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Almost two decades ago, tumor necrosis factor (TNF) was identified as a protein produced by the immune system that played a major role in suppression of tumor cell proliferation. Extensive research since then has revealed that TNF is a major mediator of inflammation, viral replication, tumor metastasis, transplant rejection, rheumatoid arthritis, and septic shock. As of today, 18 different members of the TNF superfamily have been identified, and most of them have been found to mediate a wide variety of diseases including cancer, arthritis, bone resorption, allergy, diabetes, atherosclerosis, myocardial infarction, graft versus host disease, and acquired immune deficiency disease. All the cytokines of the TNF superfamily mediate their effects through the activation of the transcription factor NF-kappaB, c-Jun N-terminal kinase, apoptosis, and proliferation. Thus, agents that can either suppress the production of these cytokines or block their action have therapeutic value for a wide variety of diseases. In this review, we have elucidated the signal transduction pathways used by the members of the TNF family and the effects of deletion of genes that mediate the pathways. Our current understanding of the signaling pathways for TNF and other family members could serve as a target for the development of therapeutics.
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PMID:The role of TNF and its family members in inflammation and cancer: lessons from gene deletion. 1456 Nov 80

This final rule refines the resource-based practice expense relative value units (RVUs) and makes other changes to Medicare Part B payment policy. These policy changes concern: supplemental survey data for practice expense; updated geographic practice cost indices for physician work and practice expense; updated malpractice RVUs; revised requirements for supervision of therapy assistants; revised payment rules for low osmolar contrast media; changes to payment policies for physicians and practitioners managing dialysis patients; clarification of care plan oversight requirements; revised requirements for supervision of diagnostic psychological testing services; clarifications to the policies affecting therapy services; revised requirements for assignment of Medicare claims; addition to the list of telehealth services; and, several coding issues. We are making these changes to ensure that our payment systems are updated to reflect changes in medical practice and the relative value of services. This final rule also addresses the following provisions of the Medicare Prescription Drug, Improvement, and Modernization Act of 2003 (Pub. L. 108-17) (MMA): coverage of an initial preventive physical examination; coverage of cardiovascular (CV) screening blood tests; coverage of diabetes screening tests; incentive payment improvements for physicians in shortage areas; payment for covered outpatient drugs and biologicals; payment for renal dialysis services; coverage of routine costs associated with certain clinical trials of category A devices as defined by the Food and Drug Administration; hospice consultation service; indexing the Part B deductible to inflation; extension of coverage of intravenous immune globulin (IVIG) for the treatment in the home of primary immune deficiency diseases; revisions to reassignment provisions; and, payment for diagnostic mammograms, physicians' services associated with drug administration services and coverage of religious nonmedical health care institution items and services to the beneficiary's home. In addition, this rule updates the codes subject to the physician self-referral prohibition, discusses payment for set-up of portable x-ray equipment, discusses the third five-year refinement of work RVUs, and solicits comments on potentially misvalued work RVUs. We are also finalizing the calendar year (CY) 2004 interim RVUs and are issuing interim RVUs for new and revised procedure codes for CY 2005. As required by the statute, we are announcing that the physician fee schedule update for CY 2005 is 1.5 percent, the initial estimate for the sustainable growth rate for CY 2005 is 4.3, and the conversion factor for CY 2005 is $37.8975.
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PMID:Medicare program; revisions to payment policies under the physician fee schedule for calendar year 2005. Final rule with comment period. 1555 93

Gene therapy is defined as the introduction of genetic material in a patient's cells with resulting therapeutic benefit. It is a promising new biomedical discipline that could potentially lead to new treatments for hereditary diseases, cardiovascular and neurologic disorders, cancer, diabetes and even infectious diseases. The introduction of genetic material into somatic cells requires gene delivery vectors. Since viruses have developed efficient means to introduce their own genetic material into cells they can be readily adapted as viral vectors for gene therapy. Preclinical studies in animal models have shown that therapeutic effects can be achieved after gene therapy for genetic, acquired and complex disorders. Furthermore, therapeutic effects have been obtained in several phase I/II gene therapy clinical trials for hemophilia, severe combined immune deficiency (SCID) and cancer. Gene transfer technology has improved significantly over the past few years and has led to the development of vectors which have fewer side-effects without compromising their efficacy, at least partly due the development of cell-type specific targetable vectors. Nevertheless, the success of gene therapy is still very much depending upon the continuous development of improved vector technologies which would hopefully and ultimately cure diseases which are refractory to current treatment paradigms.
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PMID:[Recent developments in gene therapy]. 1555 1

Necrotizing fasciitis is a rare, rapidly progressing soft tissue infection, characterised by extensive necrosis of subcutaneous fat and fascia with relative sparing of skin and underlying muscle. It is usually caused by toxin producing virulent bacteria. Although it can occur in otherwise healthy patients, the disease is usually seen in conjunction with immune deficiency disorders, intravenous drug abuse, peripheral vascular disease and diabetes. Necrotizing fasciitis is more frequent in abdominal wall, perineum and extremities. Involvement of the head and neck structures and especially the scalp is rare. We treated a diabetic and chronic renal failure patient with necrotizing fasciitis of the scalp without any complication.
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PMID:Necrotizing fasciitis of the scalp: a case of an uneventful healing. 1568 72

Rhinocerebral mucormycosis is an invasive, opportunistic fungal infection usually seen in immunocompromised patients, and particularly in the setting of diabetes or immune deficiency. It is assumed that the port of entry is colonization of the nasal mucosa, allowing the fungus to spread via the paranasal sinuses into the orbit. Involvement of the brain and cavernous sinus occurs by way of the orbital apex; therefore, spheno-ethmoidectomy with or without maxillectomy seems to be the definitive method to eradicate this infection. We conducted a prospective study of ten patients with rhinocerebral mucormycosis from February 2000 to April 2004. Rhinocerebral mucormycosis was clinically diagnosed in 11 patients, 10 of whom were included in our study upon histopathological confirmation. Diabetes was the most common underlying disorder seen in nine out of ten patients. In this study, the patients were assessed for predisposing factors, presenting signs and symptoms, sites of extension, the number and sites of surgical debridement, as well as the outcome. Ocular, sinonasal and facial soft tissue involvement was common. Involvement of the pterygopalatine fossa at the time of debridement was evident in all patients. No invasion through the lamina papiracea or the walls of the maxillary sinus was identified. At the time of this communication, six out of ten patients were alive. For the four who died, the causes were hypokalemia, cardiac arrythmia and refractory pneumonia. Pterygopalatine fossa is considered to be the main reservoir for rhinocerebral mucormycosis, and extension into the orbit and facial soft tissues usually follows this route. After proliferation in the nasal cavity, the mucor reaches the pterygo-palatine fossa, inferior orbital fissure and finally the retroglobal space of the orbit, resulting in ocular signs. The facial soft tissues, palate and infratemporal fossa can be infected through connecting pathways from the pterygo-palatine fossa; therefore, debridement of the pterygopalatine fossa seems to be the definitive method of managing this infection.
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PMID:Rhinocerebral mucormycosis: pathways of spread. 1589 27

Thirty three consecutive patients with chronic osteomyelitis and deficient soft tissue coverage treated with a muscle flap from 1991-1998 were reviewed retrospectively. Osteomyelitis was diagnosed by positive bone cultures and radiographic changes consistent with osteomyelitis. Osteomyelitis was divided into localized <50% diameter: 24 patients and diffuse >50% diameter or infected nonunion: 9 patients. The average age was 38 (18-74). The cause of the osteomyelitis was open fracture 23, closed fracture and open reduction internal fixation 5, gunshot wound 3, burn 1, and chronic venous stasis ulcer 1. Localized osteomyelitis was treated with saucerization and coverage with a free or rotational muscle flap. Pandiaphyseal osteomyelitis was treated with a complete diaphysectomy in 3, and wide saucerization in 2. Twenty three patients were treated with a free flap and 10 with a rotational flap.A reconstructive success was considered a limb that allowed full weight bearing with a stable wound, no drainage and no recurrence of infection. Patients were evaluated for risk factors: malnutrition, renal or liver failure, alcohol abuse, immune deficiency, chronic hypoxia, malignancy, diabetes, age over 70, steroid therapy, tobacco abuse, or drug abuse. Patients were followed an average of 34 months (12-58) after surgery. A reconstructive success was achieved in 91% (20/22) of patients with local osteomyelitis and in 56% (5/9) of patients with diffuse osteomyelitis (p < 0.05). A reconstructive success was achieved in 88% (7/8) patients with no risk factors and in 78% (18/23) of patients with one or more risk factors (not significant p = 0.05).
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PMID:Muscle flaps in the treatment of osteomyelitis of the lower extremity. 1592 Apr 18

Today we know there are four different types of ATPases that operate within biological membranes with the purpose of moving many different types of ions or molecules across these membranes. Some of these ions or molecules are transported into cells, some out of cells, and some in or out of organelles within cells. These ATPases span the biological world from bacteria to eukaryotic cells and have become most simply and commonly known as "transport ATPases." The price that each cell type pays for transport work is counted in molecules of hydrolyzed ATP, a metabolic currency that is itself regenerated by a transport ATPase working in reverse, i.e., the ATP synthase. Four major classes of transport ATPases, the P, V, F, and ABC types are now known. In addition to being involved in many different types of biological/physiological processes, mutations in these proteins also account for a large number of diseases. The purpose of this introductory article to a mini-review series on transport ATPases is to provide the reader with a very brief and focused look at this important area of research that has an interesting history and bears significance to cell physiology, biochemistry, immunology, nanotechnology, and medicine, including drug discovery. The latter involves potential applications to a whole host of diseases ranging from cancer to those that affect bones (osteoporosis), ears (hearing), eyes (macromolecular degeneration), the heart (hypercholesterolemia/cardiac arrest,), immune system (immune deficiency disease), kidney (nephrotoxicity), lungs (cystic fibrosis), pancreas (diabetes and cystic fibrosis), skin (Darier disease), and stomach (ulcers).
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PMID:Transport ATPases: structure, motors, mechanism and medicine: a brief overview. 1669 64

Neonatal diabetes mellitus is a rare (1/400 000 newborns) but potentially devastating condition, which may be transient or permanent; typical symptoms occur within the first 4 wk of life. The transient form is a developmental insulin production disorder that resolves postnatally. Fifty to 60% of cases can be seen as transient form. Cases that require lifelong insulin therapy can be described as permanent condition. This fraction of cases is less common than the transient form. There are no clinical features that can predict whether a neonate with diabetes mellitus but no other dysmorphology will eventually have permanent neonatal diabetes mellitus (PNDM) or transient neonatal diabetes mellitus. Some metabolic or genetic defects such as complete deficiency of glucokinase or heterozygous activating mutations of KCNJ11, encoding Kir6.2, were found in patients with PNDM. A preterm female infant with a gestational age of 36 wk was admitted to the neonatal intensive care unit in the first hours of life due to prematurity and intra-uterine growth retardation. She was diagnosed as having arthrogryposis multiplex congenita on the first day. Hyperglycemia was detected on the third day of life, and she required insulin treatment. The patient is now 6 yr old with PNDM, arthrogryposis multiplex, neurogenic bladder, immune deficiency, constipation, and ichthyosis. Is this a new form of neonatal diabetes mellitus?
Pediatr Diabetes 2006 Oct
PMID:Permanent neonatal diabetes with arthrogryposis multiplex congenita and neurogenic bladder - a new syndrome? 1705 50

This report presents the case of a healed 5-month-old infant with necrotising (malignant) bilateral otitis externa from acute mastoiditis on the right side and sepsis caused by Pseudomonas aeruginosa infection. Despite of immediately performed mastoidectomy, targeted antibiotics and intensive local treatment, two third of both external auditory canal's epithelium had shown subcutaneous concentric necrosis and ejection which have been removed with repeated necretomies. After the remission of inflammatory symptoms, successful bilateral auditory canal reconstructions were performed. The observed right peripheral facial paresis at the beginning of disease remained stationary. The patient healed with residual symptoms after 2 months of treatment. Neither immune deficiency, nor diabetes could have been proven.
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PMID:[Necrotizing otitis externa in a 5-month-old infant]. 1798 26

Transport ATPases can be lumped into four distinct types, P, F, V, and ABC, with the first three designated 20 years ago (Pedersen, P.L. and Carafoli, E., Trends Biochem. Sci. 12, 146-150, 1987) and the ABC type included more recently. The mini-reviews (>20) that comprise this volume of the Journal of Bioenergetics and Biomembranes describe work presented at the 2007 FASEB Conference (6th) on Transport ATPases (Kathleen Sweadner, Chair; Rajini Rao, Co-Chair). Since these conferences began in 1997, the "transport ATPase field" has seen tremendous progress. Advances include a much better understanding of the structure, mechanism, and regulation of each of the four major ATPase types as well as their physiological and medical relevance. In fact, the transport ATPase field has entered a new era in which work on these enzymes is likely to contribute to new therapies for multiple diseases that affect both people and animals. Among these are cancer and heart disease, mitochondrial diseases, osteoporosis, macromolecular degeneration, immune deficiency, cystic fibrosis, diabetes, ulcers, nephro-toxicity, hearing loss, skin disorders, lupus, and malaria. In addition, as several members of the transport ATPase family include those involved in drug resistance their study may help alleviate this recurring problem in drug development. Finally, the transport ATPase field is also paving the way for nanotechnology focused on nano-motors with work on the F-type ATPases (F(0)F(1)) leading the way. These ATPases driven in reverse by a proton gradient have the capacity to interconvert electrochemical energy into mechanical energy and finally into chemical energy conserved in the terminal bond of ATP. In mammalian mitochondria these events occur on a larger complex or "nano-machine" called the "ATP synthasome" that consists of the ATP synthase in complex formation with carriers for P(i) and ADP/ATP.
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PMID:Transport ATPases into the year 2008: a brief overview related to types, structures, functions and roles in health and disease. 1817 9


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