Ports and their influence on local air pollution and public health: A global analysis.

Despite the skyrocketing growth in recent decades of environmental studies on ports and shipping, their local health impacts remain largely under-researched. This article tackles this gap in research by statistically analyzing data on global shipping flows across nearly 5000 ports in 35 OECD countries between 2001 and 2018. The different traffic types, from containers to bulk and passengers, are analyzed jointly with data on natural conditions, air pollution, socio-economic indicators, and public health. The principal results show that port regions pollute more than non-port regions on average, while health impacts vary according to the size and specialization of the port region. Three types of port regions are clearly differentiated: industrial, intermediate, and metropolitan port regions.

[Systemic inflammation in COPD and asthma: similarities and differences].

While recent studies have shown that patients with COPD and patients with asthma exhibit evidence of airway and systemic inflammation, markers of systemic inflammation have not been compared between the two diseases. To evaluate circulating inflammatory markers, blood was sampled from 111 patients with COPD, 75 control subjects and 46 asthmatic patients (some of whom were smokers). Measurements of WCC, serum levels of fibrinogen, high-sensitivity c-reactive protein (hs-CRP), interleukin-8 (IL-8), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), transforming growth factor (TGF)-beta1, tissue inhibitors of metalloproteinase (TIMP)-1, neutrophil elastase and alphal-antitrypsin (alpha1-AT) were done. Serum TNF-alpha, IL-6, and TIMP-1 concentrations were significantly higher in patients with stable COPD and patients with asthma than in control patients. Serum alpha1-AT levels were significantly higher in COPD patients than in asthmatic patients and control subjects and serum TGF-beta1 levels were higher in asthma patients than in COPD patients. Smoking status had no effect on markers in COPD and asthmatic patients. Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-beta1 and alpha1-AT may reflect differences between the diseases.

Systemic inflammation in chronic obstructive pulmonary disease and asthma: Similarities and differences.

BACKGROUND AND OBJECTIVE: While recent studies have shown that patients with COPD and patients with asthma exhibit evidence of airway and systemic inflammation, markers of systemic inflammation have not been compared between the two diseases. METHODS: To evaluate circulating inflammatory markers, blood was sampled from 111 patients with COPD, 75 control subjects and 46 asthmatic patients (some of whom were smokers). Measurements of WCC, serum levels of fibrinogen, high-sensitivity (hs)-CRP, IL-8, IL-6, tumour necrosis factor-alpha (TNF-alpha), transforming growth factor (TGF)-beta1, tissue inhibitors of metalloproteinase (TIMP)-1, neutrophil elastase and alpha1-antitrypsin (alpha1-AT) were performed. RESULTS: Serum TNF-alpha, IL-6 and TIMP-1 concentrations were significantly higher in patients with stable COPD and patients with asthma than in control patients. Serum alpha1-AT levels were significantly higher in COPD patients than in asthmatic patients and control subjects, and serum TGF-beta1 levels were higher in asthma patients than in COPD patients. Smoking status had no effect on markers in COPD and asthmatic patients. CONCLUSIONS: Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-beta1 and alpha1-AT may reflect differences between the diseases.

Complex effect of adenovirus early region proteins on innate immune system.

Adenoviruses (Ads) cause acute and persistent infections. The genome of Ads has five early transcription units that are the first viral genes expressed during an active infection. The Early Region 1A (E1A) gene of the adenovirus genome is crucial for adenovirus transformation of the host cell. Ads E1A block some aspects of the innate immune system to enable viruses to invade the host cell. E1A suppresses nitric oxide (NO) production through transcriptional control of the inducible NO synthase (iNOS) gene. This inhibition of NO production may enable the virus to persist in human tissue because NO is an antiviral effector of the innate immune system. E1A also blocks secretory leukoprotease inhibitor (SLPI) and elafin/skin-derived antileukoproteinase (SKALP) secretion by alveolar epithelial cells. Recent scientific evidence suggests that SLPI and elafin/SKALP have broad-spectrum antibiotic activities that include bactericidal and antifungal properties. The inhibition of inflammation by Ad early region proteins is complex, as certain early region proteins can promote as well as inhibit inflammation depending on the genetic context of the virus. E1A DNA and protein are frequently detected in the lungs of chronic obstructive pulmonary disease (COPD) patients and it is associated with an increased inflammatory response. E1A enhances intercellular adhesion molecule-1 and interleukin-8 mRNA expression with lipopolysaccharide stimulation. Understanding the roles of the Ad gene products in the induction and inhibition of innate inflammatory functions will help us to clarify the pathogenesis of the chronic respiratory illness including COPD.

Adenoviral E1A suppresses secretory leukoprotease inhibitor and elafin secretion in human alveolar epithelial cells and bronchial epithelial cells.

BACKGROUND: An imbalance between neutrophil protease and surrounding antiprotease levels has been shown to be important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Adenoviral E1A DNA and protein are frequently detected in the lungs of COPD patients. As secretory leukoprotease inhibitor (SLPI) and elafin/skin-derived antileukoproteinase (SKALP) are locally produced in the lung and inhibit neutrophil elastase activity, we hypothesized that adenoviral E1A might affect the production of these antiproteases. OBJECTIVES: To examine the effect of E1A on SLPI and elafin/SKALP secretion in A549 (alveolar epithelial) cells and primary human bronchial epithelial (HBE) cells. METHODS: SLPI and elafin/SKALP were quantitated from cell culture supernatants using an ELISA. SLPI mRNA expression was examined by Northern blotting, and SLPI promoter activity was measured using a reporter gene assay. RESULTS: E1A significantly suppressed SLPI and elafin/SKALP secretion by A549 cells upon interleukin (IL)-1beta stimulation. E1A also suppressed SLPI and elafin/SKALP secretion by HBE cells. SLPI mRNA expression in A549 cells was suppressed by E1A regardless of IL-1beta stimulation. IL-1beta-induced SLPI promoter activity was suppressed by E1A gene transfection into A549 cells. CONCLUSIONS: Our findings of adenoviral E1A-mediated suppression of SLPI and elafin/SKALP secretion suggest that E1A may be involved in the enhancement of alveolar damage and play a role in the COPD process.

Immunological rapid urease test using monoclonal antibody for Helicobacter pylori.

BACKGROUND AND AIM: The current diagnostic methods for detecting Helicobacter pylori infection include rapid urease test (RUT), urea breath test (UBT), histology, culture, and serum antibody detection. The present study evaluated the efficacy of a novel highly specific test, an immunological RUT (IRUT), that uses a monoclonal antibody against H. pylori urease. METHODS: The clinical evaluation of the IRUT was performed in 100 subjects. Each gastric mucus sample obtained during endoscopic examination was incubated for 15 min with a solid tip coated with monoclonal antibody for H. pylori urease, and then the tip was introduced into a pH-monitoring cell containing urea solution. The change in pH of the solution after the enzymatic reaction (delta pH) was measured. The performance of the IRUT was compared with culture, histology, RUT, and UBT. RESULTS: Of the 47 H. pylori-positive subjects, 43 were IRUT positive (sensitivity, 91.5%), and of the 53 H. pylori-negative subjects, 52 were negative (specificity, 98.1%). Compared with the usual diagnostic methods, IRUT had high sensitivity and specificity for the detection of H. pylori and was no less efficient. CONCLUSIONS: IRUT is a sensitive, specific and very rapid (within 20 min) method of detecting H. pylori infection.

Myoclonus and metabolic alkalosis from licorice in antacid.

A 90-year-old woman with hypertension developed metabolic alkalosis and myoclonus. Her medications included diltiazem hydrochloride, benidipine hydrochloride, kallidinogenase, procaterol hydrochloride, sennoside, dihydrocodeine phosphate, and KM powder antacid that contained 354 mg of licorice and 900 mg of sodium bicarbonate per 3.9 g of powder. Endocrinological studies showed slightly reduced plasma renin activity and normal plasma aldosterone concentration. A provisional diagnosis of licorice-induced metabolic alkalosis was established and the patient was successfully treated after correction of serum pH and cessation of the medications. Licorice-induced metabolic alkalosis must be considered in the differential diagnosis of myoclonus.

[A case of tuberculosis pleuritis developing contralateral pleural effusion during anti-tuberculosis chemotherapy, falling into chronic respiratory failure].

The patient was a 74 year-old male presenting right pleural effusion with mild fever. His temperature was 37.0 degrees C. Culture of a pleural biopsy specimen revealed Mycobacterium tuberculosis, although culture of sputum and pleural effusion were negative. Therapy was begun with 300 mg of isoniazid (INH) per day, 600 mg of rifampicin (RFP) per day, and 1200 mg of pyrazinamide (PZA) per day. His temperature improved temporarily. One week after beginning of the therapy he had a fever over 38.0 degrees C. On the 17th day after starting chemotherapy, a chest radiological examination showed left pleural effusion in which numerous lymphocytes were found but Mycobacterium tuberculosis was negative. We assumed that the left pleural effusion was due to a paradoxical reaction to the anti-tuberculosis chemotherapy. After 3 days' discontinuation, the same regimen was resumed with an addition of prednisolone, but bilateral pleural effusion remained and the case finally fell into chronic respiratory failure.

Endoscopic Dilatation Therapy Using a Small Caliber Balloon for Esophageal Achalasia.

Balloon dilation therapy under direct endoscopic vision was performed in three patients with esophageal achalasia. The Rigiflex through-the-scope balloon dilator, with a maximum diameter of 10-25 mm, was used for dilatation, with a 10-min inflation period. In all patients, dysphagia and regurgitation improved, body weight increased, and esophagography revealed a decrease in esophageal diameter. Our approach differs from standard methods used in Europe and America, in that the balloon has a smaller diameter and the duration of inflation is longer. Although our balloon dilator was small caliber, satisfactory results were obtained because of the longer duration of inflation. We conclude that balloon dilatation is the first choice for treatment of esophageal achalasia, and that to increase the safety of this technique, it is necessary to begin such treatment with a small caliber balloon under direct endoscopic vision.