BACKGROUND:Hereditary factor occupies a certain position in suicidal behavior of depression. The researches in the past are focused on the hereditary effect on bipolar depression suicide.How do hereditary patterns and effects work in suicidal behavior in unipolar depression?OBJECTIVE: To probe into hereditary patterns and effects on suicidal behavior in unipolar depression.DESIGN:Retrospective investigation.SETTING:A municipal psychiatric hygienic centerPARTICIPANTS:Unipolar depression group included 115 outpatients and inpatients diagnosed in Wuxi Psychiatric Hygienic Center from June 1st 1983 to May 31st 2002.The diagnosis tallied with Standards on Depression Onset in Categories and Diagnostic Standards on Psychiatric Disturbance in China of 3rd Edition and with Standards on Severe Depression Onset in Manual of Diagnosis and Statistics of Psychiatric Disturbance in America of 4th Edition.The attack frequency of all the cases ≥ 3 times or the cases had been relieved ≥8 years after a couple of attacks.METHODS:The patients who tallied with the standards on unipolar depression received the investigation in every family tree under the instruction of 2 physicians-in-charge and more than 2 physicians and filled up the self-made investigation form of psychiatric family tree,including mainly the data of social demography of patients and their first grade relatives,characters of disease onset,frequency of attack,history of treatment and suicide. After re-diagnosed by 2 physicians-incharge and more than 2 physicians and checked by one physician-incharge,the cases were collected in patient group. The interview was carried on for the patients with suicidal behavior among all of the survived patients (107 cases) and first grade relatives (14 cases).The interview (337 cases) and investigation with letter (380 cases) were carried on for the first grade relatives without suicidal behavior. The investigation forms of 13 dead cases (8 cases of patients, 5 cases of first-grade relatives) were provided and filled-up by one or two first grade relatives. Two researchers interviewed the cases in the control,inquired the first grade relatives and filled up the investigation form of family tree.Single factor analysis was used for all the data and Falconer pattern of polygenetic threshold-value theory was used to estimate hereditary rate and standard error in suicidal behavior.Separation analysis in medical hereditary mathematic method and polygenetic threshold-value theory were applied to discuss the hereditary patterns.MAIN OUTCOME MEASURES:Hereditary effects and patterns of suicidal behavior in unipolar depressed patients.RESULTS:Suicidal risk of unipolar depressed patients(51.30%,59/115)was higher than their first grade relatives (2.58%,19/736) (x2=283.16,P ＜ 0.01).Suicidal risk of the first grade relatives (2.58%,19/736) of unipolar depressed patients was higher than the control (0.12%,3/2469)(x2=50.36,P ＜ 0.01).Suicidal risk of the first grade relatives of the patients with suicidal behavior (3.8%,14/372) was higher than that of the first grade relatives of the patients without suicidal behavior (1.4%,5/363)(x2=4.14,P＜ 0.05).The weighted average hereditary rate and standard error was (70.16±0.79)% for suicidal behavior in unipolar depression.The predictive morbidity of suicidal behavior in the first grade relatives was 3.1% and the real morbidity was 2.6%,which did not indicate significant difference (u =0.766, P ＞ 0.05).CONCLUSION:Suicidal behavior of unipolar depression presents obvious hereditary effects and its hereditary patterns tally with polygenetic inheritance.

As a neurological disorder in the brain, epilepsy is not only associated with abnormal synchronized discharging of neurons, but also inseparable from non-neuronal elements in the altered microenvironment. Anti-epileptic drugs (AEDs) merely focusing on neuronal circuits frequently turn out deficient, which is necessitating comprehensive strategies of medications to cover over-exciting neurons, activated glial cells, oxidative stress and chronic inflammation synchronously. Therefore, we would report the design of a polymeric micelle drug delivery system that was functioned with brain targeting and cerebral microenvironment modulation. In brief, reactive oxygen species (ROS)-sensitive phenylboronic ester was conjugated with poly-ethylene glycol (PEG) to form amphiphilic copolymers. Additionally, dehydroascorbic acid (DHAA), an analogue of glucose, was applied to target glucose transporter 1 (GLUT1) and facilitate micelle penetration across the blood‒brain barrier (BBB). A classic hydrophobic AED, lamotrigine (LTG), was encapsulated in the micelles via self-assembly. When administrated and transferred across the BBB, ROS-scavenging polymers were expected to integrate anti-oxidation, anti-inflammation and neuro-electric modulation into one strategy. Moreover, micelles would alter LTG distribution in vivo with improved efficacy. Overall, the combined anti-epileptic therapy might provide effective opinions on how to maximize neuroprotection during early epileptogenesis.

Metastasis accounts for 90% of breast cancer deaths, where the lethality could be attributed to the poor drug accumulation at the metastatic loci. The tolerance to chemotherapy induced by breast cancer stem cells (BCSCs) and their particular redox microenvironment further aggravate the therapeutic dilemma. To be specific, therapy-resistant BCSCs can differentiate into heterogeneous tumor cells constantly, and simultaneously dynamic maintenance of redox homeostasis promote tumor cells to retro-differentiate into stem-like state in response to cytotoxic chemotherapy. Herein, we develop a specifically-designed biomimic platform employing neutrophil membrane as shell to inherit a neutrophil-like tumor-targeting capability, and anchored chemotherapeutic and BCSCs-differentiating reagents with nitroimidazole (NI) to yield two hypoxia-responsive prodrugs, which could be encapsulated into a polymeric nitroimidazole core. The platform can actively target the lung metastasis sites of triple negative breast cancer (TNBC), and release the escorted drugs upon being triggered by the hypoxia microenvironment. During the responsiveness, the differentiating agent could promote transferring BCSCs into non-BCSCs, and simultaneously the nitroimidazole moieties conjugated on the polymer and prodrugs could modulate the tumor microenvironment by depleting nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) and amplifying intracellular oxidative stress to prevent tumor cells retro-differentiation into BCSCs. In combination, the BCSCs differentiation and tumor microenvironment modulation synergistically could enhance the chemotherapeutic cytotoxicity, and remarkably suppress tumor growth and lung metastasis. Hopefully, this work can provide a new insight in to comprehensively treat TNBC and lung metastasis using a versatile platform.