We studied apoptosis in a human ileocecal adenocarcinoma tumor cell line (HCT-8) infected with Cryptosporidium parvum, from 2 to 72 h postinfection (h.p.i.). At 2 h.p.i., the percentage of annexin V-positive cells in the cell culture had increased to 10% compared to 2.5% in noninfected control culture; sorted infected cells expressed mRNA of FasL, the active form of caspase 3, and high caspase 3 activity, whereas the noninfected neighboring cells sorted from the same culture showed no signs of apoptosis. At 24 h.p.i., the percentages of early (annexin V positive) and late (DNA fragment) apoptotic cells were 13 and 2%, respectively, in the entire cell culture, and these percentages were not statistically significant in comparison with those from noninfected control cultures. At this time, sorted infected cells expressed the inactive form of caspase 3, a low caspase 3 activity, and the antiapoptotic protein Bcl-2. Noninfected cells sorted from the same culture showed expression of the active form of caspase 3, a moderate caspase 3 activity, and no Bcl-2 expression. At 48 h.p.i., the percentages of early and late apoptotic cells and caspase 3 activity had increased in the total cell culture, and both sorted infected and noninfected cells showed the active form of caspase 3. These results show that C. parvum, depending on its developmental stage, can inhibit (at the trophozoite stage) or promote (at the sporozoite and merozoite stages) host cell apoptosis, suggesting that it is able to interact with and regulate the host-cell gene expression.

Bismuth subcitrate-based b.i.d. quadruple therapy was an excellent primary and salvage therapy and should be considered as first line therapy.

A longitudinal study was conducted to assess the value of quantitative ultrasound (QUS) measurement in predicting the risk of fracture and to evaluate how QUS parameters change with ageing and the climacteric. A group of 211 female subjects underwent assessment by QUS at the distal metaphysis of the first phalanx of the last four fingers of the hand on two occasions 3 years apart. The subjects were selected from outpatients attending the orthopaedic clinic, provided they were not affected by metabolic disease or under treatment with drugs known to interfere with bone metabolism. In vivo the coefficient of variation and the standardized coefficient of variation of the QUS device were respectively 0.5% and 3.5%. The correlation between the values of the amplitude-dependent speed of sound (AD-SoS) in the two measurements was r = 0.92. In 77.3% of the subjects during the observation period we recorded a reduction in AD-SoS. During the study 22 fractures were observed in peripheral sites, 8 of which were associated with 'low-energy trauma'. By multiple logistic regression analysis we found that the relative risk of fracture for a 1 SD reduction in AD-SoS was 1.5 (95% CI 1.1-1.7) (p < 0.03). The percentage of low-energy fractures significantly increased among those subjects with an AD-SoS value lower than 1850 m/s (T-score < -3.5) at the first examination (p <0.0001). QUS investigation proved to be especially sensitive to hormonal changes associated with the climacteric: we observed a mean decrease of 56 m/s in the AD-SoS for women who entered the menopause between the first and the second QUS test (average time since menopause 2 years), as against 10 m/s in subjects remaining premenopausal. In a group of 146 subjects with 'normal' Ad-SoS at the first examination, we observed a significant reduction in AD-SoS only after 40 years of age. This study demonstrates that measurement of the AD-SoS at the phalanx is reproducible, can be employed to assess the risk of fracture, and is able to detect age-related alterations in bone tissue.

No abstract

Cell-mediated immunity during the muscular phase of Trichinella infection in humans was studied. Cell proliferation, the phenotypic changes in the T-cell population, and expression and production of cytokines were examined by using peripheral blood mononuclear cells (PBMC) collected at different times postinfection from 10 individuals who had acquired Trichinella spiralis and five individuals who had acquired Trichinella britovi in two distinct outbreaks. T. spiralis and T. britovi crude worm extracts induced proliferation of PBMC from T. spiralis-and T. britovi-infected donors. Cytokine gene expression showed a predominant type 2 pattern for the entire period of infection studied, although gamma interferon (IFN-␥) was expressed. Interleukin-2 (IL-2), IL-5, IL-10, and IFN-␥ production was found in PBMC of all donors. There was a good correspondence between the cytokine expression and production patterns. Changes in PBMC composition, with a trend toward an increase in CD8 ؉ lymphocyte counts, were observed.The genus Trichinella is a group of nematodes which have a worldwide distribution and which cause trichinellosis in humans (15). Humans are infected by eating raw or undercooked meat or meat products (sausages, salami, etc.) from swine, horses, or game animals that are infected with larvae of these worms. In Italy, the main etiological agent of human trichinellosis is Trichinella britovi; however, some human infections have been attributed to consumption of products from imported animals infected with Trichinella spiralis (17).From 4 to 5 days after ingestion of infected meat, the larvae develop to the adult stage in a row of columnar epithelial cells in the small intestine. Six days after ingestion, the adult worms begin to reproduce, and the newborn larvae migrate across the lamina propria of the villus into the lymph and bloodstream. However, only the newborn larvae that reach striated muscles develop to the infective stage. In laboratory mice, the intestinal phase is longer for T. spiralis than for T. britovi and the female fecundity of T. spiralis is at least twice than that of T. britovi. These differences explain the different clinical pictures obtained for humans infected with these two species (20). Intestinal symptomatology (diarrhea, abdominal pain, and vomiting) occurs more frequently and lasts longer in human T. spiralis infections than in human T. britovi infections (20).When a larva penetrates a muscle cell, it causes the cell to become what is known as a nurse cell, and it becomes infective 15 to 16 days later (i.e., 21 to 22 days after ingestion of infected meat) (6).After ingestion of larvae, a host develops an immunity-mediated inflammatory response at the intestinal level, and this is followed by rapid expulsion of some of the larvae from the intestine (3). Studies conducted with mouse and rat models have suggested that antibodies play the most important role in this response, which depends on type Th2 cytokines derived from CD4 ϩ cells, and that mucosal mast cells also play an important rol...