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Neonatal seizures in term infants are rare but have important potential implications for brain development. Risk factors for neonatal seizures in term infants have been less well defined than those among preterm infants. To evaluate the relationship between maternal risk factors and neonatal seizures in the first 72 hours of life in term infants, a case-control study using the Colorado Birth Certificate Registry was conducted. Term neonates in all hospitals in Colorado with and without seizures in the first 72 hours were studied. After adjusting for vaginal delivery in the setting of herpes infection and post-term delivery, preexisting diabetes in the mother (odds ratio 4.30, 95% confidence interval 1.64-11.27, P < .01) and fetal distress (odds ratio 5.88, 95% confidence interval 4.60-7.13, P < .0001) were independent risk factors for neonatal seizures in term infants. These findings are confirmatory of previous reports that maternal preexisting diabetes and fetal distress increase the risk of neonatal seizure in term infants. Although we cannot establish the pathophysiology of neonatal seizures from this analysis, hypoxic-ischemic brain injury and hypoglycemia in infants of diabetic mothers are known causes of neonatal seizures that can be represented in this analysis by fetal distress and maternal preexisting diabetes, respectively. Maternal diabetic vasculopathy can also be a contributing factor.
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PMID:Maternal risk factors for term neonatal seizures: population-based study in Colorado, 1989-2003. 1697 Aug 88

Peripheral neuropathy is a common medical problem with numerous aetiologies. Unfortunately, for the majority of cases there is no available medical solution for the underlying cause, and the only option is to try to treat the resulting symptoms. Treatment options exist when neuropathy results in positive symptoms such as pain, but there is a significant lack of treatments for negative symptoms such as numbness and weakness. Systemic application of growth factor peptides has shown promise in protecting nerves from neuropathic insults in preclinical animal studies, but translation into human trials has been problematic and disappointing. Significant advancements have been made in the past few years in utilising gene therapy approaches to treat peripheral neuropathy by expressing neuroprotective gene products either systemically or in specific nervous tissues. For example, plasmids expressing vascular endothelial growth factor injected into muscle, or herpes-simplex-virus-based vectors expressing neurotrophin gene products delivered to dorsal root ganglion neurons, have been used to protect peripheral nerve function in animal models of diabetes-associated peripheral neuropathy. Many published studies support the feasibility of this approach, although several questions still need to be addressed as gene therapy to treat peripheral neuropathy moves out of the laboratory and into the clinic.
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PMID:The therapeutic potential of gene transfer for the treatment of peripheral neuropathies. 1736 56

It is assumed that various infectious agents play direct or indirect roles in the pathogenesis of atherosclerosis which is accepted as a chronic inflammatory phenomenon. However, the data obtained from different studies are contradictory. The aim of this study was to investigate the roles of herpes virus group [Herpes simplex virus (HSV), Epstein-Barr virus (EBV), Cytomegalovirus (CMV)] and hepatitis A virus (HAV) which are debated in terms of their impact in the pathogenesis of coronary arterial diseases. For this purpose, atherome plaque samples collected from 28 patients (23 were male; age range: 43-74 years) with atherosclerotic heart disease and vein samples from 22 control patients (19 were male; age range: 37-85 years) who had vascular diseases other than atherosclerosis, were investigated by means of the presence of nucleic acids of the above mentioned viruses by real-time polymerase chain reaction (PCR). Besides, classical cardiovascular risk factors (hypertension, hyperlipidemia, hypercholestrolemia, diabetes mellitus, smoking habits, gender, age and familial background) were questioned in both patient and control groups. As a result, no positivity were detected for nucleic acids of HSV type 1 and 2, EBV and HAV, whereas CMV-DNA was found positive in three of 28 (10.7%) atheromateous plaques (viral loads were 21, 188 and 288 copies/mg). Amongst 22 vascular samples from controls, two (9.1%) yielded positive results for EBV-DNA (viral loads were 5 and 10 copies/mg), while the other samples were found negative for nucleic acids of HSV type 1 and 2, CMV and HAV. The evaluation of the known risk factors for atherosclerosis revealed that, the difference between the presence of hypertension and hyperlipidemia which are the major risk factors, was statistically important (p < 0.05) in patient group (64% and 50%, respectively) and control group (32% and 23%, respectively). In conclusion, the hypothesis concerning the possible relationship between these viral agents and the progression of atherosclerosis, have not been supported by our data which are similar to the results obtained from various other studies. Actually, further studies are needed to clarify such direct or indirect roles of infectious agents in the pathogenesis of coronary arterial diseases.
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PMID:[Investigation of herpes group and hepatitis A virus nucleic acids in the atherome plaque samples of patients with coronary arterial disease]. 1817 72

A 64-years-old man referred to a hospital because of high-grade fever. He was diagnosed as having influenza B by "POCTEM Influenza A/B", a rapid influenza diagnostic kit which detect some antigens of influenza virus. Six days after medication of oseltamivir phosphate, his flu-symptoms disappeared, but he complained sever thirsty. And after 2days, he suffered from loss of consciousness and was admitted to the hospital. Laboratory data on admission showed diabetes ketoacidosis, slight elevation of HbA1c level despite sever hyperglycemia, and increase of serum amylase concentration. Anti GAD antibody and anti IA-2 antibody were not detected. Urinary C-peptide excretion was undetectable and serum C-peptide levels were also undetectable after glucagon and arginin load, suggesting disappearance of endogeneous insulin secretion. Class II HLA was susceptible to fulminant type1 diabetes. Based on these findings, we diagnosed him with fulminant type1 diabetes. In Japan, only three viruses in three cases have been reported to be the trigger in the development of fulminant type 1 diabetes. They were human herpes virus 6, herpes simplex virus and Coxsackie B3 virus. This is the fourth report of fulminant type 1 diabetes developed after the established diagnosis of viral infection and the first after influenza B virus infection. The fact that fulminant type 1 diabetes developed after the infection of such a common virus suggest that factors within host will play more important roles than virus itself in the etiology of fulminant type 1 diabetes.
Diabetes Res Clin Pract 2008 Mar
PMID:A case of fulminant type 1 diabetes mellitus after influenza B infection. 1817 74

Diabetes Mellitus (DM) is a serious medical problem that causes long-term systemic complications and considerable associated morbidity. DM can cause retinopathy (DRP), maculopathy, cataract, optic neuropathy, defects of eye muscles. DM is a risk factor for acute infectious conjunctivitis, bacterial keratitis, herpes virus infections and endophtalmitis. Elevated blood glucose induces structural, physiological and hormonal changes which affect retinal capillaries. DRP is recognized by loss of pericyte function and capillary occlusions together leading to breakdown of blood-retinal barrier, edematous changes and proliferation of vessels and fibrous tissue. Depending on stage of DRP, there are different preferable therapeutic approaches applied. In the case of ETDRS, in the area of leakage focal treatment should be performed, while panretinal photocoagulation is applied towards ischemic areas or beginning proliferations. Vitreal haemorrhage followed by fibroproliferative changes or tractional retinal detachment is treated by vitrectomy alone or in combination with ILM peeling. In pathogenesis of DRP, Insulin Growth Factor (IGF-1) can play an important role in production of VEGF (Vascular Endothelial Growth Factor). Hypoxia can up-regulate VEGF expression levels leading to pathologic ocular neovascularisation. An application of intravitreal corticosteroid treatment modulates vascular permeability by suppressing the production of VEGF, reducing both extracellular matrix metalloproteinase activity and basic fibroblast growth factor, decreasing major histocompatibility complex 2 Ag expression levels, and inhibiting activity of inflammatory cells. Clinical effects of treatment using intravitreal corticosteroids are evaluated by reduction of macular thickness and visual improvement. Intravitreal use of Anti-VEGF drugs, Pegaptanib, Ranibizumab and Bevacizumab can modify vasoproliferation, trigger macular edema, and, therefore, influence a prognosis for visual loss.
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PMID:Eye disorders in diabetes: potential drug targets. 1853 2

The XXth century is marked by the substantial increase in human life expectancy. Historically, main reasons for that are four achievements of medicine: (1) improvements in common hygiene, such as waste disposal and water purification which led to the significant reduction of communicable diseases; (2) common recognition of Pasteur's Germ Theory followed by improvements in occupational and personal hygiene as well as introduction of antiseptic and aseptic measures; (3) decrease in childhood mortality due to the discovery and widespread application of vaccination; and (4) the discovery and clinical application of antibiotics. An epidemiological transition took place, i.e. the shift from communicable infectious diseases, as a main cause of morbidity and mortality, to chronic degenerative diseases, mainly considered non-infectious. Experimental evidence has been accumulated on a significant number of microorganisms, including viruses (such as a group of herpes viruses, hepatitis viruses, etc.), bacteria (Chlamydia, Helicobacter, periodontal pathogens, etc.), fungi and parasites, as an underlying reason for many of diseases, such as atherosclerosis, various cancers, type 1 and 2 diabetes, neurodegenerative and some psychiatric diseases, osteoporosis, autoimmune diseases and others. On the other hand, most of these diseases have been traditionally associated with age, together with other "age-related" disorders, such as immune system suppression, thymus involution, pathologic calcification, etc. Taken together, these facts suggest that aging, among others, has infectious origins, and that burden of infections may lead to enhanced senescence and premature death. In fact, infections may serve as a trigger of senescence, presumably via the mechanisms of chronic oxidative stress, low-grade inflammation, telomere shortening, and autoimmune processes due to the molecular mimicry. We believe that next step in human longevity increase can be possible by common appreciation of the role of infections as the main trigger of age-related diseases and disorders, and by efforts to cure and/or eradicate these infections.
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PMID:[Fifth revolution in medicine: on the role of infections in pathogenesis of aging and chronic diseases]. 1882 37

We report a 90-year-old man who was given a diagnosis of pleural effusion lymphoma (PEL) based on the detailed immunochemical and DNA analyses of the pleural effusion. He was bed-ridden and on enteral nutrition due to severe Alzheimer's disease, and also had diabetes mellitus. He was transferred to our hospital with fever and massive pleural effusion. A cytological examination of the pleural effusion revealed class 5 atypical lymphocytes with a high nucleus/cytoplasm ratio. The origin of the atypical cells could not be determined by flow cytometry of the pleural effusion, which only suggested the existence of inflammatory changes. Considering his general physical status, further investigations were not performed. The respiratory failure progressed, and he died on the 45(th) hospital day. At autopsy, no atypical cells were identified in his organs other than in the right thoracic space. We conducted immunochemical staining after making a cell block from the effusion sample. Most of the atypical cells were CD30 positive, with human herpes virus-8 (HHV-8)-associated protein. A PCR analysis of the immunoglobulin heavy chain gene detected monoclonal rearrangement, thus indicating the atypical cells to be involved in the B-cell lineage. These findings led to a final diagnosis of PEL. PEL is a rare type of lymphoma confined to the body cavities without any prominent tumor mass, and its pathogenesis is related to HHV-8 infection. PEL develops mostly in immunocompromised patients, such as those with AIDS. However, it may also occur in elderly patients as well. We should therefore also consider the possibility of PEL in elderly patients presenting with pleural effusion of unknown origin.
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PMID:[A case of a primary effusion lymphoma in the elderly]. 2013 53

A 36-year-old woman with neuromyelitis optica had been treated with steroids for the prevention of relapse. However, her treatment was not effective and she showed adverse effects such as diabetes mellitus, osteoporosis, compression fractures, and Pneumocystis carinii pneumonia. Therefore, we started her on mitoxantrone treatment. After five courses of mitoxantrone injection, she developed a herpes zoster infection in her thigh followed by aseptic meningitis. PCR for varicella zoster virus (VZV)-DNA was positive in the cerebrospinal fluid. The mechanisms that caused VZV reactivation by mitoxantrone are not known. Opportunistic herpes virus reactivation may occur easily with increasing use of immunosuppressive drugs for both neuromyelitis optica and multiple sclerosis. These drugs must be used under careful supervision.
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PMID:[A case of neuromyelitis optica with varicella zoster virus meningitis during mitoxantrone treatment]. 2194 29

Classical population genetics shows that varying permutations of genes and risk factors permit or disallow the effects of causative agents, depending on circumstance. For example, genes and environment determine whether a fox kills black or white rabbits on snow or black ash covered islands. Risk promoting effects are different on each island, but obscured by meta-analysis or GWAS data from both islands, unless partitioned by different contributory factors. In Alzheimer's disease, the foxes appear to be herpes, borrelia or chlamydial infection, hypercholesterolemia, hyperhomocysteinaemia, diabetes, cerebral hypoperfusion, oestrogen depletion, or vitamin A deficiency, all of which promote beta-amyloid deposition in animal models-without the aid of gene variants. All relate to risk factors and subsets of susceptibility genes, which condition their effects. All are less prevalent in convents, where nuns appear less susceptible to the ravages of ageing. Antagonism of the antimicrobial properties of beta-amyloid by Abeta autoantibodies in the ageing population, likely generated by antibodies raised to beta-amyloid/pathogen protein homologues, may play a role in this scenario. These agents are treatable by diet and drugs, vitamin supplementation, pathogen detection and elimination, and autoantibody removal, although again, the beneficial effects of individual treatments may be tempered by genes and environment.
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PMID:The Fox and the Rabbits-Environmental Variables and Population Genetics (1) Replication Problems in Association Studies and the Untapped Power of GWAS (2) Vitamin A Deficiency, Herpes Simplex Reactivation and Other Causes of Alzheimer's Disease. 2238 16

We describe a case of primary hypertensive iridocyclitis with biopsy-proven Cytomegaloviral retinitis. It is an observational case report of a 69-year-old diabetic gentleman on azathioprine for Crohn's disease who presented with recurrent episodes of hypertensive iridocyclitis. On the 4 th attendance in 5 months, a granular white lesion was noted in the temporal periphery of the mid-peripheral fundus and a chorioretinal and vitreous biopsy performed. Vitreous PCR was positive for Cytomegalovirus (CMV). Hematoxylin and eosin staining revealed cytomegalic-like inclusions within necrotic neural retina. Transmission electron microscopy revealed herpes family virus particles and immunohistochemistry demonstrated CMV protein. This case provides further evidence implicating CMV infection in the etiology of hypertensive iridocyclitis. With hindsight, the cumulative effect of diabetes and azathioprine on the immune surveillance system proved sufficient to render the patient susceptible to CMV retinitis.
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PMID:Hypertensive iridocyclitis associated with delayed onset biopsy proven Cytomegalovirus retinitis. 2354 20


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