therapy and complete video-assisted thoracic surgery (VATS) resection, is presented. The VATS approach permitted accurate diagnosis and definitive therapy using lung-sparing techniques in a minimally invasive manner.

Comparison of folding rates of homologous prokaryotic and eukaryotic proteins.

The rate of polypeptide chain elongation is up to one order of magnitude faster in prokaryotic cells than in eukaryotes. Here we report that the rates of in vitro refolding of orthologous prokaryotic and eukaryotic proteins correlate with their differential rates of biosynthesis. The mitochondrial and cytosolic aspartate aminotransferases of chicken and aspartate aminotransferase of Escherichia coli show pairwise sequence identities of 41-48% and nearly identical three-dimensional structures. Nevertheless, the prokaryotic enzyme refolded 6 times faster (at 25 degrees C) than the eukaryotic isoenzymes after denaturation in 6 m guanidine hydrochloride. Prokaryotic malate dehydrogenase and lactate dehydrogenase also renatured faster than their orthologous eukaryotic counterparts, suggesting that evolutionary pressure has adapted the rate of folding to the rate of elongation of polypeptide chains.

Video-assisted thoracic surgery resection of chest wall en bloc for lung carcinoma.

A video-assisted thoracic surgery approach to en bloc resection of lung cancer invading the chest wall is described. Using a minimally invasive surgical approach combined with neoadjuvant external beam radiotherapy, complete resection of an upper lobe carcinoma invading two rib segments was performed in a manner that permitted complete resection with curative intent and allowed for rapid recovery.

Video-assisted thoracic surgical non-rib spreading simultaneously stapled lobectomy: a more patient-friendly oncologic resection.

OBJECTIVE: To evaluate the outcomes from a new surgical technique for lobectomy. PATIENTS: Two hundred fifty consecutive patients with an average age of 67.3 years underwent simultaneously stapled lobectomy. METHODS: Video-assisted thoracic surgical non-rib spreading lobectomy (VNSSL) is a new technique that has been evolving for approximately 6.5 years. During 1990, we began using video-assisted thoracic surgery (VATS) for simple, benign diseases. Throughout 1991, VATS was applied to malignant problems, ie, mediastinal masses, staging of lymph nodes, malignant effusions, and coin lesions. As experience was acquired, more complex procedures were attempted, such as lobectomy. On September 9, 1991, our first VATS lobectomy, using anatomic hilar dissection and lymph node sampling, was performed for primary carcinoma of the lung. One year later, we performed our first VNSSL using simultaneous stapling. RESULTS: Currently, 400 VNSSLs have been performed. In this entire series, there have been no surgical mortality, bronchopleural fistulas, port implantations, or transfusions. Bronchial stumps have averaged 4 mm in length, and all have been microscopically negative for neoplasm. In order to evaluate long-term survival for primary carcinoma of the lung in patients with an adequate duration of follow-up, the first 250 consecutive VNSSLs have been reviewed. There were 120 male and 130 female patients ranging in age from 20 to 92 years old who had 62 right upper lobe, 20 right middle lobe, 58 right lower lobe, 63 left upper lobe, and 33 left lower lobe lobectomies, and 14 bilobectomies. The lesions consisted of 214 primary carcinomas, 8 metastatic lesions, and 28 benign problems. Seven to 18 lymph nodes could be resected during staging of the primary neoplasms. The tumors ranged in size from 1 to 9 cm, and operating times averaged 78.6 min. Hospitalization averaged 2.83 days. No patient was admitted to the ICU. Intensive monitoring or narcotic analgesia were not needed. No epidural or intercostal anesthesia was used. Complications were infrequent and minor. Most patients returned to preoperative levels of physical activity within 7 to 10 days. Overall survival at a mean of 34 months, when all stages of neoplasms were combined, is 83%. For stage I, overall survival is 92%. The cost of VNSSL is approximately 50% less than the traditional open thoracotomy. CONCLUSIONS: VNSSL is an oncologic technique that has been clinically rewarding and economically beneficial for patients with malignant lesions. Long-term survival for primary carcinoma currently exceeds reports being published for the traditional open thoracotomy. Scientific reasons for this extraordinary survival are emerging. Complications, surgical mortality, pain, and length of stay have all been reduced. Patient recovery, comfort, and satisfaction have been extraordinary.

[Crisis and decline of bath houses]. / Krise und Untergang der Badstube.

For centuries bath-houses and barber-surgeons formed such an integral part of public life that one is mystified by their vanishing from modern view with hardly any trace left. Previous authors have offered a variety of reasons for this disappearance: the bath-houses' notorious reputation, developing fuel-shortage, the "new" fashion of taking the waters and the outbreak of previously unknown contagious diseases are among those mentioned most frequently. While these factors may be valid reasons for a crisis afflicting the "hot-houses" they would hardly explain why fate overtook the barber-surgeons' entire trade. Judging from the sources available one cannot help but feel that the philosophers of the Enlightenment were largely responsible for such a dramatic change of society. Sceptical philosophy discarded the wisdom of the ancient medical authorities replacing traditional steam-bathing with "modern" cold-bathing. Society itself was subject to equally revolutionary changes: the local masters of the trade had to make room for surgeons educated at medical schools setting the stage for a new reality which has become "normal" to us.

Secondary structure of bacteriorhodopsin fragments. External sequence constraints specify the conformation of transmembrane helices.

The secondary structure of bacteriorhodopsin polypeptides comprising two (AB, CD, DE, FG), three (AC, CE, EG), four (AD, DG), or five (AE, CG) of the seven transmembrane segments has been analyzed by circular dichroism spectroscopy. A comparison of the alpha-helix content with that predicted from the high resolution structure of the native protein revealed that the N-terminal AB, AC, AD, and AE fragments and the C-terminal CG fragment are completely refolded in the presence of mixed phospholipid micelles. In contrast, the DG, EG, FG, CD, CE, and DE fragments did not form alpha-helices of the expected lengths at pH 6. Each of the latter fragments displayed, however, an increased helicity upon lowering the pH to 4. Fluorescence measurements with the CD and FG fragments suggest that this helix formation occurs within transmembrane segments C and G, respectively, and thus is likely to originate from the protonation of carboxyl residues that participate in proton translocation. The partial misfolding at neutral pH observed for the shorter fragments from the central and C-terminal part of bacteriorhodopsin indicates that the conformation of some transmembrane segments is specified by interactions with neighboring helices in the assembled structure. Moreover, the data demonstrate that two stable helices at the N terminus of a multihelical membrane protein are sufficient as a folding template to induce a native conformation to the following transmembrane domains.

Reversal of renal failure and paraplegia after thoracoabdominal aneurysm repair.

Repair of ruptured thoracoabdominal aortic aneurysms is complicated by high rates of perioperative paraplegia, renal insufficiency, and mortality. This report describes a patient with a ruptured thoracoabdominal aortic aneurysm in whom preoperative acute renal failure was reversed with hemodialysis, aortic replacement, and renal revascularization. Prompt cerebrospinal fluid drainage reversed delayed-onset postoperative paraplegia and led to immediate, complete neurologic recovery.

Cytochrome P-450 pathway in acetylcholine-induced canine coronary microvascular vasodilation in vivo.

In the canine coronary microcirculation, acetylcholine (ACh)-induced vasodilation of large (> or = 100 microns) epicardial arterioles (LgA), but not small (< 100 microns) epicardial arterioles (SmA), is blocked by nitric oxide (NO) synthase inhibitors in vivo. We hypothesized that the ACh-induced vasodilation of SmA is mediated by a cytochrome P-450 metabolite of arachidonic acid (AA). Epicardial coronary microvascular diameters in dogs were measured at baseline and after treatment with topically applied ACh (1, 10, and 100 microM), AA (1, 5, and 10 microM), or sodium nitroprusside (SNP; 10-100 microM). Coronary microvascular diameters were compared among control dogs (group OO); dogs pretreated with N omega-nitro-L-arginine (L-NNA; 70 microM topically) (group NO); dogs pretreated with L-NNA plus clotrimazole (Clo; 1.6 microM topically) or 17-octadecynoic acid (ODYA; 2 microM topically), cytochrome P-450 monooxygenase inhibitors (groups NC and NY, respectively); dogs pretreated with Clo alone (group OC); and dogs pretreated with L-NNA plus Clo with AA as the agonist (group AA). ACh-induced vasodilation of LgA was abolished by L-NNA alone, whereas in SmA, L-NNA was without effect. Clo alone did not inhibit ACh-induced dilation in either SmA or LgA. However, the combinations of L-NNA plus either Clo or ODYA abolished ACh- and AA-induced dilation of SmA (100 microM ACh: NC, 3 +/- 5%; NY, 8 +/- 2%; 10 microM AA: 6 +/- 3%) but did not affect responses to SNP. These results suggest that the ACh-induced vasodilation of SmA is mediated in part by cytochrome P-450 metabolites of AA and provide the first evidence that the cytochrome P-450 pathway contributes to the regulation of coronary resistance vessels in vivo.

Neuroprotection against oxidative stress by estrogens: structure-activity relationship.

Oxidative stress-induced neuronal cell death has been implicated in different neurological disorders and neurodegenerative diseases; one such ailment is Alzheimer's disease. Using the Alzheimer's disease-associated amyloid beta protein, glutamate, hydrogen peroxide, and buthionine sulfoximine, we investigated the neuroprotective potential of estrogen against oxidative stress-induced cell death. We show that 17-beta-estradiol, its nonestrogenic stereoisomer, 17-alpha-estradiol, and some estradiol derivatives can prevent intracellular peroxide accumulation and, ultimately, the degeneration of primary neurons, clonal hippocampal cells, and cells in organotypic hippocampal slices. The neuroprotective antioxidant activity of estrogens is dependent on the presence of the hydroxyl group in the C3 position on the A ring of the steroid molecule but is independent of an activation of estrogen receptors.

Glucocorticoids enhance oxidative stress-induced cell death in hippocampal neurons in vitro.

In patients with Alzheimer's disease, hippocampal cells are among the first neuronal cells of the brain to degenerate. Both rat primary hippocampal neurons and cells of the clonal mouse hippocampal cell line HT22 express endogenous functional glucocorticoid receptors (GRs), as shown by transient transfection of cells with a luciferase reporter plasmid containing GR-responsive elements. The influence of activated GRs on oxidative stress-induced neuronal cell death in vitro was investigated employing these hippocampal model systems. Two oxidative stressors were investigated, the free radical-inducing Alzheimer's disease-associated amyloid beta-protein, which is toxic to hippocampal neurons, and the excitatory amino acid glutamate, which induces oxidative cell death in HT22 cells via an increase in intracellular peroxides. Cellular viability was assessed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide test and trypan exclusion staining, followed by microscopical cell counting. Glucocorticoids strongly increased the vulnerability of the hippocampal cells to amyloid beta-protein and glutamate. This increase could be blocked by the specific GR antagonist RU486. Our data suggest that changes in hippocampal GR homeostasis and regulation may render hippocampal neurons more vulnerable to oxidative stress-induced neuronal degeneration.

Melatonin prevents oxidative stress-induced cell death in hippocampal cells.

The pineal hormone melatonin has been suggested to be a very effective antioxidant in the brain. Oxidative stress may play a role in certain neuropathological conditions and the hippocampus is an early target of neurodegeneration. Using cells of the clonal hippocampal cell line HT22 and organotypic hippocampal rat brain slice cultures, we investigated a possible protective role of melatonin against oxidative stress-induced hippocampal cell death. Glutamate alone induced oxidative apoptotic cell death in HT22 cells as detected with Hoechst staining and DNA fragmentation analysis. Preincubation with 1 mM melatonin protected HT22 cells against glutamate-induced cell death and protected organotypic hippocampal slices against H2O2-induced cell death. These findings suggest that this neurohormone may be useful in the prevention of neurodegenerative diseases.

Oxidative stress-resistant cells are protected against haloperidol toxicity.

The neuroleptic drug haloperidol is cytotoxic to cells of different origin in high doses. The mechanism of haloperidol toxicity may involve oxidative stress resulting in necrosis. In the present study, we show that rat pheochromocytoma PC12 cell clones which were selected for resistance to the toxicity of the oxidative stressor amyloid beta-protein (A beta), were also resistant to haloperidol toxicity. This data strongly supports the causative involvement of free radicals in haloperidol-induced cell death.

Differential effects of molecular chaperones on refolding of homologous proteins.

Three homologous aspartate aminotransferases with virtually identical spatial structures and pairwise amino acid sequence identities of > 40% differ markedly with respect to the yield of renaturation upon dilution from 6 M guanidine hydrochloride (mitochondrial << cytosolic < Escherichia coli). The enzymes also respond differently to molecular chaperones. GroEL/GroES, the Hsp60 homolog of E. coli, increased considerably the yield of renaturation of mitochondrial aspartate aminotransferase and to a lesser extent that of its cytosolic counterpart, but not that of the E. coli enzyme. DnaK/DnaJ/GrpE, the Hsp70 system of E. coli, also increased the yield of renaturation of mitochondrial aspartate aminotransferase. Apparently, specific features in the amino acid sequence or the folding pathway which are independent of the final secondary and tertiary structure determine the interactions of the folding proteins with the chaperone systems.

17-beta estradiol protects neurons from oxidative stress-induced cell death in vitro.

The potential antioxidant activity of 17-beta estradiol and other steroid hormones in neuronal cells was investigated by studying oxidative stress-induced cell death caused by the neurotoxins amyloid beta protein, hydrogen peroxide and glutamate in the clonal mouse hippocampal cell line HT22. Preincubation of the cells with 10(-5) M 17-beta estradiol prior to addition of the neurotoxins prevented oxidative stress-induced cell damage and ultimately cell death, as detected with cell viability (MTT) and cell lysis (trypan blue exclusion/cell counting; propidium iodide staining) assays. At the DNA level, 17-beta estradiol blocked the DNA degradation caused by glutamate. Other steroid hormones, such as progesterone, aldosterone, corticosterone and the steroid precursor cholesterol, did not protect the cells. The neuronal protection afforded by 17-beta estradiol was estrogen receptor-independent. These data demonstrate a potent neuroprotective activity of the antioxidant 17-beta estradiol, which may have implications for the prevention and treatment of Alzheimer's disease.

[Inadvertant suture fixation of a Swan-Ganz catheter to the pulmonary artery following heart surgery]. / Unbemerkte Nahtfixation eines Swan-Ganz-Katheters in der Arteria pulmonalis während Herzoperation.

We report a patient undergoing redo cardiac surgery for combined replacement of the aortic and mitral valves. During the course of the operation, a Swan-Ganz catheter - positioned preoperatively - was accidentally fixed to the wall of the pulmonary artery. As this did not interfere with cardiac output measurement or the pulmonary artery pressure wave form, the fixation was not noticed until an attempt was made to remove the catheter. Fluoroscopy revealed both the catheter's immobility and the location of the suture fixation. The patient required a sternotomy to remove the catheter. In order to avoid this complication, the indications for pulmonary artery catheters during cardiac surgery should be carefully considered. If catheters are inserted, their mobility should by all means be ensured before the chest is closed.

Cyclic strain increases endothelial nitric oxide synthase activity.

BACKGROUND: Endothelial nitric oxide synthase (eNOS) is an important enzyme that controls the production of a potent vascular smooth muscle relaxing factor, nitric oxide. However, the role of hemodynamic forces (blood pressure, cyclic strain, and shear stress) on the regulation of eNOS has not been fully elucidated. Recently, we showed that cyclic strain increases eNOS gene and protein in cultured bovine aortic endothelial cells (EC). Because an increase in gene transcription and protein synthesis may not necessarily translate into an increase in functional activity, the aim of this study was to determine the effects of cyclic strain on eNOS activity. METHODS: EC were seeded onto plates with flexible bottoms that can be deformed by vacuum and were then exposed to 60 cycles/minute of either 24% maximum strain (-20 kPa vacuum) or 10% maximum strain (-5 kPa vacuum) for 24 hours. eNOS activity was assessed, and nitric oxide production was determined (as nitrite) by the Greiss reaction. RESULTS: Twenty-four percent strain, at 60 cycles/min, but not 10% strain significantly increases eNOS activity compared with stationary controls. Both strain regimens increased nitric oxide (as nitrite) in culture media compared with stationary controls, although nitrite in media of EC exposed to high strain were significantly increased compared with the lower strain. CONCLUSIONS: Cyclic strain increases eNOS activity in cultured bovine aortic EC. These results may indicate the importance of hemodynamic forces in the regulation of eNOS in vivo.

Increased ambient pressure stimulates proliferation and morphologic changes in cultured endothelial cells.

Very little is known about the effects of pressure within the vascular system on EC phenotype. To study this, bovine aortic EC were seeded on rat type I collagen plates (2,000/cm2) and allowed to attach for 24 hours. The cells were exposed to either atmospheric, 40, 80, or 120 mm Hg pressure by placing them in a plexiglass pressure chamber loaded with 5% CO2/air and maintained at 37 degrees C inside an incubator. Chamber pressure was continuously monitored with an amplified voltage transducer connected to a digital monitor. EC were maintained in DMEM supplemented with 10% calf serum and substrates for up to 9 days. The results indicate that EC proliferation is influenced by their ambient pressure. EC subjected in vitro to pressures comparable to mean systemic blood pressures had a significant increase in cell number compared to EC exposed to atmospheric pressures. EC were elongated and appeared to align randomly. We hypothesize that the systemic pressure which the endothelium is exposed to in vivo may have a significant regulatory influence on the ability of the endothelium to proliferate which may affect the endothelial cell response to injury.