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Yuan-zhi Zhang

Publications and source records attributed to Yuan-zhi Zhang.

7 recordsLinked to original sources
PubMed2006

[Quantitative method to describe the inner characteristics of hereditary nonpolyposis colorectal cancer family].

OBJECTIVE: To establish a quantitative method to describe the inner characteristics of hereditary nonpolyposis colorectal cancer (HNPCC) family. METHODS: All members of 25 HNPCC families with assembly of malignant tumors therein [with at least one patients with colorectal cancer (CRC)] in China underwent questionnaire survey. Other 32 HNPCC families with complete clinical data were collected from the published Chinese and foreign literatures related to clinical phenotype of Chinese HNPCC family. Altogether 57 HNPCC families fulfilling the Amsterdam Criteria (AC) I or II underwent analysis of the inner characteristics cumulatively. The following parameters were analyzed: familial median age when diagnosed as with the first malignant tumor (FMA-DFMT), familial median age when diagnosed as with the first CRC (FMA-DFCRC), familial proportion of CRC in first malignant tumors (FPCRC-FMT), familial proportion of CRC patients (FP-CRCP), number of involved generations, number of cancer patients, and type of family. RESULTS: In the ACI HNPCC families, the distribution patterns of both FMA-DFMT and FMA-DFCRC were not normal distribution. Most of the FMA-DFMT and FMA-DFCRC were from 35 years to 50 years with the medians of 44.0 years and 43.5 years respectively. The FPCRC-FMT and FP-CRCP were less than 0.6 in 13.2% (7/53) and 7.5% (4/53) of the families respectively. The FMA-DFMT and FMA-DFCRC were not correlated with FPCRC-FMT, FP-CRCP, number of involved generations and cancer patients, and type of family (all P > 0.05). CONCLUSION: Compared to the traditional methods, the features of HNPCC families can be accurately described by a series of quantitative parameters.

Adult↗
PubMed2006

Identification of HIV-1 specific T lymphocyte responses in highly exposed persistently seronegative Chinese.

BACKGROUND: Studies of highly exposed persistently seronegative (HEPS) individuals may provide valuable information on mechanisms of protection and on vaccine design. Cellular immune responses play a critical role in containing human immunodeficiency virus. However, the cellular immune responses in HEPS individuals have not been thoroughly assessed at the entire viral genome level. METHODS: Ten HEPS Chinese with a history of frequent penetrative vaginal intercourse (mean frequency, at least once a week), with some unprotected sexual contact occurring in the weeks or days immediately before enrollment, 25 HIV-1 seropositive individuals, 10 HIV-1-seronegative healthy individuals with low-risk sexual behavior and no history suggestive of exposure to HIV-1 infection were enrolled. HIV-1-specific T cell responses were comprehensively analyzed by an interferon-gamma Elispot assay against 770 overlapping peptides spanning all HIV-1 proteins. RESULTS: HIV-1-specific T-cell responses of interferon-gamma secretion were identified in 3 (30%) out of 10 HEPS individuals; the specific cytotoxic T lymphocytes were targeted at Pol (2/10), Env (2/10), and Tat (1/10). HIV-1-specific T-cell responses of interferon-gamma secretion were identified in 20 (80%) out of 25 seropositive intravenous drug users (IDUs), revealing that all HIV-1 proteins and protein subunits could serve as targets for HIV-1-specific CD8(+) T cell responses with 85% recognizing Gag, 80% recognizing Nef, 75% recognizing Pol, 60% recognizing Env, 55% recognizing Vpu, 45% recognizing Vpr, 20% recognizing Vif, 20% recognizing Tat and 15% recognizing Rev in these seropositive individuals. None of the seronegative healthy individuals gave the positive T-cell responses. CONCLUSIONS: About 30% of HEPS Chinese mounted HIV-1 specific T cell immune responses. Cell-mediated immunity against HIV-1 may be developed through non-productive infections.

Adult↗
PubMed2006

No mutation was detected in the LMNA gene among sporadic Charcot-Marie-Tooth patients.

OBJECTIVE: To intensively investigate sporadic CMT patients, we have analyzed the LMNA gene in this study in a series of 32 unrelated CMT patients. METHODS: Twelve exons of the LMNA gene were amplified from genetic DNA. PCR products of each exon were analyzed by single strand conformational polymorphism (SSCP). RESULTS: No abnormal SSCP pattern, suggesting no mutation in our CMT patients, was detected. CONCLUSION: The CMT diseases resulted from the mutations of LMNA gene were rare.

Charcot-Marie-Tooth Disease↗
PubMed2005

[Hereditary predisposition of colorectal cancer and prevalence of hereditary nonpolyposis colorectal cancer in general population of colorectal cancer patients in China].

OBJECTIVE: To analyze hereditary predisposition of CRC and the prevalence of HNPCC in general population of CRC patients in China. METHODS: CRC patients were from two sources. One is that we consecutively investigated 594 patients by ourselves. They were proved to be colorectal cancer by histology. The following data of all patients should be registered: sex, age diagnosed colorectal cancer, site, number and histological type of primary cancer. The other was the published Chinese and foreign literatures related to Chinese HNPCC prevalence, and there were cumulatively 3596 patients in all. Hereditary predisposition of CRC (or malignant tumors) is that CRC patients have two or more first- or second-degree relatives (or both) with CRC (or malignant tumors). HNPCC was diagnosed by Amsterdam Criteria I (AC I) or Amsterdam Criteria II (AC II), Japanese Criteria of HNPCC (JC). RESULTS: Hereditary predisposition of both malignant tumors and CRC were 17.2% and 5.2% in 594 patients with CRC, respectively. Multiple primary cancers and multiple CRC were 13.1% and 10.1% , respectively. Among them, multiple primary cancers and multiple CRCs without familial history were 9.1% and 6.7%, respectively. There was a correlation between familial history of malignant tumors and multiple primary cancers and multiple CRCs (both P < 0.01). Patients with familial history of malignant tumors had more frequently multiple primary cancers and multiple CRCs than patients without history of malignant tumors. Younger patients (< or = 50) were 21.4% in all CRC patients. there was a correlation between younger patients (< or =50) and familial history of malignant tumors and familial history of CRC (both P < 0.05). When CRC was diagnosed, patients with familial history of malignant tumors and familial history were younger than patients without them. In the population of CRC patients in China, prevalence of HNPCC diagnosed AC I, AC II and JC were 1.24%, 2.15% and 2.93%, respectively. CONCLUSIONS: Hereditary predispositions of malignant tumors and CRC were 17.2% and 5.2% in CRC patients, respectively. Familial history of malignant tumors, multiple primary cancers and younger patients with CRC (< or =50) were the clinical markers of hereditary predisposition of malignant tumors including CRC. Multiple primary cancers and younger patients with CRC (< or =50) were all correlated with familial history of malignant tumors. The prevalence of HNPCC in China was similar to that in Western countries.

Adult↗
PubMed2005

[Laminopathies--one gene, multiple diseases].

Laminopathies are genetic diseases that encompass a wide spectrum of phenotypes with diverse tissue pathologies and result mainly from mutations in the LMNA gene encoding nuclear lamin A/C. To date, at least 9 different human diseases, which superficially seem to share little with one another, result from LMNA mutations. The position of the mutation within LMNA appears to be associated with the phenotypes. This review gives an overview of genotype-phenotype relationship and describes recent advances in animal models and pathogenic mechanisms.

Animals↗
PubMed2005

[Molecular genetics of Charcot-Marie-Tooth disease].

Charcot-Marie-Tooth disease (CMT) affects the peripheral nervous system. It is generally inherited in an autosomal dominant pattern, but also is inherited in recessive or an X-linked pattern. The degree of severity can vary greatly from patient to patient, even within the same family. Traditionally, the different classes of CMT have been divided into demyelinating forms and axonal forms. Until 10 years ago, the genetic basis of CMT disease was largely unknown. An intrachromosomal duplication on chromosome 17 was found in 1991, and a point mutation in the peripheral myelin protein-22 gene was discovered in 1992. The work starts a new stage of the molecular basis of this large group of peripheral neuropathies. In this review, we will summarize what is known today about the genetics of CMT, and what we have learned about the underlying disease mechanisms.

Animals↗