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Navigating through the bronchial tree and visualizing all bronchial segments is the initial step toward learning flexible bronchoscopy. A novel bronchial segment identification system based on artificial intelligence (AI) has been developed to help guide trainees toward more effective training.

Die ultraschallgestützte Feinnadelaspiration mit Zugang über den Ösophagus unter Verwendung eines endobronchialen Endoskops (EUS-B-FNA) wird von Pneumologen zunehmend für die Diagnose von Lungentumoren angewendet. Bislang liegen uns jedoch nur wenige Erfahrungen und Daten aus der Literatur über das Staging der Erkrankung vor. Wir stellen hier 2 Fälle einer EUS-B-gestützten Aspiration eines malignen Perikardergusses vor, die unter denselben Bedingungen wie eine Bronchoskopie und endobronchiale Ultraschalluntersuchung durchgeführt wurden. Es traten keine Komplikationen auf. Wir ziehen den Schluss, dass es sich bei der EUS-B-FNA vermutlich um ein sicheres und wirksames Verfahren zur Beurteilung eines Perikardergusses im Rahmen der Lungentumor-Diagnostik handelt. Somit könnte die EUS-B-FNA bei der diagnostischen Abklärung Zeit sparen, das Tumorstaging verbessern und eine transthorakale Perikardpunktion überflüssig machen.

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To assess the diagnostic accuracy and the safety of medical thoracoscopy (MT) performed with the semirigid thoracoscope.

We analysed single nucleotide polymorphisms in two transmembrane genes (TMEM98and TMEM132E) in panic disorder (PD) patients and control individuals from the Faroe Islands, Denmark and Germany. The genes encode single-pass membrane proteins and are located within chromosome 17q11.2–q12, a previously reported candidate region for PD. Three single nucleotide polymorphisms (rs887231, rs887230 and rs4795942) located upstream and within TMEM132Eshowed a nominal significant association with PD primarily in the Danish cohort. No nominal significant associations were observed between TMEM98and PD. Our data indicate that TMEM132Emight contribute moderately towards the risk of developing PD.

Mediastinoscopy is the gold standard for preoperative mediastinal staging of patients with suspected or proven lung cancer. Since the development of endoscopic ultrasound-guided biopsy via the trachea (EBUS-TBNA), this status has been challenged. The purpose of the study was to examine whether mediastinoscopy is necessary, when EBUS-TBNA is performed in a center with (1) a high level of expertise, (2) “bed side” microscopy by a pathologist, (3) general anesthesia, and (4) achievement of representative tissue from station 4R, 7 and 4L, that is, the same mediastinal stations that mediastinoscopy gives access to.

To compare internal fixation with no fixation of the medial malleolus after open reduction and internal fixation of the lateral malleolus and if needed, the posterior malleolus.

Purpose. To compare the thrombosis markers for thrombosis and fibrinolysis in patients undergoing hip versus knee arthroplasty.Methods. Seven women aged 38 to 61 years who underwent total hip arthroplasty (THA) and 7 women aged 57 to 67 years who underwent total knee arthroplasty (TKA) were studied. Thromboprophylaxis was given before and after surgery. In patients undergoing TKA, an automatic pneumatic tourniquet was used. Blood samples were drawn (1) before surgery (control value), (2) at wound closure (immediately before release of the tourniquet in TKA), and (3) 4 hours after surgery. Thrombosis markers (prothrombin fragment 1.2 [F1.2], plasmin/a2-antiplasmin complex [PAP], and D-dimer) of the 2 groups were compared.Results. The F1.2 level increased significantly at wound closure and remained elevated 4 hours after surgery in the THA group, whereas it was unchanged at wound closure but increased significantly 4 hours after surgery in the TKA group. The PAP level was constant peri- and post-operatively in the THA group, whereas it increased significantly 4 hours after surgery in the TKA group. The D-dimer level increased significantly at wound closure and 4 hours after surgery in the THA group, whereas it was unchanged at wound closure but increased significantly 4 hours after surgery in the TKA group.Conclusion. Systemic thrombin generation starts perioperatively in THA and after tourniquet deflation in TKA, indicating that wound blood must reach the systemic circulation to activate the relevant mediators.

Abstract: Venous thrombosis is common in elective hip surgery, and prophylactic treatment is used up to 12 hours before or after surgery. Recent clinical trials suggested that the timing of initiating prophylaxis significantly influenced the antithrombotic effectiveness. Furthermore, the timing of initiating antifibrinolytic treatment to reduce blood loss has been a question of debate. We studied the time course of coagulation and fibrinolysis at all phases during total hip arthroplasty. Specific markers of thrombosis (prothrombin fragment F1.2) and of fibrinolysis (plasminantiplasmin (PAP) and D-dimer) were examined in eight female and two male patients aged 16–62 years. There was a progressive increase in plasma concentrations of F1.2 during the operation. From the end of operation to 4 hours afterwards, there was no further increase in F1.2. Levels of D-dimer did not change until wound closure, when they began to increase up to 4 hours postoperatively, but there were no changes in PAP during the operation or during the 4-h postoperative period. Therefore, surgery for total hip arthroplasty activates thrombin generation during operation with fibrin degradation at a later stage. These observations harmonize with the notion that the interval between surgery and first administration of antithrombotic treatment is a critical variable.

The objective was to evaluate the influence of treatment with rhG‐CSF on allergic indexes. This was done by open trial of 5 days' treatment with rhG‐CSF (5 μg/kg/day s. c.). 10 patients (6 men), aged 28 to 54 years, with rhinoconjunctivitis due to grass pollen allergy, participated in the investigation. Main measures were blood count, basophil histamine release, skin test and conjunctival provocation test. Results: The treatment resulted in significant increases in numbers of neutrophils (590%), basophils (280%), eosinophils (250%) and lymphocytes (71%). Total blood histamine was increased, but basophil histamine releasability was decreased. Serum alkaline phosphatase increased 92% and serum lactate dehydrogenase increased 35% (both significant). There were no significant changes in the skin tests and the conjunctival provocation tests. Two months after the treatment all tests had returned to baseline levels. Five of the patients (50%) reported side effects, one withdrew. In conclusion treatment with rhG‐CSF increases the number of circulating blood cells other than neutrophils without causing changes in indexes of allergic reactivity.

Chlamydia pneumoniae(C.pn.) is claimed to be of importance for the development of bronchial asthma in previously healthy individuals. This is a new and speculative theory. Earlier studies have mainly focused on C.pn. and exacerbation of asthma. If this new theory were true, one would expect titres of C.pn.‐specific IgG to be higher or more common in patients compared with controls. It would also seem probable that pathobiological mechanisms as found in connection with other microorganisms could be demonstrated, i.e. presence of C.pn.‐specific IgE and the capability of C.pn. to induce or enhance histamine release from basophil leukocytes. We therefore examined C.pn.‐specific IgE, IgG and IgM in sera from 22 adults with bronchial asthma and 25 healthy controls. IgE was verified by passive sensitization of basophils from umbilical cord blood. The prevalence of IgE was approx. 69% and IgG approx. 23% in both groups. IgG‐titres were between 1:16 and 1:64 in both groups. No IgM was found. Further, C.pn. could neither induce nor enhance histamine release from basophil leukocytes of patients or controls. We conclude that patients with bronchial asthma and healthy controls do not differ in relation to 1) C.pn.‐specific IgE in sera, 2) the capability of C.pn. to induce or enhance histamine release from basophil leukocytes, since no such effect was found, or 3) previous C.pn. infection judged by the presence of specific IgG antibodies. Our results cannot support the theory that C.pn. is a cause of adult‐onset asthma.

Histamine release was examined in leukocyte suspensions from patients allergic to grass pollen, mite or cat dander or to bacteria (antigen). When the cells were challenged with specific antigen plus bacteria to which the person was not sensitized, these bacteria were found to potentiate the allergic histamine release. The potentiating effect by bacteria might be due to the bacterial cell wall components, peptidoglycan and teichoic acid, which mimic the effect of bacteria.

Haemophilus influenzae and its extracellular products (EP) did not release histamine in leukocyte suspensions from normal individuals. However, the EP were found to enhance basophil histamine release triggered by anti-IgE and by the calcium ionophore A23187. Experiments with EP indicate that it is the content of endotoxins which is responsible for the potentiating effect. Removal of endotoxin from the EP thus completely abolished the potentiating effect, whereas inactivation of its protease and proteins by heat-treatment or by proteinase K did not change the potentiation. A reinforcement of mediator release by the extracellular products ofH. influenzae might play a pathophysiological role in chronic obstructive pulmonary disease.

Histamine release caused by calcium ionophore A23187 and anti-IgE was examined in leukocyte suspensions from 8 healthy individuals.Staphylococcus aureus, lipopolysaccharide (LPS) fromSalmonella typhimurium and influenza A virus were found to enhance the histamine release but did not release histamineper se. The potentiation of mediator release depends on a non-transient signal since the potentiating effect was also obtained by preincubation of the cells with LPS followed by wash-out and stimulation of the cells with anti-IgE. The potentiation was abolished or reduced by galactose, N-acetyl-glucosamine, α-methyl-d-glucoside, α-methyl-d-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. These findings indicate that the enhancement of mediator release by bacteria, endotoxin, and virus depends on a sugar-mediated reaction.

Experimentsin vitro have shown that bacteria induce histamine release and potentiate IgE-mediated histamine release. In the present study, these events were examined in allergic patients by anin vivo model using nasal challenge. Nasal spray with 56 mgStaphylococcus aureus triggered histamine release in the nasal cavity in 4 of 13 patients, whereas no response was obtained by 28 and 112 mg bacterium. These findings indicate that bacteria containing peptidoglycan may release histaminein vivo. To avoid allergens, we used anti-IgE antiserum. In six patients nasal challenge with anti-IgE (112000 IU) caused an, increased histamine level in the nasal fluid which was not obtained by a control preparation without anti-IgE antibodies. The IgE-mediated mediator release was potentiated by the bacterium in only 2 of 22 patients.

Histamine release caused by anti-IgE was examined in leukocyte suspensions from 10 healthy individuals. Influenza A virus was found to enhance the histamine release but did not release histamineper se. When monoclonal antibodies directed against the viral neuraminidase were included in the samples, the potentiating effect of the virus was completely abolished. The same occurred using a neuraminidase inhibitor. However, monoclonal antibodies directed against the viral haemagglutinin also abolished the potentiation. A binding of virus to the basophil cell surface by haemagglutinin therefore seems to be necessary for the viral neuraminidase to cause potentiation of mediator release.

Histamine release from human basophil leukocytes was triggered byStaph. aureus or by complement activation caused by endotoxins isolated fromE. coli or Salmonella bacteria. Influenza A virus was found to enhance the mediator release and the effects was caused by synergism, since the virus itself did not release histamine. The potentiating effect of the virus was abolished by a potent neuraminidase inhibitor. Furthermore, a purified neuraminidase preparation obtained fromVibrio cholerae caused a similar potentiating effect, which was also abolished by the neuraminidase inhibitor. These findings indicate that the neuraminidase on the surface of influenza A virus is responsible for the potentiating effect of the virus on basophil histamine release.

Mediator release was examined from superficially lying cells in the airway epithelium obtained by bronchoalveolar lavage (BAL) in 13 non-atopic individuals. The BAL-cells were incubated (20 min, 37°C) withStaphylococcus (Staph.) aureus or with human influenza A virus.Staph. aureus was found to release histamine from cells from 7 of the 13 individuals and influenza A virus in 3 of 5 persons. Furthermore,Staph. aureus stimulated the BAL-cells to release leukotriene B4 in 7 of 11 subjects, whereas no release was found by influenza A virus in 7 examined persons. When cells from 4 persons were stimulated withStaph. aureus no release of leukotriene C4 was found. The mediator release caused by bacteria and virus might be of importance for the exacerbation of bronchial asthma in upper respiratory tract infections, since histamine is assumed to increase the epithelial permeability with entrance of allergens and other insulting particles, and leukotriene B4 facilitates airway inflammation.

A patient with bilateral pulmonary abscesses caused by Streptococcus pyogenes is described. This bacterium is an uncommon cause of pneumonia. Metastatic foci of infection, e.g. abscess formation, may follow bacteremic spread of S. pyogenes. However, such complications are rare and the occurrence of bilateral pulmonary abscesses has not been described earlier. In the present case the diagnosis was established by fiberoptic bronchoscopy with bronchial washing.

The effects of whole spores from moulds were examined concerning histamine release using leukocyte suspensions from normal (non-atopic) individuals and grass pollen-allergic patients. Spores fromChaetomium globosum, Mucor racemosus andAspergillus terreus caused no histamine release in concentrations up to 0.1 or 1 mg/ml, but they enhanced mediator release triggered by both IgE-dependent stimuli (grass-pollen allergen and anti-IgE antibody) and non-immunological stimuli (Staphylococcus aureus and calcium ionophore). Organic dust contains microfungi as well as bacteria and endotoxins. Earlier we have shown that bacteria release mediators from human lung cells and that bacteria and their endotoxins potentiate mediator release. It is now demonstrated that fungal spores also have potentiating ability. The content of all these microorganisms in dust may therefore be responsible for the symptoms observed after occupational exposure to organic dusts.

Preliminary studies in hematological patients have indicated that treatment with rhG-CSF reduces basophil releasabilityex vivo. We examined this phenomenon further, in allergic patients. Ten patients with grass pollen rhinoconjunctivitis were given rhG-CSF (5 μg/kg/day s.c.) for 5 days, and examined before and after treatment. Basophil counts increased from 5 to 19×109/l (P<0.01). Total blood histamine increased from 80 to 160 μg/l (P<0.01), corresponding to a decrease in average basophil histamine content from 1.5 to 0.81 pg/cell (P<0.01). Isolated mononuclear cells showed a significantly decreased histamine release (HR) when stimulated with A23187 and grass. Whole blood experiments showed a similar decreased HR to grass and anti-IgE (P<0.01). However, we found an increase in total blood histamine. We conclude that treatment with rhG-CSF (1) increases the number of circulating blood basophils, (2) reduces the average histamine content per basophil, and (3) reduces the basophil releasability. These findings could be due to the mobilization of immature basophils from the bone marrow.

Purpose:To examine the value of PET in diagnosis and staging of suspected lung cancer.