Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis obliterance and critical lower limb ischemia lead to immunodeficiency and disbalance of T- and B- components of immune system. Surgical treatment doesn't eliminate but in a number of cases aggravates immune disorders. Immunocorrection stimulates anti-infectious protection. Indications to different variants of immunocorrection are formulated.
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PMID:[Immunological disorders and correction of them in surgical patients with atherosclerosis obliterance]. 1688 38

Human immunodeficiency virus (HIV)-1 infection of the central nervous system occurs in the vast majority of HIV-infected patients. HIV-associated dementia (HAD) represents the most severe form of HIV-related neuropsychiatric impairment and is associated with neuropathology involving HIV proteins and activation of proinflammatory cytokine circuits. Interferon-gamma (IFN-gamma) activates the JAK/STAT1 pathway, a key regulator of inflammatory and apoptotic signaling, and is elevated in HIV-1-infected brains progressing to HAD. Recent reports suggest green tea-derived (-)-epigallocatechin-3-gallate (EGCG) can attenuate neuronal damage mediated by this pathway in conditions such as brain ischemia. In order to investigate the therapeutic potential of EGCG to mitigate the neuronal damage characteristic of HAD, IFN-gamma was evaluated for its ability to enhance well-known neurotoxic properties of HIV-1 proteins gp120 and Tat in primary neurons and mice. Indeed, IFN-gamma enhanced the neurotoxicity of gp120 and Tat via increased JAK/STAT signaling. Additionally, primary neurons pretreated with a JAK1 inhibitor, or those derived from STAT1-deficient mice, were largely resistant to the IFN-gamma-enhanced neurotoxicity of gp120 and Tat. Moreover, EGCG treatment of primary neurons from normal mice reduced IFN-gamma-enhanced neurotoxicity of gp120 and Tat by inhibiting JAK/STAT1 pathway activation. EGCG was also found to mitigate the neurotoxic properties of HIV-1 proteins in the presence of IFN-gamma in vivo. Taken together, these data suggest EGCG attenuates the neurotoxicity of IFN-gamma augmented neuronal damage from HIV-1 proteins gp120 and Tat both in vitro and in vivo. Thus EGCG may represent a novel natural copound for the prevention and treatment of HAD.
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PMID:EGCG mitigates neurotoxicity mediated by HIV-1 proteins gp120 and Tat in the presence of IFN-gamma: role of JAK/STAT1 signaling and implications for HIV-associated dementia. 1707 33

The evaluation of patients with colitis of recent onset is a relatively common clinical challenge. The main considerations are infectious colitides, idiopathic IBD, ie, ulcerative and Crohn's colitis, and colonic ischemia. An initial risk assessment on the basis of such factors as concurrent symptoms in contacts, travel history, medications, and human immunodeficiency virus risk factors should be followed by a thorough clinical history, physical examination, stool studies, blood tests, and, in selected cases, endoscopic examination and serologic tests. Biopsies can be decisive in distinguishing among the different types of acute colitis and might help identify specific etiologies. The diagnostic yield of biopsies is maximized by appropriate sampling of the colonic mucosa and by sharing the clinical and endoscopic findings with the pathologist, eg, via a copy of the endoscopy report.
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PMID:Diagnosis of colitis: making the initial diagnosis. 1791 88

A 42-year-old woman presented to the emergency department with progressive painful discoloration of the digits of her right foot and symptoms previously diagnosed as neuroma. She was admitted to the hospital for dorsalis pedis arterial occlusion and ischemic foot pain. Despite attempts to restore perfusion to the right leg, ischemia of the right foot persisted and progressed to digital gangrene. The patient subsequently required right transmetatarsal amputation and eventually below-the-knee amputation. After extensive inpatient vascular and hematologic work-up of this otherwise healthy woman, test results revealed that she had protein S deficiency, hepatitis C, and human immunodeficiency virus type 1. In addition to describing this patient's evaluation and treatment, we review protein S deficiency, including its correlation with human immunodeficiency virus type 1 infection and laboratory diagnosis. This case promotes awareness of protein S deficiency and serves as a reminder to the physician treating patients with vascular compromise and a history of human immunodeficiency virus type 1 to include protein S deficiency in the differential diagnosis.
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PMID:Protein S deficiency and lower-extremity arterial thrombosis: complicating a common presentation. 1736 23

Glutamate is an essential neurotransmitter regulating brain functions. Excitatory amino acid transporter (EAAT)-2 is one of the major glutamate transporters primarily expressed in astroglial cells. Dysfunction of EAAT2 is implicated in acute and chronic neurological disorders, including stroke/ischemia, temporal lobe epilepsy, amyotrophic lateral sclerosis, Alzheimer disease, human immunodeficiency virus 1-associated dementia, and growth of malignant gliomas. Ceftriaxone, one of the beta-lactam antibiotics, is a stimulator of EAAT2 expression with neuroprotective effects in both in vitro and in vivo models based in part on its ability to inhibit neuronal cell death by glutamate excitotoxicity. Based on this consideration and its lack of toxicity, ceftriaxone has potential to manipulate glutamate transmission and ameliorate neurotoxicity. We investigated the mechanism by which ceftriaxone enhances EAAT2 expression in primary human fetal astrocytes (PHFA). Ceftriaxone elevated EAAT2 transcription in PHFA through the nuclear factor-kappaB (NF-kappaB) signaling pathway. The antibiotic promoted nuclear translocation of p65 and activation of NF-kappaB. The specific NF-kappaB binding site at the -272 position of the EAAT2 promoter was responsible for ceftriaxone-mediated EAAT2 induction. In addition, ceftriaxone increased glutamate uptake, a primary function of EAAT2, and EAAT2 small interference RNA completely inhibited ceftriaxone-induced glutamate uptake activity in PHFA. Taken together, our data indicate that ceftriaxone is a potent modulator of glutamate transport in PHFA through NF-kappaB-mediated EAAT2 promoter activation. These findings suggest a mechanism for ceftriaxone modulation of glutamate transport and for its potential effects on ameliorating specific neurodegenerative diseases through modulation of extracellular glutamate.
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PMID:Mechanism of ceftriaxone induction of excitatory amino acid transporter-2 expression and glutamate uptake in primary human astrocytes. 1832 97

Compartment Syndrome (CS) is a disease that has 2 etiologies, that of acute events and that of chronic. It occurs when the pressure in a fascia-encased compartment exceeds the profusion pressure in tissue. The end result, when left untreated, is muscle and nerve ischemia that can cause significant morbidity. Nerve paralysis, muscle necrosis and fibrosis and, when occurring in an extremity, loss of the limb are some of the potential outcomes of missed diagnosis. This case series involves 2 cases of CS that where caused by vasculitis with etiologies of human immunodeficiency virus and systemic lupus erythematosis. Autoimmune vasculitis has many systemic and local manifestations, but to our knowledge CS has not been described as one of its sequelae. The following is literature review and presentation of these 2 cases.
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PMID:Acquired immune deficiency syndrome and systemic lupus erythematosis: potential causes of surgical emergencies of the hand. 1858 Jan 47

Mycotic femoral pseudoaneurysms, particularly in the drug-abusing population, pose a difficult problem to the vascular surgeon. Management ranges from ligation with debridement to extra-anatomical bypass. This study reviewed the management of mycotic femoral pseudoaneurysms presenting in intravenous drug abusers to an inner city tertiary referral center. Between 2001 and 2006, 11 cases presenting in nine patients were treated. The mean age was 30.7 years with a male-to-female ratio of 1:2. Eight patients had a positive viral status for the human immunodeficiency virus and/or hepatitis C. Two patients re-presented with a contralateral pseudoaneurysm. A combination of groin pain and swelling was the most common presentation. Two patients presented with significant hemorrhage. The diagnosis was confirmed by ultrasound in the majority of cases. Nine cases were managed with arterial ligation and debridement of the necrotic tissue. The two remaining cases were managed with ultrasound-guided thrombin injection and arterial puncture closure. On follow-up, one patient required a below-knee amputation following reinjection into the postoperative wound site. One further patient underwent a fifth metatarsal amputation due to ischemia. Ligation and debridement are well tolerated in the majority of drug-abusing patients diagnosed with mycotic femoral pseudoaneurysms.
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PMID:The management of mycotic femoral pseudoaneurysms in intravenous drug abusers. 1987 20

Pneumatosis intestinalis has been described in association with many gastrointestinal tract disorders including infection, ischemia and obstruction. It has also been described in patients with chronic obstructive pulmonary disease, connective tissue disorders, organ transplantation, leukemia and various states of immunodeficiency. In the present paper, the case of a 66-year-old woman with chronic bronchiectasis who subsequently developed pneumatosis intestinalis is described.
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PMID:Pneumatosis intestinalis in a patient with chronic bronchiectasis. 1892 10

We describe a protocol for establishing mouse models of periventricular leukomalacia (PVL). PVL is the predominant form of brain injury in premature infants and the most common antecedent of cerebral palsy. PVL is characterized by periventricular white matter damage with prominent oligodendroglial injury. Hypoxia/ischemia with or without systemic infection/inflammation are the primary causes of PVL. We use P6 mice to create models of neonatal brain injury by the induction of hypoxia/ischemia with or without systemic infection/inflammation with unilateral carotid ligation followed by exposure to hypoxia with or without injection of the endotoxin lipopolysaccharide (LPS). Immunohistochemistry of myelin basic protein (MBP) or O1 and electron microscopic examination show prominent myelin loss in cerebral white matter with additional damage to the hippocampus and thalamus. Establishment of mouse models of PVL will greatly facilitate the study of disease pathogenesis using available transgenic mouse strains, conduction of drug trials in a relatively high throughput manner to identify candidate therapeutic agents, and testing of stem cell transplantation using immunodeficiency mouse strains.
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PMID:Mouse models of periventricular leukomalacia. 2048 63

Membrane-permeable peptide carriers are attractive drug delivery tools. Among such carriers, the protein transduction domain (PTD) of the human immunodeficiency virus-type 1 Tat protein is most frequently used and has been successfully shown to deliver a large variety of cargoes. The Tat PTD can facilitate the uptake of large, biologically active molecules into mammalian cells, and recent studies have shown that it can mediate the delivery of different cargoes into tissues throughout a living organism. Given that the Tat PTD-mediated delivery is size-independent, this technology could make previously non-applicable large molecules usable to modulate biological function in vivo and treat human diseases. It is likely that the peptide carrier-mediated intracellular delivery process encompasses multiple mechanisms, but endocytic pathways are the predominant internalization routes. Tat PTD has been successfully used in preclinical models for the study of cancer, ischemia, inflammation, analgesia, and anesthesia. Our recent studies have shown that intraperitoneally injected fusion Tat peptide Tat-PSD-95 PDZ2 can be delivered into the spinal cord to dose-dependently disrupt protein-protein interactions between PSD-95 and NMDA receptors. This peptide significantly inhibits chronic inflammatory pain and reduces the threshold for halothane anesthesia. The ability of the Tat PTD to target any cell is advantageous in some respects. However, the drug delivery system will be more attractive if we can modify the Tat PTD to deliver cargo only into desired organs to avoid possible side effects.
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PMID:Tat-Mediated Peptide Intervention in Analgesia and Anesthesia. 2071 10


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