Healthy Family Members Of Patients Research Articles

Objective To investigate the community structure of intestinal bacteria from patients with cirrhosis and its influencing factors. Methods From 2016 to 2017, 24 patients with liver cirrhosis (the LC group) and 23 healthy family members of patients (the HC group) were enrolled at the First Hospital of Lanzhou University. A comparative analysis of the community structure of intestinal bacteria was performed using 16S rRNA gene sequencing in LC and HC groups. Combined with LEfSe analysis and NMDS analysis, the differential markers were screened and the factors affecting the intestinal community structure of subjects were studied. Results The dominant six phylum of bacteria in intestines in LC and HC groups included Firmicutes, Bacteroides, Proteobacteria, Actinobacteria, Fusobacteria and Tenericumes. However, in the LC sample, Firmicutes was significantly reduced, while Bacteroides was significantly increased. The diversity of intestinal bacteria was significantly reduced, and the Firmicutes/Bacteroides ratio was significantly decreased, suggesting a variation of the community structure in intestinal bacteria of cirrhosis patients. The LEfSe result indicated that the abundance of Enterococcus, Lactobacillales, Bacilli, and Bacteroidetes showed a significant difference in the LC sample, which may be used as potential marked bacterial groups for cirrhosis. The NMDS analysis revealed a positive relationship between the concentration of Cd and Pb and the abundance of intestinal bacteria in the LC sample. Conclusion The community structure of intestinal bacteria from patients with cirrhosis has changed. Enterococcus, Lactobacillales, Bacilli, and Bacteroidetes are potential marked bacterial groups. The concentration of Cd and Pb in the intestinal tract of cirrhosis patients may interact with the abundance and structure of bacteria, and further affect the occurrence and development of cirrhosis. Key words: Cirrhosis; Intestinal bacteria; Bacterial community structure; Influencing factor

Distinct and Synergistic Contributions of Epithelial Stress and Adaptive Immunity to Functions of Intraepithelial Killer Cells and Active Celiac Disease

Delusional beliefs among subjects with schizophrenia, their healthy relatives, and normal subjects

Predictors of Subjective Memory Complaint in Cognitively Normal Relatives of Patients with Alzheimer's Disease

Introduction: Crohn's disease (CD) is a polygenic multifactorial heterogeneous disease. Anti-Saccharomyces cerevisiae antibodies (ASCA) are present in 50-80% of CD patients. The reason for the generation of ASCA remains unclear. Recently, some studies have shown that ASCA occur in 25% of healthy family members of patients with CD. Thus, the generation of these antibodies may be genetically determined. Mutations in the NOD2/CARD15 gene are found to be associated with susceptibility to Crohn's disease. So far, there are no reports on the relationship between ASCA and mutations of NOD2/CARD15 gene in the pediatric CD population. Aim: The aim of our study was to investigate the relationship between ASCA, disease phenotype (location of the inflammation, disease activity and body mass index at the time of diagnosis) and NOD2/CARD15 genotype in pediatric Crohn's disease patients. Methods: 38 patients with CD (6-18 years, M/F = 2,3/1) were tested for ASCA (IgA and/or IgG) by enzyme-linked immunosorbent assay. Disease location, body mass index and disease activity at the time of diagnosis were determined. All patients had genotyping performed using sequence specific PCR directed against the wild tipe and the R702W, G908R and 3020insC variants of NOD2/CARD15 gene. Results: 26 of 38 (68,4%) CD patients were ASCA positive (IgG and/or IgA). 12 of 38 (31,6%) CD patients had at least one of the three major mutations of NOD2/CARD15 gene. ASCA positive patients had significantly lower BMI (p = 0,012) and higher pediatric Crohn's disease activity index -PCDAI (p = 0,022) at the time of diagnosis compared to ASCA negative patients. We found a negative association between the presence of ASCA and ileal location of the disease (p = 0,001). There was no association between positive ASCA and the R702W, G908R and 3020insC mutations of NOD2/CARD15 gene (p = 0,926). Summary: In our study ASCA positive patients had significantly lower body mass index and higher disease activity at the time of diagnosis, however, we didn't find the positive correlation between ileal location of the disease and positive ASCA. There was also no association between positive ASCA and the three major mutations of NOD2/CARD15 gene. Conclusion: Although some studies have shown that generation of ASCA may be genetically determined, our study did not confirm the association between the presence of ASCA and the major mutations of NOD2/CARD15 gene in the pediatric CD population. This finding suggests some other genetic factors may be involved in the generation of ASCA.

Childhood onset schizophrenia: familial neurocognitive measures

There is a substantial genetic contribution to schizophrenia but no way to readily identify individuals at risk. Biological abnormalities reflecting greater genetic vulnerability may be discovered by examining healthy family members of patients with schizophrenia. There is evidence that olfactory impairments are common in patients. The authors previously reported that patients have abnormal olfactory bulbs, assessed by magnetic resonance imaging (MRI). This study examined olfactory bulbs in patients' relatives to determine whether low bulb volume represents an endophenotypic marker of genetic vulnerability. Olfactory psychophysical measures and MRI scans of olfactory bulbs were acquired from 19 healthy first-degree relatives, 20 healthy comparison subjects with similar age and gender distributions, and the 11 patient probands of these relatives. Olfactory bulb volumes were measured by using a reliable region-of-interest procedure. The patients had impaired ability to detect odors and had lower olfactory bulb volumes than the comparison subjects. Although the family members had normal olfactory ability, they exhibited low right bulb volume. The patients had smaller left, but not right, olfactory bulbs than their own healthy relatives. The findings in family members suggest that structural abnormalities of the olfactory system in schizophrenia may partly reflect preexisting genetic vulnerability to illness. Preliminary analyses suggest that right olfactory bulb volume may serve as an endophenotypic marker of genetic vulnerability, while left bulb volume may reflect overt disease among individuals who share genetic vulnerability. Bulb abnormalities in patients are consistent with reports of cellular abnormalities affecting peripheral olfactory receptor neurons.

Healthy family members of patients with insulin-dependent diabetes mellitus (IDDM) are known to share a number of immunological abnormalities with their affected relatives. Since monocyte and type 1 T-cell-derived cytokines contribute to the pathogenesis of IDDM, we studied the production of these cytokines in the healthy first degree relatives of 29 children with IDDM. We report that circulating tumour necrosis factor-alpha (TNF-alpha) and soluble interleukin-2 (sIL-2) receptor were present in increased amounts in non-diabetic family members at levels similar to those found in the diabetic children (duration of disease 3 months-5 years). Furthermore, marked hypersecretion of IL-1alpha and TNF-alpha by mitogen-stimulated peripheral blood mononuclear cells was found in both diabetic and healthy family members. Abnormalities of cytokine production in healthy relatives did not correlate with the presence of islet cell antibodies or with HLA DR type. These data indicate that healthy family members of patients with IDDM exhibit overproduction of a number of cytokines that have been implicated in diabetogenesis.

To determine if patients with the Guillain-Barré syndrome are likely to have had Campylobacter jejuni infection before onset of neurologic symptoms. A case-control study. Several university medical centers. Case patients met clinical criteria for the Guillain-Barré syndrome between 1983 and 1990 and had a serum sample collected and frozen within 3 weeks after onset of neurologic symptoms (n = 118). Disease controls were patients with other neurologic illnesses (n = 56); healthy controls were hospital employees or healthy family members of patients (n = 47). Serum IgA, IgG, and IgM antibodies to C. jejuni were determined by enzyme-linked immunosorbent assays. Assays were done in a blinded manner. Optical density ratios > or = 2 in two or more immunoglobulin classes were seen in 43 (36%) of patients with the Guillain-Barré syndrome and in 10 (10%) of controls (odds ratio, 5.3; 95% CI, 2.4 to 12.5; P < 0.001). Increasing the optical density ratio or the number of immunoglobulin classes necessary to yield a positive result increased the strength of the association. The number of patients with the Guillain-Barré syndrome who had positive serologic responses was greatest from September to November (P = 0.02). Male patients were three times more likely to have serologic evidence of C. jejuni infection (P = 0.009); the proportion of patients with the syndrome who had a positive serologic response increased with age. Patients with the Guillain-Barré syndrome are more likely than controls to have serologic evidence of C. jejuni infection in the weeks before onset of neurologic symptoms. Campylobacter jejuni may play a role in the initiation of the Guillain-Barré syndrome in many patients.

To evaluate the intrafamilial clustering of HTLV‐I, we examined the sera or plasma of 296 healthy family members of patients with adult T‐cell leukemia (ATL) for anti‐HTLV‐I antibodies. Of 296 subjects, 132 (44.6%) had anti‐HTLV‐I antibodies. Fifty‐nine (41.0%) out of 144 males and 73 (48.0%) out of 152 females were seropositive. The positive rates of antibody to HTLV‐I increased with age, especially between the 30–39 and the 40–49 age groups. Five out of 6 fathers, 3 out of 4 mothers, 31 (60.8%) out of 51 spouses, 40 (63.5%) out of 63 siblings and 46 (33.8%) out of 136 children of patients with ATL had anti‐HTLV‐I antibodies. Of 74 children with an ATL father, 14 (18.9%) were seropositive, while 32 (51.6%) out ot 63 children with an ATL mother were seropositive. This difference was statistically significant (P<0.001). Of those children with an ATL father, 12 (26.1%) out of 46 whose mothers were HTLV‐I carriers had antibodies to HTLV‐I. In contrast, none of the 13 children whose mothers were not carriers were seropositive. These results supported the hypothesis that the mother‐to‐child transmission is one of the most important modes of HTLV‐I transmission. In wives of male patients with ATL, the positive rate of antibody to HTLV‐I was 65.6% (21/32), and in husbands of female patients, it was 52.6% (10/19). The high positive rate of antibody to HTLV‐I not only in wives of male patients but also in husbands of female patients suggests that either HTLV‐I is more frequently transmitted from wives to their husbands than we had originally expected, or that ATL may develop even in wives who acquire HTLV‐I from their husbands after marriage.

We examined several immunological parameters such as the number of T cells with CD4 antigen and the receptor for the Fc portion of IgA (T alpha cells), in vitro immunoglobulin production by peripheral blood lymphocytes with or without pokeweed mitogen and serum levels of immune complexes in 19 healthy family members of patients with IgA nephropathy (IgAN). It was shown that the levels of serum IgA, T4 cells, CD4/CD8 ratio of T cell subsets, T alpha cells, IgA circulating immune-complexes and spontaneous synthesis of immunoglobulins were significantly increased in family members of patients with IgAN. No family members had proteinuria or hematuria. It was concluded that immunological abnormalities, including abnormalities of T cells and B cells, were found not only in patients with IgAN but also in their healthy family members. It was suggested that some factors in addition to these immunological abnormalities may be involved in the development of IgAN.