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Because Pseudallescheria boydii vertebral osteomyelitis is rare and frequently resistant to available antifungal agents, the proper treatment of this lesion has not been defined. To better determine the best treatment of this lesion, the authors evaluated a case P. boydii vertebral osteomyelitis and reviewed the literature. A 48-year-old man had isolated thoracic vertebral osteomyelitis resulting from P. boydii and associated severe thoracic back pain and proximal lower extremity pain and weakness. Magnetic resonance imaging studies revealed continued collapse of the T6--T7 vertebrae despite previous posterior debridement and appropriate antifungal chemotherapy. On admission to the authors' institution, the patient underwent a right thoracotomy, anterior debridement with transthoracic T6--T7 corpectomies and strut grafting, followed by posterior fusion and stabilization with pedicle screws. After operation, the patient's pain, hyperalgesia, and lower extremity symptoms resolved. He was treated with a 12-month course of itraconazole. Imaging and laboratory studies show no evidence of recurrence. P. boydii vertebral osteomyelitis can have devastating neurologic sequelae if not treated properly. The frequent lack of response of this unusual fungal infection to systemic therapy requires frequent serial follow-up examinations. Patients with evidence of progression on imaging studies or neurologic findings should undergo early and aggressive surgical debridement.
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PMID:Vertebral osteomyelitis secondary to Pseudallescheria boydii. 1148 61

Abnormalities of tracheal rigidity, which may lead to the collapse of the airway during expiration and consequent complications, characterize two groups of disorders: tracheomalacia (weakness of the anterior cartilaginous arc of the trachea) and tracheal dyskinesia (dysfunction of the posterior membranous trachea). Tracheal dyskinesia can either be isolated or associated with a more complex syndrome of malformations: esophageal atresia, tracheoesophageal fistula and laryngotracheal cleft. Although our knowledge of the embryological development of the tracheoesophageal axis remains limited, the existence of these associations suggests that tracheal dyskinesia is of congenital origin. The presentation of three clinical cases demonstrates that the coexistence of a midline malformation and of tracheal dyskinesia complicates the therapeutic management of the first malformation. In particular, the postoperative follow-up is often more difficult, and a long-term tracheostomy is often required (sometimes for several years). However, it must be pointed out that tracheal dyskinesia, even in the associated forms, has a good long-term prognosis, since spontaneous resolution as the child grows up is the rule.
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PMID:Tracheal dyskinesia associated with midline abnormality: embryological hypotheses and therapeutic implications. 1188 3

Tracheomalacia is a condition of the neonatal and infant airway, characterized by weakness of the supporting tracheal cartilage and widening of the posterior membranous wall. Together, these factors cause tracheal collapse, especially during times of increased airflow. The diagnosis of major airway collapse depends upon an accurate history combined with proper endoscopic evaluation. Tracheomalacia can be caused by a diffuse process of congenital origin or by a localized abnormality. The cases of acquired tracheomalacia occur with increasing frequency both in children and adults and are often not clearly recognized. These lesions may result from indwelling tracheostomy and endobronchial tube, chest trauma, chronic tracheobronchitis, inflammation (relapsing polychondritis), secondary to pulmonary resection, tracheal malignancy (cylindroma), and idiopathically. We present the case of a 59 years old male with acquired tracheobronchomalacia, associated with tracheopatia osteochondroplasica, secondary to COPD and a chronic parenchimal infection, on a diabetes mellitus type II background.
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PMID:[Tracheomalacia and secondary tracheopatia osteocondroplasica - a case report]. 1197 2

Histological, cytochemical and ultrastructural changes in giant black tiger shrimp Penaeus monodon were investigated at various time intervals after injection with yellow head virus (YHV). Hemocytes, lymphoid organs (LO) and gills were the main focus of the study. After injection with YHV, onset of mortality varied from 36 h onward. By normal hematoxylin and eosin staining, the 3 tissues showed clear and increasing prevalence of nuclear condensation, pyknosis and karyorrhexis from approximately 36 h post-injection (p.i.) until death, although pathology was evident in the LO as early as 12 h p.i. in some shrimp. By nuclear DNA staining with 4',6-diamidino-2-phenylindole (DAPI) and by specific labeling of 3'-OH ends of nuclear DNA using a technique called terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick-end labeling (TUNEL), cells of the 3 tissues showed evidence of chromatin condensation and DNA fragmentation, respectively. Both are generally considered to be characteristic of apoptosis. In addition to TUNEL labeling, evidence for DNA fragmentation was supported by the appearance of approximately 200 base pair DNA ladders at approximately 48 h p.i. in hemocytes of YHV-infected but not uninfected shrimp. Transmission electron microscopy (TEM) of LO tissue revealed features of apoptosis in tissues of YHV-infected shrimp only. These included marginated, condensed and fragmented chromatin without concurrent cytoplasmic damage. Histological, cytochemical, ultrastructural and biochemical data were consistent with the hypothesis that widespread and progressive apoptosis occurred in susceptible shrimp infected with YHV. Although no specific tests were carried out to determine whether this purported apoptosis was the cause of mortality, moribund shrimp had extensive deterioration of vital tissues such as the hemolymph, gills, heart and LO, suggesting that many essential bodily functions had been severely compromised. This probably resulted in the gross signs of lethargy and weakness seen, and it is reasonable to suggest that further, progressive deterioration could have led to the collapse of vital functions followed by death.
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PMID:Evidence for apoptosis correlated with mortality in the giant black tiger shrimp Penaeus monodon infected with yellow head virus. 1200 39

There are a growing number of reports of bone problems (avascular necrosis and osteonecrosis) among people with HIV. These problems are caused by a lack of blood supply in the bone, which leads to the deterioration and death of bone tissue. Generally, bones try to repair themselves. But bones that support a lot of weight, like the hip, can weaken when this condition occurs. This may cause the bone to fracture or collapse. This condition can also lead to severe pain and inflammation or overgrowth of bone in and around the joints (osteoarthritis). While still relatively uncommon, people should be aware of reports of avascular necrosis that have led to hip fracture or dislocation. Symptoms of pain associated with avascular necrosis also commonly affect the shoulder and/or knee. Avascular necrosis is different from osteoporosis, a general term for a progressive loss in bone density that results in skeletal (bones that make up the framework of the body) weakness.
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PMID:Bone problems. 1217 Oct 7

This discussion of the issues relating to the problem posed by population explosion in the developing countries and economic growth in the contemporary world covers the following: predictions of economic and social trends; the Malthusian theory of population; the classical or stationary theory of population; the medical triage model; ecological disaster; the Global 2000 study; the limits to growth; critiques of the Limits to Growth model; nonrenewable resources; food and agriculture; population explosion and stabilization; space and ocean colonization; and the limits perspective. The Limits to Growth model, a general equilibrium anti-growth model, is the gloomiest economic model ever constructed. None of the doomsday models, the Malthusian theory, the classical stationary state, the neo-Malthusian medical triage model, the Global 2000 study, are so far reaching in their consequences. The course of events that followed the publication of the "Limits to Growth" in 1972 in the form of 2 oil shocks, food shock, pollution shock, and price shock seemed to bear out formally the gloomy predictions of the thesis with a remarkable speed. The 12 years of economic experience and the knowledge of resource trends postulate that even if the economic pressures visualized by the model are at work they are neither far reaching nor so drastic. Appropriate action can solve them. There are several limitations to the Limits to Growth model. The central theme of the model, which is overshoot and collapse, is unlikely to be the course of events. The model is too aggregative to be realistic. It exaggerates the ecological disaster arising out of the exponential growth of population and industry. The gross underestimation of renewable resources is a basic flaw of the model. The most critical weakness of the model is its gross underestimation of the historical trend of technological progress and the technological possiblities within industry and agriculture. The model does correctly emphasize the exponential growth of population as the source of several complications for economic growth and human welfare. Stabilization of population by reducing fertility is conducive for improving the quality of population and also advances the longterm management of the population growth and work force utilization. The perspective of longterm economic management involves populatio n planning, control of environmental pollution, conservation of scarce resources, exploration of resources, realization of technological possibilities in agriculture and industry and in farm and factory, and achievement of economic growth and its equitable distribution.
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PMID:Population growth and economic growth. 1231 95

Multiple myeloma (MM) is a plasma cell malignancy characterized by infiltration of bone marrow, bone destruction, infiltration of soft tissues with plasma cells, and suppression of normal hematopoiesis. The production of monoclonal immunoglobulins with or without light chains is a major feature of the disease. Full spectrum of plasma cell dyscrasias include monoclonal gammapathy of undetermined significance, smouldering myeloma, indolent multiple myeloma, and fully developed, symptomatic multiple myeloma. The usual presenting features of MM include bone pain, weakness, fatigue, fever and infection. Neurologic symptoms are less common but one must not forget that MM may present with a neurologic disease. Careful neurologic history and examination are mandatory in patients with MM. Neurologic symptoms may be a direct manifestation of MM or may be due to the immune effect of monoclonal proteins directed against different neural structures. Finally, metabolic consequences (uremia, hypercalcemia, hyperviscosity) of MM may produce a broad spectrum of different neurologic symptoms including headache, blurring of vision, drowsiness, precoma, coma, vertigo, ataxia, hemiparesis and epileptiform seizures. The most common location of bone changes in MM is the thoracic spine, where it causes osteolytic changes with consequent compressive fractures. The most disastrous sequel is paraplegia. Multiple vertebral involvement with the evidence of osteolytic changes in other bones is usual, but solitary vertebral myeloma may occur. Myeloma usually involves the bone of the vertebral body and then spreads into the extradural space. However, patients with solitary extradural myeloma have been reported. Skull myeloma is frequently asymptomatic. It may grow externally or, rarely, there is intracranial expansion. Involvement of the cranial nerves is not rare, with II, V, VI, VII and VIII cranial nerves being most often affected. Isolated intracerebral plasmacytomas are extremely rare. Diagnostic approach includes plain X-rays of the skeleton, which was found to be the method of choice for demonstration of osteolytic changes, whereas magnetic resonance with gadolinium enhancement most reliably displays the degree of vertebral involvement and demonstrates any associated soft tissue mass. Current treatment of osteolytic changes in multiple myeloma include chemotherapy, radiotherapy in combination with dexamethasone, monthly infusions of bisphosphonates, surgical decompression, and kyphoplasty. Therapeutic approach is dictated by the presenting symptoms. In case of pain as the predominant symptom, treatment with chemotherapy and radiotherapy may be appropriate. Compressive symptoms are relieved with dexamethasone followed by radiotherapy and chemotherapy. Surgical decompression is used in patients with vertebral collapse and vertebral instability. Kyphoplasty is a new method used in the treatment of osteolytic changes of vertebral bodies. A viscous cement is injected into the cavity by a balloon-like inflatable bone tampon. It has been successfully employed to improve the quality of life, to reduce pain, and to increase overall functioning in patients with vertebral compression fractures by restoring most of the original height of the vertebral body. Bisphosphonates reduce pain associated with osteolytic changes in multiple myeloma, but also significantly reduce skeletal events (pathologic fracture, spinal cord compression, surgery or irradiation of bone) via unknown mechanism. It seems that bisphosphonates, by inhibiting bone resorption, alter the microenvironment in which the MM cells grow.
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PMID:[Neurologic sequelae of bone changes in multiple myeloma and its therapy]. 1263 Mar 41

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
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PMID:Carbon monoxide and the nervous system. 1266 97

Ambulatory electrocardiography techniques are superior to standard electrocardiography in evaluating rhythm disturbances in dogs with episodic weakness or collapse. Disadvantages include cumbersome equipment, short recording periods and an inherent delay in trace analysis. A small programmable cardiac event recorder with combined automatic and owner-triggered recording capability was evaluated in 13 healthy dogs in a hospital environment. The unit was well tolerated and produced diagnostic recordings directly to a personal computer, with useful information about continuous heart rate. It detects premature complexes, pauses and bradycardias according to programmed detection thresholds. These events were counted frequently but trace review revealed concerns regarding specificity. Recordings were often triggered by sinus arrhythmia, sinus tachycardia and unclassifiable rate changes rather than by clinically significant arrhythmias. Correct detection of ventricular ectopic complexes, a single supraventricular premature complex, sinus arrest and second-degree atrioventricular block occurred in individual dogs. Visual review of all automatically recorded events was essential and significantly increased the time required for event recording analysis. Manual recordings might be more useful and the overall results suggest that further studies are warranted to evaluate the system in clinical cases in the home environment.
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PMID:Assessment of an ECG event recorder in healthy dogs in a hospital environment. 1270 67

A 10-year-old collie-cross presented with intermittent episodes of pelvic limb weakness and collapse. Hypoglycemia, secondary to an insulin-secreting beta cell tumor, was suspected on the basis of clinical signs and serum biochemistry. Conservative dietary therapy consisted of multiple small meals, limited exercise, and avoidance of foods containing simple sugars.
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PMID:Insulin-secreting beta cell neoplasia in a 10-year-old dog. 1289 92


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