Alzheimer's disease(AD) is one of the most common causes of mental deterioration in elderly individuals, accounting for around 45~60% of the overall cases of dementia over 65 years of age. Although there is presently no "cure" for AD, a large number of potential therapeutic interventions have emerged to correct cholinergic dysfunctions. Currently, cholinergic therapy, particularly cholinesterase inhibition, represents the most realistic approach to the symptomatic treatment of AD. Modest efficacy for mild to moderate AD has been shown in well-designed clinical trials for tacrine, donepezil, rivastigmine, and galantimine. Among other treatment options, estrogen replacement therapy in postmenopausal women is under active investigation, but recent studies showed somewhat disappointing results. Epidemiological and clinical data suggest that nonsteroidal anti-inflammatory drugs are beneficial in the treatment and prevention of AD. But prednisone and COX-2 inhibitor, celecoxib showed no clinical benefit in recent studies. Alpha-tocopherol and gingko biloba showed some beneficial effect in delaying the progression of AD and enhancing cognitive functions. Immunization with beta amyloid peptide was considered to be the only method to prevent and halt disease progression in patients with AD. Recently, phase II clinical trial using synthetic beta amyloid peptide (AN-1792) was discontinued because some patients showed neuro-inflammation which may be caused by autoimmune responses.
Aged ; alpha-Tocopherol ; Alzheimer Disease* ; Amyloid ; Autoimmunity ; Celecoxib ; Cholinesterases ; Cognition ; Dementia ; Disease Progression ; Estrogen Replacement Therapy ; Female ; Ginkgo biloba ; Humans ; Immunization ; Methods ; Prednisone ; Rivastigmine ; Tacrine

No abstract available.
Hypertension, Renovascular*

No abstract available.
Child* ; Humans ; Male*

No abstract available.
Diabetes Mellitus* ; Insulin*

No abstract available.
Child* ; Humans

No abstract available.
Diagnosis*

No abstract available.
Animals ; Growth Hormone* ; Hypothyroidism* ; Rats*

No abstract available.

Multiple symmetric lipomatosis is a rare disease and affects almost exclusively middle aged man, usually with a background of excessive a alcohol intake. The disease is characterized by progressive growth of subcutaneous fat masses which are located symmetrically at neck, shoulders, chest, abdomen and groin, and which subsequently penetrate deeply into the surrounding spaces and structures with symptomatic compression of deep organs, such as trachea. A recent survey revealed a high incidence of sometic and autonomic neuropathy. The exact cause of the disease is not known, but a hyperplastic mechanism has been postulated, with in vitro studies demonstrating a defect in adrenergic-stimulated lipolysis of lipomatous tissue. We have experienced two cases of multiple symmetric lipomatosis. Case 1 was a 59-year-old male, complaining of slowly enlarging doughunt ring-shaped mass at his neck. He had a habit of excessive alcohol intake for many years. The subcutaneous mass at the neck was excised. The pathology report described the specimen as "normal adipose tissue". Case 2 was a 49-year-old male, complanining of slowly enlarging multiple symmetric masses at the neck, shoulders, chest, abdomen, flank and groin over a period of 6 years. He also complained of mild muscular weakness. He had a habit of excessive alcohol intake for many years. The subcutaneous mass in the neck was excised. The specimen had a tendency to form globular masses and microscopically indistinguishable from mature adipose tissue.
Incidence

The diagnostic value of GHRH in assessing GH secretion in biochemical GH sufficient short children was examined. GHRH (1microgram/kg i.v bolus) was given to three groups (upslope, trough, downslope) arbitrarily classified according to the basal pulsatile GH secretory pattern before GHRH administration. Cmax following GHRH administration were variable and overlapping. Two children in downslope group, three children in trough group, and one child in upslope group showed subnormal GH responses to GHRH administration despite of normal GH response to more than two classical GH provocative tests (Fig.1). The time of maximal GH response after GHRH administration (Tmax) in upslope group was significantly faster than those in other two groups (Fig.2). There was a highly significant correlation between AUC and Cmax (p<0.001) after GHRH administration (Fig.3) which suggests that AUC or Cmax can be used for parameters of GH response to GHRH each other. The AUC and Cmax after GHRH administration between three groups were significantly different (2764+/-579.1ng/ml min, 52.6 ng/ml, respectively in upslope group; 1645+/-383.9ng/ml min, 37.7+/-9.4ng/ml, respectively in downslope group; 1098+/-150.2ng/ml min, 26.3+/-4.5ng/ml, respectively in trough group)(p<0.005) (Fig.4, Table 1). In conclusion, GH responses to GHRH adminstration could be variable according to the basal GH secretory rhythm. Therefore, we should be cautious in interpreting the GH response to GHRH to evaluate the GH secretory capacity because subnormal GH response to GHRH administration could be observed even if normal GH response to classical GH provocative tests. In addition, the classification of these arbitary three groups (upslope, trough, and downslope) is remained to defined so as to promote the diagnostic value of GHRH in GH deficiency.
Area Under Curve ; Child* ; Classification ; Growth Hormone* ; Humans