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  • CURED FROM HERPES VIRUS Elizabeth Robbin is my name i am here to give my testimony of how i was cured from HERPES VIRUS i thought my life has ended because of the pains i went through. I spent alot in the hospital on drugs, i was so devastated, not until one faithful day as i was surfing the internet i came through a testimony of a cure on HERPES VIRUS with the help of Dr. AHMED USMAN herbal medicine, at first I thought it was a scam and I neglected it, the next day i also came across another testimony of a man cured from genital Herpes, which i found surprising so i made up my mind to give him a try, i contacted him with the email i found on the testimony. I emailed Dr. AHMED USMAN and explained what i am going through to him, and he ask me some few questions and he said a thing i will never forget that anyone who contacted him always get his or her healing in just three weeks after doing all he ask you, so i was amazed all the time i heard that from him, so i did all he ask to do and he prepare the herbal medicine and send it to me through courier service which i received after two weeks, he prescribed the intake of the medicine to me, so after 3 weeks all the strength that left me before rushed back and i became very strong and healthy, this disease almost killed me, so i went to the hospital for the final test and the doctor said there is no trace of the disease in me, i was very happy about the healing of Dr. AHMED USMAN from the ancient part of Africa, thank you sir for your great work. If you also need his help in any kind of diseases you can reach him on (drahmedusman5104@gmail) or you can call or Whatsapp him on +2348064460510. he is also specialized on curing, BREAST CANCER, HIV, PAINFUL MENSTRUATION, VIRGINAL DRYNESS, ALS, AUTISM, ASTHMA, TYPHOID, MEASLES, GONORRHEA, TUBERCULOSIS, he also can Bring back your EX. Thanks to Dr. AHMED USMAN for saving my life

  • [Abstract]

    Obesity and depression are among the most pressing health problems in the contemporary world. Obesity and depression share a bidirectional relationship, whereby each condition increases the risk of the other. By inference, shared pathways may underpin the comorbidity between obesity and depression. Activation of cell-mediated immunity (CMI) is a key factor in the pathophysiology of depression. CMI cytokines, including IFN-γ, TNFα and IL-1β, induce the catabolism of tryptophan (TRY) by stimulating indoleamine 2,3-dioxygenase (IDO) resulting in the synthesis of kynurenine (KYN) and other tryptophan catabolites (TRYCATs). In the CNS, TRYCATs have been related to oxidative damage, inflammation, mitochondrial dysfunction, cytotoxicity, excitotoxicity, neurotoxicity and lowered neuroplasticity. The pathophysiology of obesity is also associated with a state of aberrant inflammation that activates aryl hydrocarbon receptor (AHR), a pathway involved in the detection of intracellular or environmental changes as well as with increases in the production of TRYCATs, being KYN an agonists of AHR. Both AHR and TRYCATS are involved in obesity and related metabolic disorders. These changes in the TRYCAT pathway may contribute to the onset of neuropsychiatric symptoms in obesity.

    This paper reviews the role of immune activation, IDO stimulation and increased TRYCAT production in the pathophysiology of depression and obesity. Here we suggest that increased synthesis of detrimental TRYCATs is implicated in comorbid obesity and depression and is a new drug target to treat both diseases.

  • Study used a silk thread to create an animal model of “bladder outlet obstruction (BOO),” which is a condition affecting nearly 30% of men over the age of 60 and usually caused by benign prostatic hyperplasia (BPH).

    FTA:

    The bladder pressure was significantly increased in obstructed rats relative to sham rats. However, the peak voiding pressure of bladders in obstructed rats treated by SFN is lower than obstructed rats at the 4-week time point. Bladder capacity was significantly higher in BOO rats compared to sham rats. Rats of the BOO+SFN group showed the highest bladder capacity among all groups. Bladder compliance decreased significantly at the 4-week time point after BOO. However, SFN treatment rescued the compliance increase in bladder capacity. Moreover, we found that the interval of micturition was shorter in BOO rats than in sham rats. The micturition interval in BOO+SFN rats was significantly increased compared to BOO rats (Table 2).

  • Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD in mice subjected to 14 d chronic unpredictable stress (CUS). Repeated administration of CBD (30 mg/kg i.p., 2 h after each daily stressor) increased hippocampal progenitor proliferation and neurogenesis in wild-type mice. Ganciclovir administration to GFAP-thymidine kinase (GFAP-TK) transgenic mice, which express thymidine kinase in adult neural progenitor cells, abrogated CBD-induced hippocampal neurogenesis. CBD administration prevented the anxiogenic effect of CUS in wild type but not in GFAP-TK mice as evidenced in the novelty suppressed feeding test and the elevated plus maze. This anxiolytic effect of CBD involved the participation of the CB1 cannabinoid receptor, as CBD administration increased hippocampal anandamide levels and administration of the CB1–selective antagonist AM251 prevented CBD actions. Studies conducted with hippocampal progenitor cells in culture showed that CBD promotes progenitor proliferation and cell cycle progression and mimics the proliferative effect of CB1 and CB2 cannabinoid receptor activation. Moreover, antagonists of these two receptors or endocannabinoid depletion by fatty acid amide hydrolase overexpression prevented CBD-induced cell proliferation. These findings support that the anxiolytic effect of chronic CBD administration in stressed mice depends on its proneurogenic action in the adult hippocampus by facilitating endocannabinoid-mediated signalling.