Hypertension and Nephrosclerosis: A Reappraisal and a New Theory of Renal Ischemia

An observation in human autopsy material showing a statistically close relationship between complicated atherosclerosis of the aorta, at or above the renal artery take-off, and nephrosclerosis of usual type (i.e. the “granular kidney” of essential hypertension) led to a study of platelet aggregates as a cause of renal lesions. The renal cortical surface is peculiarly sensitive to ischemic damage. When an embolic source, which sheds repeatedly, was placed in the thoracic aorta of rabbits, they became hypertensive. The hypertension persisted for six months, at which time the kidneys showed nephrosclerosis characterized by surface cortical lesions consisting of shrunken glomeruli and atrophical tubules, subtended by arterioles whose intimas showed fibrous thickening. It is suggested that the renal component of the hypertension so induced is transitory, serving as a trigger mechanism for sustained hypertension.     

A review of projection radiography of plasma and biological objects in X-Pinch radiation

A review of studies on the X-pinch as a radiation source for X-ray projection shadow radiography (XPSR) and X-ray absorption spectroscopy (XAS) is presented. The ultimate capabilities of the techniques and ways of their achievement are considered. XPSR has been successfully used to study high-energy-density plasma objects, in particular, exploding wires and wire arrays. Using XPSR, the internal structure and dynamics of a wire explosion and wire array implosion have been investigated for the first time, which has made it possible to develop an adequate consistent theory of the processes occurring in the wire loads of generators with currents from several units of kiloamperes to a few tens of megamperes. The use of XAS for diagnostics of wire loads has allowed one for the first time to measure the parameters of matter in the wire core and plasma corona of the load. X-ray images of various biological objects have obtained, including those with the use of the phase contrast method. This review is a logical continuation of the review “Х-Pinch” [Plasma Phys. Rep. 41, 319, 493 (2015)], in which the Х-pinch as a physical object was considered.     

Frequency of micronucleated exfoliated cells in oral lichen planus

OBJECTIVE: The purpose of this study was to determine the frequency of micronucleated exfoliated cells (MEC) in atrophic and erosive oral lichen planus (OLP). MATERIALS AND METHODS: Twenty-two patients with atrophic and/or erosive OLP participated in this study. Lesions were scored ranging from 0 (no lesion) to 5 (large erosion) according to the severity and assessed for MEC. Exfoliated cells were obtained by swabbing the lesions and normal-appearing mucosa adjacent to the lesions. Swabbing was also performed in age-sex-matched normal individuals. Five hundred exfoliated cells were screened for nuclear anomalies including micronuclei, karyorhexis, pycnosis, and chromatid clumping. RESULTS: The severity score of OLP ranged from 2 to 4 with the average of 2. The frequency of MEC in OLP patients was 3.79% and 0.37% in the lesions and normal-appearing mucosa, respectively. In normal individuals, the frequency of MEC was also 0.37%. Using a paired t-test, it was found that the MEC frequency in the OLP lesions was significantly elevated (p<0.01) as compared to that in normal-appearing mucosa adjacent to lesions and that in normal individuals. There were no statistically significant differences in the MEC frequency of the three severity scores as analyzed by Kruskal-Wallis one way analysis of variance on ranks (p>0.05). CONCLUSION: This study revealed an increase in micronuclei in OLP lesions. The results indicate genotoxic damage in atrophic and erosive OLP.     

Difference in chromatin sensitivity to heparin of chronic atrophic gastritis, of carcinoma-free and carcinoma-bearing stomach in comparison with normal gastric mucosa and gastric carcinoma as revealed by flow cytometry

DNA distribution patterns from gastric mucosal cells corresponding to four groups defined by histological examination were measured by flow cytometry before and after treatment with heparin, a polyanion. Group I comprised normal gastric mucosal cells; group II, chronic atrophic gastric mucosal cells originating from a carcinoma free stomach; group III, chronic atrophic gastric mucosal cells originating from a carcinoma bearing stomach; and group IV, malignant gastric mucosal cells. The heparin concentrations used were 1.25, 1.5, and 5 U/ml cell suspension. Heparin caused increases in fluorescence intensity and in coefficients of variation, which are interpreted as a reflection of alterations in chromatin structure. For the four groups investigated, the heparin-initiated changes were dependent, in varying degree, on concentration and time. Group I showed a much more extensive sensitivity to heparin than group IV. Group II and III reacted similarly to group I or group IV, depending on the source, i.e., either a carcinoma-free stomach or a carcinoma-bearing stomach. Further extension of this method might yield information concerning the real premalignant potential of a specific case of chronic atrophic gastritis.     

Computerized tomography of the head in patients with epilepsy

A detection of structural changes in the brain of epileptic patients is of importance to the choice of therapeutical management. Incidence and character of lesions in CT-scans of the skull were analysed in the random group of epileptic patients. Normal areas in CT-scans were prevailing in young patients. Atrophic lesions to the brain increased with the patients' age and duration of the disease. Normal results were obtained in post-traumatic epilepsy and that of unknown etiology similarly to atrophic lesions whereas localized lesions were found in all patients with cerebral tumors. Partial epilepsy, especially of short duration, was characterized by high incidence of localized lesions. Normal EEG records were rare in patients with localized lesions detected with CT-scans whereas normal CT-scans may be related to abnormal EEG record. Presence of the localized lesions in some patients and atrophic areas did not limit clinical results of monitored therapy. CT-scanning of the skull should be performed in case of all patients with epilepsy even if there are no significant changes in EEG records or clinical status.     

Diagnosis of early gastric cancer based on fluorescence hyperspectral imaging technology combined with partial‐least‐square discriminant analysis and support vector machine

This study investigated the feasibility of using fluorescence hyperspectral imaging technology to diagnose of early‐stage gastric cancer. Fluorescence spectral images of 76 patients who were pathologically diagnosed as non‐atrophic gastritis, premalignant lesions and gastric cancer were collected. Fluorescence spectra at 100‐pixel points were randomly extracted after binarization. Diagnostic models of non‐atrophic gastritis, premalignant lesions and gastric cancer were constructed through partial‐least‐square discriminant analysis (PLS‐DA) and support vector machine (SVM) algorithms. The prediction effects of PLS‐DA and SVM models were compared. Results showed that the average spectra of normal, precancerous and gastric cancer tissues significantly differed at 496, 546, 640 and 670 nm, and regular changes in fluorescence intensity at 546 nm were in the following order: normal > precancerous lesions > gastric cancer. Additionally, the effect of the diagnostic model established by SVM is significantly better than PLS‐DA which accuracy, specificity and sensitivity are above 94%. Experimental results revealed that the fast diagnostic model of early gastric cancer by combining fluorescence hyperspectral imaging technology and improved SVM was effective and feasible, thereby providing an accurate and rapid method for diagnosing early‐stage gastric cancer.      

Hypertension,Thrombosis, and Atherosclerosis in the Rat

A simple high fat diet containing cholic acid has been devised for producing hyperlipemia and an increased incidence of thrombosis in the small coronary vessels of the rat, but without producing significant atherosclerotic lesions. The influence on this syndrome induced by six weeks of desoxycorticosterone administration, 2 mg. daily, and 10 weeks of oral saline (1%) ingestion was investigated in 30 115-g. male rats. Marked hypertension developed only when it was induced prior to beginning the dietary feeding. In comparison to the control groups, the group that was both hyperlipemic and hypertensive had severer hypertension, severer hyperlipemia, double the mortality due to thrombosis and fatty streaks in the aorta but very few lesions of periarteritis nodosa. However, the early atherosclerotic lesions did not seem to be responsible for the increased production of thrombosis. It is therefore probable that under these experimental conditions hypertension has a more direct action on the production of thrombotic effect than that of worsening the atherosclerotic lesions.     

A novel double lesion in X-irradiated DNA consists of a strand break and a base modification.

A single free radical-initiating event can produce a pair of base lesions in DNA oligomers exposed to ionizing radiation. Whereas double base lesions have been observed previously, the present study shows that double lesions may sometimes consist of a base lesion and an associated strand break. The mechanism for the formation of double lesions is discussed. A redox process is postulated in which guanine is the source of the electron. It is suggested that double lesions may be formed in DNA either on adjacent nucleotides or, alternatively, on nucleotides separated by one, two or possibly more intervening nucleotides. It is hypothesized that intramolecular electron transfer facilitates the formation of double lesions on nonadjacent nucleotides.     

Strokes among black people in Harare,Zimbabwe: results of computed tomography and associated risk factors.

Computed tomography was performed and risk factors evaluated in 100 consecutive adult patients presenting to the two teaching hospitals in Harare with a clinical diagnosis of stroke. The mean age of the patients was 52; only 28 were 65 or older. Non-stroke lesions were found in seven patients and were predicted by a recent history of convulsions (p less than 0.0001). Five lesions (four subdural haematomas and one cerebral cysticercosis) were remediable. Hypertension was present in 27 (93%) of the 29 patients with cerebral haemorrhage and in 49 (53%) of the 93 patients with stroke lesions. In 22 (45%) of these patients the hypertension had not been diagnosed, and another 22 had defaulted from treatment. All 13 patients who died before computed tomography had hypertension, and over half showed evidence of haemorrhagic stroke. There was a cardiac source for all 12 cases of cerebral embolism. In eight of the 100 patients cerebral infarction was attributed to neurosyphilis. None of the patients had clinical evidence of atherosclerosis. Smoking and oral contraceptives did not seem important risk factors for stroke. Detection and control of hypertension remain the most important measures needed to reduce the incidence of and mortality from stroke in Zimbabwe.     

Mammography in management of breast lesions

Comparison of the clinical and mammography findings in 101 histologically proved breast lesions showed that the accuracy of each method in diagnosing carcinoma was about 90%, but when taken together an accuracy of 98% was reached. Though mammography was less accurate in the diagnosis of benign lesions, it was found to be a valuable complement in the management of a lesion in the large atrophic breast and for showing an impalpable carcinoma. In mammography of the young dense breast a negative result must be interpreted with caution.     

Cobalt Tumor of the Thyroid Gland

Diminutive kidney, hypoplasia or atrophic pyelonephritis, may be the cause of hypertension, lumbar or abdominal pain, obscure gastrointestinal symptoms or chronic urinary infection accompanied by chills and fever. A hypoplastic kidney is prone to infection and stone formation.Diagnosis includes meticulous x-ray examination and renal function studies employing the more accurate quantitative phenolsulfonphthalein test of each kidney.Nephrectomy is the treatment for unilateral disease causing symptoms; localized atrophic pyelonephritis is amenable to partial resection.Since urinary stasis invites infection, obstructing ureteral strictures should be dilated. Pyelectasis, secondary to ptosis, and ureteropelvic obstruction should be corrected by nephropexy or plastic repair. These conservative measures may prevent renal destruction.Sixteen patients were subjected to nephrectomy: Six because of persistent pain and chronic infection and ten because of hypertension. The six with pain and chronic urinary infection were relieved. In six of the ten with hypertension, the disease recurred within six months to seven years.     

Cobalt tumor of the thyroid gland

Diminutive kidney, hypoplasia or atrophic pyelonephritis, may be the cause of hypertension, lumbar or abdominal pain, obscure gastrointestinal symptoms or chronic urinary infection accompanied by chills and fever. A hypoplastic kidney is prone to infection and stone formation.Diagnosis includes meticulous x-ray examination and renal function studies employing the more accurate quantitative phenolsulfonphthalein test of each kidney. Nephrectomy is the treatment for unilateral disease causing symptoms; localized atrophic pyelonephritis is amenable to partial resection. Since urinary stasis invites infection, obstructing ureteral strictures should be dilated. Pyelectasis, secondary to ptosis, and ureteropelvic obstruction should be corrected by nephropexy or plastic repair. These conservative measures may prevent renal destruction.SIXTEEN PATIENTS WERE SUBJECTED TO NEPHRECTOMY: Six because of persistent pain and chronic infection and ten because of hypertension. The six with pain and chronic urinary infection were relieved. In six of the ten with hypertension, the disease recurred within six months to seven years.     

Hypertension exacerbates coronary artery disease in transgenic hyperlipidemic Dahl salt-sensitive hypertensive rats

BACKGROUND: The mechanisms underlying the known interaction of two complex polygenic traits, hypertension and hyperlipidemia, resulting in exacerbation of coronary artery disease have not been elucidated. Identification of critical pathways underlying said exacerbation could identify mechanism-based targets for intervention and prevention. MATERIALS AND METHODS: To investigate hypertension- atherosclerosis interaction, we studied the inbred transgenic atherosclerosis-polygenic hypertension Dahl salt-sensitive (S) rat model (Tg53), which over-expresses human cholesteryl ester transfer protein (hCETP) in the liver, and exhibits coronary artery disease and decreased survival compared with control non-transgenic Dahl S rats. Using serial-section histopathological and immunohistochemical analyses, we analyzed the coronary artery disease phenotype of Tg53 rats at end-stage marked by cardio-respiratory compromise as the experimental equivalent of acute coronary syndromes, and determined the effects of reduction of blood pressure through low salt diet (0.008% NaCl) on the coronary artery disease phenotype and survival. RESULTS: End-stage Tg53 rats exhibit coronary artery lesions in the proximal right coronary artery system which exhibit "culprit plaque" features such as plaque inflammation, matrix degradation, apoptosis, neovascularization, thrombosis and hemorrhage recapitulating said features and heterogeneity of human coronary "culprit plaques". Comparative analysis of 6 month vs end-stage lesions reveals distinct lesion development profiles of proximal coronary lesions which quickly progress from eccentric non-occlusive foam-cell rich lesions at 6 months to occlusive "culprit plaques", compared with more distal coronary lesions which exhibit occlusive thick-cap atheroma that remain relatively unchanged from 6 months to end stage. Reduction of hypertension through a low-salt (0.008% NaCl) diet increased survival (P < 0.0001) of Tg53 rats and significantly attenuated the coronary artery disease phenotype detected at 10 months of age marked by diminished apoptosis, neovascularization, matrix degradation compared with end-stage lesions detected at <8 months of age. CONCLUSIONS: End stage coronary lesions in the Tg53 rats recapitulate many, albeit not all, features of "culprit plaques" in humans supporting proposed paradigms of plaque vulnerability implicating lesion macrophage enrichment, apoptosis, matrix degradation and pathological neovascularization. Comparative time course analysis of coronary lesions reveals that plaques which develop into end-stage "culprit plaques" are distinct from "stable plaques" by location and early lesion morphology, suggesting distinct lesion development and progression pathways. The significant effects of low-salt diet-induced decrease in hypertension on right coronary disease phenotype provides compelling evidence that polygenic hypertension accelerates coronary plaque progression and complication independent of cardiac hypertrophy, and more importantly provides paradigmatic support for public health policy.     

Familial primary pulmonary hypertension (gene PPH1) is caused by mutations in the bone morphogenetic protein receptor-II gene

Familial primary pulmonary hypertension is a rare autosomal dominant disorder that has reduced penetrance and that has been mapped to a 3-cM region on chromosome 2q33 (locus PPH1). The phenotype is characterized by monoclonal plexiform lesions of proliferating endothelial cells in pulmonary arterioles. These lesions lead to elevated pulmonary-artery pressures, right-ventricular failure, and death. Although primary pulmonary hypertension is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs, including phentermine-fenfluramine. We genotyped 35 multiplex families with the disorder, using 27 microsatellite markers; we constructed disease haplotypes; and we looked for evidence of haplotype sharing across families, using the program TRANSMIT. Suggestive evidence of sharing was observed with markers GGAA19e07 and D2S307, and three nearby candidate genes were examined by denaturing high-performance liquid chromatography on individuals from 19 families. One of these genes (BMPR2), which encodes bone morphogenetic protein receptor type II, was found to contain five mutations that predict premature termination of the protein product and two missense mutations. These mutations were not observed in 196 control chromosomes. These findings indicate that the bone morphogenetic protein-signaling pathway is defective in patients with primary pulmonary hypertension and may implicate the pathway in the nonfamilial forms of the disease.     

Hypertension from compression and/or enucleation of the adrenal glands in the rat.

Previos studies have shown that compression of the adrenal glands is as effective as adrenal enucleation in causing hypertension in rats. Unilateral adrenal enucleation is ineffective, however, if a normal contralateral adrenal gland is present. The studies reported herein demonstrate that unilateral compression also fails to cause hypertension in the presence of a normal contralateral gland. When present singly, either enucleate or compressed adrenals cause hypertension; when either is present with a normal contralateral gland, the blood pressure is unaffected. When compressed or enucleate glands constitute the pair, in any combination, hypertension ensues. However, whereas an enucleate gland remains extremely atrophic in the presence of a normal gland, compressed glands attain a much larger size under this circumstance. Furthermore, a compressed gland is less inhibitory to the regeneration of a contralateral enucleate gland than is a normal adrenal. Whereas enucleate glands, whether bilateral or unilateral, are always smaller than normal glands, compressed adrenals may be enlarged. The hypertensogenic function of compressed adrenals is, like that of enucleate glands, suppressed by the presence of a normal gland. The growth response of compressed or enucleate glands, whether bilateral or single, appears to depend upon the degree of injury inflicted upon them. There is a considerable discrepancy in the size of individual members of a pair when one or both have been injured, that members of a normal pair do not exhibit.     

Pathological Lesions in Swine at Slaughter

An extended disease recording programme in pigs has been carried out by the meat inspection service at Sentralslakteriet, Forus, Stavanger. A data system including 57 disease codes has been applied. In the period 1975–1977 an average of 85,000 baconers were slaughtered yearly. About 39 % of these were given disease remarks; 42–47 % of the lesions were directly related to the parasites Sarcoptes scabiei (rind lesions) and Ascaris suum (white spots in the livers). The thoracic cavity was the most commonly affected part of the body with 30–35 % of all recorded lesions. Sixteen disease codes occurred at frequencies above 0.3 %, and they encompassed approx. 97 % of all recorded lesions. Scabies occurred at an average of 12 % of the fatteners. Parasitic hepatitis of severe and moderate degrees were seen in about 11 %, pleurisy in 7 %, pneumonia — severe and moderate — in 5.4 %, pericarditis in 4.3 %, pyaemia and abscess/-es in 2.5 %, tail lesions in 2.3 %, perihepatitis and other non-parasitic liver lesions in 2.2 %, polyarthritis and arthritis in 1.7 %, tuberculous lesions in the cervical lymph nodes in 0.9 %, peritonitis in 0.9 % and atrophic rhinitis — external lesions — in 0.8 % of the carcasses. The majority of the other 41 disease codes occurred at frequencies below 0.1 %. A seasonal variation was pronounced in scabies, numerous white spots in the liver, and tuberculous lesions in the cervical lymph nodes. It could be noted in pleurisy, pericarditis, perihepatitis and other non-parasitic liver lesions, arthritis and atrophic rhinitis, but not in pneumonias, moderate number of white spots in the liver, tail lesions, pyaemia, abscess/-es, peritonitis and polyarthritis.     

树突状细胞对胃癌前病变的免疫保护分析

摘要 目的：探究树突状细胞(Dendritic cells,DC)对胃癌的免疫保护作用。方法：选择2016年1月至2018年1月于我院接受治疗的145例胃癌、39例慢性萎缩性胃炎、21例不典型增生、27例肠上皮化生以及20例正常对照组患者为研究对象,分别采集其胃粘膜标本进行染色,记录和比较其胃粘膜中S100⁺、CD4⁺和CD8⁺细胞的数量、平均面积以及平均吸光度,并将胃癌患者分为中分化腺癌(49例)、低分化腺癌(53例)和未分化癌(43例)进行对比。结果：(1)胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组的胃粘膜S100⁺阳性细胞计数明显高于正常对照组（P<0.05）,胃癌组平均吸光度低于对照组,其他3组平均吸光度显著高于对照组,(P<0.05);胃癌组平均面积与正常对照组相比无差异(P>0.05),其他三组平均面积显著高于对照组（P<0.05）;(2)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD4⁺细胞数均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、肠上皮化生组患者平均面积均低于对照组(P<0.05);胃癌组、慢性萎缩性胃炎组、不典型增生、肠上皮化生组平均吸光度均低于对照组(P<0.05);(3)慢性萎缩性胃炎组、肠上皮化生组、不典型增生组患者CD8⁺细胞数明显高于对照组(P<0.05),胃癌组稍低于对照组(P>0.05);胃癌组患者平均面积低于对照组(P<0.05);胃癌组患者平均吸光值低于对照组,慢性萎缩性胃炎组、肠上皮化生组患者高于对照组(P均<0.05);(4)随着胃癌分化程度的降低,胃癌患者DC细胞数有降低趋势。结论：胃癌前病变患者胃粘膜中DC数量会显著增多,免疫功能加强,DC细胞数量会随胃癌分化程度的降低而减少,分析其原因与DC细胞能够抑制癌前病变有关。     

The detection, surveillance and treatment of premalignant gastric lesions related to Helicobacter pylori infection

Gastric cancer is an important worldwide health problem and causes considerable morbidity and mortality. It represents the second leading cause of cancer-related death worldwide. A cascade of recognizable precursor lesions precedes most distal gastric carcinomas. In this multistep model of gastric carcinogenesis, Helicobacter pylori causes chronic active inflammation of the gastric mucosa, which slowly progresses through the premalignant stages of atrophic gastritis, intestinal metaplasia and dysplasia to gastric carcinoma. Detection and treatment of premalignant lesions may thus provide a basis for gastric cancer prevention. However, at present, premalignant changes of the gastric mucosa are frequently disregarded in clinical practice or result in widely varying follow-up frequency or treatment. This review provides an overview of current knowledge on detection, surveillance and treatment of patients with premalignant gastric lesions, and identifies the uncertainties that require further research.     

Description of a new computer wire coding method and its application to evaluate potential control selection bias in the Savitz et al. childhood cancer study

We developed a new computer wire coding method and then applied it to investigate the suggestion that control selection bias might explain the observed association between wire codes and childhood cancer made in the study conducted by Savitz et al. in the Denver area. The computer wire coding method used a geographic information system approach with data on the local distribution electric system and from tax assessor records. Individual residences were represented as a circle scaled to the ground floor area of the residence and centered on the lot centroid. The wire code of the residence was determined from the distance between the circle and the relevant power line, and from the current carrying capacity of that line. Using this method, wire codes were generated for 238 290 residences built before 1986, the time of the Savitz et al. study, in the Denver metropolitan area. We then attempted to reconstruct the 1985 population of hypothetically eligible control children in the Denver metropolitan area by using 1980 census data. Since data were not available to locate the children in each residence within a census block, uniform, Poisson, and negative binomial distributions were used to randomly assign children to residences. To evaluate the likelihood of the wire code distribution of the controls selected by Savitz et al., 100 random trials were conducted for each distribution, matching two controls to each case. The odds ratios between childhood cancer and very high current configuration (VHCC) wire codes were reduced when the assigned controls were used, suggesting control selection bias may have been present. However, control selection bias is unlikely to account for all the reported association between childhood cancer and wire codes in the Savitz et al. study.     

Cell membrane permeability in hypertension

A great deal of evidence has been presented which suggests that a generalized increase in cell membrane permeability to various ions is a fundamental defect associated with hypertension. In addition, some of the evidence is supportive of a central role of this defect in the pathogenesis of hypertension. The source of this defect may lie in the reduced calcium binding capacity of the cell membrane. Because of this reduced capacity the membrane is less stable and is more permeable to various ions.