While it is unlikely that Major Depressive Disorder (MDD) is a primary and pure 'inflammatory' disease, evidence is accumulating to show that depression and inflammation are closely connected and may fuel each other. Specifically: 1) patients with inflammatory diseases are more likely to show greater rates of MDD; 2) a large number (approximately one-third) of people with major depression show elevated peripheral inflammatory biomarkers, even in the absence of a medical illness, and 3) patients treated with cytokines (i.e. for chronic infective hepatitis) are at increased risk of developing depression. Indeed, inflammatory mediators have been found to alter glutamate and monoamine neurotransmission, glucocorticoid receptor resistance and hippocampal neurogenesis. Also, inflammation is able to alter brain signalling patterns, to affect cognition and to contribute to the production of a pattern of symptoms, clustering in a syndrome named 'sickness behaviour' and closely related to depression. Moreover, it is becoming increasingly clear that inflammation may increase the complexity and severity of illness presentation, as well as treatment response, at least among a subpopulation of individuals with MDD. Not surprisingly, a number of illnesses, including diabetes, metabolic syndrome, rheumatoid arthritis, asthma, multiple sclerosis, cardiovascular disease, chronic pain, and psoriasis, are characterized by increased risk for depression. This paper provides a review on the mechanisms by which inflammation may interact with neurotransmitters and neurocircuits to influence the risk for depression. The links between depression and inflammation are analyzed with special reference to the presence of increased inflammatory markers in patients with depression, to the relationship between inflammation and cognitive symptoms of depression, to the relationship between depression and medications that may promote or halt inflammation and to the relationship between depression and certain inflammatory diseases.

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Objective: Bipolar disorder is a heritable chronic mental disorder that causes psychosocial impairment through depressive/manic episodes. Familial transmission of bipolar disorder does not follow simple Mendelian patterns of inheritance. The aim of this study was to describe a large family with 12 members affected by bipolar disorder. Whole-exome sequencing was performed for eight members, three of whom were diagnosed with bipolar disorder, and another reported as “borderline.” Methods: Whole-exome sequencing data allowed us to select variants that the affected members had in common, including and excluding the “borderline” individual with moderate anxiety and obsessive-compulsive traits. Results: The results favored designating certain genes as predispositional to bipolar disorder: a heterozygous missense variant in CLN6 resulted in a “borderline” phenotype that, if combined with a heterozygous missense variant in ZNF92 , is responsible for the more severe bipolar disorder phenotype. Both rare missense changes are predicted to disrupt protein function. Conclusions: Loss of both alleles in CLN6 causes neuronal ceroid lipofuscinosis, a severe progressive childhood neurological disorder. Our results indicate that heterozygous CLN6 carriers, previously reported as healthy, may be susceptible to bipolar disorder later in life if associated with additional variants in ZNF92 .

Twenty-eight patients affected by advanced non-small cell lung cancer (NSCLC) were enrolled in a feasibility study evaluating toxicity and activity of carboplatin-vindesine combination chemotherapy, according to two different schedules. Fourteen patients were treated with carboplatin 350 mg/m2 monthly and vindesine 3 mg/m2 weekly for 5 doses, then every other week (schedule 1). The activity observed was promising with 3 partial remissions, but the toxicity was substantial, preventing full dose administration in 11 out of 14 patients. The subsequent 14 patients were treated with carboplatin 350 mg/m2 monthly and vindesine 3 mg/m2 on days 1 and 8 of each cycle. Activity was maintained with 4 partial remissions and toxicity was quite tolerable, allowing all patients to receive the planned treatment. The combination of carboplatin 350 mg/m2 on day 1 and vindesine 3 mg/m2 on days 1 and 8 seems active and well tolerated in advanced NSCLC patients and deserves further evaluation in a larger phase II study.

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A case of lung cancer presenting with cardiac tamponade is reported. Lasting control of the malignant effusion was achieved by means of intracavitary cisplatin following pericardiocentesis. The patient presented an objective response to subsequent systemic chemotherapy and died 10 months after the diagnosis because of disseminated cancer, without clinical or instrumental findings of pericardial effusion.