HEART RATE RESPONSE HABITUATION IN HIGH-RISK PREMATURE INFANTS

The hypothesis suggested by Luria (1963) that infants with central nervous system damage fail to habituate to repeated stimulation was tested using an experimental group whose clinical course suggested a relatively high probability of CNS damage, a control group matched for age in weeks since conception, and a group of normal, fullterm infants. An auditory stimulus at 80 db SPL was presented for 3 sec at 20-sec intervals. Heart rate change averaged across time on Trials 1–5 and Trials 26–30 were compared. The hypothesis was not confirmed, since significant habituation was found on Trials 26–30 for all groups. However, latency of response was significantly longer in high-risk Ss. A developmental trend toward decreased latency of response with increasing gestational age was identified.     

AECA AND ANCA IN PATIENTS WITH PREMATURE ATHEROSCLEROSIS

Autoimmunity is suggested to play a pathogenetic role in premature atherosclerosis. Since atherosclerosis and vasculitis seem pathogenetically related, we hypothesized that ANCA, an important antibody in vasculitis, plays a role in atherosclerosis as well. We therefore investigated the prevalence of ANCA in patients with premature atherosclerosis and related the presence of these antibodies to levels of AECA and markers of inflammation. Methods & Results: In a cohort of 286 patients with premature atherosclerosis the prevalence of ANCA was 5.6% (16/286). All had perinuclear ANCA. More females were ANCA-positive (8M/8F vs. 200M/70F, p=0.03). In a nested case-control study, comparing the 16 ANCA-positive patients with 32 controls, levels of AECA were higher in the first (7.32±0.91U vs. 5.52±0.41U, p<0.05). Conclusion: ANCA does not seem to play a major role in premature atherosclerosis. Whether elevated levels of AECA in ANCA-positive patients with premature atherosclerosis reflect more extended vascular disease remains to be determined.     

DIROFILARIAL INFECTION IN HUMAN LUNGS

Two cases of dirofilarial infection in the human being were reported. Dirofilarial infection is common in dogs but rather rare in human. A review of Japanese literature disclosed 13 cases of human dirofilarial infection. Scarcity of symptoms and its morphological similarity to tuberculosis or infarction as well as the popularity in pets suggest that the true incidence of infection may actually be higher than the above figure. Our cases alert us for the recognition of human dirofilarial infection, and careful examination of multiple sections in granulomatous or nonspecific infarcted lesions is suggested.     

室性早搏80例心电图分析

室性早搏(以下简室早)是临床上最常见的一种心律失常。要判断系功能性或器质性,有时殊不易。本文通过分析80例室早在心电图上的起源部位、频率、时限、电压、切迹的变化,结合临床资料探讨功能性与器质性室早在心电图上的表现。     

ALIMENTARY TRACT LESIONS IN CYTOMEGALOVIRUS INFECTION

Ten autopsy and 2 biopsy cases of cytomegalovirus (CMV) infection of the alimentary tract were studied. CMV infection was microscopically determined by the presence of cytomegalic inclusion as well as by the immunofluorescent method. Clinical manifestations such as abdominal pain, diarrhea, hema-temesis, bloody stool, perforation, and/or abdominal distension with paralytic ileus were observed in 8 autopy cases and 1 biopsy case. Disappearance of cytomegalic cells was confirmed by the follow-up study in the biopsy cases. Macroscopically, mucosal hemorrhage or ulceration was found in the gastrointestinal tract from the esophagus to the colon. Ulceration showed a characteristic well-defined punched-out appearance. The esophagus was the most frequently involved organ. However, no cytomegalic cells were found in the squamous epithelium. In the stomach, regenerated epithelial cells were frequently involved in the deeper part of glands. Numerous endothelial cells transformed into cytomegalic cells in the mucosa surrounding the ulcer in the esophagus, stomach, and intestine. Ischemia caused by cytomegalic changes of vascular endothelial cells is thought to play an important role in the pathogenesis of the ulcer of the gastrointestinal tract.     

CYTOKINES IN EXPERIMENTAL HERPES SIMPLEX VIRUS INFECTION

Herpes simplex virus (HSV) causes productive and latent forms of infection in humans and experimental animals. The primary infection and reactivation of the latent infection evoke an immune response in the host organism, involving activities of macrophages, CD4+ and CD8+ lymphocytes, and B lymphocytes. Strong cytokine responses are associated with the acute and recurrent phases of HSV infection. Also, during the latent phase of HSV infection in the senory ganglia, expression of certain cytokines can be detected. The cytokine response to HSV infection is dominated by proinflammatory and Th1 type cytokines; however, Th2 type cytokines such as interleukin-4 also are expressed in the infected tissue. The use of novel HSV-derived, cytokine-expressing gene therapy vectors necessitates studies on the possible modulation of the host responses by the virus-encoded cytokine transgenes. This review focuses on the roles of certain Th1 and Th2 type cytokines in different phases of the experimental HSV infections.