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BackgroundThe attention of international agencies and scientific community on bullying and work-related stress is increasing. This study describes the gender differences found in victims of bullying and work-related stress in an Italian case series and analyzes the critical issues in the diagnostic workup.MethodsBetween 2001 and 2009 we examined 345 outpatients (148 males, 197 females; mean age: 41 ± 10.49) for suspected psychopathological work-related problems. Diagnosis of bullying was established using international criteria (ICD-10 and DSM-IV).ResultsAfter interdisciplinary diagnostic evaluation (Occupational Medicine Unit, Psychology and Psychiatry Service), the diagnosis of bullying was formulated in 35 subjects, 12 males and 23 females (2 cases of Post-Traumatic Stress Disorder and 33 of Adjustment Disorder). Fifty-four (20 males, 34 females) suffered from work-related anxiety, while work-unrelated Adjustment Disorder and other psychiatric disorders were diagnosed in 7 and 112 subjects, respectively. Women between 34 and 45 years showed a high prevalence (65%) of "mobbing syndrome" or other work-related stress disorders.ConclusionsAt work, women are more subject to harassment (for personal aspects related to emotional and relational factors) than men. The knowledge of the phenomenon is an essential requisite to contrast bullying; prevention can be carried out only through effective information and training of workers and employers, who have the legal obligation to preserve the integrity of the mental and physical status of their employees during work.

Glutamate dehydrogenase (GDH) activity and its allosteric modulation by purine nucleotides were studied in platelet preparations from 4 patients with a nondominant form of adult-onset olivopontocerebellar atrophy (OPCA) and in affected and nonaffected members of two families with a dominant form of OPCA. A partial deficiency of GDH activity (40 to 50% of control values) was present in 3 patients with nondominant OPCA and in 2 patients, father and son, with a dominant form of OPCA. Platelet GDH from these patients and controls was regularly inactivated by 2 mM guanosine-5'-triphosphate (GTP) and simulated one- to twofold by 2 mM adenosine-5'-diphosphate (ADP). In the presence of 0.2% Triton X-100, the activating effect of ADP was enhanced four- to sixfold. The partial deficiency in maximum catalytic activity observed in these patients persisted under all conditions used for enzyme assay. In affected members, but not in one unaffected member of another family with a dominant type of OPCA, GDH activity was in the control range but was not activated by ADP in either the presence or absence of Triton. These results suggest that there may be at least two possible alterations of GDH in patients with OPCA: one which decreases the maximum catalytic activity and one which impairs the regulatory properties of the enzyme. Furthermore, this study suggests that platelet GDH determination in patients with OPCA may provide a simple and useful tool to classify these disorders and to understand the basic pathophysiological mechanisms involved.

Objectives: Vocal cord dysfunction (VCD) is an uncommon respiratory disease characterized by the paradoxical adduction of vocal cords during inspiration, that may mimic bronchial asthma. The pathogenesis of VCD has not been clearly defined but it is possible to recognize non-psychologic and psychologic causes. The majority of patients are female but, interestingly, a high incidence of VCD has been documented in health care workers. A misdiagnosis with asthma leads to hospitalisation, unnecessary use of systemic steroids with related adverse effects, and sometimes tracheostomy and intubation. In a subset of VCD patients, the disease can be attributed to occupational or environmental exposure to inhaled irritants. Materials and Methods: We report the case of a 45-year-old woman, working as a nurse, who complained of wheezing, cough, dyspnoea related to inhalation of irritating agents (isopropylic alcohol, formaldehyde, peracetic acid). She underwent chest radiography, pulmonary function assessment both in the presence and in the absence of symptoms, bronchial provocation with methacholine and bronchodilation test with salbutamol to recognize asthma's features, allergy evaluation by skin prick tests and patch tests and video-laryngoscopy. Results: VCD diagnosis was made on the basis of video-laryngoscopy, that visualized the paradoxical motion of the vocal cords during symptoms, in the absence of other pathologic processes. Conclusions: This case fulfils the proposed criteria for the diagnosis of irritant VCD (IVCD). This is the first report of VCD onset following exposure to several irritants: formaldehyde, glutaraldehyde, isopropylic alcohol, peracetic acid-hydrogen performaldehyde, glutaraldehyde, isopropylic alcohol, peracetic acid-hydrogen perisopropylic alcohol, peracetic acid-hydrogen perisopropylic alcohol, peracetic acid-hydrogen peroxide mixture. These substances are used as cleaning and antiseptic agents in healthcare settings and some ones can also be found in many indoor environments. A correct diagnosis is important both to give the appropriate treatment and for medical legal implications.

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Background and purpose: Nitric oxide (NO) and vasoactive intestinal peptide (VIP) are considered transmitters of nonadrenergic, non-cholinergic (NANC) relaxations in guinea-pig trachea, whereas the role of carbon monoxide (CO) is unknown. This study was designed to assess the participation of CO, and to investigate the localization of haem oxygenase-2 (HO-2), the CO-producing enzyme, in tracheal neurons. Experimental approach: NANC responses to electrical field stimulation (EFS) at 3 and 10 Hz were evaluated in epithelium-free whole tracheal segments as intraluminal pressure changes. Drugs used were: L-nitroarginine methyl ester (L-NAME, 100 mM) to inhibit NO synthase (NOS), a-chymotrypsin (2 U ml À1 ) to inactivate VIP, zinc protoporphyrin-IX (ZnPP-IX, 10 mM) to inhibit HO-2, and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 mM), a soluble guanylyl cyclase inhibitor. For immunohistochemistry, tissues were exposed to antibodies to PGP 9.5, a general neuronal marker, HO-2 and NOS, and processed with an indirect immunofluorescence method. Key results: a-Chymotrypsin did not affect NANC relaxations. ODQ inhibited NANC responses by about 60%, a value similar to that obtained by combining L-NAME and ZnPP-IX. The combination of ODQ, L-NAME and ZnPP-IX reduced the responses by 90%. Subpopulations of HO-2 positive neurons containing NOS were detected in tracheal sections. Conclusions and Implications: In the guinea-pig trachea, NANC inhibitory responses at 3 and 10 Hz use NO and CO as main transmitters. Their participation is revealed following inhibition of NOS, HO-2 and soluble guanylyl cyclase. The involvement of CO as a relaxing transmitter paves the way for novel therapeutic approaches in the treatment of airway obstruction.

The activity of 7 mitochondrial enzymes, fumarase, NAD-malate dehydrogenase (MDH), citrate synthase (CS), valine dehydrogenase (VDH), succinate dehydrogenase (SDH), glutamate dehydrogenase (GDH), pyruvate dehydrogenase complex (PDHC) has been measured in platelet preparations from patients affected by Friedreich's ataxia (FA), dominant and non-dominant olivopontocerebellar atrophy (DOPCA, NDOPCA) and normal individuals. Significant decreases of GDH (P less than 0.01), PDHC (P less than 0.01), VDH (P less than 0.05) and SDH (P less than 0.05) activities were observed in FA patients. Significant decreases of GDH (P less than 0.01), PDHC (P less than 0.01), VDH (P less than 0.05), SDH (P less than 0.05) and CS (P less than 0.05) activities were Observed in ND-OPCA patients, whereas in DOPCA patients only GDH activity was significantly (P less than 0.05) decreased. In 8 of 10 patients with FA and in all patients with NDOPCA the activity of one or more of 4 enzymes, i.e. GDH, VDH, SDH, PDHC, was lower than the lowest of control values. Four of 6 patients with DOPCA had GDH activity lower than the lowest of control values. These results indicate that abnormalities of mitochondrial metabolism is a constant element in hereditary ataxia and suggest that the alteration primary leading to the different types of ataxias should be related to mitochondrial oxidative metabolism, at least at a regulatory level.

Background: Persulphates can act both as irritants and sensitizers in inducing occupational asthma. A dysfunction of nervous control regulating the airway tone has been hypothesized as a mechanism underlying bronchoconstriction in asthma. Objectives: It was the aim of this study to investigate whether inhaled ammonium persulphate affects the non-adrenergic, non-cholinergic (NANC) inhibitory innervation, the cholinergic nerve-mediated contraction or the muscular response to the spasmogens, carbachol or histamine, in the guinea pig epithelium-free, isolated trachea. Methods: Male guinea pigs inhaled aerosols containing ammonium persulphate (10 mg/m³ for 30 min for 5 days during 3 weeks). Control animals inhaled saline aerosol. NANC relaxations to electrical field stimulation at 3 Hz were evaluated in whole tracheal segments as intraluminal pressure changes. Drugs inactivating peptide transmission, nitric oxide synthase, carbon monoxide production by haem oxygenase-2 and soluble guanylyl cyclase were used to assess the involvement of various inhibitory neurotransmitters. Carbachol and histamine cumulative concentration-response curves were obtained. Results: In both groups, nitric oxide and carbon monoxide participated to the same extent as inhibitory neurotransmitters. In exposed animals, the tracheal NANC relaxations were reduced to 45.9 ± 12.1% (p < 0.01). The cholinergic nerve-mediated contractions to electrical field stimulation and the muscular response to histamine were not modified by ammonium persulphate exposure. The muscular response to carbachol was unaffected up to 1 µM. Conversely, the response to the maximal concentration of carbachol (3 µM) was increased (p < 0.01). Conclusion: Ammonium persulphate inhalation at high concentrations impairs the nervous NANC inhibitory control in the guinea pig airways. This may represent a novel mechanism contributing to persulphate-induced asthma.