the occurrence of clinically evident cerebral hyperperfusion. Crossed cerebellar hypoperfusion (CCH) is a reduction in blood flow in the cerebellar hemisphere contralateral to a supertentorial lesion. This phenomenon can be seen after CEA. The authors sought to clarify the significance of postoperative CCH in patients with cerebral hyperperfusion using SPECT scanning and tests of cognitive impairment.Brain perfusion was measured using SPECT scanning before and immediately after CEA and on postoperative day 3 in 80 patients who underwent CEA for Ͼ70% stenosis. Postoperative CCH was determined by differences between asymmetry of perfusion in the cerebellar hemispheres before and after CEA. Patients also underwent neuropsychologic testing preoperatively and at 1 month after CEA.The authors used a definition of a 100% increase in cerebral blood flow for cerebral hyperperfusion and found that it had developed in 11 of 80 patients after CEA. SPECT scans were performed immediately after CEA and on postoperative day 3. Of the 11 patients in whom cerebral hyperperfusion developed, CCH was observed in seven on postoperative day 3. Three patients had cerebral hyperperfusion syndrome and exhibited cerebral hyperperfusion and CCH on postoperative day 3, and postoperative cognitive impairment developed. Four of eight patients with asymptomatic cerebral hyperperfusion exhibited CCH. Three of these patients exhibited postoperative cognitive impairment. The four patients with asymptomatic cerebral hyperperfusion who did not have CCH did not experience postoperative cognitive impairment.Comment: Cerebral hyperperfusion after CEA is more complicated than most are aware. The article points out that it occurs more frequently than is generally thought, has different patterns of hyperperfusion, and can result, at least when measured using sophisticated neuropsychiatric testing, in cognitive impairment even in the absence of clinical hyperperfusion syndrome.

The role of immune mechanisms in the pathogenesis of Ebola hemorrhagic fever (EHF) remains to be elucidated. In this report, the serum cytokine levels of patients who died of EHF were compared with those of patients who recovered and those of control patients. A marked elevation of interferon (IFN)-gamma levels (>100 pg/mL) was observed in sequential serum samples from all fatal EHF cases compared with patients who recovered or controls. Markedly elevated serum levels of interleukin (IL)-2, IL-10, tumor necrosis factor (TNF)-alpha, and IFN-alpha were also noted in fatal EHF cases; however, they had a greater degree of variability. No differences were noted in serum levels of IL-4 and IL-6. mRNA quantitation from blood clots of the same patients showed relatively elevated levels of TNF-alpha and IFN-alpha in samples from EHF patients. Taken together, these results suggest that a high degree of immune activation accompanies and potentially contributes to a fatal outcome in EHF patients.

Plasma markers of inflammation were significantly elevated and correlated with increased LV dimensions and lower LVEF at presentation. Baseline Fas/Apo-1 and higher NYHA FC were the only predictors of mortality. Normalization of LVEF was only observed in 23% of this African cohort.

The major significance of the capsular polysaccharide of C. neoformans is its role in potentiating opportunistic infections by the yeast. It has the ability to exert a broad spectrum of influences on the immune response, from activation of phagocytic cells and complement components of the alternative pathway, to the induction of specific antibody, T-suppressor cells, DTH responses, and cytokines (51). These biological properties along with the serotype specificities are all determined by the physical properties and chemical structures of the polysaccharide antigens that compose the capsule. There is evidence not only for an association of lethal infections with serotype A in patients with advanced AIDS (34, 56), but also for a role for the capsule in directly influencing the infection of CD4+ cells by HIV (57). Together, these phenomena raise intriguing questions about the possible connection between the chemistry of these capsular antigens and cryptococcal infections in AIDS patients. One speculation is that AIDS creates the optimal physiological conditions for the establishment and spread of cryptococcosis. It has been observed that during the progression of AIDS there is a shift towards a T-2 response (14). This could lead to conditions that would inhibit the cellular immune responses that block dissemination of cryptococcal infections. Thus, an important consideration in the application of vaccine or immune modulation therapies in the treatment of cryptococcosis in AIDS victims would be the design of vaccines that could boost the T-1 immune response. It has been shown that the form and dose of an antigenic challenge can influence the induction of a T-1 or T-2 immune response (61). Recently, Murphy has reported that gamma interferon and interleukin 2 are up-regulated in the spleens of mice that produce anticryptococcal TDH and TAMP cells in response to immunogenic doses of cryptococcal culture filtrate antigen given with Freund's complete adjuvant (49). Perhaps purified cryptococcal antigens (e.g., MP) conjugated to an appropriate carrier or adjuvant could be used in therapeutic strategies to limit cryptococcosis in immunocompromised individuals. Future investigations of virulence and pathogenicity in the context of defined polysaccharide antigens from encapsulated strains of C. neoformans will contribute to a better understanding of the regulation of cryptococcal infection and immunity at the cellular and molecular levels.(ABSTRACT TRUNCATED AT 400 WORDS)