No abstract available.
Diagnosis* ; Leptospirosis* ; Scrub Typhus*

No abstract available.
Brain* ; Craniocerebral Trauma* ; Head* ; Humans

No abstract available.
DNA* ; Nucleic Acid Hybridization*

We have experienced a case of plexiform neurofibrorna of the right upper eyelid and orbit in a 12-year-old girl who had typical skin features of neurofibromatosis and no family history. The non-pulsating proptosis of the right eye and diffuse thickening with hypertrophy of the upper lid, had increased insiduciusly since the birth on. Biopsy taken from eyelirl lesion showed the features of plexiform neurofibroma. Skull X-ray and brain computerized tomogram showed that the right orbit was wider, with the enlarged mass and defects in orbital roof and lesser and greater wings of the sphenoid bone. The surgical excision of the right eyelid lesion was performed.
Biopsy ; Brain ; Child ; Exophthalmos ; Eyelids* ; Female ; Humans ; Hypertrophy ; Neurofibroma, Plexiform* ; Neurofibromatoses* ; Orbit* ; Parturition ; Skin ; Skull ; Sphenoid Bone

No abstract available.
Arteriovenous Malformations*

Pulmonary agenesis is a very rare anomaly. It is defined as total absence of the pulmonary parenchyma, vascular structures, and bronchi beyond the carina. We experienced a case of right pulmonary agenesis in association with other congenital defects who died at 1 day of age. The other defects included: esophageal atresia, tracheoesophageal fistula, cardiac malformation, anal atresia and a malformed left thumb. The cardiac malformations were a type of Pentalogy of Fallot, composed of right ventricular hypertrophy, ventricular septal defect, an overiding of aorta, pulmonary atresia, and an atrial septal defect. Hand roentgenograms of the malformed left thumb showed an unarticulated metacarpopharyngeal joint. This unique combination of anomalies is extremely rare.

To a better understanding for molecular mechanism of oncogenesis in hepatoma, primary hepatocellular carcinoma and hepatoma cell lines (Hep 3B, PLC/PRP/5, Hep G2) were subjected to detailed cytogenetic analysis with G-banding method after cell cultures. No cloned chromosomal abnormalities were found in the primary hepatoma (below 100%). On the other hand, all hepatoma cell lines were cloned, the specific chromosomal abnormalities in Hep 3B were del(1p21), del(6q14) and t(1 ; 11)(pll ; q13). Genes of AMY1A, CGA, SEA and HSTF1 were located on 1p21 and 6q14 respectively. SEA and HSTF1 were located on 11q13. Regions of chromosome abnormalities in PLC/PRF/5 were the same found in Hep 3B. Besides, del(1q32) and del(1p32) were also cloned. Gene of CR1 and MYCL1 were located on 1q32 and 1p32 respectively. The characteristic findings of chromosome abnormalities in Hep G2 were del(1p31) and del(1q22). And GST1 and DAF were located on these regions each other Del(6q11) and del(1p22) were also found in Hep G2. From the above results, it is presumed that HBV may integrate to AMY1A gene or near this gene and leads to loss of functions to this gene. And impaired regulation of CGA occurs in next step. SEA, HSTF1 and MYCL1 oncogenes may act as a progressing factor of tumourgenesis in HBsAg(+) hepatoma. Some factors like chemical agents may cause functional loss of GST1 and DAF at first and functional loss of cell regulation of CGA occurs in next step. SKI oncogene may promote the progression of carcinogenesis in this cell line. Whether any causative agents are involved in carcinogenesis of hepatoma, functional loss of CGA gene is the most important factor in tumour-genesis in hepatoma.
Carcinogenesis ; Carcinoma, Hepatocellular* ; Cell Culture Techniques ; Cell Line ; Chromosome Aberrations* ; Clone Cells ; Cytogenetic Analysis ; Hand ; Humans* ; Methods ; Oncogenes

No abstract available.
Colorectal Neoplasms* ; Humans ; Male*

No abstract available.

No abstract available.
Anesthesia* ; Humans ; Outpatients*