No abstract available.

We have examined the regenerative capabilities of the human scalp hair follicle after grafting the lower half of the follicle. Twenty-eight of 32 intact whole-hair follicles isolated from the human scalp regenerated hairs when grafted onto the forehead of the same person. Seven of the 15 lower-half follicles regenerated complete hair follicles 8 months after grafting showed that the lower-half follicle implant reconstituted the complete hair follicle. The sebaceous gland was not regenerated, but there was an outgrowth in the sebaceous gland regPark ion. Some grafts formed epithelial cysts. Two years after grafting, the histological examination of the regenerated follicle from the lower-half implant showed that the sebaceous gland was completely regenerated. While an intact follicle shows prominent naked shaft outgPark Park Parkrowth, the sheath grows concomitantly with the shaft in lower-half follicles in culture. If grafted lower-half follicles were located too deep, the regrown sheath could not reach the epidermal layer. In this situation, the formation of an epidermal cyst was likely.
Epidermal Cyst ; Forehead ; Hair Follicle* ; Hair* ; Humans ; Scalp ; Sebaceous Glands ; Transplants*

Cutaneous horn is a clinical diagnosis based upon the presence of a large protuberant mass of keratin. We report a case of cutaneous horn arising from dermatofibroma in a 31-year old woman. A silver whitish colored comical hyperkeratotic protruding lesion (1.0  0.7 cm size) from the red brown colored nodule was observed. Histopathologic findings showed characteristic findings of dermatofibroma and cutaneous horn. The lesion was removed by surgical excision.
Animals ; Diagnosis ; Female ; Histiocytoma, Benign Fibrous* ; Horns* ; Humans ; Silver

By means of hospital-based data over 8 years we sought to evaluate the clinical indications and incidence of emergency peripartum hysterectomy by demographic characteristic and reproduction history. From the obstetric record of all deliveries at Chung Goo Hospital between Jan. 1, 1990, and Nov. 31, 1997, we identified all women undergoing emergency cesarean hysterectomy, calculated incidence rates, conducted statistical tests of linear trends and heterogenety, and observed the clinical indicatons preceding the onset of this procedure. There were 16731 deliveries during this period, Cesarean hysterectomy was performed in 24 of 5993 cesarean sections(0.40%) and in 10 of 10738 vaginal deleveries(0.09%), so more frequently after cesarean section than vaginal delivery. The age of patients varied from 22 to 40 years old. The higher the age and the parity of patients, the higher incidence of cesarean hysterectomy was noted. The most common indication of cesarean hysterectomy was uterine atony(52.94%) followed by placental disorders(41.18%), uterine myoma with pregnancy(2.9%) and uterine rupture (2.9%). All patients who had hysterectomy received transfusion from 1 pint to 57 pints. The postoperative complications were bladder injury, febrile morbidity, disseminated intravascular coaguolopathy and wound disruption. There were three maternal deaths, the cause was disseminated intravascular coaguolopathy and amniotic embolism. The data identifiy uterine atony as the primary cause for gravid hysterctomy. The data also illustrated how the incidence of emergency peripartum hysterectomy increases significantly with increasing parity, especially when influenced by a current placenta previa or a prior cesarean section. Maternal morbidity remained high.
Adult ; Cesarean Section ; Embolism ; Emergencies ; Female ; Humans ; Hysterectomy* ; Incidence ; Leiomyoma ; Maternal Death ; Parity ; Peripartum Period* ; Placenta Previa ; Postoperative Complications ; Pregnancy ; Reproduction ; Urinary Bladder ; Uterine Inertia ; Uterine Rupture ; Wounds and Injuries

A 49-year-old woman with anemia who developed headache and seizure after blood transfusion was diagnosed with posterior reversible encephalopathy syndrome (PRES). Magnetic resonance imaging showed typical PRES findings including lesions in bilateral parieto-occipital subcortical white matter and overlying cortex. Only a few cases of PRES after transfusion have been reported and this case is unique in that there was a latent period between infusion and development of PRES. We postulate that rapid change of hemoglobin level may disrupt cerebral autoregulation and result in delayed PRES. We suggest that neurological symptoms after blood transfusion should be appropriately investigated.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.