[Applied anatomical study and clinical application of the caudate lobe boundary and ductal system of the liver].

Objective: To explore the relationship between the hepatic caudate lobe boundary and the ductal system so as to guide the identification of the anatomical relationship during liver surgery. Methods: The specific parts were observed and the liver parenchyma was removed according to 41 cadaveric liver autopsy specimens. The critical relationship between the hepatic caudate lobe and other ducts was observed to explore the reticular duct structure. Results: The plane formed by the hepatic hilar plate and Arantius ligament served as the boundary between the caudate lobe and other hepatic lobes. The caudate lobe hepatic portal vein was composed of numerous small branches from its left and right branches. The portal vein adjacent to the vena cava was mainly derived from the left branch, and to a lesser extent from the right branch. Blood was drained straight from the caudate lobe vein into the inferior vena cava via the short hepatic vein. There were three or four bile duct branches in the caudate lobe. The main source of arterial blood flow were the left and right branches of the hepatic artery. An avascular zone of loose connective tissue was found between the caudate lobe and the retrohepatic inferior vena cava. Conclusion: The hepatic caudate lobe is an independent lobe. During hepatic caudate lobe surgery, the plane formed by the hepatic hilar plate and Arantius ligament can serve as the boundary between the caudate lobe and other hepatic lobes and be used for anatomical site identification. The duct system of the caudate lobe's is complicated, but it also has its own distinct regularity.

Identification of a novel HLA-A*33 allele, HLA-*33:03:13, in a Chinese family.

A*33:03:13 differs from A*33:03:01 by one nucleotide change at nucleotide 714 in exon 4 from A to G.

Human leukocyte antigen-B27 alleles in Xinjiang Uygur patients with ankylosing spondylitis.

We investigated the distribution of human leukocyte antigen (HLA)-B27 subtypes in Uygur ankylosing spondylitis patients in Xinjiang. B27-positive patients with ankylosing spondylitis were subtyped by using polymerase chain reaction-sequence-based typing. The HLA-B27 subtype frequencies of Uygur patients were compared with those in Han patients in Xinjiang and the other areas of China. B*2705 was the predominant subtype in Uygur patients with a frequency of 58.95%, which was much higher than that in Han patients in Xinjiang (31.58%, P < 0.05) and the other areas of China (excluding the Shandong region, which was 63.89%). The frequency of B*2704 (27.37%) in Uygur patients was the lowest and significantly lower than that in Han patients (61.18%, P < 0.05) and in 8 other areas of China. B*2710 has not been previously reported in Uygur ankylosing spondylitis patients; B*2704 was the main (61.18%) subtype in Han patients in Xinjiang, followed by B*2705 (31.58%) and was similar to the characteristics of Han patients in the other areas of China. B*2724 in Han ankylosing spondylitis patients has not been previously reported. Additionally, the B*2702/B*2705 homozygote was identified in Uygur patients. B*2702/B*2704, B*2704/B*2705, and B*2705/B*2705 homozygotes were identified in 3 Han patients. The distribution of HLAB27 subtypes in Uygur ankylosing spondylitis patients in Xinjiang significantly differed from that in Han patients. Understanding the distribution of HLAB27 subtypes in ethnic minority populations of Xinjiang is important for anthropological genetic studies and for analyzing the impact of genetic background on ankylosing spondylitis susceptibility.

Detection of serum antinuclear antibodies in lymphoma patients.

We investigated the presence of serum antinuclear antibodies (ANAs) and autoantibodies and their relationship with serum prognostic indicators in lymphoma patients. The study population comprised 127 patients diagnosed with lymphoma and 138 healthy control subjects. The blood samples of the participants were assayed for ANAs by immunofluorescence, and autoantibodies were detected by western blotting. Serum ANAs were detected in 31.5 (40/127) and 6.5% (9/138) of lymphoma patients and control subjects, respectively. There was a statistically significant difference between the lymphoma and the control groups (P < 0.05). The level of lactate dehydrogenase in the ANA-positive subjects was significantly lower than in the ANA-negative subjects (P < 0.05). Low ANA titers (1:100) were commonly found in the ANA-positive subjects and the control subjects, and the fluorescence models were diverse. Autoantibodies were found in 35% (14/40) of the ANA-positive patients by western blotting. Detection of ANAs in lymphoma patients helps in determining the diagnosis and prognosis of lymphoma, but has no independent diagnostic value; there are still various autoantibodies of unknown significance that require further study.

Identification of a novel HLA-B*51 allele, HLA-B*51:144, in a Chinese individual.

The novel HLA-B*51:144 allele shows one nucleotide difference from B*51:02:02 in exon 3.

HLA-A*02:01:79, a novel allele, which has arisen by silent mutation in codon 230.

A*02:01:79 is identical to A*02:01:01:01, except for one nucleotide change at nt 762 in exon 4 from C to T.

Interleukin-1B-31 gene polymorphism in Hakka gastric cancer patients in Guangdong, China.

The aim of this study was to examine the interleukin-1B (IL-1B) gene promoter region -31 (IL-1B-31) polymorphism distribution characteristic of Hakka gastric cancer patients in Guangdong Province and to explore its association with gastric cancer. We used the 1:1 case-control method, matrix-assisted laser desorption ionization flight time mass spectrometry, and MassARRAY-IPLEX technology to genotype IL-1B-31 (-31C> T) in 52 Hakka gastric cancer patients and 52 Hakka control subjects in Meizhou. Three genotypes - CT, TT, and CC - of IL-1B-31 were found in the Meizhou Hakka population. Their distribution frequencies in the gastric cancer group were 40.38, 40.38, and 19.23%, respectively, whereas the frequencies in control subjects were 57.69, 17.31, and 25.00%, respectively. The differences in frequency distributions of the genotypes between the 2 groups were statistically significant (chi-square = 6.78, P < 0.05). Subjects with the TT genotype had a higher risk of gastric cancer compared with that in subjects carrying the CT genotype (odds ratio = 2.857, 95% confidence interval = 1.114-7.328). This risk was more apparent in male subjects. IL-1B-31 locus polymorphism may be associated with gastric cancer susceptibility in this population, but additional studies with larger sample size are needed to confirm the conclusions.

Preliminary study of the clonal characteristics of the TCR BV subfamilies in T cells in the peripheral blood from patients with uveitis.

The aim of this study was to investigate the characteristics and polymorphisms of the T-cell receptor BV complementarity-determining region 3 (TCR BV CDR3) gene in peripheral blood mononuclear cells (PBMCs) from patients with uveitis to provide an experimental basis for studying the pathogenesis of this disease. RT-PCR amplification of 26 subfamilies of the TCR BV CDR3 gene and immune spectratyping analysis were used to study the pedigree drift of TCR BV CDR3 in PBMCs from the uveitis patients. The following results were obtained: 1) the vast majority of the TCR BV CDR3 spectra in PBMCs in 5 healthy subjects fit the normal (or Gaussian) distribution. The distributions of the TCR BV CDR3 spectra in 4 patients with uveitis were non-normal and showed an abnormal peak including a widowed peak trend, a partial peak, and an irregular abnormal peak. 2) In the 26 TCR BV subfamilies, the abnormal peak frequency was different in the various subfamilies. The BV2 and BV17 (both 3/4) subfamilies had higher frequencies of the non-normally distributed abnormal peak. The BV5.2, BV6, BV15, and BV18 subfamilies showed no abnormal peaks. 3) TCR BV2 and BV17 yielded an abnormal peak in 3 HLA-B27-negative patients; however, no such abnormalities were detected in HLA-B27-positive patients. The abnormal expression of some TCR BV subfamilies in PBMCs from patients with uveitis may be associated with the immune pathogenesis of the disease. Our study provides the basis for further investigations into the pathogenesis of uveitis.

Identification of a new HLA-DQB1*03 variant, DQB1*03:39, by sequence-based typing in a Chinese Han individual.

HLA-DQB1*03:39 is identical to HLA-DQB1*03:03:02, except for one nucleotide change at nt 477 (C→G) in exon 3.

HLA-B*40:06:06, a novel allele, which has arisen by silent mutation in codon 45.

Exons 2, 3 and 4 of HLA-B*40:06:06 allele are identical to those of HLA-B*40:06:01:01, except for one nucleotide change.

Full-length sequence of a novel HLA-A*02:230 allele.

The full-length sequences of exons 1-8 of this novel HLA-A*02:230 allele are identical to those of HLA-A*02:03:01, except for one nucleotide change at nt 858 in exon 3 from G to A.

A HLA-A null allele (A*24:132N) with a stop codon in exon 3 generated by a point mutation.

Exons 1-8 of HLA-A*24:132N allele are identical to those of HLA-A*24:02:01:01, except for one nucleotide change at nt 746 in exon 3 from C to A.

Identification of a novel HLA-C*04 allele, HLA-C*04:107, in a Chinese individual.

The novel HLA-C*04:107 allele shows one nucleotide difference from C*04:03 in exon 2 at nucleotide position 341.

Identification of a new HLA-DRB1 *16 variant, DRB1*16:19 by sequence-based typing in a Chinese Han.

The sequence of the novel allele is identical to HLA-DRB1*16:02:01 except for one nucleotide change at nt203 (G→A), resulting in a coding change, 39 R (CGC)→H (CAC).

Identification of a novel HLA-Cw*08 variant allele, Cw*0824.

A novel HLA-C allele, Cw*0824, which was identified from an individual of the Han Chinese, differs from Cw*080101 at codon 222 (GAG > AAG ) in exon 4, which results in an amino acid change Glu222Lys.

Characterization of a new HLA-C allele in a Chinese family by sequence-based typing: HLA-Cw*0348.

The novel human leukocyte antigen (HLA)-Cw*0348 allele was identified by sequence-based typing in a Chinese family. This allele shows that the sequences of exons 1-3 of HLA-Cw*0348 are identical to those of HLA-Cw*030401 except for a nucleotide substitution that changes CCG to CTG at codon 57, resulting in an amino acid change from Pro to Leu in the protein, and this is a unique nucleotide change among the HLA-C alleles, suggesting a point mutation mechanism. The extended haplotype carrying the new allele was deduced from the family group typing and defined as A*110101, B*1301, Cw*0348, DRB1*0405, and DQB1*0402.

A novel allele, HLA-A*110203, was identified in a Chinese individual.

This allele is characterized by a nucleotide substitution (C>T) in exon 4 at position nt 672, codon 200 (ACC>ACT), no coding change.

Full-length sequence of a novel allele, HLA-Cw*070205.

The full-length sequences of exons 1-8 of this novel HLA-Cw*070205 allele are identical to those of HLA-Cw*07020101, except for one nucleotide change at nt 498 in exon 3 from C to T, which result in a synonymous amino acid substitution from ATC to ATT at codon 142 in exon 3.

Identification of a new HLA-B*40 allele, HLA-B*4081, in a Chinese individual.

A novel human leukocyte antigen (HLA)-B*40 allele, officially named B*4081, was identified during routine high-resolution sequence-based typing in a Chinese potential hematopoietic stem cell transplantation donor. The HLA-B*4081 allele shows one nucleotide difference from B*400101 in exon 2 at nucleotide position 124 where G-->C (codon 18 GGG-->CGG) resulting in a coding change, 18Gly is changed to Arg, this is a unique nucleotide change among the HLA class I alleles, suggesting a point mutation mechanism.

A novel HLA-DRB1 allele, DRB1*112802, was identified in a Chinese individual.

We report here a novel human leukocyte antigen-DRB1 allele, DRB1*112802, which was identified from a Chinese individual during sequence-based typing. The new allele is identical to DRB1*112801 except for one nucleotide change at nucleotide 189 (A --> G ), codon 34 Q (CAA) --> Q (CAG), no coding change.