Laser technology, characterized by its precision and high-intensity applications, is being used increasingly in medical treatments, ranging from oncology to dermatology and ophthalmology. Neutropenia, a hematological condition marked by a critically low neutrophil count, presents significant clinical challenges because of its association with increased infection risk. This review explores the intricate relationship between laser technology and neutropenia, emphasizing the mechanisms through which laser treatments can induce neutropenia, their clinical implications, and strategies for mitigation. High-intensity laser therapies, such as photodynamic therapy, can generate systemic inflammatory responses and oxidative stress, potentially impairing the bone marrow function and reducing neutrophil production. Clinically, managing the risk of neutropenia involves pre-treatment evaluation, continuous monitoring of blood counts, and prophylactic measures such as granulocyte colony-stimulating factor. Recent advancements, including the development of selective photosensitizers and personalized treatment protocols, show promise in enhancing the safety and efficacy of laser treatments. This review underscores the need for comprehensive patient management and ongoing research to balance the therapeutic benefits of laser technology with potential hematological risks, ultimately aiming to optimize patient outcomes while minimizing the adverse effects.

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.

Bart's syndrome was initially described as a genodermatosis characterized by congenital localized absence of the skin with blistering and nail deformities 1-3. However, it is considered as any type of epidermolysis bullosa(EB) with localized congenital absence of the skin on the extremities. A 33-day-old fbmale baby was presented with congenital absence of the skin over the left shin and dorsa of both feet which were covered with the thin, translucent, and brown-red glistening membranes. Blistering of the right calf and left great toe nail deformity were also noted. She was diagnosed as a recessive dystrophic EB by the histopathological, ultra- structural and immunomapping studies.
Blister ; Congenital Abnormalities ; Extremities ; Foot ; Membranes ; Skin ; Toes

The final degrees of education for the third and fourth authors were mutually misplaced.

No abstract available.
Lipomatosis*

Cryosupernatant which is the residual plasma fraction after removing cryoprecipitate has been used for plasma exchange in thrombotic thrombocytopenic purpura and hemolytic uremic syndrome replacing the fresh frozen plasma. Recently, the unusually large yon Willebrand factor multireefs (ULvWFM) has been observed in patients with refractory or chronic relapsing hemolytic uremic syndrome as well as thrombotic thrombocytopenic purpura which disappeared by infusion or plasma exchange with cryosupernatant, and infusion of fresh frozen plasma, the largest multimers of yon Willebrand factor were replenished that it might be a cause of refractoriness. This study was conducted to investigate the characteristics of home-made cryosupernatant from thawed fresh frozen plasma and its thehrapeutic effect in a hemolytic uremic syndrome patient. The level of fibrinogen, coagulation factor VIII, vWF antigen, and ristocetin cofactor activity was decreased and yon Willebrand factor multimers were barely seen in cryosupernatant than those of in fresh frozen plasma. A hemolytic uremic syndrome patient tried with exchange and infusion of cryosupernatant showed excellent recovery. It is concluded that home-made cryosupernatant shares many of the features of fresh frozen plasma except factor VIII, especially von Willebrand factor multimers, and thus it could be a useful alternative to fresh frozen plasma in case of refractory hemolytic uremic synydrome.
Factor VIII ; Fibrinogen ; Hemolytic-Uremic Syndrome ; Humans ; Plasma Exchange* ; Plasma* ; Purpura, Thrombotic Thrombocytopenic ; von Willebrand Factor